BAY1217389;BAY-1217389|Mps1/TTK inhibitor
BAY1217389 is an orally bioavailable, selective inhibitor of the serine/threonine kinase monopolar spindle 1 (Mps1, TTK), with potential antineoplastic activity.
Product Name: BAY1217389|Cat No: DC9679|Cas: 1554458-53-5 |Molecule Formular: C27H24F5N5O3 |Molecule Weight: 561.51|Other names: BAY1217389
BAY1217389 is an orally bioavailable, selective inhibitor of the serine/threonine kinase monopolar spindle 1 (Mps1, TTK), with potential antineoplastic activity. Upon administration, the Mps1 inhibitor BAY 1217389 selectively binds to and inhibits the activity of Mps1. This inactivates the spindle assembly checkpoint (SAC), accelerates mitosis, causes chromosomal misalignment and missegregation, and mitotic checkpoint complex destabilization. This induces cell death in Mps1-overexpressing cancer cells.
For research only, not for human use.
2016年6月13日星期一
HLCL-61,HLCL61|PRMT5 inhibitor
HLCL-61,HLCL61|PRMT5 inhibitor
HLCL-61 is a first-in-class small-molecule inhibitor of PRMT5 for treatment of acute myeloid leukemia.
Product Name: HLCL-61 hydrochloride|Cat No: DC9678|Cas: 586395-74-6|Molecule Formular: C23H25ClN2O |Molecule Weight: 344.18|Other names: HLCL-61 hydrochloride
HLCL-61 is a potent and selective PRMT5 inhibitor for treatment of acute myeloid leukemia. HLCL-61 resulted in significantly increased expression of miR-29b and consequent suppression of Sp1 and FLT3 in AML (acute myeloid leukemia) cells. As a result, significant antileukemic activity was achieved. The increased PRMT5 activity enhanced AML growth in vitro and in vivo while PRMT5 downregulation reduced it. In AML cells, PRMT5 interacted with Sp1 in a transcription repressor complex and silenced miR-29b preferentially via dimethylation of histone 4 arginine residue H4R3.
For research only, not for human use.
HLCL-61 is a first-in-class small-molecule inhibitor of PRMT5 for treatment of acute myeloid leukemia.
Product Name: HLCL-61 hydrochloride|Cat No: DC9678|Cas: 586395-74-6|Molecule Formular: C23H25ClN2O |Molecule Weight: 344.18|Other names: HLCL-61 hydrochloride
HLCL-61 is a potent and selective PRMT5 inhibitor for treatment of acute myeloid leukemia. HLCL-61 resulted in significantly increased expression of miR-29b and consequent suppression of Sp1 and FLT3 in AML (acute myeloid leukemia) cells. As a result, significant antileukemic activity was achieved. The increased PRMT5 activity enhanced AML growth in vitro and in vivo while PRMT5 downregulation reduced it. In AML cells, PRMT5 interacted with Sp1 in a transcription repressor complex and silenced miR-29b preferentially via dimethylation of histone 4 arginine residue H4R3.
For research only, not for human use.
AL 082D06(D-06)|CAS 256925-03-8
AL 082D06(D-06)|CAS 256925-03-8
AL 082D06(D-06) is the first selective, nonsteroidal glucocorticoid receptor (GR) antagonist with Ki of 210 nM, exhibits excellent selectivity against AR, PR, MR and ER(Ki > 10 uM).
Product Name: AL 082D06(D-06)|Cat No: DC9677|Cas: 256925-03-8|Molecule Formular: C23H24ClN3O2|Molecule Weight: 409.91|Other names: AL 082D06(D-06)
AL 082D06(D-06) is the first selective, nonsteroidal glucocorticoid receptor (GR) antagonist with Ki of 210 nM, exhibits excellent selectivity against AR, PR, MR and ER(Ki > 10 uM).The antagonists NET, DO6 and UDCA, as well as the dissociated GC ligand CpdA (14%) resulted in little to no increase in S226 phosphorylation. The antagonists NET, DO6 and UDCA (13%, 8% and 21%), as well as the dissociated GC ligand CpdA (24%) resulted in little increase in S211 phosphorylation. D06 competes with 3H-Dex for baculovirus-expressed GR with nanomolar affinity. Other intracellular receptors (AR, ER, PR, and MR) have no affinity for D06 in a similarly structured binding assay with the appropriate receptor and tritiated ligand (>2500 nM). D06 can antagonize steroid-mediated induction of glutamine synthetase RNA in MG63 cells (data not shown) and TAT enzyme in human skin fibroblasts.
For research only, not for human use.
AL 082D06(D-06) is the first selective, nonsteroidal glucocorticoid receptor (GR) antagonist with Ki of 210 nM, exhibits excellent selectivity against AR, PR, MR and ER(Ki > 10 uM).
Product Name: AL 082D06(D-06)|Cat No: DC9677|Cas: 256925-03-8|Molecule Formular: C23H24ClN3O2|Molecule Weight: 409.91|Other names: AL 082D06(D-06)
AL 082D06(D-06) is the first selective, nonsteroidal glucocorticoid receptor (GR) antagonist with Ki of 210 nM, exhibits excellent selectivity against AR, PR, MR and ER(Ki > 10 uM).The antagonists NET, DO6 and UDCA, as well as the dissociated GC ligand CpdA (14%) resulted in little to no increase in S226 phosphorylation. The antagonists NET, DO6 and UDCA (13%, 8% and 21%), as well as the dissociated GC ligand CpdA (24%) resulted in little increase in S211 phosphorylation. D06 competes with 3H-Dex for baculovirus-expressed GR with nanomolar affinity. Other intracellular receptors (AR, ER, PR, and MR) have no affinity for D06 in a similarly structured binding assay with the appropriate receptor and tritiated ligand (>2500 nM). D06 can antagonize steroid-mediated induction of glutamine synthetase RNA in MG63 cells (data not shown) and TAT enzyme in human skin fibroblasts.
