PAC-14028|cas 1005168-10-4
DC Chemicals, Website: www.dcchemicals.com
Product Name: PAC-14028|Cas Number: 1005168-10-4| Catalog Number: DC10399|Other Nmaes: PAC14028; PAC 14028
PAC-14028 is a potent and selective transient receptor potential vanilloid type I (TRPV1) antagonist.
PAC-14028 could prevent barrier damages, accelerate skin barrier recovery and suppress pruritus, showing a potential for the treatment of atopic dermatitis. It could suppress serum IgE increase, epidermal infiltration of inflammatory cells and mast cell degranulation associated with atopic dermatitis[1]. PAC-14028 shows efficacies against diverse disease models including visceral pain, inflammatory bowel disease, and inflammatory pain[2].PAC-14028 shows a plasma half-life of 2.1 h in rats while it is extended slightly to 3.8 h in minipigs. Oral bioavailability at 10 mg/kg dose is determined to be 52.7% and 64.2% in rats and minipigs, respectively suggesting that PAC-14028 is relatively well-absorbed through oral route[1]. PAC-14028 could inhibit capsaicin-evoked calcium influx in keratinocytes at sub-micromolar concentrations. This potent TRPV1 antagonistic activity in keratinocytes is manifested in vivo as the blockade of capsaicin-induced blood perfusion increase, and the accelerated barrier recovery from tape-stripping-induced barrier damages in hairless mice[3].
2017年11月30日星期四
MELK-8a hydrochloride
MELK-8a hydrochloride
DC Chemicals, Website: www.dcchemicals.com
Product Name: MELK-8a hydrochloride| Catalog Number: DC10398
MELK-8a hydrochloride is a novel maternal embryonic leucine zipper kinase (MELK) inhibitor with an IC50 of 2 nM.
MELK-8a remains very potent (IC50=140 nM) when the ATP concentration in the biochemical assay is shifted from 20 μM to 2 mM. Its potency is well tracked between full-length MELK versus catalytic domain construct (5 nM versus 2 nM). It only inhibits seven off-target kinases in addition to MELK with >85% inhibition of binding at 1 μM demonstrating great selectivity. The compound is at least 90-fold more selective in targeting MELK in all cases. MELK-8a is fairly soluble (0.22 g/L at pH 6.8) and shows a good permeability in the Caco-2 assay. MELK-8a inhibits the growth of MDA-MB-468 cells and MCF-7 cells with an IC50 of approximately 0.06 and 1.2 μM, respectively[1].Subcutaneous administration of MELK-8a at 30 mg/kg in C57BL/6 mice results in good plasma exposure. The compound adsorption into the systemic circulation is rapid (Tmax=0.4 h) and peak plasma concentration reaches 6.6 μM. An ascending dose PK study in female athymic nude mice shows that the rate of compound release is maximal at 120 mg/kg and all clearance mechanisms can be saturated at 240 mg/kg. However, when administered orally at 10 mg/kg in C57BL/6 male mice, it shows very poor PK (3.6% oral bioavailability) consistent with very high in vivo clearance[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: MELK-8a hydrochloride| Catalog Number: DC10398
MELK-8a hydrochloride is a novel maternal embryonic leucine zipper kinase (MELK) inhibitor with an IC50 of 2 nM.
MELK-8a remains very potent (IC50=140 nM) when the ATP concentration in the biochemical assay is shifted from 20 μM to 2 mM. Its potency is well tracked between full-length MELK versus catalytic domain construct (5 nM versus 2 nM). It only inhibits seven off-target kinases in addition to MELK with >85% inhibition of binding at 1 μM demonstrating great selectivity. The compound is at least 90-fold more selective in targeting MELK in all cases. MELK-8a is fairly soluble (0.22 g/L at pH 6.8) and shows a good permeability in the Caco-2 assay. MELK-8a inhibits the growth of MDA-MB-468 cells and MCF-7 cells with an IC50 of approximately 0.06 and 1.2 μM, respectively[1].Subcutaneous administration of MELK-8a at 30 mg/kg in C57BL/6 mice results in good plasma exposure. The compound adsorption into the systemic circulation is rapid (Tmax=0.4 h) and peak plasma concentration reaches 6.6 μM. An ascending dose PK study in female athymic nude mice shows that the rate of compound release is maximal at 120 mg/kg and all clearance mechanisms can be saturated at 240 mg/kg. However, when administered orally at 10 mg/kg in C57BL/6 male mice, it shows very poor PK (3.6% oral bioavailability) consistent with very high in vivo clearance[1].
Proguanil |cas 500-92-5
Proguanil |cas 500-92-5
DC Chemicals, Website: www.dcchemicals.com
Product Name: Proguanil|Cas Number: 500-92-5| Catalog Number: DC10397
Proguanil is an antimalarial prodrug that is metabolized to the active metabolite cycloguanil, a dihydrofolate reductase (DHFR) inhibitor.
Proguanil per se has only weak antimalarial activity in vitro (IC50=2.4-19 μM), and its effectiveness depends on the active metabolite cycloguanil (IC50=0.5-2.5 nM). The cycloguanil is a dihydrofolate reductase (DHFR) inhibitor. The combination of atovaquone and proguanil is synergistic in vitro. Both drugs also have activity against gametocytes and pre-erythrocytic (hepatic) stages of malaria parasites[1]. Proguanil acts as a biguanide rather than as its metabolite cycloguanil (a parasite dihydrofolate reductase [DHFR] inhibitor) to enhance the atovaquone effect; proguanil-mediated enhancement is specific for atovaquone, since the effects of other mitochondrial electron transport inhibitors, such as myxothiazole and antimycin, are not altered by inclusion of proguanil[2]. 5-HT3 receptor responses are reversibly inhibited by proguanil, the metabolite 4-chlorophenyl-1-biguanide (CPB) and the active metabolite cycloguanil (CG), with an IC50 of 1.81, 1.48 and 4.36 μM, respectively[3].Proguanil could induce infertility in rats which may act by distorting the blood-testis barrier formed by the Sertoli cells. Duration dependent significant decrease in body and organ weights and also in sperm parameters is observed. Serum testosterone level is significantly decreased for proguanil treatment rats[4]. Administration of Malarone (atovaquone and proguanil) to experimentally B. gibsoni infected two dogs in chronic stage and three dogs in acute stage results in decrease in parasitemia, and clinical improvements are observed[5].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Proguanil|Cas Number: 500-92-5| Catalog Number: DC10397
Proguanil is an antimalarial prodrug that is metabolized to the active metabolite cycloguanil, a dihydrofolate reductase (DHFR) inhibitor.
Proguanil per se has only weak antimalarial activity in vitro (IC50=2.4-19 μM), and its effectiveness depends on the active metabolite cycloguanil (IC50=0.5-2.5 nM). The cycloguanil is a dihydrofolate reductase (DHFR) inhibitor. The combination of atovaquone and proguanil is synergistic in vitro. Both drugs also have activity against gametocytes and pre-erythrocytic (hepatic) stages of malaria parasites[1]. Proguanil acts as a biguanide rather than as its metabolite cycloguanil (a parasite dihydrofolate reductase [DHFR] inhibitor) to enhance the atovaquone effect; proguanil-mediated enhancement is specific for atovaquone, since the effects of other mitochondrial electron transport inhibitors, such as myxothiazole and antimycin, are not altered by inclusion of proguanil[2]. 5-HT3 receptor responses are reversibly inhibited by proguanil, the metabolite 4-chlorophenyl-1-biguanide (CPB) and the active metabolite cycloguanil (CG), with an IC50 of 1.81, 1.48 and 4.36 μM, respectively[3].Proguanil could induce infertility in rats which may act by distorting the blood-testis barrier formed by the Sertoli cells. Duration dependent significant decrease in body and organ weights and also in sperm parameters is observed. Serum testosterone level is significantly decreased for proguanil treatment rats[4]. Administration of Malarone (atovaquone and proguanil) to experimentally B. gibsoni infected two dogs in chronic stage and three dogs in acute stage results in decrease in parasitemia, and clinical improvements are observed[5].
S107 |cas 927871-76-9
S107 |cas 927871-76-9
DC Chemicals, Website: www.dcchemicals.com
Product Name: S107|Cas Number: 927871-76-9| Catalog Number: DC10395|Other Nmaes: S-107; S 10
S107 is a RyR-selective 1,4-benzothiazepine derivative that stabilizes RyR2 channels by enhancing the binding affinity of calstabin2 to mutant and/or PKA-phosphorylated channels.
S107 is a small compound that enhances calstabin2 binding to RyR2 at low nanomolar concentrations and failed to interact with over 400 receptors, enzymes, and ion channels in screens using up to 10 μM of the compound. S107 has no effect on cardiac ion channels including the voltage-gated Na+, K+, and Ca2+ channels at concentrations up to 10 μM, and S107 had no effect on normal Ca2+ signaling in cells[1]. S107 is a promising candidate drug for treating catecholaminergic polymorphic ventricular tachycardia (CPVT). S107 exerts an antiarrhythmic effect on CPVT-hiPSC-CMs. Pre-incubation with 10 μM S107, which stabilizes the closed state of the ryanodine receptor 2, significantly decreases the percentage of CPVT-hiPSC-CMs presenting DADs to 25%[2]. S107 is thought to improve skeletal muscle function by stabilizing the RyR1-FKBP12 complex. S107 increases FKBP12 binding to RyR1 in SR vesicles in the presence of reduced glutathione and the NO-donor NOC12, with no effect in the presence of oxidized glutathione. S107 can reverse the harmful effects of redox active species on SR Ca2+ release in skeletal muscle by binding to RyR1 low affinity sites[3].S107, which prevents a leak in the channel but does not block the channel or alter normal Ca2+ signaling, is able to inhibit both seizures and arrhythymias in the mutant mice[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: S107|Cas Number: 927871-76-9| Catalog Number: DC10395|Other Nmaes: S-107; S 10
S107 is a RyR-selective 1,4-benzothiazepine derivative that stabilizes RyR2 channels by enhancing the binding affinity of calstabin2 to mutant and/or PKA-phosphorylated channels.
S107 is a small compound that enhances calstabin2 binding to RyR2 at low nanomolar concentrations and failed to interact with over 400 receptors, enzymes, and ion channels in screens using up to 10 μM of the compound. S107 has no effect on cardiac ion channels including the voltage-gated Na+, K+, and Ca2+ channels at concentrations up to 10 μM, and S107 had no effect on normal Ca2+ signaling in cells[1]. S107 is a promising candidate drug for treating catecholaminergic polymorphic ventricular tachycardia (CPVT). S107 exerts an antiarrhythmic effect on CPVT-hiPSC-CMs. Pre-incubation with 10 μM S107, which stabilizes the closed state of the ryanodine receptor 2, significantly decreases the percentage of CPVT-hiPSC-CMs presenting DADs to 25%[2]. S107 is thought to improve skeletal muscle function by stabilizing the RyR1-FKBP12 complex. S107 increases FKBP12 binding to RyR1 in SR vesicles in the presence of reduced glutathione and the NO-donor NOC12, with no effect in the presence of oxidized glutathione. S107 can reverse the harmful effects of redox active species on SR Ca2+ release in skeletal muscle by binding to RyR1 low affinity sites[3].S107, which prevents a leak in the channel but does not block the channel or alter normal Ca2+ signaling, is able to inhibit both seizures and arrhythymias in the mutant mice[1].
Org-26576|cas 1026791-61-6
Org-26576|cas 1026791-61-6
DC Chemicals, Website: www.dcchemicals.com
Product Name: Org-26576|Cas Number: 1026791-61-6| Catalog Number: DC10394|Other Nmaes: Org26576; Org 26576
Org 26576 is a AMPA receptor positive allosteric modulator.
Org 26576 represents structurally a distinct chemical series derived from the first generation ampakine CX516 and displays 10-30 fold greater potency when compared to CX516 in potentiating AMPA-mediated electrophysiological responses with an EC50 of 8-16 μM in rat hippocampal primary cultured neurons. Org 26576 demonstrates selectivity for AMPA receptors when tested at 10 μM against >60 molecular targets including G-Protein Coupled Receptors, ion channels and kinases[1].Org 26576 (1 mg/kg) produces significant increases in the anteroventral and laterodorsal thalamus, cingulate cortex, dentate gyrus and CA3 subfield of the hippocampus in mice[1]. Chronic administration of Org 26576 increases progenitor cell proliferation in dentate gyrus (approximately 40%) and in prelimbic cortex (approximately 35%) at the 10-mg/kg dosage. Cells born in response to chronic Org 26576 in dentate gyrus exhibits increased rates of survival (approximately 30%) with the majority of surviving cells expressing a neuronal phenotype[2]. AMPA receptor potentiation by Org 26576 exerts a positive modulatory influence on brain derived neurotrophic factor (BDNF) expression during ongoing neuronal activity. Total BDNF mRNA levels are significantly increased in the hippocampus of animals exposed to the combination of Org 26576 and stress[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Org-26576|Cas Number: 1026791-61-6| Catalog Number: DC10394|Other Nmaes: Org26576; Org 26576
Org 26576 is a AMPA receptor positive allosteric modulator.
Org 26576 represents structurally a distinct chemical series derived from the first generation ampakine CX516 and displays 10-30 fold greater potency when compared to CX516 in potentiating AMPA-mediated electrophysiological responses with an EC50 of 8-16 μM in rat hippocampal primary cultured neurons. Org 26576 demonstrates selectivity for AMPA receptors when tested at 10 μM against >60 molecular targets including G-Protein Coupled Receptors, ion channels and kinases[1].Org 26576 (1 mg/kg) produces significant increases in the anteroventral and laterodorsal thalamus, cingulate cortex, dentate gyrus and CA3 subfield of the hippocampus in mice[1]. Chronic administration of Org 26576 increases progenitor cell proliferation in dentate gyrus (approximately 40%) and in prelimbic cortex (approximately 35%) at the 10-mg/kg dosage. Cells born in response to chronic Org 26576 in dentate gyrus exhibits increased rates of survival (approximately 30%) with the majority of surviving cells expressing a neuronal phenotype[2]. AMPA receptor potentiation by Org 26576 exerts a positive modulatory influence on brain derived neurotrophic factor (BDNF) expression during ongoing neuronal activity. Total BDNF mRNA levels are significantly increased in the hippocampus of animals exposed to the combination of Org 26576 and stress[3].
Bicyclomycin benzoate|cas 37134-40-0
Bicyclomycin benzoate|cas 37134-40-0
DC Chemicals, Website: www.dcchemicals.com
Product Name: Bicyclomycin benzoate|Cas Number: 37134-40-0| Catalog Number: DC10393|Other Nmaes: FR2054
Bicyclomycin benzoate is an antibiotic exhibiting activity against a broad spectrum of Gram-negative bacteria and against the Gram-positive bacterium.
The primary action of bicyclomycin is due to interference with the biosynthesis of lipoprotein and its assembly to peptidoglycan in the cell envelope of E. coli. At the lethal level, bicyclomycin is shown to inhibit the synthesis of RNA and protein in the growing cells of E. coli 15 THU[1]. Bicyclomycin targets the rho transcription termination factor in Escherichia coli. Bicyclomycin is a modest rho inhibitor, can disrupt the rho molecular machinery thereby leading to a catastrophic effect caused by the untimely overproduction of proteins not normally expressed constitutively, thus leading to a toxic effect on the cells[2]. The inhibition of rho poly(C)-stimulated hydrolysis of ATP by bicyclomycin has been found to proceed by a non-competitive, reversible pathway with respect to ATP (Ki=20 μM)[3].Bicyclomycin has low excretion rate after a single intramuscular dose of 50 mg/kg in rats. Bicyclomycin is well distributed in various tissues, and the highest concentration is observed in the kidney at 100 mg/kg[4].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Bicyclomycin benzoate|Cas Number: 37134-40-0| Catalog Number: DC10393|Other Nmaes: FR2054
Bicyclomycin benzoate is an antibiotic exhibiting activity against a broad spectrum of Gram-negative bacteria and against the Gram-positive bacterium.
The primary action of bicyclomycin is due to interference with the biosynthesis of lipoprotein and its assembly to peptidoglycan in the cell envelope of E. coli. At the lethal level, bicyclomycin is shown to inhibit the synthesis of RNA and protein in the growing cells of E. coli 15 THU[1]. Bicyclomycin targets the rho transcription termination factor in Escherichia coli. Bicyclomycin is a modest rho inhibitor, can disrupt the rho molecular machinery thereby leading to a catastrophic effect caused by the untimely overproduction of proteins not normally expressed constitutively, thus leading to a toxic effect on the cells[2]. The inhibition of rho poly(C)-stimulated hydrolysis of ATP by bicyclomycin has been found to proceed by a non-competitive, reversible pathway with respect to ATP (Ki=20 μM)[3].Bicyclomycin has low excretion rate after a single intramuscular dose of 50 mg/kg in rats. Bicyclomycin is well distributed in various tissues, and the highest concentration is observed in the kidney at 100 mg/kg[4].
S1p receptor agonist 1 |cas 1514888-56-2
S1p receptor agonist 1 |cas 1514888-56-2
DC Chemicals, Website: www.dcchemicals.com
Product Name: S1p receptor agonist 1|Cas Number: 1514888-56-2| Catalog Number: DC10392
S1p receptor agonist 1 is an S1P receptor agonist extracted from patent WO 2015039587 A1, compound example 2.
DC Chemicals, Website: www.dcchemicals.com
Product Name: S1p receptor agonist 1|Cas Number: 1514888-56-2| Catalog Number: DC10392
S1p receptor agonist 1 is an S1P receptor agonist extracted from patent WO 2015039587 A1, compound example 2.
GSK682753A |cas 1334294-76-6
GSK682753A |cas 1334294-76-6
DC Chemicals, Website: www.dcchemicals.com
Product Name: GSK682753A|Cas Number: 1334294-76-6| Catalog Number: DC10391|Other Nmaes: GSK 682753A; GSK-682753
GSK682753A is a selective and highly potent inverse agonist of the epstein-barr virus-induced receptor 2 (EBI2) with an IC50 of 53.6 nM.
GSK682753 is a selective and highly potent inverse agonist for murine as well as human EBI2 with inhibition of G protein-dependent signals as well as signals that are probably G protein-independent. In cAMP-response element-binding protein-based reporter and guanosine5'-3-O-(thio)-triphosphate (GTPγS) binding assays, the potency of this compound is 2.6-53.6 nM, and its inhibitory efficacy is 75%. GSK682753A dose-dependently inhibits EBI2 with an IC50of 53.6 nM. GSK682753A inhibits ERK phosphorylation, GTPγS binding, and cAMP-response element-binding protein activation with similar potency[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: GSK682753A|Cas Number: 1334294-76-6| Catalog Number: DC10391|Other Nmaes: GSK 682753A; GSK-682753
GSK682753A is a selective and highly potent inverse agonist of the epstein-barr virus-induced receptor 2 (EBI2) with an IC50 of 53.6 nM.
GSK682753 is a selective and highly potent inverse agonist for murine as well as human EBI2 with inhibition of G protein-dependent signals as well as signals that are probably G protein-independent. In cAMP-response element-binding protein-based reporter and guanosine5'-3-O-(thio)-triphosphate (GTPγS) binding assays, the potency of this compound is 2.6-53.6 nM, and its inhibitory efficacy is 75%. GSK682753A dose-dependently inhibits EBI2 with an IC50of 53.6 nM. GSK682753A inhibits ERK phosphorylation, GTPγS binding, and cAMP-response element-binding protein activation with similar potency[1].
TD139 |cas 1450824-22-2
TD139 |cas 1450824-22-2
DC Chemicals, Website: www.dcchemicals.com
Product Name: TD139|Cas Number: 1450824-22-2| Catalog Number: DC10390|Other Nmaes: TD-139; TD 139
TD139 is a novel high-affinity inhibitor of the galectin-3 carbohydrate binding domain with a Kd of 14 nM.
TD139 is a novel synthetic inhibitor of galectin-3. TD139 has high affinity for galectin-3 with a Kd of 14 nM and 10 nM for galectin-1, but low affinity for galectins 2, 4N, 4C, 7, 8N, or 9N[1].In primary lung AECs TD139 reduces TGF-β1–induced β-catenin translocation to the nucleus, with most of the β-catenin remaining at the cell surface. TD139 blocks TGF-β1–induced β-catenin phosphorylation. A marked reduction in fibrosis and β-catenin activation accompanied by decreased galectin-3 expression is observed in the lungs of WT mice treated with TD139[1]. Pretreatment of WT C57BL/6 mice with TD139 leads to the attenuation of liver injury and milder infiltration of IFNγ- and IL-17- and -4-producing CD4(+) T cells, as well as an increase in the total number of IL-10-producing CD4(+) T cells and F4/80(+) CD206(+) alternatively activates macrophages and preventes the apoptosis of liver-infiltrating MNCs[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: TD139|Cas Number: 1450824-22-2| Catalog Number: DC10390|Other Nmaes: TD-139; TD 139
TD139 is a novel high-affinity inhibitor of the galectin-3 carbohydrate binding domain with a Kd of 14 nM.