For research only, not for human use.
AT7519|AT 7519CAS 844442-38-2
AT7519|AT 7519CAS 844442-38-2
AT7519 is a multi-CDK inhibitor for CDK1, 2, 4, 6 and 9 with IC50 of 10-210 nM; less potent to CDK3 and little active to CDK7.
Product Name: AT7519|Cat No: DC9676|Cas: 844442-38-2|Molecule Formular: C16H17Cl2N5O2|Molecule Weight: 382.24|Other names: AT7519
AT7519 is a multi-CDK inhibitor for CDK1, 2, 4, 6 and 9 with IC50 of 10-210 nM; less potent to CDK3 and little active to CDK7.in vitro: AT7519 is an ATP competitive CDK inhibitor with a Ki value of 38 nM for CDK1. AT7519 is inactive against all non-CDK kinases with the exception of GSK3β (IC50 = 89 nM). AT7519 shows potent antiproliferative activity in a variety of human tumor cell lines with IC50 values ranging from 40 nM for MCF-7 to 940 nM for SW620 consistent with the inhibition of CDK1 and CDK2. AT7519 induces dose-dependent cytotoxicity in multiple myeloma (MM) cell lines with IC50 values ranging from 0.5 to 2 μM at 48 hours, with the most sensitive cell lines being MM.1S (0.5 μM) and U266 (0.5 μM) and the most resistant MM.1R (>2 μM). It does not induce cytotoxicity in peripheral blood mononuclear cells (PBMNC). AT7519 partially overcomes the proliferative advantage conferred by IL6 and IGF-1 as well as the protective effect of bone marrow stromal cells (BMSCs). AT7519 induces rapid dephosphorylation of RNA pol II CTD at serine 2 and serine 5 sites, and leads to the inhibition of transcription, partially contributing to AT7519 induced cytotoxicity of MM cells. AT7519 induces activation of GSK-3β by down-regulating GSK-3β phosphorylation, which also contributes to AT7519 induced apoptosis independent of the inhibition of transcription.
in vivo: A twice daily dosing of AT7519 (9.1 mg/kg) causes tumor regression of both early-stage and advanced-stage s.c. tumors in the HCT116 and HT29 colon cancer xenograft models. AT7519 treatment (15 mg/kg) inhibits tumor growth and prolongs the median overall survival of mice in the human MM xenograft mouse model in association with increased caspase 3 activation.
For research only, not for human use.
AT7519 is a multi-CDK inhibitor for CDK1, 2, 4, 6 and 9 with IC50 of 10-210 nM; less potent to CDK3 and little active to CDK7.
Product Name: AT7519|Cat No: DC9676|Cas: 844442-38-2|Molecule Formular: C16H17Cl2N5O2|Molecule Weight: 382.24|Other names: AT7519
AT7519 is a multi-CDK inhibitor for CDK1, 2, 4, 6 and 9 with IC50 of 10-210 nM; less potent to CDK3 and little active to CDK7.in vitro: AT7519 is an ATP competitive CDK inhibitor with a Ki value of 38 nM for CDK1. AT7519 is inactive against all non-CDK kinases with the exception of GSK3β (IC50 = 89 nM). AT7519 shows potent antiproliferative activity in a variety of human tumor cell lines with IC50 values ranging from 40 nM for MCF-7 to 940 nM for SW620 consistent with the inhibition of CDK1 and CDK2. AT7519 induces dose-dependent cytotoxicity in multiple myeloma (MM) cell lines with IC50 values ranging from 0.5 to 2 μM at 48 hours, with the most sensitive cell lines being MM.1S (0.5 μM) and U266 (0.5 μM) and the most resistant MM.1R (>2 μM). It does not induce cytotoxicity in peripheral blood mononuclear cells (PBMNC). AT7519 partially overcomes the proliferative advantage conferred by IL6 and IGF-1 as well as the protective effect of bone marrow stromal cells (BMSCs). AT7519 induces rapid dephosphorylation of RNA pol II CTD at serine 2 and serine 5 sites, and leads to the inhibition of transcription, partially contributing to AT7519 induced cytotoxicity of MM cells. AT7519 induces activation of GSK-3β by down-regulating GSK-3β phosphorylation, which also contributes to AT7519 induced apoptosis independent of the inhibition of transcription.
in vivo: A twice daily dosing of AT7519 (9.1 mg/kg) causes tumor regression of both early-stage and advanced-stage s.c. tumors in the HCT116 and HT29 colon cancer xenograft models. AT7519 treatment (15 mg/kg) inhibits tumor growth and prolongs the median overall survival of mice in the human MM xenograft mouse model in association with increased caspase 3 activation.
For research only, not for human use.
Pardoprunox.HCl(SLV-308)|CAS 269718-83-4
Pardoprunox.HCl(SLV-308)|CAS 269718-83-4
Pardoprunox hydrochloride is a novel partial dopamine D2 and D3 receptor agonist and serotonin 5-HT1A receptor agonist, D2 (pKi = 8.1) and D3 receptor (pKi = 8.6) partial agonist and 5-HT1A receptor (pKi = 8.5) full agonist.
Product Name: Pardoprunox.HCl(SLV-308)|Cat No: DC9675|Cas: 269718-83-4|Molecule Formular: C12H16ClN3O2|Molecule Weight: 269.73|Other names: Pardoprunox.HCl(SLV-308)
Pardoprunox hydrochloride is a novel partial dopamine D2 and D3 receptor agonist and serotonin 5-HT1A receptor agonist, D2 (pKi = 8.1) and D3 receptor (pKi = 8.6) partial agonist and 5-HT1A receptor (pKi = 8.5) full agonist.in vitro: Pardoprunox also binds to D4 (pKi = 7.8), α1-adrenergic (pKi = 7.8), α2-adrenergic (pKi = 7.4), and 5-HT7 receptors (pKi = 7.2) with lower affinity. Pardoprunox acts as a potent but partial D(2) receptor agonist (pEC50 = 8.0 and pA2 = 8.4) with an efficacy of 50% on forskolin stimulated cAMP accumulation. At human recombinant dopamine D3 receptors, Pardoprunox acts as a partial agonist in the induction of [35S]GTPgammaS binding (intrinsic activity of 67%; pEC(50) = 9.2) and antagonized the dopamine induction of [35S]GTPgammaS binding (pA2 = 9.0). Pardoprunox acts as a full 5-HT1A receptor agonist on forskolin induced cAMP accumulation at cloned human 5-HT1A receptors but with low potency (pEC50 = 6.3).
in vivo: Pardoprunox induces contralateral turning behaviour in rats with unilateral 6-hydroxydopamine-induced lesions of the substantia nigra pars compacta (SNpc) (MED=0.03mg/kg; po). In MPTP-treated common marmosets, Pardoprunox dose-dependently increases locomotor activity (MED=0.03mg/kg; po) and decreases motor disability (MED=0.03mg/kg; po). In contrast Pardoprunox attenuated novelty-induced locomotor activity (MED=0.01mg/kg; po), (+)-amphetamine-induced hyperlocomotion (MED=0.3mg/kg; po) and apomorphine-induced climbing (MED=0.6mg/kg; po) in rodents. Pardoprunox also induces 5-HT1A receptor-mediated behaviours, including flat body posture and lower lip retraction (MED=0.3mg/kg; po). Collectively, these findings demonstrate that Pardoprunox possesses dopamine D2/3 partial agonist effects, 5-HT1A agonist effects and reduces parkinsonism in animal models. functional D2 receptor partial agonist activity and is effective in experimental models predictive of efficacy in PD.
For research only, not for human use.
Pardoprunox hydrochloride is a novel partial dopamine D2 and D3 receptor agonist and serotonin 5-HT1A receptor agonist, D2 (pKi = 8.1) and D3 receptor (pKi = 8.6) partial agonist and 5-HT1A receptor (pKi = 8.5) full agonist.
Product Name: Pardoprunox.HCl(SLV-308)|Cat No: DC9675|Cas: 269718-83-4|Molecule Formular: C12H16ClN3O2|Molecule Weight: 269.73|Other names: Pardoprunox.HCl(SLV-308)
Pardoprunox hydrochloride is a novel partial dopamine D2 and D3 receptor agonist and serotonin 5-HT1A receptor agonist, D2 (pKi = 8.1) and D3 receptor (pKi = 8.6) partial agonist and 5-HT1A receptor (pKi = 8.5) full agonist.in vitro: Pardoprunox also binds to D4 (pKi = 7.8), α1-adrenergic (pKi = 7.8), α2-adrenergic (pKi = 7.4), and 5-HT7 receptors (pKi = 7.2) with lower affinity. Pardoprunox acts as a potent but partial D(2) receptor agonist (pEC50 = 8.0 and pA2 = 8.4) with an efficacy of 50% on forskolin stimulated cAMP accumulation. At human recombinant dopamine D3 receptors, Pardoprunox acts as a partial agonist in the induction of [35S]GTPgammaS binding (intrinsic activity of 67%; pEC(50) = 9.2) and antagonized the dopamine induction of [35S]GTPgammaS binding (pA2 = 9.0). Pardoprunox acts as a full 5-HT1A receptor agonist on forskolin induced cAMP accumulation at cloned human 5-HT1A receptors but with low potency (pEC50 = 6.3).
in vivo: Pardoprunox induces contralateral turning behaviour in rats with unilateral 6-hydroxydopamine-induced lesions of the substantia nigra pars compacta (SNpc) (MED=0.03mg/kg; po). In MPTP-treated common marmosets, Pardoprunox dose-dependently increases locomotor activity (MED=0.03mg/kg; po) and decreases motor disability (MED=0.03mg/kg; po). In contrast Pardoprunox attenuated novelty-induced locomotor activity (MED=0.01mg/kg; po), (+)-amphetamine-induced hyperlocomotion (MED=0.3mg/kg; po) and apomorphine-induced climbing (MED=0.6mg/kg; po) in rodents. Pardoprunox also induces 5-HT1A receptor-mediated behaviours, including flat body posture and lower lip retraction (MED=0.3mg/kg; po). Collectively, these findings demonstrate that Pardoprunox possesses dopamine D2/3 partial agonist effects, 5-HT1A agonist effects and reduces parkinsonism in animal models. functional D2 receptor partial agonist activity and is effective in experimental models predictive of efficacy in PD.
For research only, not for human use.
AJ-97166|CAS 746667-48-1
AJ-97166|CAS 746667-48-1
Product Name: AJ-97166|Cat No: DC9674|Cas: 746667-48-1|Molecule Formular: C17H13N5|Molecule Weight: 287.32|Other names: AJ-97166
For research only, not for human use.
Product Name: AJ-97166|Cat No: DC9674|Cas: 746667-48-1|Molecule Formular: C17H13N5|Molecule Weight: 287.32|Other names: AJ-97166
For research only, not for human use.
Eptapirone(F-11440)|CAS 179756-58-2
Eptapirone(F-11440)|CAS 179756-58-2
Eptapirone(F-11440) is a potent, selective, high efficacy 5-HT1A receptor agonist with marked anxiolytic and antidepressant potential.