TD139 is a novel synthetic inhibitor of galectin-3. TD139 has high affinity for galectin-3 with a Kd of 14 nM and 10 nM for galectin-1, but low affinity for galectins 2, 4N, 4C, 7, 8N, or 9N[1].In primary lung AECs TD139 reduces TGF-β1–induced β-catenin translocation to the nucleus, with most of the β-catenin remaining at the cell surface. TD139 blocks TGF-β1–induced β-catenin phosphorylation. A marked reduction in fibrosis and β-catenin activation accompanied by decreased galectin-3 expression is observed in the lungs of WT mice treated with TD139[1]. Pretreatment of WT C57BL/6 mice with TD139 leads to the attenuation of liver injury and milder infiltration of IFNγ- and IL-17- and -4-producing CD4(+) T cells, as well as an increase in the total number of IL-10-producing CD4(+) T cells and F4/80(+) CD206(+) alternatively activates macrophages and preventes the apoptosis of liver-infiltrating MNCs[2].
RIPA-56|cas 1956370-21-0
RIPA-56|cas 1956370-21-0
DC Chemicals, Website: www.dcchemicals.com
Product Name: RIPA-56|Cas Number: 1956370-21-0| Catalog Number: DC10389|Other Nmaes: RIPA56; RIPA 56
RIPA-56 is a highly potent, selective, and metabolically stable inhibitor of receptor-interacting protein 1 (RIP1) with an IC50 of 13 nM.
RIPA-56 has a half-life of 128 min in human liver microsomal stability assays and an EC50 of 28 nM in TSZ-induced HT-29 necrosis assay. RIPA-56 also demonstrates potency in protection of murine L929 cells from TZ-induced necrosis (EC50=27 nM). RIPA-56 shows efficient inhibition of RIP1 kinase activity, with an IC50 of 13 nM and no inhibition of RIP3 kinase activity at a 10 μM concentration. RIPA-56 could form tight hydrophobic interactions with RIP1 through both the phenyl group and the 2,2-dimethylbutyl group, and form two important hydrogen bonds[1].In the SIRS mice disease model, RIPA-56 efficiently reduces tumor necrosis factor alpha (TNFα)-induced mortality and multi-organ damage. Compared to known RIP1 inhibitors, RIPA-56 is potent in both human and murine cells, is much more stable in vivo, and is efficacious in animal model studies. RIPA-56 has an impressive PK profile in mice with a 3.1 h half-life, 22% oral bioavailability (P.O.), and 100% bioavailability from intraperitoneal injection (I.P.)[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: RIPA-56|Cas Number: 1956370-21-0| Catalog Number: DC10389|Other Nmaes: RIPA56; RIPA 56
RIPA-56 is a highly potent, selective, and metabolically stable inhibitor of receptor-interacting protein 1 (RIP1) with an IC50 of 13 nM.
RIPA-56 has a half-life of 128 min in human liver microsomal stability assays and an EC50 of 28 nM in TSZ-induced HT-29 necrosis assay. RIPA-56 also demonstrates potency in protection of murine L929 cells from TZ-induced necrosis (EC50=27 nM). RIPA-56 shows efficient inhibition of RIP1 kinase activity, with an IC50 of 13 nM and no inhibition of RIP3 kinase activity at a 10 μM concentration. RIPA-56 could form tight hydrophobic interactions with RIP1 through both the phenyl group and the 2,2-dimethylbutyl group, and form two important hydrogen bonds[1].In the SIRS mice disease model, RIPA-56 efficiently reduces tumor necrosis factor alpha (TNFα)-induced mortality and multi-organ damage. Compared to known RIP1 inhibitors, RIPA-56 is potent in both human and murine cells, is much more stable in vivo, and is efficacious in animal model studies. RIPA-56 has an impressive PK profile in mice with a 3.1 h half-life, 22% oral bioavailability (P.O.), and 100% bioavailability from intraperitoneal injection (I.P.)[1].
(R)-BPO-27|cas 1415390-47-4
(R)-BPO-27|cas 1415390-47-4
DC Chemicals, Website: www.dcchemicals.com
Product Name: (R)-BPO-27|Cas Number: 1415390-47-4| Catalog Number: DC10388|Other Nmaes: (R)-BPO 27; (R)-BPO27
(R)-BPO-27 is a potent CFTR inhibitor with an IC50 of 4 nM
The benzopyrimido-pyrrolo-oxazinedione BPO-27 is an analogue of PPQ-102, which inhibits CFTR with an IC50 of 8 nM. The R enantiomer of BPO-27 inhibits CFTR chloride conductance with an IC50 of 4 nM, while S enantiomer is inactive. In vitro metabolic stability in hepatic microsomes shows both enantiomers as stable, with less than 5% metabolism in 4 h[1]. (R)-BPO-27 binds near the canonical ATP binding site. Whole-cell patch-clamp studies shows linear CFTR currents with a voltage-independent (R)-BPO-27 block mechanism. At a concentration of (R)-BPO-27 that inhibits CFTR chloride current by 50%, the EC50 for ATP activation of CFTR increases from 0.27 to 1.77 mM[2].Following bolus interperitoneal administration in mice, serum (R)-1 decays with t1/2 ≈ 1.6 h and gives sustained therapeutic concentrations in kidney[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: (R)-BPO-27|Cas Number: 1415390-47-4| Catalog Number: DC10388|Other Nmaes: (R)-BPO 27; (R)-BPO27
(R)-BPO-27 is a potent CFTR inhibitor with an IC50 of 4 nM
The benzopyrimido-pyrrolo-oxazinedione BPO-27 is an analogue of PPQ-102, which inhibits CFTR with an IC50 of 8 nM. The R enantiomer of BPO-27 inhibits CFTR chloride conductance with an IC50 of 4 nM, while S enantiomer is inactive. In vitro metabolic stability in hepatic microsomes shows both enantiomers as stable, with less than 5% metabolism in 4 h[1]. (R)-BPO-27 binds near the canonical ATP binding site. Whole-cell patch-clamp studies shows linear CFTR currents with a voltage-independent (R)-BPO-27 block mechanism. At a concentration of (R)-BPO-27 that inhibits CFTR chloride current by 50%, the EC50 for ATP activation of CFTR increases from 0.27 to 1.77 mM[2].Following bolus interperitoneal administration in mice, serum (R)-1 decays with t1/2 ≈ 1.6 h and gives sustained therapeutic concentrations in kidney[1].
BPO-27 racemat|cas 1314873-02-3
BPO-27 racemat|cas 1314873-02-3
DC Chemicals, Website: www.dcchemicals.com
Product Name: BPO-27 racemat|Cas Number: 1314873-02-3| Catalog Number: DC10387|Other Nmaes: BPO 27 racemate; BPO27 racemate
BPO-27 racemate is a potent CFTR inhibitor with an IC50 of 8 nM.
The benzopyrimido-pyrrolo-oxazinedione BPO-27 is an analogue of PPQ-102, which inhibits CFTR with an IC50 of 8 nM. The R enantiomer of BPO-27 inhibits CFTR chloride conductance with an IC50 of 4 nM, while S enantiomer is inactive. In vitro metabolic stability in hepatic microsomes shows both enantiomers as stable, with less than 5% metabolism in 4 h[1]. (R)-BPO-27 binds near the canonical ATP binding site. Whole-cell patch-clamp studies shows linear CFTR currents with a voltage-independent (R)-BPO-27 block mechanism. At a concentration of (R)-BPO-27 that inhibits CFTR chloride current by 50%, the EC50 for ATP activation of CFTR increases from 0.27 to 1.77 mM[2].Following bolus interperitoneal administration in mice, serum (R)-1 decays with t1/2 ≈ 1.6 h and gives sustained therapeutic concentrations in kidney[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: BPO-27 racemat|Cas Number: 1314873-02-3| Catalog Number: DC10387|Other Nmaes: BPO 27 racemate; BPO27 racemate
BPO-27 racemate is a potent CFTR inhibitor with an IC50 of 8 nM.
The benzopyrimido-pyrrolo-oxazinedione BPO-27 is an analogue of PPQ-102, which inhibits CFTR with an IC50 of 8 nM. The R enantiomer of BPO-27 inhibits CFTR chloride conductance with an IC50 of 4 nM, while S enantiomer is inactive. In vitro metabolic stability in hepatic microsomes shows both enantiomers as stable, with less than 5% metabolism in 4 h[1]. (R)-BPO-27 binds near the canonical ATP binding site. Whole-cell patch-clamp studies shows linear CFTR currents with a voltage-independent (R)-BPO-27 block mechanism. At a concentration of (R)-BPO-27 that inhibits CFTR chloride current by 50%, the EC50 for ATP activation of CFTR increases from 0.27 to 1.77 mM[2].Following bolus interperitoneal administration in mice, serum (R)-1 decays with t1/2 ≈ 1.6 h and gives sustained therapeutic concentrations in kidney[1].
Tenapanor|cas 1234423-95-0
Tenapanor|cas 1234423-95-0
DC Chemicals, Website: www.dcchemicals.com
Product Name: Tenapanor|Cas Number: 1234423-95-0| Catalog Number: DC10386|Other Nmaes: AZD 1722; AZD1722; AZD-1722; RDX5791; RDX 5791; RDX-5791
Tenapanor is an inhibitor of the Na+/H+ exchanger NHE3 with IC50 values of 5 and 10 nM against human and Rat NHE3, respectively.
Tenapanor exhibits human and rat NHE3 with IC50 values of 5 and 10 nM, respectively. Human intestinal transporters NHE1, NHE2, TGR5, ASBT, and Pit-1 and the sodium-dependent phosphate transporter NaPiIIb are not inhibited by tenapanor at concentrations up to 10 to 30 μM[1].Tenapanor plays a prominent role in sodium handling in the gastrointestinal tract and kidney. It acts exclusively in the gastrointestinal tract to inhibit sodium uptake when administered orally to rats. Average plasma Cmax values of tenapanor in rats and humans are less than 1 ng/mL with negligible area under the curve at doses of up to 30mg/kg in rats, 10mg/kg in dogs, and 900 mg in humans. Dose-dependent reductions in urinary sodium and increases in fecal sodium and luminal fluid mass are observed upon administering single doses of tenapanor to rats. Chronic administration of tenapanor to rats fed with standard chow (0.49% NaCl) causes a sustained reduction of urinary sodium and increase in fecal sodium[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Tenapanor|Cas Number: 1234423-95-0| Catalog Number: DC10386|Other Nmaes: AZD 1722; AZD1722; AZD-1722; RDX5791; RDX 5791; RDX-5791
Tenapanor is an inhibitor of the Na+/H+ exchanger NHE3 with IC50 values of 5 and 10 nM against human and Rat NHE3, respectively.
Tenapanor exhibits human and rat NHE3 with IC50 values of 5 and 10 nM, respectively. Human intestinal transporters NHE1, NHE2, TGR5, ASBT, and Pit-1 and the sodium-dependent phosphate transporter NaPiIIb are not inhibited by tenapanor at concentrations up to 10 to 30 μM[1].Tenapanor plays a prominent role in sodium handling in the gastrointestinal tract and kidney. It acts exclusively in the gastrointestinal tract to inhibit sodium uptake when administered orally to rats. Average plasma Cmax values of tenapanor in rats and humans are less than 1 ng/mL with negligible area under the curve at doses of up to 30mg/kg in rats, 10mg/kg in dogs, and 900 mg in humans. Dose-dependent reductions in urinary sodium and increases in fecal sodium and luminal fluid mass are observed upon administering single doses of tenapanor to rats. Chronic administration of tenapanor to rats fed with standard chow (0.49% NaCl) causes a sustained reduction of urinary sodium and increase in fecal sodium[1].
BAR501 |cas 1632118-69-4
BAR501 |cas 1632118-69-4
DC Chemicals, Website: www.dcchemicals.com
Product Name: BAR501|Cas Number: 1632118-69-4| Catalog Number: DC10385|Other Nmaes: BAR 501; BAR-501
BAR501 is a potent and selective agonist of GPBAR1 with an EC50 of 1 μM.
BAR501 is a selective GPBAR1 agonist devoid of FXR agonistic activity. It effectively transactivates GPBAR1 in HEK293 cells overexpressing a CRE along with GPBAR1, with an EC50 of 1 μM. Exposure of GLUTAg cells to BAR501 (10 μM) increases the expression of GLP-1 mRNA by 2.5 folds[1].Pretreating rats for 6 days with BAR501, 15 mg/kg, reduces basal portal pressure and blunts the vasoconstriction activity of norepinephrine. Pretreatment with BAR501 attenuates the hepatic vasomotor activity induced by shear stress and methoxamine. Administration of BAR501 exerts a direct vasodilatory activity in the CCl4 model. Treating mice with BAR501 at the dose of 15 mg/Kg reduces portal pressure and AST plasma levels. BAR501 attenuates endothelial dysfunction by regulating CSE expression/activity[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: BAR501|Cas Number: 1632118-69-4| Catalog Number: DC10385|Other Nmaes: BAR 501; BAR-501
BAR501 is a potent and selective agonist of GPBAR1 with an EC50 of 1 μM.
BAR501 is a selective GPBAR1 agonist devoid of FXR agonistic activity. It effectively transactivates GPBAR1 in HEK293 cells overexpressing a CRE along with GPBAR1, with an EC50 of 1 μM. Exposure of GLUTAg cells to BAR501 (10 μM) increases the expression of GLP-1 mRNA by 2.5 folds[1].Pretreating rats for 6 days with BAR501, 15 mg/kg, reduces basal portal pressure and blunts the vasoconstriction activity of norepinephrine. Pretreatment with BAR501 attenuates the hepatic vasomotor activity induced by shear stress and methoxamine. Administration of BAR501 exerts a direct vasodilatory activity in the CCl4 model. Treating mice with BAR501 at the dose of 15 mg/Kg reduces portal pressure and AST plasma levels. BAR501 attenuates endothelial dysfunction by regulating CSE expression/activity[1].
Olodaterol |cas 868049-49-4
Olodaterol |cas 868049-49-4
DC Chemicals, Website: www.dcchemicals.com
Product Name: Olodaterol|Cas Number: 868049-49-4| Catalog Number: DC10384|Other Nmaes: BI1744
Olodaterol (BI1744) is a long acting β2-adrenoceptor agonist with an EC50 of 1.4±0.08 nM.
Olodaterol shows a potent, nearly full agonistic response at the hβ2-adrenoceptor (EC50=0.1 nM; intrinsic activity=88% compared with isoprenaline) and a significant selectivity profile (241- and 2299-fold against the hβ1- and hβ3-ARs, respectively). Likewise, olodaterol is able to potently reverse contraction induced by different stimuli in isolated human bronchi[2].Olodaterol is a long acting β2-agonist that induces bronchodilation up to 24 h after dosing in patients with chronic obstructive pulmonary disease (COPD) . Olodaterol dose-dependently attenuates cell influx and pro-inflammatory mediator release in murine and guinea pig models of pulmonary inflammation. Olodaterol attenuates pro-inflammatory mediator release from human parenchymal explants and whole blood and reduced expression of CD11b adhesion molecules on granulocytes, but without direct effects on IL-8-induced neutrophil transwell migration[3]. Once-daily olodaterol 5 μg is an effective therapy in improving lung function and symptomatic outcomes in patients with moderate to very severe (COPD) receiving other maintenance therapy, with a satisfactory safety profile[4].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Olodaterol|Cas Number: 868049-49-4| Catalog Number: DC10384|Other Nmaes: BI1744
Olodaterol (BI1744) is a long acting β2-adrenoceptor agonist with an EC50 of 1.4±0.08 nM.
Olodaterol shows a potent, nearly full agonistic response at the hβ2-adrenoceptor (EC50=0.1 nM; intrinsic activity=88% compared with isoprenaline) and a significant selectivity profile (241- and 2299-fold against the hβ1- and hβ3-ARs, respectively). Likewise, olodaterol is able to potently reverse contraction induced by different stimuli in isolated human bronchi[2].Olodaterol is a long acting β2-agonist that induces bronchodilation up to 24 h after dosing in patients with chronic obstructive pulmonary disease (COPD) . Olodaterol dose-dependently attenuates cell influx and pro-inflammatory mediator release in murine and guinea pig models of pulmonary inflammation. Olodaterol attenuates pro-inflammatory mediator release from human parenchymal explants and whole blood and reduced expression of CD11b adhesion molecules on granulocytes, but without direct effects on IL-8-induced neutrophil transwell migration[3]. Once-daily olodaterol 5 μg is an effective therapy in improving lung function and symptomatic outcomes in patients with moderate to very severe (COPD) receiving other maintenance therapy, with a satisfactory safety profile[4].
Brivudine |cas 69304-47-8
Brivudine |cas 69304-47-8
DC Chemicals, Website: www.dcchemicals.com
Product Name: Brivudine|Cas Number: 69304-47-8| Catalog Number: DC10383|Other Nmaes: Bromovinyldeoxyuridine; BVDU
Brivudine is a thymidine analogue with antiviral activity, indicated for the early treatment of acute herpes zoster.
Brivudine is an analog of thymidine, and is incorporated into the viral DNA. It blocks the action of DNA polymerases, thus inhibiting viral replication. It has a stronger antiviral effect against the varicella-zoster virus compared with reference compounds such as aciclovir or penciclovir[1]. It has high, selective activity against varicella zoster virus (VZV), inhibiting VZV replication, possibly through competitive inhibition of viral DNA polymerase, or by acting as an alternative substrate to deoxythymidine triphosphate, causing viral DNA strand breakage[2].At a dose of 125 mg once daily, brivudine has proved to be superior to aciclovir with respect to reducing the period of new blister production, and has shortened the duration of post-herpetic neuralgia[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Brivudine|Cas Number: 69304-47-8| Catalog Number: DC10383|Other Nmaes: Bromovinyldeoxyuridine; BVDU
Brivudine is a thymidine analogue with antiviral activity, indicated for the early treatment of acute herpes zoster.
Brivudine is an analog of thymidine, and is incorporated into the viral DNA. It blocks the action of DNA polymerases, thus inhibiting viral replication. It has a stronger antiviral effect against the varicella-zoster virus compared with reference compounds such as aciclovir or penciclovir[1]. It has high, selective activity against varicella zoster virus (VZV), inhibiting VZV replication, possibly through competitive inhibition of viral DNA polymerase, or by acting as an alternative substrate to deoxythymidine triphosphate, causing viral DNA strand breakage[2].At a dose of 125 mg once daily, brivudine has proved to be superior to aciclovir with respect to reducing the period of new blister production, and has shortened the duration of post-herpetic neuralgia[1].
Farampator |cas 211735-76-1
Farampator |cas 211735-76-1
DC Chemicals, Website: www.dcchemicals.com
Product Name: Farampator|Cas Number: 211735-76-1| Catalog Number: DC10382|Other Nmaes: CX-691; Org2444
Farampator (CX-691;Org24448) is an AMPA receptor positive modulator.
Farampator has potential in treating disorders characterised by cognitive deficits such as Alzheimer's disease and schizophrenia. CX691 attenuates a scopolamine-induced impairment of cued fear conditioning following acute administration (0.1 mg/kg p.o.) and a temporally induced deficit in novel object recognition following both acute (0.1 and 1.0 mg/kg p.o.) and sub-chronic (bi-daily for 7 days) administration (0.01, 0.03, 0.1 mg/kg p.o.). It also improves attentional set-shifting following sub-chronic administration (0.3 mg/kg p.o.)[1]. Farampator (500 mg) unequivocally improves short-term memory but appeares to impair episodic memory. Furthermore, it tends to decrease the number of switching errors in the CTMT. Drug-induced side effects (SEs) included headache, somnolence and nausea. Subjects with SEs has significantly higher plasma levels of farampator than subjects without SEs[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Farampator|Cas Number: 211735-76-1| Catalog Number: DC10382|Other Nmaes: CX-691; Org2444
Farampator (CX-691;Org24448) is an AMPA receptor positive modulator.
Farampator has potential in treating disorders characterised by cognitive deficits such as Alzheimer's disease and schizophrenia. CX691 attenuates a scopolamine-induced impairment of cued fear conditioning following acute administration (0.1 mg/kg p.o.) and a temporally induced deficit in novel object recognition following both acute (0.1 and 1.0 mg/kg p.o.) and sub-chronic (bi-daily for 7 days) administration (0.01, 0.03, 0.1 mg/kg p.o.). It also improves attentional set-shifting following sub-chronic administration (0.3 mg/kg p.o.)[1]. Farampator (500 mg) unequivocally improves short-term memory but appeares to impair episodic memory. Furthermore, it tends to decrease the number of switching errors in the CTMT. Drug-induced side effects (SEs) included headache, somnolence and nausea. Subjects with SEs has significantly higher plasma levels of farampator than subjects without SEs[2].
TOFA |cas 54857-86-2
TOFA |cas 54857-86-2
DC Chemicals, Website: www.dcchemicals.com
Product Name: TOFA|Cas Number: 54857-86-2| Catalog Number: DC10381|Other Nmaes: RMI14514; MDL14514
TOFA (RMI14514;MDL14514) is an allosteric inhibitor of acetyl-CoA carboxylase-α (ACCA ).