Product Name: Eptapirone(F-11440)|Cat No: DC9673|Cas: 179756-58-2|Molecule Formular: C16H23N7O2|Molecule Weight: 345.4|Other names: Eptapirone(F-11440)
F 11440 is a potent, selective, high efficacy 5-HT1A receptor agonist with marked anxiolytic and antidepressant potential.The affinity of F 11440 for 5-HT1Abinding sites (pKi, 8.33) was higher than that of buspirone (pKi , 7.50), and somewhat lower than that of flesinoxan (pKi , 8.91).In vivo, F 11440 was 4- to 20-fold more potent than flesinoxan, and 30- to 60-fold more potent than buspirone, in exerting 5-HT1A agonist activity at pre- and postsynaptic receptors in rats (measured by, for example, its ability to decrease hippocampal extracellular serotonin (5-HT) levels and to increase plasma corticosterone levels, respectively). F 11440, shown here to be a potent, selective, high efficacy 5-HT1Areceptor agonist, appears to have the potential to exert marked anxiolytic and antidepressant activity in humans.
For research only, not for human use.
Eptapirone(F-11440) is a potent, selective, high efficacy 5-HT1A receptor agonist with marked anxiolytic and antidepressant potential.
Product Name: Eptapirone(F-11440)|Cat No: DC9673|Cas: 179756-58-2|Molecule Formular: C16H23N7O2|Molecule Weight: 345.4|Other names: Eptapirone(F-11440)
F 11440 is a potent, selective, high efficacy 5-HT1A receptor agonist with marked anxiolytic and antidepressant potential.The affinity of F 11440 for 5-HT1Abinding sites (pKi, 8.33) was higher than that of buspirone (pKi , 7.50), and somewhat lower than that of flesinoxan (pKi , 8.91).In vivo, F 11440 was 4- to 20-fold more potent than flesinoxan, and 30- to 60-fold more potent than buspirone, in exerting 5-HT1A agonist activity at pre- and postsynaptic receptors in rats (measured by, for example, its ability to decrease hippocampal extracellular serotonin (5-HT) levels and to increase plasma corticosterone levels, respectively). F 11440, shown here to be a potent, selective, high efficacy 5-HT1Areceptor agonist, appears to have the potential to exert marked anxiolytic and antidepressant activity in humans.
For research only, not for human use.
NSC5844 (RE640)|CAS 140926-75-6
NSC5844 (RE640)|CAS 140926-75-6
NSC5844 (RE640) is a bisquinoline compound with C-C chemokine receptor type 1 (CCR1)-agonistic properties.
Product Name: NSC5844 (RE640)|Cat No: DC9672|Cas: 140926-75-6|Molecule Formular: C20H16Cl2N4|Molecule Weight: 383.27|Other names: NSC5844 (RE640)
NSC5844 (RE640) is a bisquinoline compound with C-C chemokine receptor type 1 (CCR1)-agonistic properties.NSC5844 shows 3-fold increased activity in MDA-MB-468 cells (GI50 = 7.35 μM), compared to Chloroquine. NSC5844 shows lower activity (GI50 = 14.80 M) in the MCF-7 cell line.
For research only, not for human use.
NSC5844 (RE640) is a bisquinoline compound with C-C chemokine receptor type 1 (CCR1)-agonistic properties.
Product Name: NSC5844 (RE640)|Cat No: DC9672|Cas: 140926-75-6|Molecule Formular: C20H16Cl2N4|Molecule Weight: 383.27|Other names: NSC5844 (RE640)
NSC5844 (RE640) is a bisquinoline compound with C-C chemokine receptor type 1 (CCR1)-agonistic properties.NSC5844 shows 3-fold increased activity in MDA-MB-468 cells (GI50 = 7.35 μM), compared to Chloroquine. NSC5844 shows lower activity (GI50 = 14.80 M) in the MCF-7 cell line.
For research only, not for human use.
Trovirdine（LY300046）|CAS 149488-17-5
Trovirdine（LY300046）|CAS 149488-17-5
Trovirdine inhibits HIV-1 RT with an IC50 of 7 nM when employing heteropolymeric primer/template (oligo-DNA/ribosomal RNA)and dGTP as substrate.
Product Name: Trovirdine（LY300046）|Cat No: DC9671|Cas: 149488-17-5|Molecule Formular: C13H13BrN4S|Molecule Weight: 337.24|Other names: Trovirdine（LY300046）
Trovirdine inhibits HIV-1 RT with an IC50 of 7 nM when employing heteropolymeric primer/template (oligo-DNA/ribosomal RNA)and dGTP as substrate.Trovirdine is currently in phase I clinical trials for potential use in thetreatment of AIDS.
For research only, not for human use.
Trovirdine inhibits HIV-1 RT with an IC50 of 7 nM when employing heteropolymeric primer/template (oligo-DNA/ribosomal RNA)and dGTP as substrate.
Product Name: Trovirdine（LY300046）|Cat No: DC9671|Cas: 149488-17-5|Molecule Formular: C13H13BrN4S|Molecule Weight: 337.24|Other names: Trovirdine（LY300046）
Trovirdine inhibits HIV-1 RT with an IC50 of 7 nM when employing heteropolymeric primer/template (oligo-DNA/ribosomal RNA)and dGTP as substrate.Trovirdine is currently in phase I clinical trials for potential use in thetreatment of AIDS.
For research only, not for human use.
BIBS39|BIBS 39|CAS 133085-33-3
BIBS39|BIBS 39|CAS 133085-33-3
BIBS 39 is a new nonpeptide angiotensin II (AII) receptor antagonist.
Product Name: BIBS39|Cat No: DC9670|Cas: 133085-33-3|Molecule Formular: C32H36N4O3|Molecule Weight: 524.65|Other names: BIBS39
BIBS 39 is a new nonpeptide angiotensin II (AII) receptor antagonist.in vitro: BIBS 39 displaces [125I] AII from its specific binding sites with a Ki value of 29 ± 7 nM for the AII subtype 1 (AT1) receptor and a Ki value of 480 ± 110 nM for the AII subtype 2 (AT2) receptor. BIBS 222 shows a Ki value of 20 ± 7 nM for the AT1 subtype and a Ki value of 730 ± 170 nM for the AT2 subtype. BIBS 39 is 17 times more selective for the AT1 subtype and BIBS 222 37 times. BIBS 39 shifts the AII concentration-contractile response curves in isolated rabbit aorta to the right in a parallel fashion.
in vivo: In pithed rats, BIBS 39 dependently shifts the dose-response curve of AII to the right without affecting the maximal response. BIBS 222 also causes parallel shifts to the right but a significant reduction of the maximal responses was observed at 3 and 10 mg/kg i.v. These results show that the benzimidazole derivatives BIBS 39 is a potent and selective AII receptor antagonists. Substitution with a benzimidazole moiety results into a considerable loss of selectivity for the AT1 receptor subtype compared with an imidazole moiety as, for instance, in DuP 753.BIBS 39 is a new nonpeptide angiotensin receptor blockers that has affinity for both AT1- and AT2-receptors, is also a potent antagonist of the cardiovascular effects of AII in pithed rabbits.
For research only, not for human use.
BIBS 39 is a new nonpeptide angiotensin II (AII) receptor antagonist.
Product Name: BIBS39|Cat No: DC9670|Cas: 133085-33-3|Molecule Formular: C32H36N4O3|Molecule Weight: 524.65|Other names: BIBS39
BIBS 39 is a new nonpeptide angiotensin II (AII) receptor antagonist.in vitro: BIBS 39 displaces [125I] AII from its specific binding sites with a Ki value of 29 ± 7 nM for the AII subtype 1 (AT1) receptor and a Ki value of 480 ± 110 nM for the AII subtype 2 (AT2) receptor. BIBS 222 shows a Ki value of 20 ± 7 nM for the AT1 subtype and a Ki value of 730 ± 170 nM for the AT2 subtype. BIBS 39 is 17 times more selective for the AT1 subtype and BIBS 222 37 times. BIBS 39 shifts the AII concentration-contractile response curves in isolated rabbit aorta to the right in a parallel fashion.
in vivo: In pithed rats, BIBS 39 dependently shifts the dose-response curve of AII to the right without affecting the maximal response. BIBS 222 also causes parallel shifts to the right but a significant reduction of the maximal responses was observed at 3 and 10 mg/kg i.v. These results show that the benzimidazole derivatives BIBS 39 is a potent and selective AII receptor antagonists. Substitution with a benzimidazole moiety results into a considerable loss of selectivity for the AT1 receptor subtype compared with an imidazole moiety as, for instance, in DuP 753.BIBS 39 is a new nonpeptide angiotensin receptor blockers that has affinity for both AT1- and AT2-receptors, is also a potent antagonist of the cardiovascular effects of AII in pithed rabbits.
For research only, not for human use.
Fluoroclebopride|CAS 154540-49-5
Fluoroclebopride|CAS 154540-49-5
Fluoroclebopride is useful chemical for PET image study.
Product Name: Fluoroclebopride|Cat No: DC9669|Cas: 154540-49-5|Molecule Formular: C20H23ClFN3O2|Molecule Weight: 391.87|Other names: Fluoroclebopride
Fluoroclebopride is useful chemical for PET image study. [18F]fluoroclebopride had been used for PET imaging of dopamine D2 receptors in monkeys
For research only, not for human use.
Fluoroclebopride is useful chemical for PET image study.
Product Name: Fluoroclebopride|Cat No: DC9669|Cas: 154540-49-5|Molecule Formular: C20H23ClFN3O2|Molecule Weight: 391.87|Other names: Fluoroclebopride
Fluoroclebopride is useful chemical for PET image study. [18F]fluoroclebopride had been used for PET imaging of dopamine D2 receptors in monkeys
For research only, not for human use.
WAY181187.HCl（WAY-181,187）|CAS 554403-49-5
WAY181187.HCl（WAY-181,187）|CAS 554403-49-5
WAY-181187 is a potent and selective 5-HT6 receptor agonist. WAY-181187 possesses high affinity binding (2.2 and 4.8 nM, respectively) at the human 5-HT6 receptor and profile as full receptor agonists (WAY-181187: EC50=6.6 nM, Emax=93%).
Product Name: WAY181187.HCl（WAY-181,187）|Cat No: DC9668|Cas: 554403-49-5 |Molecule Formular: C15H13ClN4O2S2.HCl|Molecule Weight: 417.33|Other names: WAY181187.HCl（WAY-181,187）
WAY-181187 is a potent and selective 5-HT6 receptor agonist. WAY-181187 possesses high affinity binding (2.2 and 4.8 nM, respectively) at the human 5-HT6 receptor and profile as full receptor agonists (WAY-181187: EC50=6.6 nM, Emax=93%). In the rat frontal cortex, acute administration of WAY-181187 (3-30 mg/kg, subcutaneous (s.c.)) significantly increased extracellular GABA concentrations without altering the levels of glutamate or norepinephrine.
For research only, not for human use.
WAY-181187 is a potent and selective 5-HT6 receptor agonist. WAY-181187 possesses high affinity binding (2.2 and 4.8 nM, respectively) at the human 5-HT6 receptor and profile as full receptor agonists (WAY-181187: EC50=6.6 nM, Emax=93%).
Product Name: WAY181187.HCl（WAY-181,187）|Cat No: DC9668|Cas: 554403-49-5 |Molecule Formular: C15H13ClN4O2S2.HCl|Molecule Weight: 417.33|Other names: WAY181187.HCl（WAY-181,187）
WAY-181187 is a potent and selective 5-HT6 receptor agonist. WAY-181187 possesses high affinity binding (2.2 and 4.8 nM, respectively) at the human 5-HT6 receptor and profile as full receptor agonists (WAY-181187: EC50=6.6 nM, Emax=93%). In the rat frontal cortex, acute administration of WAY-181187 (3-30 mg/kg, subcutaneous (s.c.)) significantly increased extracellular GABA concentrations without altering the levels of glutamate or norepinephrine.