TOFA (5-tetradecyloxy-2-furoic acid) is cytotoxic to lung cancer cells NCI-H460 and colon carcinoma cells HCT-8 and HCT-15, with an IC50 at approximately 5.0, 5.0, and 4.5 μg/mL, respectively. TOFA at 1.0–20.0 μg/mL effectively blocks fatty acid synthesis and induces cell death in a dose-dependent manner[1]. TOFA is found to be cytotoxic to COC1 and COC1/DDP cells with IC50 values of ~26.1 and 11.6 µg/mL, respectively. TOFA inhibits the proliferation of the cancer cells examined in a time and dose dependent manner, arrests the cells in the G0/G1 cell cycle phase and induces apoptosis[2]. Acetyl-CoA-carboxylase-α (ACCA) is a key enzyme in the regulation of fatty acids synthesis. Inhibition of ACCA by TOFA decreases fatty acid synthesis and induces caspase activation and cell death in most PCa cell lines[3].TOFA inhibits COC1/DDP cell growth in ovarian tumor mouse xenografts. The tumor growth rate is signifi¬cantly inhibited by TOFA compared with the DMSO treated control mice (1649±356.3 vs. 5128±390.4 mm3. No toxicity is observed in the heart, liver, spleen, lung, kidney and intestinal tissues. By inhibiting ACC, TOFA may be a promising small molecule agent for ovarian cancer therapy[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: TOFA|Cas Number: 54857-86-2| Catalog Number: DC10381|Other Nmaes: RMI14514; MDL14514
TOFA (RMI14514;MDL14514) is an allosteric inhibitor of acetyl-CoA carboxylase-α (ACCA ).
TOFA (5-tetradecyloxy-2-furoic acid) is cytotoxic to lung cancer cells NCI-H460 and colon carcinoma cells HCT-8 and HCT-15, with an IC50 at approximately 5.0, 5.0, and 4.5 μg/mL, respectively. TOFA at 1.0–20.0 μg/mL effectively blocks fatty acid synthesis and induces cell death in a dose-dependent manner[1]. TOFA is found to be cytotoxic to COC1 and COC1/DDP cells with IC50 values of ~26.1 and 11.6 µg/mL, respectively. TOFA inhibits the proliferation of the cancer cells examined in a time and dose dependent manner, arrests the cells in the G0/G1 cell cycle phase and induces apoptosis[2]. Acetyl-CoA-carboxylase-α (ACCA) is a key enzyme in the regulation of fatty acids synthesis. Inhibition of ACCA by TOFA decreases fatty acid synthesis and induces caspase activation and cell death in most PCa cell lines[3].TOFA inhibits COC1/DDP cell growth in ovarian tumor mouse xenografts. The tumor growth rate is signifi¬cantly inhibited by TOFA compared with the DMSO treated control mice (1649±356.3 vs. 5128±390.4 mm3. No toxicity is observed in the heart, liver, spleen, lung, kidney and intestinal tissues. By inhibiting ACC, TOFA may be a promising small molecule agent for ovarian cancer therapy[2].
Evobrutinib |cas 1415823-73-2
Evobrutinib |cas 1415823-73-2
DC Chemicals, Website: www.dcchemicals.com
Product Name: Evobrutinib|Cas Number: 1415823-73-2| Catalog Number: DC10380|Other Nmaes: M2951; MSC2364447C
Evobrutinib is an inhibitor of Bruton's tyrosin kinase (Btk) inhibitor extracted from patent US20140162983 example 0174.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Evobrutinib|Cas Number: 1415823-73-2| Catalog Number: DC10380|Other Nmaes: M2951; MSC2364447C
Evobrutinib is an inhibitor of Bruton's tyrosin kinase (Btk) inhibitor extracted from patent US20140162983 example 0174.
SDMA |cas 30344-00-4
SDMA |cas 30344-00-4
DC Chemicals, Website: www.dcchemicals.com
Product Name: SDMA|Cas Number: 30344-00-4| Catalog Number: DC10379|Other Nmaes: NG,NG'-Dimethyl-L-arginine
SDMA (Symmetric dimethylarginine) is an endogenous inhibitor of nitric oxide (NO) synthase activity.
SDMA is the structural isomer of the cardiovascular risk marker asymmetric dimethylarginine, as an endogenous marker of renal function. SDMA does not directly inhibit NOS but is a competitor of arginine transport. SDMA is primarily eliminated by renal excretion and is a promising endogenous marker of glomerular filtration rate[1]. SDMA inhibits dose dependently the NO synthesis in intact endothelial cells, whereas it has no effect on protein expression of NOS[1]. SDMA is involved in the inflammatory process of chronic kidney disease, activating NF-κB and resulting in enhanced expression of IL-6 and TNF-α[2].SDMA is highly stable in serum and plasma, and the assay demonstrates excellent analytical performance. In unaffected dogs, SDMA remains unchanged whereas in affected dogs, SDMA increases during disease progression, correlating strongly with an increase in sCr and decrease in GFR[3]. Chronic SDMA infusion leads to a significant increase of SDMA levels in mice, but the GFR did not change at 4 weeks. No histological changes are observed, particularly no effect on fibrosis or endothelias nitric oxide synthase expression. There is neither an effect of SDMA on systolic blood pressure nor on ejection fraction[4].
DC Chemicals, Website: www.dcchemicals.com
Product Name: SDMA|Cas Number: 30344-00-4| Catalog Number: DC10379|Other Nmaes: NG,NG'-Dimethyl-L-arginine
SDMA (Symmetric dimethylarginine) is an endogenous inhibitor of nitric oxide (NO) synthase activity.
SDMA is the structural isomer of the cardiovascular risk marker asymmetric dimethylarginine, as an endogenous marker of renal function. SDMA does not directly inhibit NOS but is a competitor of arginine transport. SDMA is primarily eliminated by renal excretion and is a promising endogenous marker of glomerular filtration rate[1]. SDMA inhibits dose dependently the NO synthesis in intact endothelial cells, whereas it has no effect on protein expression of NOS[1]. SDMA is involved in the inflammatory process of chronic kidney disease, activating NF-κB and resulting in enhanced expression of IL-6 and TNF-α[2].SDMA is highly stable in serum and plasma, and the assay demonstrates excellent analytical performance. In unaffected dogs, SDMA remains unchanged whereas in affected dogs, SDMA increases during disease progression, correlating strongly with an increase in sCr and decrease in GFR[3]. Chronic SDMA infusion leads to a significant increase of SDMA levels in mice, but the GFR did not change at 4 weeks. No histological changes are observed, particularly no effect on fibrosis or endothelias nitric oxide synthase expression. There is neither an effect of SDMA on systolic blood pressure nor on ejection fraction[4].
Urolithin A |cas 1143-70-0
Urolithin A |cas 1143-70-0
DC Chemicals, Website: www.dcchemicals.com
Product Name: Urolithin A|Cas Number: 1143-70-0| Catalog Number: DC10378
Urolithin A is an intestinal metabolite of ellagic acid with antioxidant and antiproliferative effects; inhibits T24 and Caco-2 cell growth with IC50 values of 43.9 and 49 μM, respectively.
Urolithins could mainly inhibit prostate cancer and colon cancer cell growth. Urolithin A increases mRNA and protein expression of Phospho-p38 MAPK, and decreases mRNA and protein expression of MEKK1 and Phospho-c-Jun in T24 cells. Caspase-3 is also activated and PPAR-γ protein expression increased in drug-induced apoptosis[1]. Urolithin A exerts a dose- and time-dependent significant arrest at G2/M and S phases after treatments with 50 and 100 μM at 24 and 48 h compared to control cells. It induces cell apoptosis with 50 and 100 μM [2]. Urolithin A shows potent antiproliferative activity on HepG2 cells. When cell death is induced by Urolithin A, the expression of β-catenin, c-Myc and Cyclin D1 are decreased and TCF/LEF transcriptional activation is notably down-regulated. Urolithin A also increases protein expression of p53, p38-MAPK and caspase-3, but suppresses expression of NF-κB p65 and other inflammatory mediators[3].The volume of paw edema is reduced at 1 h after oral administration of urolithin A. In addition, plasma in treated mice exhibited significant oxygen radical antioxidant capacity (ORAC) scores with high plasma levels of the unconjugated form at 1 h after oral administration of urolithin A[4].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Urolithin A|Cas Number: 1143-70-0| Catalog Number: DC10378
Urolithin A is an intestinal metabolite of ellagic acid with antioxidant and antiproliferative effects; inhibits T24 and Caco-2 cell growth with IC50 values of 43.9 and 49 μM, respectively.
Urolithins could mainly inhibit prostate cancer and colon cancer cell growth. Urolithin A increases mRNA and protein expression of Phospho-p38 MAPK, and decreases mRNA and protein expression of MEKK1 and Phospho-c-Jun in T24 cells. Caspase-3 is also activated and PPAR-γ protein expression increased in drug-induced apoptosis[1]. Urolithin A exerts a dose- and time-dependent significant arrest at G2/M and S phases after treatments with 50 and 100 μM at 24 and 48 h compared to control cells. It induces cell apoptosis with 50 and 100 μM [2]. Urolithin A shows potent antiproliferative activity on HepG2 cells. When cell death is induced by Urolithin A, the expression of β-catenin, c-Myc and Cyclin D1 are decreased and TCF/LEF transcriptional activation is notably down-regulated. Urolithin A also increases protein expression of p53, p38-MAPK and caspase-3, but suppresses expression of NF-κB p65 and other inflammatory mediators[3].The volume of paw edema is reduced at 1 h after oral administration of urolithin A. In addition, plasma in treated mice exhibited significant oxygen radical antioxidant capacity (ORAC) scores with high plasma levels of the unconjugated form at 1 h after oral administration of urolithin A[4].
Campesterol |cas 474-62-4
Campesterol |cas 474-62-4
DC Chemicals, Website: www.dcchemicals.com
Product Name: Campesterol|Cas Number: 474-62-4| Catalog Number: DC10377|Other Nmaes: (24R)-5-Ergosten-3β-ol
Campesterol is a plant sterol with cholesterol lowering and anticarcinogenic effects.
Campesterol shows a weak cytotoxicity in non-proliferating human umbilical vein endothelial cells (HUVECs). Within the non-cytotoxic concentration range, campesterol significantly inhibits the bFGF-induced proliferation and tube formation of HUVECs in a concentration-dependent manner, while it does not affect the motility of HUVECs. 50 μg/mL of campesterol decreases the cell viability up to about 56% of control(IC50 of over 50 μg/mL)[1].Campesterol effectively disrupts the bFGF-induced neovascularization in chick chorioallantoic membrane (CAM) in vivo[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Campesterol|Cas Number: 474-62-4| Catalog Number: DC10377|Other Nmaes: (24R)-5-Ergosten-3β-ol
Campesterol is a plant sterol with cholesterol lowering and anticarcinogenic effects.
Campesterol shows a weak cytotoxicity in non-proliferating human umbilical vein endothelial cells (HUVECs). Within the non-cytotoxic concentration range, campesterol significantly inhibits the bFGF-induced proliferation and tube formation of HUVECs in a concentration-dependent manner, while it does not affect the motility of HUVECs. 50 μg/mL of campesterol decreases the cell viability up to about 56% of control(IC50 of over 50 μg/mL)[1].Campesterol effectively disrupts the bFGF-induced neovascularization in chick chorioallantoic membrane (CAM) in vivo[1].
BAY-1143572|cas 1414943-88-6
BAY-1143572|cas 1414943-88-6
DC Chemicals, Website: www.dcchemicals.com
Product Name: BAY-1143572|Cas Number: 1414943-88-6| Catalog Number: DC10376|Other Nmaes: BAY1143572; BAY 114357
BAY 1143572 is a highly selective, potent and orally available inhibitor of PTEFb/CDK9; inhibits the proliferation of AML cell lines with a median IC50 of 385 nM.
BAY 1143572 inhibits the proliferation of 7 MLL-rearrangements positive and negative AML cell lines with a median IC50 of 385 nM (range 230-1100 nM) and induces apoptosis[1]. BAY 1143572 has potent and highly selective PTEFb-kinase inhibitory activity in the low nanomolar range against PTEFb/CDK9 and an at least 50-fold selectivity against other CDKs. BAY 1143572 shows a favorable selectivity against a panel of non-CDK kinases. It shows broad antiproliferative activity against a panel of tumor cell lines with sub-micromolar IC50 values. The concentration-dependent inhibition of the phosphorylation of the RNA polymerase II and downstream reduction of MYC mRNA and protein levels is observed[2].BAY 1143572 exhibits single agent efficacy at tolerated doses in 4 out of 5 AML xenograft tumor models in mice and in 2 out of 2 AML xenograft tumor models in rats upon once daily oral administration. Partial or even complete remissions could be achieved in several models[1].The inhibition of MYC mRNA is also observed in blood cells of BAY 1143572-treated rats indicating the potential clinical utility of MYC in blood cells as a pharmacodynamic marker in clinical development. The in vivo efficacy of BAY 1143572 is significantly enhanced in combination with several chemotherapeutics in different solid tumor models[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: BAY-1143572|Cas Number: 1414943-88-6| Catalog Number: DC10376|Other Nmaes: BAY1143572; BAY 114357
BAY 1143572 is a highly selective, potent and orally available inhibitor of PTEFb/CDK9; inhibits the proliferation of AML cell lines with a median IC50 of 385 nM.
BAY 1143572 inhibits the proliferation of 7 MLL-rearrangements positive and negative AML cell lines with a median IC50 of 385 nM (range 230-1100 nM) and induces apoptosis[1]. BAY 1143572 has potent and highly selective PTEFb-kinase inhibitory activity in the low nanomolar range against PTEFb/CDK9 and an at least 50-fold selectivity against other CDKs. BAY 1143572 shows a favorable selectivity against a panel of non-CDK kinases. It shows broad antiproliferative activity against a panel of tumor cell lines with sub-micromolar IC50 values. The concentration-dependent inhibition of the phosphorylation of the RNA polymerase II and downstream reduction of MYC mRNA and protein levels is observed[2].BAY 1143572 exhibits single agent efficacy at tolerated doses in 4 out of 5 AML xenograft tumor models in mice and in 2 out of 2 AML xenograft tumor models in rats upon once daily oral administration. Partial or even complete remissions could be achieved in several models[1].The inhibition of MYC mRNA is also observed in blood cells of BAY 1143572-treated rats indicating the potential clinical utility of MYC in blood cells as a pharmacodynamic marker in clinical development. The in vivo efficacy of BAY 1143572 is significantly enhanced in combination with several chemotherapeutics in different solid tumor models[2].
YU238259|homology-dependent DNA repair(HDR) inhibitor
YU238259|homology-dependent DNA repair(HDR) inhibitor
DC Chemicals, Website: www.dcchemicals.com
Product Name: YU238259|Cas Number: 1943733-16-1| Catalog Number: DC10375|Other Nmaes: YU-238259，YU 238259
YU238259 is a novel inhibitor of homology-dependent DNA repair(HDR), but does not inhibit non-homologous end-joining (NHEJ), in cell-based GFP reporter assays.
YU238259 exhibits potent synthetic lethality in the setting of DNA damage response and DNA repair defects. Treatment with YU238259 is not only synergistic with ionizing radiation (IR), etoposide, and PARP inhibition, but this synergism is heightened by BRCA2-deficiency. Synthetic lethality of YU238259 in HDR-deficient cells results from accumulation of unresolved DSBs following additional inhibition of residual HDR pathway activity. Inhibition of HDR activity by YU238259 has little to no effect on the NHEJ pathway. YU238259 sensitizes tumor cells to radiation therapy and DSB-inducing chemotherapy.Growth of BRCA2-deficient human tumor xenografts in nude mice is significantly delayed by YU238259 treatment even in the absence of concomitant DNA-damaging therapy.
DC Chemicals, Website: www.dcchemicals.com
Product Name: YU238259|Cas Number: 1943733-16-1| Catalog Number: DC10375|Other Nmaes: YU-238259，YU 238259
YU238259 is a novel inhibitor of homology-dependent DNA repair(HDR), but does not inhibit non-homologous end-joining (NHEJ), in cell-based GFP reporter assays.
YU238259 exhibits potent synthetic lethality in the setting of DNA damage response and DNA repair defects. Treatment with YU238259 is not only synergistic with ionizing radiation (IR), etoposide, and PARP inhibition, but this synergism is heightened by BRCA2-deficiency. Synthetic lethality of YU238259 in HDR-deficient cells results from accumulation of unresolved DSBs following additional inhibition of residual HDR pathway activity. Inhibition of HDR activity by YU238259 has little to no effect on the NHEJ pathway. YU238259 sensitizes tumor cells to radiation therapy and DSB-inducing chemotherapy.Growth of BRCA2-deficient human tumor xenografts in nude mice is significantly delayed by YU238259 treatment even in the absence of concomitant DNA-damaging therapy.
TM5441|TM-5441|TAP-1 antagonist
TM5441|TM-5441|TAP-1 antagonist
DC Chemicals, Website: www.dcchemicals.com
Product Name: TM5441|Cas Number: 1190221-43-2| Catalog Number: DC10374|Other Nmaes: TM 5441,TM-5441
TM5441 is a novel orrally active TAP-1 antagonist.
DC Chemicals, Website: www.dcchemicals.com
Product Name: TM5441|Cas Number: 1190221-43-2| Catalog Number: DC10374|Other Nmaes: TM 5441,TM-5441
TM5441 is a novel orrally active TAP-1 antagonist.
WEHI-345|WEHI345|RIPK2 inhibitor
WEHI-345|WEHI345|RIPK2 inhibitor
DC Chemicals, Website: www.dcchemicals.com
Product Name: WEHI-345|Cas Number: 1354825-58-3| Catalog Number: DC10373|Other Nmaes: WEHI345，WEHI 345
WEHI-345 is a potent and selective inhibitor of RIPK2, with IC50 of 0.13 μM.
WEHI-345 is a potent and selective inhibitor of RIPK2, with IC50 of 0.13 μM. IC50 value: 0.13 μM Target: RIPK2 in vitro: WEHI-345 is a selective RIPK2 kinase inhibitor, which delays RIPK2 ubiquitylation and NF-κB activation downstream of NOD engagement. WEHI-345 is an ATP analogue and was therefore predicted to bind in the ATP-binding pocket of RIPK2. WEHI-345 proved to be highly specific for RIPK2(Kd=46 nM) and displayed negligible activity (>10 μM) against RIPK1, RIPK4 and RIPK5. in vivo: WEHI-345 inhibits NOD signalling and has a beneficial effect on an EAE model. WEHI-345 blocks MDP-induced cytokine production. WEHI-345 ameliorates experimental autoimmune encephalomyelitis in mice. WEHI-345 also potently inhibited MDP-induced cytokine and chemokine secretion in the mouse macrophage Raw 264.7 cell line.
DC Chemicals, Website: www.dcchemicals.com
Product Name: WEHI-345|Cas Number: 1354825-58-3| Catalog Number: DC10373|Other Nmaes: WEHI345，WEHI 345
WEHI-345 is a potent and selective inhibitor of RIPK2, with IC50 of 0.13 μM.
WEHI-345 is a potent and selective inhibitor of RIPK2, with IC50 of 0.13 μM. IC50 value: 0.13 μM Target: RIPK2 in vitro: WEHI-345 is a selective RIPK2 kinase inhibitor, which delays RIPK2 ubiquitylation and NF-κB activation downstream of NOD engagement. WEHI-345 is an ATP analogue and was therefore predicted to bind in the ATP-binding pocket of RIPK2. WEHI-345 proved to be highly specific for RIPK2(Kd=46 nM) and displayed negligible activity (>10 μM) against RIPK1, RIPK4 and RIPK5. in vivo: WEHI-345 inhibits NOD signalling and has a beneficial effect on an EAE model. WEHI-345 blocks MDP-induced cytokine production. WEHI-345 ameliorates experimental autoimmune encephalomyelitis in mice. WEHI-345 also potently inhibited MDP-induced cytokine and chemokine secretion in the mouse macrophage Raw 264.7 cell line.
Amcasertib|BBI503|BBI-503|cancer stem cell
Amcasertib|BBI503|BBI-503|cancer stem cell
DC Chemicals, Website: www.dcchemicals.com
Product Name: Amcasertib(BBI503)|Cas Number: 1129403-56-0| Catalog Number: DC10372|Other Nmaes: BBI 503,BBI-503
Amcasertib(BBI503) is an orally administered investigational agent designed to inhibit cancer stem cell pathways, including Nanog, by targeting stemness kinases.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Amcasertib(BBI503)|Cas Number: 1129403-56-0| Catalog Number: DC10372|Other Nmaes: BBI 503,BBI-503
Amcasertib(BBI503) is an orally administered investigational agent designed to inhibit cancer stem cell pathways, including Nanog, by targeting stemness kinases.
Anlotinib|EGFR inhibitor
Anlotinib|EGFR inhibitor
DC Chemicals, Website: www.dcchemicals.com
Product Name: Anlotinib|Cas Number: 1058156-90-3| Catalog Number: DC10371
Anlotinib is a EGFR inhibitor extracted from patent 2015185012 A1, compound 1，which can be used to treat non-small cell lung cancer.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Anlotinib|Cas Number: 1058156-90-3| Catalog Number: DC10371
Anlotinib is a EGFR inhibitor extracted from patent 2015185012 A1, compound 1，which can be used to treat non-small cell lung cancer.