For research only, not for human use.
AZ-33(AZ33)|CAS 1370290-34-8
AZ-33(AZ33)|CAS 1370290-34-8
AZ-33 is a inhibitor LDH-A with an IC50 of 0.5 μM.
Product Name: AZ-33(AZ33)|Cat No: DC9667|Cas: 1370290-34-8|Molecule Formular: C25H27N3O6S|Molecule Weight: 497.56|Other names: AZ-33(AZ33)
AZ-33 is a inhibitor LDH-A with an IC50 of 0.5 μM.
For research only, not for human use.
AZ-33 is a inhibitor LDH-A with an IC50 of 0.5 μM.
Product Name: AZ-33(AZ33)|Cat No: DC9667|Cas: 1370290-34-8|Molecule Formular: C25H27N3O6S|Molecule Weight: 497.56|Other names: AZ-33(AZ33)
AZ-33 is a inhibitor LDH-A with an IC50 of 0.5 μM.
For research only, not for human use.
Ro 46-2005|CAS 150725-87-4
Ro 46-2005|CAS 150725-87-4
Ro 46-2005 is a novel synthetic non-peptide endothelin receptor antagonist, inhibits the specific binding of 125I-ET-1 to human vascular smooth muscle cells (ETA receptor) with IC50 of 220 nM.
Product Name: Ro 46-2005|Cat No: DC9666|Cas: 150725-87-4|Molecule Formular: C23H27N3O6S|Molecule Weight: 473.54|Other names: Ro 46-2005
Ro 46-2005 is a novel synthetic non-peptide endothelin receptor antagonist, inhibits the specific binding of 125I-ET-1 to human vascular smooth muscle cells (ETA receptor) with IC50 of 220 nM.in vitro: Ro 46-2005 proves to be equipotent (IC50 200-500 nM) for inhibition of [125I]ET-1 binding on the two known ET receptor subtypes (ETA and ETB). Ro 46-2005 also inhibits the functional consequences of ET-1 stimulation: the ET-l-induced release of arachidonic acid from rat mesangial cells was inhibited with an IC50 of 1.8 μM.
For research only, not for human use.
Ro 46-2005 is a novel synthetic non-peptide endothelin receptor antagonist, inhibits the specific binding of 125I-ET-1 to human vascular smooth muscle cells (ETA receptor) with IC50 of 220 nM.
Product Name: Ro 46-2005|Cat No: DC9666|Cas: 150725-87-4|Molecule Formular: C23H27N3O6S|Molecule Weight: 473.54|Other names: Ro 46-2005
Ro 46-2005 is a novel synthetic non-peptide endothelin receptor antagonist, inhibits the specific binding of 125I-ET-1 to human vascular smooth muscle cells (ETA receptor) with IC50 of 220 nM.in vitro: Ro 46-2005 proves to be equipotent (IC50 200-500 nM) for inhibition of [125I]ET-1 binding on the two known ET receptor subtypes (ETA and ETB). Ro 46-2005 also inhibits the functional consequences of ET-1 stimulation: the ET-l-induced release of arachidonic acid from rat mesangial cells was inhibited with an IC50 of 1.8 μM.
For research only, not for human use.
EAI045，EAI-045|EGFR(T790M/C797S) inhibitor
EAI045，EAI-045|EGFR(T790M/C797S) inhibitor
EAI045 is an allosteric inhibitor that targets selected drug-resistant EGFR mutants but spares the wild-type receptor.
Product Name: EAI045|Cat No: DC9665|Cas: N/A|Molecule Formular: C19H16FN3O3S|Molecule Weight: 385.09|Other names: EAI045
EAI045 in combination with cetuximab is effective in mouse models of lung cancer driven by EGFR(L858R/T790M) and by EGFR(L858R/T790M/C797S), a mutant that is resistant to all currently available EGFR TKIs.
For research only, not for human use.
EAI045 is an allosteric inhibitor that targets selected drug-resistant EGFR mutants but spares the wild-type receptor.
Product Name: EAI045|Cat No: DC9665|Cas: N/A|Molecule Formular: C19H16FN3O3S|Molecule Weight: 385.09|Other names: EAI045
EAI045 in combination with cetuximab is effective in mouse models of lung cancer driven by EGFR(L858R/T790M) and by EGFR(L858R/T790M/C797S), a mutant that is resistant to all currently available EGFR TKIs.
For research only, not for human use.
Doxapram,CAS 1015064-87-5
Doxapram,CAS 1015064-87-5
Doxapram inhibits TASK-1, TASK-3, TASK-1/TASK-3 heterodimeric channel function with EC50 of 410 nM, 37 μM, 9 μM, respectively.
Product Name: Doxapram|Cat No: DC9664|Cas: 309-29-5|Molecule Formular: C24H30N2O2|Molecule Weight: 378.51|Other names: Doxapram
Doxapram is a respiratory stimulant. Doxapram (15-150 microM) also evoked 3H overflow in a concentration dependent manner, and doxapram-evoked release was inhibited by the Ca2+ channel blocker nifedipine (5 microM). Analysis of released tritiated compounds suggested that doxapram preferentially stimulated the release of dopamine. Our results indicate that the mechanism of action of doxapram shares similarities with that of hypoxia in the carotid body [1]. Doxapram (1-100 microM) caused rapid, reversible and dose-dependent inhibitions of K+ currents recorded in type I cells (IC50 approximately 13 microM). doxapram was also seen to directly inhibit Ca(2+)-independent K+ currents. Doxapram was a more potent inhibitor of the Ca(2+)-activated K+ currents recorded under control conditions. Doxapram (10 microM) was without effect on L-type Ca2+ channel currents recorded under conditions where K+ channel activity was minimized and was also without significant effect on K+ currents recorded in the neuronal cell line NG-108 15, suggesting a selective effect on carotid body type I cells. The effects of doxapram on type I cells show similarities to those of the physiological stimuli of the carotid body, suggesting that doxapram may share a similar mechanism of action in stimulating the intact organ.