Olcegepant hydrochloride|cas: 586368-06-1
Olcegepant hydrochloride|cas: 586368-06-1
DC Chemicals, Website: www.dcchemicals.com
Product Name: Olcegepant hydrochloride|Cas Number: 586368-06-1| Catalog Number: DC10370|Other Nmaes: BIBN-4096 hydrochloride; BIBN-4096BS hydrochloride; BIBN4096BS hydrochloride; BIBN 4096BS hydrochloride
Olcegepant hydrochloride is the first potent and selective non-peptide antagonist of the calcitonin gene-related peptide 1 (CGRP1) receptor with IC50 of 0.03 nM and with a Ki of 14.4 pM for human CGRP.
Olcegepant possesses higher affinity for the human CGRP receptor than the endogenous ligand CGRP and 150-fold higher affinity compared to the peptidic antagonist CGRP8-37. Olcegepant reverses CGRP-mediated vasodilation in human cerebral vessels and inhibits neurogenic vasodilation in a surrogate animal model of migraine pathophysiology[1]. Olcegepant (BIBN4096BS) is extremely potent at primate CGRP receptors exhibiting an affinity (Ki) for human CGRP receptors of 14.4±6.3 (n=4) pM[2]. Several lines of evidence suggest that a calcitonin-gene related peptide (CGRP) receptor antagonist may serve as a novel abortive migraine treatment. Olcegepant (BIBN4096BS) exhibits competitive antagonism at the CGRP receptor present in SK-N-MC cells. Isolated human cerebral, coronary, and omental arteries are studied with a sensitive myograph technique. CGRP induces a concentration-dependent relaxation that is antagonized by Olcegepant in a competitive manner[3].Olcegepant (BIBN4096BS) in doses between 1 and 30 μg/kg (i.v.) inhibits the effects of CGRP, released by stimulation of the trigeminal ganglion, on facial blood flow in marmoset monkeys[2]. Pre-treatment with Olcegepant (900 μg/kg) inhibits the capsaicin-induced expression of Fos throughout the spinal trigeminal nucleus by 57%. In contrast, the expression of phosphorylated extracellular signal-regulated kinase in the trigeminal ganglion is not changed by Olcegepant pre-treatment[4]. Olcegepant (0.3 to 0.9 mg/kg, i.v.) markedly reduces mechanical allodynia in CCI-ION rats. Olcegepant (0.6 mg/kg, i.v.) significantly reduces the number of c-Fos immunolabeled cells in spinal nucleus of the trigeminal nerve and upregulation of ATF3 transcript (a marker of neuron injury) but not that of interleukin-6 in trigeminal ganglion of CCI-ION rats[5].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Olcegepant hydrochloride|Cas Number: 586368-06-1| Catalog Number: DC10370|Other Nmaes: BIBN-4096 hydrochloride; BIBN-4096BS hydrochloride; BIBN4096BS hydrochloride; BIBN 4096BS hydrochloride
Olcegepant hydrochloride is the first potent and selective non-peptide antagonist of the calcitonin gene-related peptide 1 (CGRP1) receptor with IC50 of 0.03 nM and with a Ki of 14.4 pM for human CGRP.
Olcegepant possesses higher affinity for the human CGRP receptor than the endogenous ligand CGRP and 150-fold higher affinity compared to the peptidic antagonist CGRP8-37. Olcegepant reverses CGRP-mediated vasodilation in human cerebral vessels and inhibits neurogenic vasodilation in a surrogate animal model of migraine pathophysiology[1]. Olcegepant (BIBN4096BS) is extremely potent at primate CGRP receptors exhibiting an affinity (Ki) for human CGRP receptors of 14.4±6.3 (n=4) pM[2]. Several lines of evidence suggest that a calcitonin-gene related peptide (CGRP) receptor antagonist may serve as a novel abortive migraine treatment. Olcegepant (BIBN4096BS) exhibits competitive antagonism at the CGRP receptor present in SK-N-MC cells. Isolated human cerebral, coronary, and omental arteries are studied with a sensitive myograph technique. CGRP induces a concentration-dependent relaxation that is antagonized by Olcegepant in a competitive manner[3].Olcegepant (BIBN4096BS) in doses between 1 and 30 μg/kg (i.v.) inhibits the effects of CGRP, released by stimulation of the trigeminal ganglion, on facial blood flow in marmoset monkeys[2]. Pre-treatment with Olcegepant (900 μg/kg) inhibits the capsaicin-induced expression of Fos throughout the spinal trigeminal nucleus by 57%. In contrast, the expression of phosphorylated extracellular signal-regulated kinase in the trigeminal ganglion is not changed by Olcegepant pre-treatment[4]. Olcegepant (0.3 to 0.9 mg/kg, i.v.) markedly reduces mechanical allodynia in CCI-ION rats. Olcegepant (0.6 mg/kg, i.v.) significantly reduces the number of c-Fos immunolabeled cells in spinal nucleus of the trigeminal nerve and upregulation of ATF3 transcript (a marker of neuron injury) but not that of interleukin-6 in trigeminal ganglion of CCI-ION rats[5].
TAS-102|cas: 733030-01-8
TAS-102|cas: 733030-01-8
DC Chemicals, Website: www.dcchemicals.com
Product Name: TAS-102|Cas Number: 733030-01-8| Catalog Number: DC10369|Other Nmaes: Trifluridine-tipiracil hydrochloride mixture
TAS-102 is a novel oral combination drug that consists of an antineoplastic thymidine-based nucleoside analog, trifluorothymidine, and a potent thymidine phosphorylase inhibitor, tipiracil, in a 1:0.5 molar ratio.
TAS-102, a novel antimetabolite combination chemotherapy agent, consists of a rediscovered antimetabolite agent, trifluorothymidine (trifluridine, FTD) combined with the metabolic inhibitor of thymidine phosphorylase, tipiracil (TPI), in a 1:0.5 molar ratio[1]. FTD is the active antitumor component of TAS-102; its monophosphate form inhibits thymidylate synthase, and its triphosphate form is incorporated into DNA in tumor cells. The incorporation into DNA is known to have antitumor effects, since the inhibition of thymidylate synthase caused by oral FTD rapidly disappears after the drug's elimination. When FTD is administered orally, it is rapidly degraded to its inactive form by thymidine phosphorylase in the intestines and liver (first-pass effect). Consequently, TPI is synthesized to maintain adequate plasma concentrations of orally-administered FTD and to potentiate the antitumor activity of FTD[2].TAS-102 and CPT-11 is a promising treatment option for colorectal or gastric cancer. TAS-102 monotherapy has a significant antitumor activity against KM12C/5-FUFU-bearing nude mice. The combination-treated (CPT-11-and TAS-102) group is significantly superior to monotherapy[2]. FTD systemic exposure in plasma increaseS dose-dependently. The tumor growth rate and body weight gain decreaseS dose-dependently, but FTD concentrations in the DNA of tumor tissues and white blood cells increases dose-dependently. FTD inhibits colony formation of bone marrow cells in a concentration-dependent manner[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: TAS-102|Cas Number: 733030-01-8| Catalog Number: DC10369|Other Nmaes: Trifluridine-tipiracil hydrochloride mixture
TAS-102 is a novel oral combination drug that consists of an antineoplastic thymidine-based nucleoside analog, trifluorothymidine, and a potent thymidine phosphorylase inhibitor, tipiracil, in a 1:0.5 molar ratio.
TAS-102, a novel antimetabolite combination chemotherapy agent, consists of a rediscovered antimetabolite agent, trifluorothymidine (trifluridine, FTD) combined with the metabolic inhibitor of thymidine phosphorylase, tipiracil (TPI), in a 1:0.5 molar ratio[1]. FTD is the active antitumor component of TAS-102; its monophosphate form inhibits thymidylate synthase, and its triphosphate form is incorporated into DNA in tumor cells. The incorporation into DNA is known to have antitumor effects, since the inhibition of thymidylate synthase caused by oral FTD rapidly disappears after the drug's elimination. When FTD is administered orally, it is rapidly degraded to its inactive form by thymidine phosphorylase in the intestines and liver (first-pass effect). Consequently, TPI is synthesized to maintain adequate plasma concentrations of orally-administered FTD and to potentiate the antitumor activity of FTD[2].TAS-102 and CPT-11 is a promising treatment option for colorectal or gastric cancer. TAS-102 monotherapy has a significant antitumor activity against KM12C/5-FUFU-bearing nude mice. The combination-treated (CPT-11-and TAS-102) group is significantly superior to monotherapy[2]. FTD systemic exposure in plasma increaseS dose-dependently. The tumor growth rate and body weight gain decreaseS dose-dependently, but FTD concentrations in the DNA of tumor tissues and white blood cells increases dose-dependently. FTD inhibits colony formation of bone marrow cells in a concentration-dependent manner[3].
Cyclo(his-pro)|cas: 53109-32-3
Cyclo(his-pro)|cas: 53109-32-3
DC Chemicals, Website: www.dcchemicals.com
Product Name: Cyclo(his-pro)|Cas Number: 53109-32-3| Catalog Number: DC10368|Other Nmaes: Cyclo(histidyl-proline); Histidylproline diketopiperazine
Cyclo(His-Pro) is a cyclic dipeptide structurally related to tyreotropin-releasing hormone.
Cyclo(His-Pro) is a cyclic dipeptide derived from the hydrolytic removal of the amino-terminal pyroglutamic acid residue of the hypothalamic thyrotropin-releasing hormone. Cyclo(His-Pro) is ubiquitous in the central nervous system and is a key substrate of organic cation transporters, which are strongly linked to neuroprotection. The cyclic dipeptide can also cross the brain-blood-barrier and, once in the brain, can affect diverse inflammatory and stress responses by modifying the Nrf2-NF-κB signaling axis[1]. Cyclo(His-Pro) inhibits NF-κB nuclear accumulation induced by paraquat in rat pheochromocytoma PC12 cells via the Nrf2/heme oxygenase-1 pathway[2].Mice that receives cyclo(His-Pro) pre-treatment shows a significant decrease in the oedematogenic response, confirming that the cyclic dipeptide can exert anti-inflammatory effect[2]. Cyclo(His-Pro) exerts in vivo anti-inflammatory effects in the central nervous system by down-regulating hepatic and cerebral TNFα expression thereby counteracting LPS-induced gliosis. Moreover, by up-regulating Bip, cyclo(His-Pro) increases the ER stress sensitivity andtriggers the unfolded protein response to alleviate the ER stress[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Cyclo(his-pro)|Cas Number: 53109-32-3| Catalog Number: DC10368|Other Nmaes: Cyclo(histidyl-proline); Histidylproline diketopiperazine
Cyclo(His-Pro) is a cyclic dipeptide structurally related to tyreotropin-releasing hormone.
Cyclo(His-Pro) is a cyclic dipeptide derived from the hydrolytic removal of the amino-terminal pyroglutamic acid residue of the hypothalamic thyrotropin-releasing hormone. Cyclo(His-Pro) is ubiquitous in the central nervous system and is a key substrate of organic cation transporters, which are strongly linked to neuroprotection. The cyclic dipeptide can also cross the brain-blood-barrier and, once in the brain, can affect diverse inflammatory and stress responses by modifying the Nrf2-NF-κB signaling axis[1]. Cyclo(His-Pro) inhibits NF-κB nuclear accumulation induced by paraquat in rat pheochromocytoma PC12 cells via the Nrf2/heme oxygenase-1 pathway[2].Mice that receives cyclo(His-Pro) pre-treatment shows a significant decrease in the oedematogenic response, confirming that the cyclic dipeptide can exert anti-inflammatory effect[2]. Cyclo(His-Pro) exerts in vivo anti-inflammatory effects in the central nervous system by down-regulating hepatic and cerebral TNFα expression thereby counteracting LPS-induced gliosis. Moreover, by up-regulating Bip, cyclo(His-Pro) increases the ER stress sensitivity andtriggers the unfolded protein response to alleviate the ER stress[3].
RG14620|cas: 136831-49-7
RG14620|cas: 136831-49-7
DC Chemicals, Website: www.dcchemicals.com
Product Name: RG14620|Cas Number: 136831-49-7| Catalog Number: DC10367|Other Nmaes: RG 14620; RG-14620; Tyrphostin RG14620
RG14620 is an epidermal growth factor receptor (EGFR) inhibitor, with IC50 values of 3 μM for HER 14 colony formation and 1 pM for HER 14 DNA synthesis.
RG-14620 inhibits colony formation and DNA synthesis by HER 14 cells, which are stimulated by 50 ng/mL EGF, in a dose-dependent manner. The IC50s for RG-14620 are 3 μM for HER 14 colony formation and 1 pM for HER 14 DNA synthesis[1]. RG-14620 also suppresses colony formation and DNA synthesis by EGF-stimulated MH-85 cells in a dose-dependent manner. The IC50s for RG-14620 on MH-85 cells are 4 μM for colony formation and 1.25 μM for DNA synthesis[1].RG-14620, at a dose of 200 μg/mouse/day inhibits MH-85 tumor growth in nude mice. Mice show less cachexia and hypercalcemia, eat more food, and are more active than untreated MH-85 tumor-bearing animals[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: RG14620|Cas Number: 136831-49-7| Catalog Number: DC10367|Other Nmaes: RG 14620; RG-14620; Tyrphostin RG14620
RG14620 is an epidermal growth factor receptor (EGFR) inhibitor, with IC50 values of 3 μM for HER 14 colony formation and 1 pM for HER 14 DNA synthesis.
RG-14620 inhibits colony formation and DNA synthesis by HER 14 cells, which are stimulated by 50 ng/mL EGF, in a dose-dependent manner. The IC50s for RG-14620 are 3 μM for HER 14 colony formation and 1 pM for HER 14 DNA synthesis[1]. RG-14620 also suppresses colony formation and DNA synthesis by EGF-stimulated MH-85 cells in a dose-dependent manner. The IC50s for RG-14620 on MH-85 cells are 4 μM for colony formation and 1.25 μM for DNA synthesis[1].RG-14620, at a dose of 200 μg/mouse/day inhibits MH-85 tumor growth in nude mice. Mice show less cachexia and hypercalcemia, eat more food, and are more active than untreated MH-85 tumor-bearing animals[1].
Omadacycline hydrochloride|cas: 1196800-39-1
Omadacycline hydrochloride|cas: 1196800-39-1
DC Chemicals, Website: www.dcchemicals.com
Product Name: Omadacycline hydrochloride|Cas Number: 1196800-39-1| Catalog Number: DC10365|Other Nmaes: PTK 0796 hydrochloride; PTK-0796 hydrochloride; PTK0796 hydrochloride; Amadacycline hydrochloride
Omadacycline hydrochloride is novel, aminomethyl tetracycline antibiotic being developed for the treatment of community-acquired bacterial infections. The ED50 for Escherichia coli is 2.02 mg/kg.
The omadacycline MIC90s for MRSA, VRE, and beta-hemolytic streptococci are 1.0 μg/mL, 0.25 μg/mL, and 0.5 μg/mL, respectively, and the omadacycline MIC90s for PRSP and H. influenzae are 0.25 μg/ml and 2.0 μg/mL, respectively. Omadacycline is active against organisms demonstrating the two major mechanisms of resistance, ribosomal protection and active tetracycline efflux[1]. Omadacycline inhibits protein synthesis while having no significant effect on RNA, DNA and peptidoglycan synthesis. Further, omadacycline binds to the tetracycline binding site on the 30S subunit of the bacterial ribosome with enhanced binding similar to tigecycline based on additional molecular interactions[2].In vivo efficacy of omadacycline is demonstrated using an intraperitoneal infection model in mice. A single intravenous dose of omadacycline exhibits efficacy against Streptococcus pneumoniae, Escherichia coli, and Staphylococcus aureus, including tet (M) and tet (K) efflux-containing strains and MRSA strains. The 50% effective doses (ED50s) for Streptococcus pneumoniae obtained ranged from 0.45 mg/kg to 3.39 mg/kg, the ED50s for Staphylococcus aureus obtained ranges from 0.30 mg/kg to 1.74 mg/kg, and the ED50 for Escherichia coli is 2.02 mg/kg[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Omadacycline hydrochloride|Cas Number: 1196800-39-1| Catalog Number: DC10365|Other Nmaes: PTK 0796 hydrochloride; PTK-0796 hydrochloride; PTK0796 hydrochloride; Amadacycline hydrochloride
Omadacycline hydrochloride is novel, aminomethyl tetracycline antibiotic being developed for the treatment of community-acquired bacterial infections. The ED50 for Escherichia coli is 2.02 mg/kg.
The omadacycline MIC90s for MRSA, VRE, and beta-hemolytic streptococci are 1.0 μg/mL, 0.25 μg/mL, and 0.5 μg/mL, respectively, and the omadacycline MIC90s for PRSP and H. influenzae are 0.25 μg/ml and 2.0 μg/mL, respectively. Omadacycline is active against organisms demonstrating the two major mechanisms of resistance, ribosomal protection and active tetracycline efflux[1]. Omadacycline inhibits protein synthesis while having no significant effect on RNA, DNA and peptidoglycan synthesis. Further, omadacycline binds to the tetracycline binding site on the 30S subunit of the bacterial ribosome with enhanced binding similar to tigecycline based on additional molecular interactions[2].In vivo efficacy of omadacycline is demonstrated using an intraperitoneal infection model in mice. A single intravenous dose of omadacycline exhibits efficacy against Streptococcus pneumoniae, Escherichia coli, and Staphylococcus aureus, including tet (M) and tet (K) efflux-containing strains and MRSA strains. The 50% effective doses (ED50s) for Streptococcus pneumoniae obtained ranged from 0.45 mg/kg to 3.39 mg/kg, the ED50s for Staphylococcus aureus obtained ranges from 0.30 mg/kg to 1.74 mg/kg, and the ED50 for Escherichia coli is 2.02 mg/kg[1].
(±)-Pirmenol |cas: 68252-19-7
(±)-Pirmenol |cas: 68252-19-7
DC Chemicals, Website: www.dcchemicals.com
Product Name: (±)-Pirmenol|Cas Number: 68252-19-7| Catalog Number: DC10364
Pirmenol inhibits IK.ACh by blocking muscarinic receptors. The IC50 of Pirmenol for inhibition of Carbachol-induced IK.ACh is 0.1 μM.
Pirmenol inhibits the carbachol-induced IK.ACh in a concentration-dependent manner. Pirmenol also inhibits the GTPγS-induced current although the concentrations of Pirmenol needed to inhibit the GTPγS-induced current are much higher than those to inhibit the carbachol-induced IK.ACh. The IC50 of Pirmenol for inhibition of the GTPγS-induced currents is 30 μM. The inhibitory effect of Pirmenol on these IK.ACh is almost completely reversible and the outward current reappeared upon washout of Pirmenol. Pirmenol on the muscarinic acetylcholine receptor-operated K+ current (IK.ACh) in atrial cells and on experimental atrial fibrillation in isolated guinea-pig hearts. In isolated atrial myocytes, Pirmenol concentration dependently inhibits the IK.ACh induced by carbachol or intracellular loading of GTPγS. In Langendorff-perfused hearts Pirmenol reverses the carbachol-induced decreases in effective refractory periods and atrial fibrillation threshold[1].The pyridine-methanol derivative Pirmenol is a new antiarrhythmic agent. Single-dose studies in rodents demonstrate a 10- to 15-fold difference between the po and iv LD50 values. In rats, the po LD50 is 359.9 mg/kg and the iv LD50 is 23.6 mg/kg. Mice LD50 values are 215.5 and 20.8 mg/kg for po and iv routes, respectively. Short-term subacute iv toxicity studies in rats (2.5, 5.0, and 7.5 mg/kg) and dogs (2.5, 5, and 10 mg/kg) for 4 weeks elicite minimal reactions. Cardiac effects in dogs include drug related increases in heart rate, increases QRS duration, shortening of ST interval without evidence of cardiac tissue damage and mild local reaction at the injection site. Orally, Pirmenol is well tolerated for 13 weeks in rats receiving 25, 50, and 100 mg/kg/day while dogs given 5, 10, and 15 mg/kg/day shows anticholinergic effects at high levels (dryness of mucosae, body tremors). Heart rates are significantly accelerated only at the beginning of the study and QRS changes are seen with wide individual variations. No drug-related tissue changes are elicited in these species. Teratology studies in rats (50, 100, and 150 mg/kg) and in rabbits (10, 25, and 50 mg/kg) show no overt effect on organogenesis but embryotoxicity is seen at 150 mg/kg in rats[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: (±)-Pirmenol|Cas Number: 68252-19-7| Catalog Number: DC10364
Pirmenol inhibits IK.ACh by blocking muscarinic receptors. The IC50 of Pirmenol for inhibition of Carbachol-induced IK.ACh is 0.1 μM.
Pirmenol inhibits the carbachol-induced IK.ACh in a concentration-dependent manner. Pirmenol also inhibits the GTPγS-induced current although the concentrations of Pirmenol needed to inhibit the GTPγS-induced current are much higher than those to inhibit the carbachol-induced IK.ACh. The IC50 of Pirmenol for inhibition of the GTPγS-induced currents is 30 μM. The inhibitory effect of Pirmenol on these IK.ACh is almost completely reversible and the outward current reappeared upon washout of Pirmenol. Pirmenol on the muscarinic acetylcholine receptor-operated K+ current (IK.ACh) in atrial cells and on experimental atrial fibrillation in isolated guinea-pig hearts. In isolated atrial myocytes, Pirmenol concentration dependently inhibits the IK.ACh induced by carbachol or intracellular loading of GTPγS. In Langendorff-perfused hearts Pirmenol reverses the carbachol-induced decreases in effective refractory periods and atrial fibrillation threshold[1].The pyridine-methanol derivative Pirmenol is a new antiarrhythmic agent. Single-dose studies in rodents demonstrate a 10- to 15-fold difference between the po and iv LD50 values. In rats, the po LD50 is 359.9 mg/kg and the iv LD50 is 23.6 mg/kg. Mice LD50 values are 215.5 and 20.8 mg/kg for po and iv routes, respectively. Short-term subacute iv toxicity studies in rats (2.5, 5.0, and 7.5 mg/kg) and dogs (2.5, 5, and 10 mg/kg) for 4 weeks elicite minimal reactions. Cardiac effects in dogs include drug related increases in heart rate, increases QRS duration, shortening of ST interval without evidence of cardiac tissue damage and mild local reaction at the injection site. Orally, Pirmenol is well tolerated for 13 weeks in rats receiving 25, 50, and 100 mg/kg/day while dogs given 5, 10, and 15 mg/kg/day shows anticholinergic effects at high levels (dryness of mucosae, body tremors). Heart rates are significantly accelerated only at the beginning of the study and QRS changes are seen with wide individual variations. No drug-related tissue changes are elicited in these species. Teratology studies in rats (50, 100, and 150 mg/kg) and in rabbits (10, 25, and 50 mg/kg) show no overt effect on organogenesis but embryotoxicity is seen at 150 mg/kg in rats[2].
Coumestrol|cas: 479-13-0
Coumestrol|cas: 479-13-0
DC Chemicals, Website: www.dcchemicals.com
Product Name: Coumestrol|Cas Number: 479-13-0| Catalog Number: DC10363
Coumestrol, a phytoestrogen present in soybean products, exhibits activities against cancers, neurological disorders, and autoimmune diseases. It suppresses proliferation of ES2 cells with an IC50 of 50 μM.
Coumestrol exerts chemotherapeutic effects via PI3K and ERK1/2 MAPK pathways. Coumestrol inhibits viability and invasion, and induces apoptosis of ES2 (clear cell-/serous carcinoma origin) cells. In addition, immunoreactive PCNA and ERBB2, markers of proliferation of ovarian carcinoma, are attenuated in their expression in coumestrol-induced death of ES2 cells. Phosphorylation of AKT, p70S6K, ERK1/2, JNK1/2 and p90RSK is inactivated by coumestrol treatment in a dose- and time-dependent manner[1]. Coumestrol inhibits proliferation and induces apoptosis in MCF-7 cells, which is prevented by copper chelator neocuproine and ROS scavengers. Coumestrol treatment induces ROS generation coupled to DNA fragmentation, up-regulation of p53/p21, cell cycle arrest at G1/S phase, mitochondrial membrane depolarization and caspases 9/3 activation[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Coumestrol|Cas Number: 479-13-0| Catalog Number: DC10363
Coumestrol, a phytoestrogen present in soybean products, exhibits activities against cancers, neurological disorders, and autoimmune diseases. It suppresses proliferation of ES2 cells with an IC50 of 50 μM.
Coumestrol exerts chemotherapeutic effects via PI3K and ERK1/2 MAPK pathways. Coumestrol inhibits viability and invasion, and induces apoptosis of ES2 (clear cell-/serous carcinoma origin) cells. In addition, immunoreactive PCNA and ERBB2, markers of proliferation of ovarian carcinoma, are attenuated in their expression in coumestrol-induced death of ES2 cells. Phosphorylation of AKT, p70S6K, ERK1/2, JNK1/2 and p90RSK is inactivated by coumestrol treatment in a dose- and time-dependent manner[1]. Coumestrol inhibits proliferation and induces apoptosis in MCF-7 cells, which is prevented by copper chelator neocuproine and ROS scavengers. Coumestrol treatment induces ROS generation coupled to DNA fragmentation, up-regulation of p53/p21, cell cycle arrest at G1/S phase, mitochondrial membrane depolarization and caspases 9/3 activation[2].
Palmitelaidic Acid |cas: 10030-73-6
Palmitelaidic Acid |cas: 10030-73-6
DC Chemicals, Website: www.dcchemicals.com
Product Name: Palmitelaidic Acid|Cas Number: 10030-73-6| Catalog Number: DC10362|Other Nmaes: 9-trans-Hexadecenoic acid; trans-Palmitoleic acid
Palmitelaidic acid is the trans isomer of palmitoleic acid. Palmitoleic acid is one of the most abundant fatty acids in serum and tissue.
The monounsaturated fatty acid palmitoleate (palmitoleic acid) is one of the most abundant fatty acids in serum and tissues, particularly adipose tissue and liver. Its endogenous production by stearoyl-CoA desaturase 1 gives rise to its cis isoform, cis-palmitoleate. Palmitoleic acid has been correlated with multiple cardiometabolic risk factors, including high blood pressure, total cholesterol, TGs, apoA-I, apoB, and endothelial dysfunction[1].Palmitoleic acid promotes a faster uptake of glucose in the body, associated with higher insulin concentration. Palmitoleic acid increases the phosphorylation of AMPK, up-regulates glucokinase and down-regulates SREBP-1. Regarding AMPK downstream, palmitoleic acid increases the production of FGF-21 and stimulates the expression of PPARα[2]. Palmitoleic acid reduces body weight increase, ameliorates the development of hyperglycemia and hypertriglyceridemia, and improves insulin sensitivity. Furthermore, palmitoleic acid down-regulates mRNA expressions of proinflammatory adipocytokine genes (TNFα and resistin) in white adipose tissue and lipogenic genes (SREBP-1, FAS, and SCD-1) in liver[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Palmitelaidic Acid|Cas Number: 10030-73-6| Catalog Number: DC10362|Other Nmaes: 9-trans-Hexadecenoic acid; trans-Palmitoleic acid
Palmitelaidic acid is the trans isomer of palmitoleic acid. Palmitoleic acid is one of the most abundant fatty acids in serum and tissue.
The monounsaturated fatty acid palmitoleate (palmitoleic acid) is one of the most abundant fatty acids in serum and tissues, particularly adipose tissue and liver. Its endogenous production by stearoyl-CoA desaturase 1 gives rise to its cis isoform, cis-palmitoleate. Palmitoleic acid has been correlated with multiple cardiometabolic risk factors, including high blood pressure, total cholesterol, TGs, apoA-I, apoB, and endothelial dysfunction[1].Palmitoleic acid promotes a faster uptake of glucose in the body, associated with higher insulin concentration. Palmitoleic acid increases the phosphorylation of AMPK, up-regulates glucokinase and down-regulates SREBP-1. Regarding AMPK downstream, palmitoleic acid increases the production of FGF-21 and stimulates the expression of PPARα[2]. Palmitoleic acid reduces body weight increase, ameliorates the development of hyperglycemia and hypertriglyceridemia, and improves insulin sensitivity. Furthermore, palmitoleic acid down-regulates mRNA expressions of proinflammatory adipocytokine genes (TNFα and resistin) in white adipose tissue and lipogenic genes (SREBP-1, FAS, and SCD-1) in liver[3].
Iberin |cas: 505-44-2
Iberin |cas: 505-44-2
DC Chemicals, Website: www.dcchemicals.com
Product Name: Iberin|Cas Number: 505-44-2| Catalog Number: DC10361
Iberin, a sulfoxide analogue of sulforaphane, is a naturally occurring member of isothiocyanate family. It inhibits cell survival with an IC50 of 2.3 μM in HL60 cell.
Iberin inhibits the growth of neuroblastoma cells in a dose- and time-dependent manner. The iberin-induced cell cycle arrest in neuroblastoma cells is associated with inhibition of expression of cyclin-dependent kinase Cdk2, Cdk4, and Cdk6 proteins. There is an increase in apoptotic cell death in iberin treated cells as compared with control cells. The iberin-induced apoptosis is found to be associated with activation of caspase-9, caspase-3, and PARP[2]. Iberin inhibits growth of human glioblastoma cells in cell proliferation assays, enhances cytotoxicity, and induces apoptosis by activation of caspase-3 and caspase-9[3].Iberin is tested in an in vivo foreign-body infection mouse model, and the results show no significantly difference in bacterial clearance between treated and nontreated miced[4]. Iberin increases tissue levels of the phase II detoxification enzymes quinone reductase and glutathione S-transferase in a variety of rat tissues[5].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Iberin|Cas Number: 505-44-2| Catalog Number: DC10361
Iberin, a sulfoxide analogue of sulforaphane, is a naturally occurring member of isothiocyanate family. It inhibits cell survival with an IC50 of 2.3 μM in HL60 cell.
Iberin inhibits the growth of neuroblastoma cells in a dose- and time-dependent manner. The iberin-induced cell cycle arrest in neuroblastoma cells is associated with inhibition of expression of cyclin-dependent kinase Cdk2, Cdk4, and Cdk6 proteins. There is an increase in apoptotic cell death in iberin treated cells as compared with control cells. The iberin-induced apoptosis is found to be associated with activation of caspase-9, caspase-3, and PARP[2]. Iberin inhibits growth of human glioblastoma cells in cell proliferation assays, enhances cytotoxicity, and induces apoptosis by activation of caspase-3 and caspase-9[3].Iberin is tested in an in vivo foreign-body infection mouse model, and the results show no significantly difference in bacterial clearance between treated and nontreated miced[4]. Iberin increases tissue levels of the phase II detoxification enzymes quinone reductase and glutathione S-transferase in a variety of rat tissues[5].
MLi-2|cas: 1627091-47-7
MLi-2|cas: 1627091-47-7
DC Chemicals, Website: www.dcchemicals.com
Product Name: MLi-2|Cas Number: 1627091-47-7| Catalog Number: DC10360|Other Nmaes: MLi2; Mli 2
MLi-2 is an a potent, highly selective, orally available, brain penetrant inhibitor of LRRK2 with an IC50 of 0.76 nM.
MLi-2 exhibits exceptional potency in a purified LRRK2 kinase assay in vitro( IC50=0.76 nM), a cellular assay monitoring dephosphorylation of LRRK2 pSer935 LRRK2 (IC50=1.4 nM), and a radioligand competition binding assay (IC50=3.4 nM). MLi-2 has greater than 295-fold selectivity for over 300 kinases in addition to a diverse panel of receptors and ion channels[1].Acute oral and subchronic dosing in MLi-2 mice results in dose-dependent central and peripheral target inhibition over a 24-hour period as measured by dephosphorylation of pSer935 LRRK2. Treatment of MitoPark mice with MLi-2 is well tolerated over a 15-week period at brain and plasma exposures. Morphologic changes in the lung, consistent with enlarged type II pneumocytes, are observed in MLi-2-treated MitoPark mice[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: MLi-2|Cas Number: 1627091-47-7| Catalog Number: DC10360|Other Nmaes: MLi2; Mli 2
MLi-2 is an a potent, highly selective, orally available, brain penetrant inhibitor of LRRK2 with an IC50 of 0.76 nM.
MLi-2 exhibits exceptional potency in a purified LRRK2 kinase assay in vitro( IC50=0.76 nM), a cellular assay monitoring dephosphorylation of LRRK2 pSer935 LRRK2 (IC50=1.4 nM), and a radioligand competition binding assay (IC50=3.4 nM). MLi-2 has greater than 295-fold selectivity for over 300 kinases in addition to a diverse panel of receptors and ion channels[1].Acute oral and subchronic dosing in MLi-2 mice results in dose-dependent central and peripheral target inhibition over a 24-hour period as measured by dephosphorylation of pSer935 LRRK2. Treatment of MitoPark mice with MLi-2 is well tolerated over a 15-week period at brain and plasma exposures. Morphologic changes in the lung, consistent with enlarged type II pneumocytes, are observed in MLi-2-treated MitoPark mice[1].
N2-Methylguanine|cas: 10030-78-1
N2-Methylguanine|cas: 10030-78-1
DC Chemicals, Website: www.dcchemicals.com
Product Name: N2-Methylguanine|Cas Number: 10030-78-1| Catalog Number: DC10359
N2-Methylguanine is a modified nucleoside. N2-Methylguanine is an endogenous methylated nucleoside found in human fluids.
N2-methylguanine is found within both helical and looped regions of RNA secondary structure, and it can exist in either the s-cis or the s-trans rotamer. If there is a rotational preference for the methyl group, the effect of N2-methylguanine substitution may be specific to the sequence context depending upon which face of the base participates in hydrogen bonding[1]. N2-methylguanine is the principal kinetic barrier for reverse transcription in the 1340 bases proximal to the 5' end of E. coli 16S rRNA. Transcription intermediates correspond to attenuation at the positions of N2-methylguanine in the rRNA sequence. The relaxation time for elongation of the cDNA through m2G is approximately 3 min[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: N2-Methylguanine|Cas Number: 10030-78-1| Catalog Number: DC10359
N2-Methylguanine is a modified nucleoside. N2-Methylguanine is an endogenous methylated nucleoside found in human fluids.
N2-methylguanine is found within both helical and looped regions of RNA secondary structure, and it can exist in either the s-cis or the s-trans rotamer. If there is a rotational preference for the methyl group, the effect of N2-methylguanine substitution may be specific to the sequence context depending upon which face of the base participates in hydrogen bonding[1]. N2-methylguanine is the principal kinetic barrier for reverse transcription in the 1340 bases proximal to the 5' end of E. coli 16S rRNA. Transcription intermediates correspond to attenuation at the positions of N2-methylguanine in the rRNA sequence. The relaxation time for elongation of the cDNA through m2G is approximately 3 min[2].
Lys01 trihydrochloride|cas: 1391426-24-6
Lys01 trihydrochloride|cas: 1391426-24-6
DC Chemicals, Website: www.dcchemicals.com
Product Name: Lys01 trihydrochloride|Cas Number: 1391426-24-6| Catalog Number: DC10358|Other Nmaes: Lys05
Lys01 trihydrochloride (Lys05) is a novel lysosomal autophagy inhibitor with IC50 values of 3.6, 3.8, 6 and 7.9 μM for 1205Lu, c8161, LN229 and HT-29 cell line in the MTT assay.
Lys01, is a 10-fold more potent autophagy inhibitor than HCQ. Compared with HCQ, Lys05, a water-soluble salt of Lys01, more potently accumulates within and deacidifies the lysosome. Lys01 and lys01 trihydrochloride produce equivalent dose-dependent increases in the LC3II/LC3I ratio, accumulation of the autophagy cargo protein p62, and identical IC50 values in the MTT assay[1].With this high-dose, short-term treatment, no mice die, but after 2 d of dosing, mice treated with lys01 trihydrochloride 76 mg/kg i.p. are observed to have arched backs and lethargy. Morphologically, EM show that cells with intact nuclear and cytoplasmic membranes contain large AVs in lys01 trihydrochloride-treated tumors. Tumor growth is significantly impaired in lys01 trihydrochloride-treated tumors compared with controls. Lys01 trihydrochloride treatment results in a 53% reduction in the average daily tumor growth rate compared with vehicle-treated controls. A significant three- and six-fold accumulation of AV is observed at the end of 14 d of treatment in HCQ- and lys01 trihydrochloride-treated tumors, respectively, compared with control-treated tumors[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Lys01 trihydrochloride|Cas Number: 1391426-24-6| Catalog Number: DC10358|Other Nmaes: Lys05
Lys01 trihydrochloride (Lys05) is a novel lysosomal autophagy inhibitor with IC50 values of 3.6, 3.8, 6 and 7.9 μM for 1205Lu, c8161, LN229 and HT-29 cell line in the MTT assay.
Lys01, is a 10-fold more potent autophagy inhibitor than HCQ. Compared with HCQ, Lys05, a water-soluble salt of Lys01, more potently accumulates within and deacidifies the lysosome. Lys01 and lys01 trihydrochloride produce equivalent dose-dependent increases in the LC3II/LC3I ratio, accumulation of the autophagy cargo protein p62, and identical IC50 values in the MTT assay[1].With this high-dose, short-term treatment, no mice die, but after 2 d of dosing, mice treated with lys01 trihydrochloride 76 mg/kg i.p. are observed to have arched backs and lethargy. Morphologically, EM show that cells with intact nuclear and cytoplasmic membranes contain large AVs in lys01 trihydrochloride-treated tumors. Tumor growth is significantly impaired in lys01 trihydrochloride-treated tumors compared with controls. Lys01 trihydrochloride treatment results in a 53% reduction in the average daily tumor growth rate compared with vehicle-treated controls. A significant three- and six-fold accumulation of AV is observed at the end of 14 d of treatment in HCQ- and lys01 trihydrochloride-treated tumors, respectively, compared with control-treated tumors[1].
Cenerimod|cas: 1262414-04-9
Cenerimod|cas: 1262414-04-9
DC Chemicals, Website: www.dcchemicals.com
Product Name: Cenerimod|Cas Number: 1262414-04-9| Catalog Number: DC10357|Other Nmaes: ACT-334441; ACT334441; ACT 334441
Cenerimod (ACT-334441) is a potent and orally available sphingosine 1-phosphate 1 receptor (S1P1) agonist extracted from patent WO 2016184939 A1 and WO 2011007324 A1, example 1, with an EC50 of 2.7 nM.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Cenerimod|Cas Number: 1262414-04-9| Catalog Number: DC10357|Other Nmaes: ACT-334441; ACT334441; ACT 334441
Cenerimod (ACT-334441) is a potent and orally available sphingosine 1-phosphate 1 receptor (S1P1) agonist extracted from patent WO 2016184939 A1 and WO 2011007324 A1, example 1, with an EC50 of 2.7 nM.
PF 03716556|cas: 928774-43-0
PF 03716556|cas: 928774-43-0
DC Chemicals, Website: www.dcchemicals.com
Product Name: PF 03716556|Cas Number: 928774-43-0| Catalog Number: DC10356|Other Nmaes: PF-03716556; PF03716556
PF 03716556 is a potent, and selective acid pump (H+,K+ ATPase) antagonist, with pIC50 value of 6.009.
DC Chemicals, Website: www.dcchemicals.com
Product Name: PF 03716556|Cas Number: 928774-43-0| Catalog Number: DC10356|Other Nmaes: PF-03716556; PF03716556
PF 03716556 is a potent, and selective acid pump (H+,K+ ATPase) antagonist, with pIC50 value of 6.009.
Nelfinavir |cas: 159989-64-7
Nelfinavir |cas: 159989-64-7
DC Chemicals, Website: www.dcchemicals.com
Product Name: Nelfinavir|Cas Number: 159989-64-7| Catalog Number: DC10355|Other Nmaes: AG 1341; AG-1341; AG1341
Nelfinavir(AG-1341) is a potent and orally bioavailable human immunodeficiency virus HIV-1 protease inhibitor (Ki=2 nM) and is widely prescribed in combination with HIV reverse transcriptase inhibitors for the treatment of HIV infection.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Nelfinavir|Cas Number: 159989-64-7| Catalog Number: DC10355|Other Nmaes: AG 1341; AG-1341; AG1341
Nelfinavir(AG-1341) is a potent and orally bioavailable human immunodeficiency virus HIV-1 protease inhibitor (Ki=2 nM) and is widely prescribed in combination with HIV reverse transcriptase inhibitors for the treatment of HIV infection.
HBX 19818|cas: 1426944-49-1
HBX 19818|cas: 1426944-49-1
DC Chemicals, Website: www.dcchemicals.com
Product Name: HBX 19818|Cas Number: 1426944-49-1| Catalog Number: DC10354|Other Nmaes: HBX19818; HBX-19818
HBX 19818 is a selective USP7 inhibitor with IC50 of 28.1 uM .
DC Chemicals, Website: www.dcchemicals.com
Product Name: HBX 19818|Cas Number: 1426944-49-1| Catalog Number: DC10354|Other Nmaes: HBX19818; HBX-19818
HBX 19818 is a selective USP7 inhibitor with IC50 of 28.1 uM .
MCOPPB triHydrochloride|cas: 1108147-88-1
MCOPPB triHydrochloride|cas: 1108147-88-1
DC Chemicals, Website: www.dcchemicals.com
Product Name: MCOPPB triHydrochloride|Cas Number: 1108147-88-1| Catalog Number: DC10353|Other Nmaes: MCOPPB 3HCl
MCOPPB 3Hcl is a nociceptin receptor agonist with pKi of 10.07; weaker activity at other opioid receptors
DC Chemicals, Website: www.dcchemicals.com
Product Name: MCOPPB triHydrochloride|Cas Number: 1108147-88-1| Catalog Number: DC10353|Other Nmaes: MCOPPB 3HCl
MCOPPB 3Hcl is a nociceptin receptor agonist with pKi of 10.07; weaker activity at other opioid receptors
Varenicline Hydrochloride|cas: 230615-23-3
Varenicline Hydrochloride|cas: 230615-23-3
DC Chemicals, Website: www.dcchemicals.com
Product Name: Varenicline Hydrochloride|Cas Number: 230615-23-3| Catalog Number: DC10352|Other Nmaes: CP 526555 hydrochloride; Champix hydrochloride; Chantix hydrochloride
Varenicline Hcl(CP 526555;Champix) is a nicotinic receptor partial agonist; it stimulates nicotine receptors more weakly than nicotine itself does.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Varenicline Hydrochloride|Cas Number: 230615-23-3| Catalog Number: DC10352|Other Nmaes: CP 526555 hydrochloride; Champix hydrochloride; Chantix hydrochloride
Varenicline Hcl(CP 526555;Champix) is a nicotinic receptor partial agonist; it stimulates nicotine receptors more weakly than nicotine itself does.