For research only, not for human use.
Doxapram inhibits TASK-1, TASK-3, TASK-1/TASK-3 heterodimeric channel function with EC50 of 410 nM, 37 μM, 9 μM, respectively.
Product Name: Doxapram|Cat No: DC9664|Cas: 309-29-5|Molecule Formular: C24H30N2O2|Molecule Weight: 378.51|Other names: Doxapram
Doxapram is a respiratory stimulant. Doxapram (15-150 microM) also evoked 3H overflow in a concentration dependent manner, and doxapram-evoked release was inhibited by the Ca2+ channel blocker nifedipine (5 microM). Analysis of released tritiated compounds suggested that doxapram preferentially stimulated the release of dopamine. Our results indicate that the mechanism of action of doxapram shares similarities with that of hypoxia in the carotid body [1]. Doxapram (1-100 microM) caused rapid, reversible and dose-dependent inhibitions of K+ currents recorded in type I cells (IC50 approximately 13 microM). doxapram was also seen to directly inhibit Ca(2+)-independent K+ currents. Doxapram was a more potent inhibitor of the Ca(2+)-activated K+ currents recorded under control conditions. Doxapram (10 microM) was without effect on L-type Ca2+ channel currents recorded under conditions where K+ channel activity was minimized and was also without significant effect on K+ currents recorded in the neuronal cell line NG-108 15, suggesting a selective effect on carotid body type I cells. The effects of doxapram on type I cells show similarities to those of the physiological stimuli of the carotid body, suggesting that doxapram may share a similar mechanism of action in stimulating the intact organ.
For research only, not for human use.
ZL004,ZL-004,CAS 1015064-87-5
ZL004,ZL-004,CAS 1015064-87-5
ZL-004 could protect mice against 5-fluorouracil damage and raise peripheral blood leukocyte
Product Name: ZL-004|Cat No: DC9663|Cas: 1015064-87-5|Molecule Formular: C16H16N2O5S2|Molecule Weight: 380.05|Other names: ZL-004
For research only, not for human use.
ZL-004 could protect mice against 5-fluorouracil damage and raise peripheral blood leukocyte
Product Name: ZL-004|Cat No: DC9663|Cas: 1015064-87-5|Molecule Formular: C16H16N2O5S2|Molecule Weight: 380.05|Other names: ZL-004
For research only, not for human use.
JNJ-42165279|JNJ42165279|FAAH inhibitor
JNJ-42165279|JNJ42165279|FAAH inhibitor
JNJ-42165279 is a potent and selective inhibitor of the enzyme fatty acid amide hydrolase (FAAH), with an IC50 of 70nM.
Product Name: JNJ-42165279|Cat No: DC9662|Cas: 1346528-50-4|Molecule Formular: C18H17ClF2N4O3|Molecule Weight: 410.8|Other names: JNJ-42165279
JNJ-42165279 exhibited excellent ADME and pharmacodynamic properties as evidenced by its ability to block FAAH in the brain and periphery of rats and thereby cause an elevation of the concentrations of anandamide (AEA), oleoyl ethanolamide (OEA), and palmitoyl ethanolamide (PEA). The compound was also efficacious in the spinal nerve ligation (SNL) model of neuropathic pain. The combination of good physical, ADME, and PD properties of JNJ-42165279 supported it entering the clinical portfolio.
For research only, not for human use.
JNJ-42165279 is a potent and selective inhibitor of the enzyme fatty acid amide hydrolase (FAAH), with an IC50 of 70nM.
Product Name: JNJ-42165279|Cat No: DC9662|Cas: 1346528-50-4|Molecule Formular: C18H17ClF2N4O3|Molecule Weight: 410.8|Other names: JNJ-42165279
JNJ-42165279 exhibited excellent ADME and pharmacodynamic properties as evidenced by its ability to block FAAH in the brain and periphery of rats and thereby cause an elevation of the concentrations of anandamide (AEA), oleoyl ethanolamide (OEA), and palmitoyl ethanolamide (PEA). The compound was also efficacious in the spinal nerve ligation (SNL) model of neuropathic pain. The combination of good physical, ADME, and PD properties of JNJ-42165279 supported it entering the clinical portfolio.
For research only, not for human use.
PIK-293|PIK293|cas 900185-01-5
PIK-293|PIK293|cas 900185-01-5
PIK-293 is a PI3K inhibitor, mostly for PI3Kδ with IC50 of 0.24 μM, 500-, 100- and 50-fold less potent to PI3Kα/β/γ, respectively.
Product Name: PIK-293|Cat No: DC9661|Cas: 900185-01-5|Molecule Formular: C22H19N7O|Molecule Weight: 397.43|Other names: PIK-293
PIK-293 is a PI3K inhibitor, mostly for PI3Kδ with IC50 of 0.24 μM, 500-, 100- and 50-fold less potent to PI3Kα/β/γ, respectively.PIK-293 is a pyrazolopyrimidine analog of IC87114. PIK-293 is synthesized by replacing the adenine of IC87114 with the isosteric pyrazolopyrimidine.
For research only, not for human use.
PIK-293 is a PI3K inhibitor, mostly for PI3Kδ with IC50 of 0.24 μM, 500-, 100- and 50-fold less potent to PI3Kα/β/γ, respectively.
Product Name: PIK-293|Cat No: DC9661|Cas: 900185-01-5|Molecule Formular: C22H19N7O|Molecule Weight: 397.43|Other names: PIK-293
PIK-293 is a PI3K inhibitor, mostly for PI3Kδ with IC50 of 0.24 μM, 500-, 100- and 50-fold less potent to PI3Kα/β/γ, respectively.PIK-293 is a pyrazolopyrimidine analog of IC87114. PIK-293 is synthesized by replacing the adenine of IC87114 with the isosteric pyrazolopyrimidine.