Y-33075 dihydrochloride|cas: 173897-44-4
Y-33075 dihydrochloride|cas: 173897-44-4
DC Chemicals, Website: www.dcchemicals.com
Product Name: Y-33075 dihydrochloride|Cas Number: 173897-44-4| Catalog Number: DC10351|Other Nmaes: Y39983 hydrochlorid
Y-33075 dihydrochloride is a selective ROCK inhibitor derived from Y-27632, and is more potent than Y-27632.
In the examination of inhibition of PKC and CaMKII, the IC50s of Y-27632 and Y-39983 for PKC is 9.0 μM and 0.42 μM, respectively, whereas the IC50s of Y-27632 and Y-39983 for CaMKII is 26 μM and 0.81 μM, respectively. The IC50s of Y-27632 and Y-39983 for PKC is 82 and 117 times those for ROCK, respectively, whereas the IC50s of Y-27632 and Y-39983 for CaMKII is 236 and 225 times those for ROCK, respectively[1]. Y-39983 (10 μM) extends neurites in the RGCs compared with those in RGCs treated without Y-39983[2].In rabbits and in monkeys, Y-39983 lowers IOP in a dose-dependent fashion[1]. An increase in regenerating axons of RGCs in 100 mM Y-39983-treated eyes is observed compared with saline-treated eyes. Y-39983 dose-dependently increases the number of RGCs with regenerating axons[2]. Both Y-27632 and Y-39983 induces a concentration-dependent relaxation in rabbit ciliary arteries precontracted with a high-potassium (high-K) solution. The amplitude of relaxation induced by Y-27632 and Y-39983 is not affected by either 100 μM N (G)-nitro-L: -arginine methyl ester (L: -NAME) or 10 μM indomethacin. In Ca2+-free solution, Y-27632 and Y-39983 significantly inhibits the transient contraction of ciliary arteries induced by 10 μM histamine. However, neither Y-27632 nor Y-39983 affects the elevation of [Ca2+](i) induced by high-K solution and histamine[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Y-33075 dihydrochloride|Cas Number: 173897-44-4| Catalog Number: DC10351|Other Nmaes: Y39983 hydrochlorid
Y-33075 dihydrochloride is a selective ROCK inhibitor derived from Y-27632, and is more potent than Y-27632.
In the examination of inhibition of PKC and CaMKII, the IC50s of Y-27632 and Y-39983 for PKC is 9.0 μM and 0.42 μM, respectively, whereas the IC50s of Y-27632 and Y-39983 for CaMKII is 26 μM and 0.81 μM, respectively. The IC50s of Y-27632 and Y-39983 for PKC is 82 and 117 times those for ROCK, respectively, whereas the IC50s of Y-27632 and Y-39983 for CaMKII is 236 and 225 times those for ROCK, respectively[1]. Y-39983 (10 μM) extends neurites in the RGCs compared with those in RGCs treated without Y-39983[2].In rabbits and in monkeys, Y-39983 lowers IOP in a dose-dependent fashion[1]. An increase in regenerating axons of RGCs in 100 mM Y-39983-treated eyes is observed compared with saline-treated eyes. Y-39983 dose-dependently increases the number of RGCs with regenerating axons[2]. Both Y-27632 and Y-39983 induces a concentration-dependent relaxation in rabbit ciliary arteries precontracted with a high-potassium (high-K) solution. The amplitude of relaxation induced by Y-27632 and Y-39983 is not affected by either 100 μM N (G)-nitro-L: -arginine methyl ester (L: -NAME) or 10 μM indomethacin. In Ca2+-free solution, Y-27632 and Y-39983 significantly inhibits the transient contraction of ciliary arteries induced by 10 μM histamine. However, neither Y-27632 nor Y-39983 affects the elevation of [Ca2+](i) induced by high-K solution and histamine[3].
UK-383367|cas: 348622-88-8
UK-383367|cas: 348622-88-8
DC Chemicals, Website: www.dcchemicals.com
Product Name: UK-383367|Cas Number: 348622-88-8| Catalog Number: DC10350|Other Nmaes: UK 383367; UK383367
UK-383367 (UK 383367) is a potent and selective inhibitor of BMP-1 (procollagen C-proteinase) with IC50 of 44 nM; Selective for BMP-1 over MMPs 1, 2, 3, 9 and 14 (IC50 values are >10,000 nM for listed MMPs).
DC Chemicals, Website: www.dcchemicals.com
Product Name: UK-383367|Cas Number: 348622-88-8| Catalog Number: DC10350|Other Nmaes: UK 383367; UK383367
UK-383367 (UK 383367) is a potent and selective inhibitor of BMP-1 (procollagen C-proteinase) with IC50 of 44 nM; Selective for BMP-1 over MMPs 1, 2, 3, 9 and 14 (IC50 values are >10,000 nM for listed MMPs).
Sumanirole maleate|cas: 179386-44-8
Sumanirole maleate|cas: 179386-44-8
DC Chemicals, Website: www.dcchemicals.com
Product Name: Sumanirole maleate|Cas Number: 179386-44-8| Catalog Number: DC10349|Other Nmaes: U95666E; PNU 95666; PNU 95666E; Sumanirole
Sumanirole maleate(PNU 95666E; U95666E) is a highly selective D2 receptor full agonist with an ED50 of about 46 nM.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Sumanirole maleate|Cas Number: 179386-44-8| Catalog Number: DC10349|Other Nmaes: U95666E; PNU 95666; PNU 95666E; Sumanirole
Sumanirole maleate(PNU 95666E; U95666E) is a highly selective D2 receptor full agonist with an ED50 of about 46 nM.
Vapreotide acetate|cas: 849479-74-9
Vapreotide acetate|cas: 849479-74-9
DC Chemicals, Website: www.dcchemicals.com
Product Name: Vapreotide acetate|Cas Number: 849479-74-9| Catalog Number: DC10348|Other Nmaes: RC-160 acetate; BMY-41606 acetate; RC160 acetate; BMY41606 acetate; RC 160 acetate; BMY 41606 acetate
Vapreotide acetate is a synthetic analog of somatostatin for the treatment of variceal bleeding; also exhibits antitumor activity.
Somatostatin is a peptide hormone which is distributed in many tissues including the immune system and the nervous system. Vapreotide attenuates the Substance P (SP)-triggered intracellular calcium increases and NF-κB activation in a dose-dependent manner. Vapreotide also inhibits SP-induced IL-8 and MCP-1 production in HEK293-NK1R and U373MG cell lines. Vapreotide inhibits HIV-1 infection of human MDM in vitro, an effect that is reversible by SP pretreatment[1]. Vapreotide significantly inhibits GH-, PRL, and/or alpha-subunit release by human GH-secreting pituitary adenoma cells in concentrations as low as 10-12-10-14 M. Vapreotide inhibits GH release with an IC50 of 0.1 pM[2]. Vapreotide exhibits moderate-to-high affinities for SSTR2, -3, and -5 (IC50=0.17, 0.1 and 21 nM, respectively) and low affinity for SSTR1 and -4 (IC50=200 and 620 nM, respectively). RC-160 inhibits serum-induced proliferation of CHO cells expressing SSTR2 and SSTR5 (EC50=53 and 150 pM, respectively)[3].In cirrhosis, bleeding by rupture of oesophagogastric varices is a severe complication of portal hypertension. The acute administration of vapreotide to rats decreases collateral circulation blood flow while chronic administration attenuated its development[4]. Tumor volumes and weights are reduced by about 40% by RC-160 by s.c. injections at doses of 100 μg/day/animal. Vapreotide can inhibit the growth of androgen-independent prostate cancer when the therapy is started at an early stage of tumor development[5].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Vapreotide acetate|Cas Number: 849479-74-9| Catalog Number: DC10348|Other Nmaes: RC-160 acetate; BMY-41606 acetate; RC160 acetate; BMY41606 acetate; RC 160 acetate; BMY 41606 acetate
Vapreotide acetate is a synthetic analog of somatostatin for the treatment of variceal bleeding; also exhibits antitumor activity.
Somatostatin is a peptide hormone which is distributed in many tissues including the immune system and the nervous system. Vapreotide attenuates the Substance P (SP)-triggered intracellular calcium increases and NF-κB activation in a dose-dependent manner. Vapreotide also inhibits SP-induced IL-8 and MCP-1 production in HEK293-NK1R and U373MG cell lines. Vapreotide inhibits HIV-1 infection of human MDM in vitro, an effect that is reversible by SP pretreatment[1]. Vapreotide significantly inhibits GH-, PRL, and/or alpha-subunit release by human GH-secreting pituitary adenoma cells in concentrations as low as 10-12-10-14 M. Vapreotide inhibits GH release with an IC50 of 0.1 pM[2]. Vapreotide exhibits moderate-to-high affinities for SSTR2, -3, and -5 (IC50=0.17, 0.1 and 21 nM, respectively) and low affinity for SSTR1 and -4 (IC50=200 and 620 nM, respectively). RC-160 inhibits serum-induced proliferation of CHO cells expressing SSTR2 and SSTR5 (EC50=53 and 150 pM, respectively)[3].In cirrhosis, bleeding by rupture of oesophagogastric varices is a severe complication of portal hypertension. The acute administration of vapreotide to rats decreases collateral circulation blood flow while chronic administration attenuated its development[4]. Tumor volumes and weights are reduced by about 40% by RC-160 by s.c. injections at doses of 100 μg/day/animal. Vapreotide can inhibit the growth of androgen-independent prostate cancer when the therapy is started at an early stage of tumor development[5].
Gestrinone|cas: 16320-04-0
Gestrinone|cas: 16320-04-0
DC Chemicals, Website: www.dcchemicals.com
Product Name: Gestrinone|Cas Number: 16320-04-0| Catalog Number: DC10347
Gestrinone (R2323) is a synthetic steroid hormone used to treat endometriosis. It inhibits leiomyoma cells with an IC50 of 43.67 μM.
Gestrinone binds to endometrial receptors for estrogen, progesterone and androgen, occupies all specific binding sites of steroids in the steroid target cells despite the presence of endogenous steroids[1]. Gestrinone exhibits stronger inhibitory effects on the growth of leiomyoma cells at 60 h than that at 20 and 40 h. Leiomyoma cells appears less dense, the cytoplasm is atrophic, the intercellular connections dwindled and nuclear aggregations are observed with more than 10 μM gestrinone treatment. Gestrinone treatment reduces the relative mRNA levels of estrogen α in a concentration dependent manner at concentrations of 0.1-3.0 μM[2].The estrogen-sensitive endpoints, vaginal keratinization and uterine progesterone receptor concentration, are enhanced by treatment with a combination of flutamide and either danazol or gestrinone. These data indicate that danazol and gestrinone have estrogenic activity that is masked by the androgenic component of these drugs[3]. The mean hormone binding globulin treated with gestrinone fell from 56.4 nM to 28.1 nM after one week’s treatment and to 7.1 nM after 4 weeks respectively[4].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Gestrinone|Cas Number: 16320-04-0| Catalog Number: DC10347
Gestrinone (R2323) is a synthetic steroid hormone used to treat endometriosis. It inhibits leiomyoma cells with an IC50 of 43.67 μM.
Gestrinone binds to endometrial receptors for estrogen, progesterone and androgen, occupies all specific binding sites of steroids in the steroid target cells despite the presence of endogenous steroids[1]. Gestrinone exhibits stronger inhibitory effects on the growth of leiomyoma cells at 60 h than that at 20 and 40 h. Leiomyoma cells appears less dense, the cytoplasm is atrophic, the intercellular connections dwindled and nuclear aggregations are observed with more than 10 μM gestrinone treatment. Gestrinone treatment reduces the relative mRNA levels of estrogen α in a concentration dependent manner at concentrations of 0.1-3.0 μM[2].The estrogen-sensitive endpoints, vaginal keratinization and uterine progesterone receptor concentration, are enhanced by treatment with a combination of flutamide and either danazol or gestrinone. These data indicate that danazol and gestrinone have estrogenic activity that is masked by the androgenic component of these drugs[3]. The mean hormone binding globulin treated with gestrinone fell from 56.4 nM to 28.1 nM after one week’s treatment and to 7.1 nM after 4 weeks respectively[4].
Coproporphyrin III|cas: 14643-66-4
Coproporphyrin III|cas: 14643-66-4
DC Chemicals, Website: www.dcchemicals.com
Product Name: Coproporphyrin III|Cas Number: 14643-66-4| Catalog Number: DC10346
Coproporphyrin III is a porphyrin derivative.
Coproporphyrin III methyl ester is repeatedly isolated in considerable amount from both feces and urine. A great increase of coproporphyrin III excretion is unaccompanied by symptoms or signs of porphyria, metal or chemical poisoning or liver disease[1]. Primary cultures of chick embryo hepatocytes have been used to study the mechanism by which chemicals cause accumulation of intermediates of the heme synthetic pathway. In the presence of the porphyrin precursor, 5-aminolevulinate (ALA), addition of insulin causes a striking increase in accumulation of uroporphyrin I and coproporphyrin III. Antioxidants abolishes the uroporphyrin I accumulation and increases coproporphyrin III[2].Urinary DMA and porphyrin profile can be used as an early warning biomarker for chronic MMA exposure before the onset of cancer. After 4 weeks the level of coproporphyrin III concentration significantly increases in all the treatment groups compared to the control[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Coproporphyrin III|Cas Number: 14643-66-4| Catalog Number: DC10346
Coproporphyrin III is a porphyrin derivative.
Coproporphyrin III methyl ester is repeatedly isolated in considerable amount from both feces and urine. A great increase of coproporphyrin III excretion is unaccompanied by symptoms or signs of porphyria, metal or chemical poisoning or liver disease[1]. Primary cultures of chick embryo hepatocytes have been used to study the mechanism by which chemicals cause accumulation of intermediates of the heme synthetic pathway. In the presence of the porphyrin precursor, 5-aminolevulinate (ALA), addition of insulin causes a striking increase in accumulation of uroporphyrin I and coproporphyrin III. Antioxidants abolishes the uroporphyrin I accumulation and increases coproporphyrin III[2].Urinary DMA and porphyrin profile can be used as an early warning biomarker for chronic MMA exposure before the onset of cancer. After 4 weeks the level of coproporphyrin III concentration significantly increases in all the treatment groups compared to the control[3].
PDE1-IN-2|cas: 1904611-63-7
PDE1-IN-2|cas: 1904611-63-7
DC Chemicals, Website: www.dcchemicals.com
Product Name: PDE1-IN-2|Cas Number: 1904611-63-7| Catalog Number: DC10345
PDE1-IN-2 is an inhibitor of PDE1 extracted from patent WO2016/55618 A1, example 31; has IC50 values of 6, 140 and 164 nM for PDE1C, PDE1B and PDE1A, respectvely.
DC Chemicals, Website: www.dcchemicals.com
Product Name: PDE1-IN-2|Cas Number: 1904611-63-7| Catalog Number: DC10345
PDE1-IN-2 is an inhibitor of PDE1 extracted from patent WO2016/55618 A1, example 31; has IC50 values of 6, 140 and 164 nM for PDE1C, PDE1B and PDE1A, respectvely.
HSP70-IN-1 |cas: 1268273-90-0
HSP70-IN-1 |cas: 1268273-90-0
DC Chemicals, Website: www.dcchemicals.com
Product Name: HSP70-IN-1|Cas Number: 1268273-90-0| Catalog Number: DC10344
HSP70-IN-1 is a heat shock protein (HSP) inhibitor; inhibits the growth of Kasumi-1 cells with an IC50 of 2.3 μM.
The heat shock protein 70 (Hsp70) is a molecular chaperone which plays an important function in protein homeostasis as well as in cell signaling and survival. Hsp70 is frequently overexpressed in cancer, where the elevated expression is furthermore believed to be a cause of or to lead to resistance to chemotherapy and other treatments. HSP70-IN-1 interferes with the formation of functional Hsp70-HOP-Hsp90 machinery by its ability to dose-dependently alter the megacomplex components and to destabilize an Hsp70-Hsp90 machinery client, Raf-1. In cells, the refolding of heat-denatured luciferase by endogenous as well as transfected Hsp70 is inhibited by HSP70-IN-1. HSP70-IN-1 also results in induction of apoptosis in cancer cells. Addition of HSP70-IN-1to cancer cells dose-dependently alters the formation of the Hsp70-HOP complex, a phenomenon associated with their destabilization and reduction in half-life[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: HSP70-IN-1|Cas Number: 1268273-90-0| Catalog Number: DC10344
HSP70-IN-1 is a heat shock protein (HSP) inhibitor; inhibits the growth of Kasumi-1 cells with an IC50 of 2.3 μM.
The heat shock protein 70 (Hsp70) is a molecular chaperone which plays an important function in protein homeostasis as well as in cell signaling and survival. Hsp70 is frequently overexpressed in cancer, where the elevated expression is furthermore believed to be a cause of or to lead to resistance to chemotherapy and other treatments. HSP70-IN-1 interferes with the formation of functional Hsp70-HOP-Hsp90 machinery by its ability to dose-dependently alter the megacomplex components and to destabilize an Hsp70-Hsp90 machinery client, Raf-1. In cells, the refolding of heat-denatured luciferase by endogenous as well as transfected Hsp70 is inhibited by HSP70-IN-1. HSP70-IN-1 also results in induction of apoptosis in cancer cells. Addition of HSP70-IN-1to cancer cells dose-dependently alters the formation of the Hsp70-HOP complex, a phenomenon associated with their destabilization and reduction in half-life[1].
Diquafosol tetrasodium|cas: 211427-08-6
Diquafosol tetrasodium|cas: 211427-08-6
DC Chemicals, Website: www.dcchemicals.com
Product Name: Diquafosol tetrasodium|Cas Number: 211427-08-6| Catalog Number: DC10343|Other Nmaes: INS365
Diquafosol tetrasodium is a P2Y2 receptor agonist that stimulates fluid and mucin secretion on the ocular surface, as a topical treatment of dry eye disease.
Cell viability significantly decreased after treatment with 30% diluted diquafosol for 1 hour and 6 hours after treatment with 10% and 20% diluted diquafosol. Twenty-four hours after wounding monolayers, 3% diquafosol, and 0.3% HCECs exhibits significantly more wound healing than the control[1].In a rat dry eye model, the P2Y2 agonist diquafosol tetrasodium is found to improve surface health, based on increases in tear fluid secretion, corneal epithelial resistance, and release of glycoprotein-containing moieties from goblet cells. Beginning at 2 weeks and continuing for an additional 2 weeks, maximal declines in dye penetrance of approximately 50% occurred with doses of diquafosol tetrasodium as low as 1%[2]. INS365 significantly suppresses corneal damage at concentrations of more than 0.1% w/v[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Diquafosol tetrasodium|Cas Number: 211427-08-6| Catalog Number: DC10343|Other Nmaes: INS365
Diquafosol tetrasodium is a P2Y2 receptor agonist that stimulates fluid and mucin secretion on the ocular surface, as a topical treatment of dry eye disease.
Cell viability significantly decreased after treatment with 30% diluted diquafosol for 1 hour and 6 hours after treatment with 10% and 20% diluted diquafosol. Twenty-four hours after wounding monolayers, 3% diquafosol, and 0.3% HCECs exhibits significantly more wound healing than the control[1].In a rat dry eye model, the P2Y2 agonist diquafosol tetrasodium is found to improve surface health, based on increases in tear fluid secretion, corneal epithelial resistance, and release of glycoprotein-containing moieties from goblet cells. Beginning at 2 weeks and continuing for an additional 2 weeks, maximal declines in dye penetrance of approximately 50% occurred with doses of diquafosol tetrasodium as low as 1%[2]. INS365 significantly suppresses corneal damage at concentrations of more than 0.1% w/v[3].
CHZ868 |cas: 1895895-38-1
CHZ868 |cas: 1895895-38-1
DC Chemicals, Website: www.dcchemicals.com
Product Name: CHZ868|Cas Number: 1895895-38-1| Catalog Number: DC10341|Other Nmaes: CHZ 868; CHZ-868
CHZ868 is a type II JAK2 inhibitor with an IC50 of 0.17 μM in EPOR JAK2 WT Ba/F3 cell.
CHZ868 potently inhibits constitutive JAK2 and STAT5 phosphorylation in JAK2V617F SET2 cells. CHZ868 potently inhibits the proliferation of SET2 cells (GI50=59nM), and has 6-fold less growth inhibitory activity against CMK cells (GI50=378nM)[1]. At 100 nM CHZ868 has activity against 26 kinases, including JAK2 and TYK2. CHZ868 is thought to engage with the hinge region of JAK2 through two H-bonds, formed between the amino-pyridine of CHZ868 and the backbone-NH/CO of L932, while the pyridine is occupying the adenine pocket of the ATP binding site. CHZ868 potently suppresses the growth of CRLF2-rearranged human B-ALL cells, abrogates JAK2 signaling[2].CHZ868 is characterized by high passive permeability, good metabolic stability, and low water solubility, as well as by moderate blood clearance and good oral bioavailability, making it suitable for in vivo use. CHZ868 improves survival in mice with human or murine B-ALL. CHZ868 and dexamethasone synergistically induces apoptosis in JAK2-dependent B-ALLs and further improves survival compared to CHZ868 alone[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: CHZ868|Cas Number: 1895895-38-1| Catalog Number: DC10341|Other Nmaes: CHZ 868; CHZ-868
CHZ868 is a type II JAK2 inhibitor with an IC50 of 0.17 μM in EPOR JAK2 WT Ba/F3 cell.
CHZ868 potently inhibits constitutive JAK2 and STAT5 phosphorylation in JAK2V617F SET2 cells. CHZ868 potently inhibits the proliferation of SET2 cells (GI50=59nM), and has 6-fold less growth inhibitory activity against CMK cells (GI50=378nM)[1]. At 100 nM CHZ868 has activity against 26 kinases, including JAK2 and TYK2. CHZ868 is thought to engage with the hinge region of JAK2 through two H-bonds, formed between the amino-pyridine of CHZ868 and the backbone-NH/CO of L932, while the pyridine is occupying the adenine pocket of the ATP binding site. CHZ868 potently suppresses the growth of CRLF2-rearranged human B-ALL cells, abrogates JAK2 signaling[2].CHZ868 is characterized by high passive permeability, good metabolic stability, and low water solubility, as well as by moderate blood clearance and good oral bioavailability, making it suitable for in vivo use. CHZ868 improves survival in mice with human or murine B-ALL. CHZ868 and dexamethasone synergistically induces apoptosis in JAK2-dependent B-ALLs and further improves survival compared to CHZ868 alone[2].
ISA-2011B|cas: 1395347-24-6
ISA-2011B|cas: 1395347-24-6
DC Chemicals, Website: www.dcchemicals.com
Product Name: ISA-2011B|Cas Number: 1395347-24-6| Catalog Number: DC10340|Other Nmaes: ISA2011B; ISA 2011B
ISA-2011B is a PIP5Kα inhibitor with promising anticancer effects .
The proliferation rate of PC-3 cells after treatment with ISA-2011B at 10, 20, and 50 μM is significantly reduced to 58.77%, 48.65%, and 21.62% of vehicle-treated controls, respectively. ISA-2011B exhibits the highest binding affinity to PIP5K1α, and to MAP/microtubule affinity-regulating kinase 1 and 4 (MARK1 and MARK4) across 460 kinases. ISA-2011B treatment inhibits PIP5K1α expression by 78.6% in PC-3 cells[1]. ISA-2011B leads to a remarkable reduction in AR-V7 and CDK1 in both nucleus and cytoplasm of 22Rv1 cells. ISA-2011B treatment also abolishes AR expression in the nucleus, without depleting the cytoplasmic AR[2].ISA-2011B significantly inhibits growth of tumor cells in xenograft mice, and is mediated by targeting PIP5K1α-associated PI3K/AKT and the downstream survival, proliferation, and invasion pathways[1]. Overexpression of AR-V7 increases PIP5K1α, promotes rapid growth of PCa in xenograft mice, whereas inhibition of PIP5K1α by its inhibitor ISA-2011B suppresses the growth and invasiveness of xenograft tumors overexpressing AR-V7. ISA-2011B disrupts protein stabilization of AR-V7 which is dependent on PIP5K1α, leading to suppression of invasive growth of AR-V7-high tumors in xenograft mice[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: ISA-2011B|Cas Number: 1395347-24-6| Catalog Number: DC10340|Other Nmaes: ISA2011B; ISA 2011B
ISA-2011B is a PIP5Kα inhibitor with promising anticancer effects .
The proliferation rate of PC-3 cells after treatment with ISA-2011B at 10, 20, and 50 μM is significantly reduced to 58.77%, 48.65%, and 21.62% of vehicle-treated controls, respectively. ISA-2011B exhibits the highest binding affinity to PIP5K1α, and to MAP/microtubule affinity-regulating kinase 1 and 4 (MARK1 and MARK4) across 460 kinases. ISA-2011B treatment inhibits PIP5K1α expression by 78.6% in PC-3 cells[1]. ISA-2011B leads to a remarkable reduction in AR-V7 and CDK1 in both nucleus and cytoplasm of 22Rv1 cells. ISA-2011B treatment also abolishes AR expression in the nucleus, without depleting the cytoplasmic AR[2].ISA-2011B significantly inhibits growth of tumor cells in xenograft mice, and is mediated by targeting PIP5K1α-associated PI3K/AKT and the downstream survival, proliferation, and invasion pathways[1]. Overexpression of AR-V7 increases PIP5K1α, promotes rapid growth of PCa in xenograft mice, whereas inhibition of PIP5K1α by its inhibitor ISA-2011B suppresses the growth and invasiveness of xenograft tumors overexpressing AR-V7. ISA-2011B disrupts protein stabilization of AR-V7 which is dependent on PIP5K1α, leading to suppression of invasive growth of AR-V7-high tumors in xenograft mice[2].
Vadadustat |cas: 1000025-07-9
Vadadustat |cas: 1000025-07-9
DC Chemicals, Website: www.dcchemicals.com
Product Name: Vadadustat|Cas Number: 1000025-07-9| Catalog Number: DC10339|Other Nmaes: PG-1016548; PG1016548; PG 1016548; AKB-6548
Vadadustat is a novel, titratable, oral hypoxia-inducible factor prolyl hydroxylase (HIF-PH) inhibitor in development for the treatment of anemia.
Vadadustat induces endogenous erythropoietin synthesis and enhances iron mobilization. Vadadustat is well-tolerated in healthy volunteers and patients with chronic kidney disease, where it increases reticulocytes, plasma EPO, and Hb levels in a dose-dependent manner. The increase in plasma EPO levels seen with vadadustat is comparable in magnitude to that occurring physiologically at moderate altitude and shows a normal diurnal pattern with a return to baseline levels prior to the next dose. Vadadustat improves iron homeostasis by decreasing hepcidin and increasing transferrin levels. once-daily oral administration of vadadustat, titrated to increase and maintain Hb in the target range, may provide multiple advantages over conventional ESAs[1]. Vadadustat is observed to have a half-life of approximately 4.5 hours. Overall, patients demonstrate an increase in Hb levels, from 9.91 g/dL at baseline to 10.54 g/dL by day 29. Ferritin levels decrease from 334.1 ng/mL at baseline to 271.7 ng/mL by day 29[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Vadadustat|Cas Number: 1000025-07-9| Catalog Number: DC10339|Other Nmaes: PG-1016548; PG1016548; PG 1016548; AKB-6548
Vadadustat is a novel, titratable, oral hypoxia-inducible factor prolyl hydroxylase (HIF-PH) inhibitor in development for the treatment of anemia.
Vadadustat induces endogenous erythropoietin synthesis and enhances iron mobilization. Vadadustat is well-tolerated in healthy volunteers and patients with chronic kidney disease, where it increases reticulocytes, plasma EPO, and Hb levels in a dose-dependent manner. The increase in plasma EPO levels seen with vadadustat is comparable in magnitude to that occurring physiologically at moderate altitude and shows a normal diurnal pattern with a return to baseline levels prior to the next dose. Vadadustat improves iron homeostasis by decreasing hepcidin and increasing transferrin levels. once-daily oral administration of vadadustat, titrated to increase and maintain Hb in the target range, may provide multiple advantages over conventional ESAs[1]. Vadadustat is observed to have a half-life of approximately 4.5 hours. Overall, patients demonstrate an increase in Hb levels, from 9.91 g/dL at baseline to 10.54 g/dL by day 29. Ferritin levels decrease from 334.1 ng/mL at baseline to 271.7 ng/mL by day 29[2].
Bradykinin|cas: 58-82-2
Bradykinin|cas: 58-82-2
DC Chemicals, Website: www.dcchemicals.com
Product Name: Bradykinin|Cas Number: 58-82-2| Catalog Number: DC10338
Bradykinin is an active peptide that is generated by the kallikrein-kinin system. It is a inflammatory mediator and also recognized as a neuromediator and regulator of several vascular and renal functions.
Bradykinin is a potent vasodilator peptide that exerts its vasodilatory action through stimulation of specific endothelial B2 receptors, thereby causing the release of prostacyclin, NO, and EDHF[1]. Bradykinin has been reported to be involved in the progression of many types of cancer. Bradykinin treatment promotes the invasion and migration of colorectal cancer cells. Bradykinin treatment stimulates ERK1/2 activation and IL-6 production[2]. Exogenous bradykinin markedly inhibits TF expression in mRNA and protein level induced by LPS in a dose-dependent manner. The NO synthase antagonist L-NAME and PI3K inhibitor LY294002 dramatically abolish the inhibitory effects of bradykinin on tissue factor expression[3].Application of 1 μM bradykinin to the ovary produces significant decreases in heart rate and mean arterial pressure. In vagotomized animals, application of 1 μM bradykinin to the ovary produces bradycardia and hypotension similar to the responses evoked when vagal innervation is intact[4]. Vascular bradykinin can improve pancreatic microcirculation and hemorheology in rats with severe acute pancreatitis. The pancreatic microcirculatory blood flow volume and velocity in the vascular bradykinin treatment group increases gradually after 48 h[5]. PI3K/Akt signaling pathway activation induced by bradykinin administration reduces the activity of GSK-3β and MAPK, and reduces NF-x03BA;B level in the nucleus, thereby inhibiting TF expression. Consistent with this, intraperitoneal injection of C57/BL6 mice with bradykinin also inhibits the thrombus formation induced by ligation of inferior vena cava[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Bradykinin|Cas Number: 58-82-2| Catalog Number: DC10338
Bradykinin is an active peptide that is generated by the kallikrein-kinin system. It is a inflammatory mediator and also recognized as a neuromediator and regulator of several vascular and renal functions.
Bradykinin is a potent vasodilator peptide that exerts its vasodilatory action through stimulation of specific endothelial B2 receptors, thereby causing the release of prostacyclin, NO, and EDHF[1]. Bradykinin has been reported to be involved in the progression of many types of cancer. Bradykinin treatment promotes the invasion and migration of colorectal cancer cells. Bradykinin treatment stimulates ERK1/2 activation and IL-6 production[2]. Exogenous bradykinin markedly inhibits TF expression in mRNA and protein level induced by LPS in a dose-dependent manner. The NO synthase antagonist L-NAME and PI3K inhibitor LY294002 dramatically abolish the inhibitory effects of bradykinin on tissue factor expression[3].Application of 1 μM bradykinin to the ovary produces significant decreases in heart rate and mean arterial pressure. In vagotomized animals, application of 1 μM bradykinin to the ovary produces bradycardia and hypotension similar to the responses evoked when vagal innervation is intact[4]. Vascular bradykinin can improve pancreatic microcirculation and hemorheology in rats with severe acute pancreatitis. The pancreatic microcirculatory blood flow volume and velocity in the vascular bradykinin treatment group increases gradually after 48 h[5]. PI3K/Akt signaling pathway activation induced by bradykinin administration reduces the activity of GSK-3β and MAPK, and reduces NF-x03BA;B level in the nucleus, thereby inhibiting TF expression. Consistent with this, intraperitoneal injection of C57/BL6 mice with bradykinin also inhibits the thrombus formation induced by ligation of inferior vena cava[3].
CEP-40783|cas: 1437321-24-8
CEP-40783|cas: 1437321-24-8
DC Chemicals, Website: www.dcchemicals.com
Product Name: CEP-40783|Cas Number: 1437321-24-8| Catalog Number: DC10337|Other Nmaes: CEP 40783; CEP40783; RXDX-1063
CEP-40783 is a potent, selective and orally available inhibitor of AXL and c-Met with IC50 values of 7 nM and 12 nM, respectively.
In AXL-transfected 293GT cells, CEP-40783 is 27-fold more active compared to recombinant enzyme with an IC50 value of 0.26 nM. CEP-40783 also demonstrates superior activity against c-Met in GTL-16 cells (IC50=6 nM). The increased inhibitory activity of CEP-40783 in cells could be attributed to its extended residence time on both AXL and c-Met, consistent with a Type II mechanism. CEP-40783 shows high kinome selectivity against 298 kinases with an S90 of 0.04 (fraction of kinases showing >90% inhibition at 1 µM)[1].CEP-40783 shows dose- and time-dependent inhibition of AXL phosphorylation using NCI-H1299 NSCL xenografts with 80% target inhibition at 0.3 mg/kg 6 h post dose and complete target inhibition to >90% inhibition at 1 mg/kg between 6-24 h, while a 10 mg/kg po dose resulted in complete AXL inhibition up to 48 h post dosing[1]. In 3/5 (60%) of the tumor models, CEP-40783 shows in vivo efficacy, including tumor regressions, significantly superior to that achieved with an optimal regimen of paclitaxel. In 4/4 (100%) of the erlotinib-insensitive tumor models, CEP-40783 demonstrates significant efficacy (66 to 118% TGI) compared to the control group at the 30 mg/kg dose. Additionally, CEP-40783 in combination with erlotinib demonstrate superior anti-tumor efficacy compared to CEP-40783 and erlotinib single agents in the one erlotinib-sensitive model evaluated. CEP-40783 as a single agent and in combination with erlotinib are well tolerated[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: CEP-40783|Cas Number: 1437321-24-8| Catalog Number: DC10337|Other Nmaes: CEP 40783; CEP40783; RXDX-1063
CEP-40783 is a potent, selective and orally available inhibitor of AXL and c-Met with IC50 values of 7 nM and 12 nM, respectively.
In AXL-transfected 293GT cells, CEP-40783 is 27-fold more active compared to recombinant enzyme with an IC50 value of 0.26 nM. CEP-40783 also demonstrates superior activity against c-Met in GTL-16 cells (IC50=6 nM). The increased inhibitory activity of CEP-40783 in cells could be attributed to its extended residence time on both AXL and c-Met, consistent with a Type II mechanism. CEP-40783 shows high kinome selectivity against 298 kinases with an S90 of 0.04 (fraction of kinases showing >90% inhibition at 1 µM)[1].CEP-40783 shows dose- and time-dependent inhibition of AXL phosphorylation using NCI-H1299 NSCL xenografts with 80% target inhibition at 0.3 mg/kg 6 h post dose and complete target inhibition to >90% inhibition at 1 mg/kg between 6-24 h, while a 10 mg/kg po dose resulted in complete AXL inhibition up to 48 h post dosing[1]. In 3/5 (60%) of the tumor models, CEP-40783 shows in vivo efficacy, including tumor regressions, significantly superior to that achieved with an optimal regimen of paclitaxel. In 4/4 (100%) of the erlotinib-insensitive tumor models, CEP-40783 demonstrates significant efficacy (66 to 118% TGI) compared to the control group at the 30 mg/kg dose. Additionally, CEP-40783 in combination with erlotinib demonstrate superior anti-tumor efficacy compared to CEP-40783 and erlotinib single agents in the one erlotinib-sensitive model evaluated. CEP-40783 as a single agent and in combination with erlotinib are well tolerated[2].
Coenzyme Q9|cas: 303-97-9
Coenzyme Q9|cas: 303-97-9
DC Chemicals, Website: www.dcchemicals.com
Product Name: Coenzyme Q9|Cas Number: 303-97-9| Catalog Number: DC10336|Other Nmaes: Ubiquinone Q9; CoQ9; Ubiquinone 9
Coenzyme Q9, a nine isoprenyl group-containing member of the ubiquinone family, is a normal constituent of human plasma.
Both CoQ9 and CoQ10 are equally cardioprotective, as evidenced by their abilities to improve left ventricular performance and to reduce myocardial infarct size and cardiomyocyte apoptosis. HPLC analysis reveals that a substantial portion of CoQ9 has been converted into CoQ10[1]. CoQ10 and CoQ9 are components of themitochondrial respiratory chain in mammals and can regulate some mitochondrial proteins/functions. Soybean, corn, and rapeseed oils are very rich sources of CoQ10, whereas CoQ9 has been found in high concentrations in corn oil[2].The lack of a functional CoQ9 protein in homozygous CoQ9 mutant (CoQ9(X/X)) mice causes a severe reduction in the CoQ7 protein and a widespread CoQ deficiency and accumulation of demethoxyubiquinone. The deficit in CoQ induces a brain-specific impairment of mitochondrial bioenergetics performance, a reduction in respiratory control ratio, ATP levels and ATP/ADP ratio and specific loss of respiratory complex I. These effects lead to neuronal death and demyelinization with severe vacuolization and astrogliosis in the brain of CoQ9 (X/X) mice that consequently die between 3 and 6 months of age[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Coenzyme Q9|Cas Number: 303-97-9| Catalog Number: DC10336|Other Nmaes: Ubiquinone Q9; CoQ9; Ubiquinone 9
Coenzyme Q9, a nine isoprenyl group-containing member of the ubiquinone family, is a normal constituent of human plasma.
Both CoQ9 and CoQ10 are equally cardioprotective, as evidenced by their abilities to improve left ventricular performance and to reduce myocardial infarct size and cardiomyocyte apoptosis. HPLC analysis reveals that a substantial portion of CoQ9 has been converted into CoQ10[1]. CoQ10 and CoQ9 are components of themitochondrial respiratory chain in mammals and can regulate some mitochondrial proteins/functions. Soybean, corn, and rapeseed oils are very rich sources of CoQ10, whereas CoQ9 has been found in high concentrations in corn oil[2].The lack of a functional CoQ9 protein in homozygous CoQ9 mutant (CoQ9(X/X)) mice causes a severe reduction in the CoQ7 protein and a widespread CoQ deficiency and accumulation of demethoxyubiquinone. The deficit in CoQ induces a brain-specific impairment of mitochondrial bioenergetics performance, a reduction in respiratory control ratio, ATP levels and ATP/ADP ratio and specific loss of respiratory complex I. These effects lead to neuronal death and demyelinization with severe vacuolization and astrogliosis in the brain of CoQ9 (X/X) mice that consequently die between 3 and 6 months of age[3].
BGB-3111|cas: 1633350-06-7
BGB-3111|cas: 1633350-06-7
DC Chemicals, Website: www.dcchemicals.com
Product Name: BGB-3111|Cas Number: 1633350-06-7| Catalog Number: DC10335|Other Nmaes: BGB3111; BGB 3111
BGB-3111 is a potent, selective and orally available Bruton's tyrosine kinase (Btk) inhibitor.
In both biochemical and cellular assays, BGB-3111 demonstrates nanomolar Btk inhibition activity. In several MCL and DLBCL cell lines, BGB-3111 inhibits BCR aggregation-triggered Btk autophosphorylation, blocks downstream PLC-γ2 signaling, and potently inhibits cell proliferation. In comparison with ibrutinib, BGB-3111 shows much more restricted off-target activities against a panel of kinases, including ITK. BGB-3111 is at least 10-fold weaker than ibrutinib in inhibiting rituximab induced ADCC, consistent with its weak ITK inhibition activity[1].BGB-3111 induces dose-dependent anti-tumor effects against REC-1 MCL xenografts engrafted either subcutaneously or systemically via tail vein injection in mice. In the subcutaneous xenografts. Preliminary 14-day toxicity study in rats shows that BGB-3111 is very well tolerated and maximal tolerate dose (MTD) is not reached when it is dosed up to 250mg/kg/day[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: BGB-3111|Cas Number: 1633350-06-7| Catalog Number: DC10335|Other Nmaes: BGB3111; BGB 3111
BGB-3111 is a potent, selective and orally available Bruton's tyrosine kinase (Btk) inhibitor.
In both biochemical and cellular assays, BGB-3111 demonstrates nanomolar Btk inhibition activity. In several MCL and DLBCL cell lines, BGB-3111 inhibits BCR aggregation-triggered Btk autophosphorylation, blocks downstream PLC-γ2 signaling, and potently inhibits cell proliferation. In comparison with ibrutinib, BGB-3111 shows much more restricted off-target activities against a panel of kinases, including ITK. BGB-3111 is at least 10-fold weaker than ibrutinib in inhibiting rituximab induced ADCC, consistent with its weak ITK inhibition activity[1].BGB-3111 induces dose-dependent anti-tumor effects against REC-1 MCL xenografts engrafted either subcutaneously or systemically via tail vein injection in mice. In the subcutaneous xenografts. Preliminary 14-day toxicity study in rats shows that BGB-3111 is very well tolerated and maximal tolerate dose (MTD) is not reached when it is dosed up to 250mg/kg/day[1].
ARV-771|cas: 1949837-12-0
ARV-771|cas: 1949837-12-0
DC Chemicals, Website: www.dcchemicals.com
Product Name: ARV-771|Cas Number: 1949837-12-0| Catalog Number: DC10334|Other Nmaes: ARV 771; ARV771
ARV-771 is a potent bromodomain and extra-terminal (BET) proteins degrader with Kd values of 4.7, 7.6, 7.6 nM against bromodomain 2, 3 and 4, respectively.
ARV-771 potently degrades BRD2/3/4 in 22Rv1 cells with a DC50 less than 5 nM. c-MYC protein is a downstream effector of BET proteins. Treatment with ARV-771 results in depletion of c-MYC with an IC50 of less than 1 nM. ARV-771 shows strong antiproliferative effect on 22Rv1, VCaP, and LnCaP95 cell lines. ARV-771 treatment has a pronounced effect on cell morphology consistent with apoptosis. FL-AR and AR-V7 mRNA are down-regulated upon treatment with 10 nM ARV-771 in VCaP cells. ARV-771 has an antiandrogenic effect on a number of AR-regulated genes in VCaP cells[1].Treatment of non castrated male Nu/Nu mice bearing AR-V7+ 22Rv1 tumor xenografts with daily subcutaneous injections of ARV-771 at 10 mg/kg for 3 d results in 37% and 76% down-regulation of BRD4 and c-MYC levels, respectively, in tumor tissue. A marked down-regulation in levels of AR-V7 is observed in the 22Rv1 tumors after ARV-771 treatment[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: ARV-771|Cas Number: 1949837-12-0| Catalog Number: DC10334|Other Nmaes: ARV 771; ARV771
ARV-771 is a potent bromodomain and extra-terminal (BET) proteins degrader with Kd values of 4.7, 7.6, 7.6 nM against bromodomain 2, 3 and 4, respectively.
ARV-771 potently degrades BRD2/3/4 in 22Rv1 cells with a DC50 less than 5 nM. c-MYC protein is a downstream effector of BET proteins. Treatment with ARV-771 results in depletion of c-MYC with an IC50 of less than 1 nM. ARV-771 shows strong antiproliferative effect on 22Rv1, VCaP, and LnCaP95 cell lines. ARV-771 treatment has a pronounced effect on cell morphology consistent with apoptosis. FL-AR and AR-V7 mRNA are down-regulated upon treatment with 10 nM ARV-771 in VCaP cells. ARV-771 has an antiandrogenic effect on a number of AR-regulated genes in VCaP cells[1].Treatment of non castrated male Nu/Nu mice bearing AR-V7+ 22Rv1 tumor xenografts with daily subcutaneous injections of ARV-771 at 10 mg/kg for 3 d results in 37% and 76% down-regulation of BRD4 and c-MYC levels, respectively, in tumor tissue. A marked down-regulation in levels of AR-V7 is observed in the 22Rv1 tumors after ARV-771 treatment[1].
PTP1B-IN-2｜PTP1B inhibitor｜cas 1919853-46-5
PTP1B-IN-2｜PTP1B inhibitor｜cas 1919853-46-5
DC Chemicals, Website: www.dcchemicals.com
Product Name: PTP1B-IN-2|Cas Number: 1919853-46-5| Catalog Number: DC10333|Other Nmaes: PTP1B-IN-2,PTP1B inhibitor 2
PTP1B-IN-2 is a novel protein tyrosine phosphatase-1B (PTP1B) inhibitor
DC Chemicals, Website: www.dcchemicals.com
Product Name: PTP1B-IN-2|Cas Number: 1919853-46-5| Catalog Number: DC10333|Other Nmaes: PTP1B-IN-2,PTP1B inhibitor 2
PTP1B-IN-2 is a novel protein tyrosine phosphatase-1B (PTP1B) inhibitor
MT-DADMe-ImmA|cas 653592-04-2
MT-DADMe-ImmA|cas 653592-04-2
DC Chemicals, Website: www.dcchemicals.com
Product Name: MT-DADMe-ImmA|Cas Number: 653592-04-2| Catalog Number: DC10332|Other Nmaes: Methylthio-DADMe-Immucillin A; MTDIA
MT-DADMe-ImmA is an inhibitor of human 5'-methylthioadenosine phosphorylase (MTAP) with a Ki of 90 pM.
Treatment of cultured cells with MT-DADMe-ImmA and MTA inhibit MTAP, increase cellular MTA concentrations, decrease polyamines, and induce apoptosis in FaDu and Cal27, two head and neck squamous cell carcinoma cell lines. The same treatment does not induce apoptosis in normal human fibroblast cell lines (CRL2522 and GM02037) or in MCF7, a breast cancer cell line with an MTAP gene deletion. MT-DADMe-ImmA alone does not induce apoptosis in any cell line, implicating MTA as the active agent[2].The t1/2 for onset of inhibition is 50 min with complete inhibition by 250 min. MTAP activity slowly returns, giving a biological half-life for the action of oral MT-DADMe-ImmA of 6.3 days. The time-dependent growth of FaDu tumors in immunodeficient mice is suppressed by oral or intraperitoneal treatment with MT-DADMe-ImmA[2].
DC Chemicals, Website: www.dcchemicals.com
Product Name: MT-DADMe-ImmA|Cas Number: 653592-04-2| Catalog Number: DC10332|Other Nmaes: Methylthio-DADMe-Immucillin A; MTDIA
MT-DADMe-ImmA is an inhibitor of human 5'-methylthioadenosine phosphorylase (MTAP) with a Ki of 90 pM.
Treatment of cultured cells with MT-DADMe-ImmA and MTA inhibit MTAP, increase cellular MTA concentrations, decrease polyamines, and induce apoptosis in FaDu and Cal27, two head and neck squamous cell carcinoma cell lines. The same treatment does not induce apoptosis in normal human fibroblast cell lines (CRL2522 and GM02037) or in MCF7, a breast cancer cell line with an MTAP gene deletion. MT-DADMe-ImmA alone does not induce apoptosis in any cell line, implicating MTA as the active agent[2].The t1/2 for onset of inhibition is 50 min with complete inhibition by 250 min. MTAP activity slowly returns, giving a biological half-life for the action of oral MT-DADMe-ImmA of 6.3 days. The time-dependent growth of FaDu tumors in immunodeficient mice is suppressed by oral or intraperitoneal treatment with MT-DADMe-ImmA[2].
Tebanicline hydrochloride|cas 203564-54-9
Tebanicline hydrochloride|cas 203564-54-9
DC Chemicals, Website: www.dcchemicals.com
Product Name: Tebanicline hydrochloride|Cas Number: 203564-54-9| Catalog Number: DC10331|Other Nmaes: Ebanicline hydrochloride; ABT594 hydrochloride; ABT-594 hydrochloride; ABT 594 hydrochloride
Tebanicline hydrochloride (ABT594 hydrochloride) is a nAChR modulator with potent, orally effective analgesic activity. It inhibits the binding of cytisine to α4β2 neuronal nAChRs with a Ki of 37 pM.
Tebanicline is a novel, potent cholinergic nAChR ligand with analgesic properties that shows preferential selectivity for neuronal nAChRs. It inhibits the binding of cytisine to α4β2 neuronal nAChRs with a Ki of 37 pM. Functionally, tebanicline is an agonist. At the transfected human α4β2 neuronal nAChR in K177 cells, with increased 86Rb+ efflux as a measure of cation efflux, ABT-594 has an EC50 value of 140 nM with an intrinsic activitycompared with (−)-nicotine of 130%; at the nAChR subtype expressed in IMR-32 cells, an EC50 of 340 nM; at the F11 dorsal root ganglion cell line, an EC50 of 1220 nM; and via direct measurement of ion currents, an EC50 value of 56,000 nM at the human α7 homo-oligimeric nAChR produced in oocytes[1]Tebanicline is a potent antinociceptive agent with full efficacy in models of acute and persistent pain and that these effects are mediated predominately by an action at central neuronal nAChRs[2]. Tebanicline produces significant antinociceptive effects in mice against both acute noxious thermal stimulation. ABT-594 is orally active, but 10-fold less potent by this route than after i.p. administration. The antinociceptive effect of ABT-594 is prevented, but not reversed, by the noncompetitive neuronal nicotinic acetylcholine receptor antagonist[3]. Tebanicline has antinociceptive effects in rat models of acute thermal, persistent chemical, and neuropathic pain. Direct injection of tebanicline into the nucleus raphe magnus (NRM) is antinociceptive in a thermal threshold test and destruction of serotonergic neurons in the NRM attenuates the effect of systemic tebanicline[4].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Tebanicline hydrochloride|Cas Number: 203564-54-9| Catalog Number: DC10331|Other Nmaes: Ebanicline hydrochloride; ABT594 hydrochloride; ABT-594 hydrochloride; ABT 594 hydrochloride
Tebanicline hydrochloride (ABT594 hydrochloride) is a nAChR modulator with potent, orally effective analgesic activity. It inhibits the binding of cytisine to α4β2 neuronal nAChRs with a Ki of 37 pM.
Tebanicline is a novel, potent cholinergic nAChR ligand with analgesic properties that shows preferential selectivity for neuronal nAChRs. It inhibits the binding of cytisine to α4β2 neuronal nAChRs with a Ki of 37 pM. Functionally, tebanicline is an agonist. At the transfected human α4β2 neuronal nAChR in K177 cells, with increased 86Rb+ efflux as a measure of cation efflux, ABT-594 has an EC50 value of 140 nM with an intrinsic activitycompared with (−)-nicotine of 130%; at the nAChR subtype expressed in IMR-32 cells, an EC50 of 340 nM; at the F11 dorsal root ganglion cell line, an EC50 of 1220 nM; and via direct measurement of ion currents, an EC50 value of 56,000 nM at the human α7 homo-oligimeric nAChR produced in oocytes[1]Tebanicline is a potent antinociceptive agent with full efficacy in models of acute and persistent pain and that these effects are mediated predominately by an action at central neuronal nAChRs[2]. Tebanicline produces significant antinociceptive effects in mice against both acute noxious thermal stimulation. ABT-594 is orally active, but 10-fold less potent by this route than after i.p. administration. The antinociceptive effect of ABT-594 is prevented, but not reversed, by the noncompetitive neuronal nicotinic acetylcholine receptor antagonist[3]. Tebanicline has antinociceptive effects in rat models of acute thermal, persistent chemical, and neuropathic pain. Direct injection of tebanicline into the nucleus raphe magnus (NRM) is antinociceptive in a thermal threshold test and destruction of serotonergic neurons in the NRM attenuates the effect of systemic tebanicline[4].
PD-1-Inhibitor-1 |cas 1673534-76-3|WO 2015033299
PD-1-Inhibitor-1 |cas 1673534-76-3|WO 2015033299
DC Chemicals, Website: www.dcchemicals.com
Product Name: PD-1-IN-1|Cas Number: 1673534-76-3| Catalog Number: DC10330
PD-1-IN-1 is an inhibitor of programmed cell dealth-1 (PD-1) extracted from patent WO 2015033299 A1, compound example 4.
DC Chemicals, Website: www.dcchemicals.com
Product Name: PD-1-IN-1|Cas Number: 1673534-76-3| Catalog Number: DC10330
PD-1-IN-1 is an inhibitor of programmed cell dealth-1 (PD-1) extracted from patent WO 2015033299 A1, compound example 4.
Glucagon|cas 16941-32-5
Glucagon|cas 16941-32-5
DC Chemicals, Website: www.dcchemicals.com
Product Name: Glucagon|Cas Number: 16941-32-5| Catalog Number: DC10329|Other Nmaes: Porcine glucagon
Glucagon is a peptide hormone, exhibits therapeutic potential for metabolic disease.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Glucagon|Cas Number: 16941-32-5| Catalog Number: DC10329|Other Nmaes: Porcine glucagon
Glucagon is a peptide hormone, exhibits therapeutic potential for metabolic disease.
Migalastat hydrochloride|cas 75172-81-5
Migalastat hydrochloride|cas 75172-81-5
DC Chemicals, Website: www.dcchemicals.com
Product Name: Migalastat hydrochloride|Cas Number: 75172-81-5| Catalog Number: DC10328|Other Nmaes: 1-Deoxygalactonojirimycin hydrochloride
Migalastat hydrochloride (1-Deoxygalactonojirimycin hydrochloride) is a potent and competitive inhibitor of α-galactosidase A (α-Gal A) with an IC50 of 0.04 μM for human α-Gal A.
Both IC50 and Ki values of migalastat hydrochloride toward human lysosomal a-Gal A are 0.04 μM[1].Fabry disease is an X-linked recessive disorder caused by the deficient activity of α-galactosidase A. α-Gal A activity in heart, kidney, spleen, and liver is increased dose- and time-dependently in transgenic mice that express human mutant alpha-Gal A with migalastat hydrochloride treatment. The half-life of DGJ is less than 1 day in all major issues and that of the enzyme synthesized during the DGJ treatment period is approximately 4 days[2]. Oral administration of migalastat hydrochloride reduces tissue GL-3 in fabry transgenic mice, and in urine and kidneys of some FD patients. Oral administration of migalastat hydrochloride to transgenic mice reduces elevated lyso-Gb3 levels up to 64%, 59%, and 81% in kidney, heart, and skin, respectively, generally equal to or greater than observed for GL-3[3].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Migalastat hydrochloride|Cas Number: 75172-81-5| Catalog Number: DC10328|Other Nmaes: 1-Deoxygalactonojirimycin hydrochloride
Migalastat hydrochloride (1-Deoxygalactonojirimycin hydrochloride) is a potent and competitive inhibitor of α-galactosidase A (α-Gal A) with an IC50 of 0.04 μM for human α-Gal A.
Both IC50 and Ki values of migalastat hydrochloride toward human lysosomal a-Gal A are 0.04 μM[1].Fabry disease is an X-linked recessive disorder caused by the deficient activity of α-galactosidase A. α-Gal A activity in heart, kidney, spleen, and liver is increased dose- and time-dependently in transgenic mice that express human mutant alpha-Gal A with migalastat hydrochloride treatment. The half-life of DGJ is less than 1 day in all major issues and that of the enzyme synthesized during the DGJ treatment period is approximately 4 days[2]. Oral administration of migalastat hydrochloride reduces tissue GL-3 in fabry transgenic mice, and in urine and kidneys of some FD patients. Oral administration of migalastat hydrochloride to transgenic mice reduces elevated lyso-Gb3 levels up to 64%, 59%, and 81% in kidney, heart, and skin, respectively, generally equal to or greater than observed for GL-3[3].
2017年11月29日星期三
Calcitonin salmon|cas 47931-85-1
Calcitonin salmon|cas 47931-85-1
DC Chemicals, Website: www.dcchemicals.com
Product Name: Calcitonin salmon|Cas Number: 47931-85-1| Catalog Number: DC10327|Other Nmaes: Salmon calcitonin
Calcitonin, Salmon is a calcium regulating hormone secreted from mammalian thyroid parafollicular cells and in non-mammalian species from the ultimobranchial gland.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Calcitonin salmon|Cas Number: 47931-85-1| Catalog Number: DC10327|Other Nmaes: Salmon calcitonin
Calcitonin, Salmon is a calcium regulating hormone secreted from mammalian thyroid parafollicular cells and in non-mammalian species from the ultimobranchial gland.
Mozavaptan |cas 137975-06-5
Mozavaptan |cas 137975-06-5
DC Chemicals, Website: www.dcchemicals.com
Product Name: Mozavaptan|Cas Number: 137975-06-5| Catalog Number: DC10326|Other Nmaes: OPC-31260; OPC31260l; OPC 31260
Mozavaptan (OPC31260) is a orally effective, nonpeptide vasopressin V2 receptor antagonist with an IC50 of 14 nM.
Mozavaptan causes a competitive displacement of [3H]-arginine vasopressin (AVP) binding to both V1 and V2 receptors with IC50 values of 1.2 μM and 14 nM, respectively. The Kd of [3H]-AVP is reduced significantly in both rat liver and kidney in the presence of mozavaptan (Kd=1.1 nM in liver, Kd=1.38 nM in kidney)[1].Mozavaptan at doses of 10 to 100 μg/kg, i.v., inhibits the antidiuretic action of exogenously administered arginine vasopressin in water-loaded, alcohol-anaesthetized rats in a dose-dependent manner. Mozavaptan does not exert an antidiuretic activity suggesting that it is not a partial V2 receptor agonist. Mozavaptan dose-dependently increases urine flow and decreases urine osmolality after oral administration at doses of 1 to 30 mg/kg in normal conscious rats[1].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Mozavaptan|Cas Number: 137975-06-5| Catalog Number: DC10326|Other Nmaes: OPC-31260; OPC31260l; OPC 31260
Mozavaptan (OPC31260) is a orally effective, nonpeptide vasopressin V2 receptor antagonist with an IC50 of 14 nM.
Mozavaptan causes a competitive displacement of [3H]-arginine vasopressin (AVP) binding to both V1 and V2 receptors with IC50 values of 1.2 μM and 14 nM, respectively. The Kd of [3H]-AVP is reduced significantly in both rat liver and kidney in the presence of mozavaptan (Kd=1.1 nM in liver, Kd=1.38 nM in kidney)[1].Mozavaptan at doses of 10 to 100 μg/kg, i.v., inhibits the antidiuretic action of exogenously administered arginine vasopressin in water-loaded, alcohol-anaesthetized rats in a dose-dependent manner. Mozavaptan does not exert an antidiuretic activity suggesting that it is not a partial V2 receptor agonist. Mozavaptan dose-dependently increases urine flow and decreases urine osmolality after oral administration at doses of 1 to 30 mg/kg in normal conscious rats[1].
Aviptadil|cas 40077-57-4
Aviptadil|cas 40077-57-4
DC Chemicals, Website: www.dcchemicals.com
Product Name: Aviptadil|Cas Number: 40077-57-4| Catalog Number: DC10325|Other Nmaes: Vasoactive Intestinal Peptide (human, rat, mouse, rabbit, canine, porcine)
Aviptadil (INN) is an analog of vasoactive intestinal polypeptide (VIP) for the treatment of erectile dysfunction.
DC Chemicals, Website: www.dcchemicals.com
Product Name: Aviptadil|Cas Number: 40077-57-4| Catalog Number: DC10325|Other Nmaes: Vasoactive Intestinal Peptide (human, rat, mouse, rabbit, canine, porcine)
Aviptadil (INN) is an analog of vasoactive intestinal polypeptide (VIP) for the treatment of erectile dysfunction.
Omapatrilat |cas 167305-00-2
Omapatrilat |cas 167305-00-2
DC Chemicals, Website: www.dcchemicals.com
Product Name: Omapatrilat|Cas Number: 167305-00-2| Catalog Number: DC10324|Other Nmaes: BMS-186716
Omapatrilat is a dual inhibitor of the metalloproteases ACE and NEP with Ki values of 0.64 and 0.45 nM, respectively.
Omapatrilat exhibits high potency for NEP, NEP2 and ACE, moderate strong activity against APP, but low activity against ECE1 (Ki=0.45, 25, 0.64, 250 nM) [1]. In vitro autoradiography using the specific NEP inhibitor radioligand 125I-RB104 and the specific ACE inhibitor radioligand 125I-MK351A show omapatril at (10 mg/kg) causes rapid and potent inhibition of renal NEP and ACE, respectively, for 24 h[4].Omapatrilat demonstrates excellent blood pressure lowering in a variety of animal models characterized by various levels of plasma renin activity and significantly potentiates urinary sodium, ANP, and cGMP excretion in a cynomolgus monkey assay. Omapatrilat decreases mean arterial pressure (MAP) approximately 40 mmHg below baseline from 10 to 24 h. Oral administration of omapatrilat at 100 μM/kg once daily results in a 38 mmHg decrease in systolic blood pressure at day three as compared to vehicle [2]. Omapatrilat is widely used in experimental protocols related to hypertension and heart failure. Chronic oral administration of omapatrilat reduces aortic leakiness and atheroma formation with enhanced endothelial independent vasorelaxation to ANP[3]. Omapatrilat causes significant inhibition of plasma ACE and increased plasma renin activity in rats[4].
DC Chemicals, Website: www.dcchemicals.com
Product Name: Omapatrilat|Cas Number: 167305-00-2| Catalog Number: DC10324|Other Nmaes: BMS-186716
Omapatrilat is a dual inhibitor of the metalloproteases ACE and NEP with Ki values of 0.64 and 0.45 nM, respectively.
Omapatrilat exhibits high potency for NEP, NEP2 and ACE, moderate strong activity against APP, but low activity against ECE1 (Ki=0.45, 25, 0.64, 250 nM) [1]. In vitro autoradiography using the specific NEP inhibitor radioligand 125I-RB104 and the specific ACE inhibitor radioligand 125I-MK351A show omapatril at (10 mg/kg) causes rapid and potent inhibition of renal NEP and ACE, respectively, for 24 h[4].Omapatrilat demonstrates excellent blood pressure lowering in a variety of animal models characterized by various levels of plasma renin activity and significantly potentiates urinary sodium, ANP, and cGMP excretion in a cynomolgus monkey assay. Omapatrilat decreases mean arterial pressure (MAP) approximately 40 mmHg below baseline from 10 to 24 h. Oral administration of omapatrilat at 100 μM/kg once daily results in a 38 mmHg decrease in systolic blood pressure at day three as compared to vehicle [2]. Omapatrilat is widely used in experimental protocols related to hypertension and heart failure. Chronic oral administration of omapatrilat reduces aortic leakiness and atheroma formation with enhanced endothelial independent vasorelaxation to ANP[3]. Omapatrilat causes significant inhibition of plasma ACE and increased plasma renin activity in rats[4].
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