For research only, not for human use.
Acalabrutinib(ACP196)|cas 20362-31-6
Acalabrutinib(ACP196)|cas 20362-31-6
Acalabrutinib (ACP-196) is a second-generation, selective, irreversible inhibitor of BTK that has improved pharmacologic features, including favorable plasma exposure, rapid oral absorption, a short half-life, and the absence of irreversible targeting to alternative kinases, such as EGFR,TEC, and ITK.
Product Name: Acalabrutinib(ACP196)|Cat No: DC9660|Cas: 1420477-60-6|Molecule Formular: C26H23N7O2|Molecule Weight: 465.51|Other names: Acalabrutinib(ACP196)
Acalabrutinib (ACP-196) is a second-generation, selective, irreversible inhibitor of BTK that has improved pharmacologic features, including favorable plasma exposure, rapid oral absorption, a short half-life, and the absence of irreversible targeting to alternative kinases, such as EGFR,TEC, and ITK. Acalabrutinib (ACP-196) is a more selective, irreversible BTK inhibitor that is specifically designed to improve on the safety and efficacy of first-generation BTK inhibitors. Acalabrutinib shows dose dependent inhibition of B-cell receptor signaling in primary CLL cells. In kinase-inhibition assays, acalabrutinib was a more selective BTK inhibitor than ibrutinib. These biochemical findings are physiologically relevant, because acalabrutinib did not
inhibit EGFR, TEC, or ITK signaling. The findings provide structural, biochemical, and in vitro differentiation of acalabrutinib from ibrutinib. These data, combined with objective clinical responses in a study of naturally occurring canine B-cell lymphomas, provided justification for the clinical development of acalabrutinib for the treatment of CLL.
Acalabrutinib (ACP-196) is a second-generation, selective, irreversible inhibitor of BTK that has improved pharmacologic features, including favorable plasma exposure, rapid oral absorption, a short half-life, and the absence of irreversible targeting to alternative kinases, such as EGFR,TEC, and ITK.
Product Name: Acalabrutinib(ACP196)|Cat No: DC9660|Cas: 1420477-60-6|Molecule Formular: C26H23N7O2|Molecule Weight: 465.51|Other names: Acalabrutinib(ACP196)
Acalabrutinib (ACP-196) is a second-generation, selective, irreversible inhibitor of BTK that has improved pharmacologic features, including favorable plasma exposure, rapid oral absorption, a short half-life, and the absence of irreversible targeting to alternative kinases, such as EGFR,TEC, and ITK. Acalabrutinib (ACP-196) is a more selective, irreversible BTK inhibitor that is specifically designed to improve on the safety and efficacy of first-generation BTK inhibitors. Acalabrutinib shows dose dependent inhibition of B-cell receptor signaling in primary CLL cells. In kinase-inhibition assays, acalabrutinib was a more selective BTK inhibitor than ibrutinib. These biochemical findings are physiologically relevant, because acalabrutinib did not
inhibit EGFR, TEC, or ITK signaling. The findings provide structural, biochemical, and in vitro differentiation of acalabrutinib from ibrutinib. These data, combined with objective clinical responses in a study of naturally occurring canine B-cell lymphomas, provided justification for the clinical development of acalabrutinib for the treatment of CLL.
For research only, not for human use.
Arctiin|cas 20362-31-6|Supplied by DC Chemicals
Arctiin|cas 20362-31-6|Supplied by DC Chemicals
Arctiin, a plant lignan that can be extracted from the Arctium lappa (burdock) seeds, is a possible environmental endocrine disruptor compounds and have been shown to influence sex hormone metabolism as well as protein synthesis, steroid biosynthesis.
Product Name: Arctiin(NSC 315527)|Cat No: DC9659|Cas: 20362-31-6|Molecule Formular: C27H34O11|Molecule Weight: 534.55|Other names: Arctiin(NSC 315527)
Arctiin, a plant lignan that can be extracted from the Arctium lappa (burdock) seeds, is a possible environmental endocrine disruptor compounds and have been shown to influence sex hormone metabolism as well as protein synthesis, steroid biosynthesis.
in vitro: Treatment of PC-3 cells with arctiin decreased the cell number in a concentration- and time-dependent manner in serum-containing condition. Arctiin preferentially induced cell detachment, but did not have anti-proliferation or cytotoxic effects in PC-3 cells. The arctiin-induced effect was inhibited by cycloheximide, indicating that protein synthesis was required [1]. Although arctiin, the active component of AL that has been described in the literature, was not able to reduce degranulation in RBL-2H3 cells, a single high-performance liquid chromatography (HPLC) fraction from the AL extract inhibited beta-hexosaminidase release (IC(50) = 22.2 microg/ml). The growth inhibition caused by arctiin is associated with the down-regulation of cyclin D1 protein expression. Furthermore, thearctiin-induced suppression of cyclin D1 protein expression occurs in various types of human tumor cells, including osteosarcoma, lung, colorectal, cervical and breast cancer, melanoma, transformed renal cells and prostate cancer. Depletion of the cyclin D1 protein using small interfering RNA-rendered human breast cancer MCF-7 cells insensitive to the growth inhibitory effects of arctiin, implicates cyclin D1 as an important target of arctiin.
in vivo: Histopathological evaluation of prostate revealed that all the rats in any group developed adenocarcinoma in dorsolateral lobe of prostate, except two rats in 0.1% arctiin treated and one rat in 0.002% arctiin treated groups without prostate adenocarcinoma development. After oral administration of arctiin (30, 60, 120 mg/kgd) for three weeks, the levels of serum creatinine (Scr) and blood urea nitrogen (BUN) and 24-h urine protein content markedly decreased, while endogenous creatinine clearance rate (ECcr) significantly increased. STZ-induced diabetic rats were treated witharctiin at the dosage of 60 or 40 mg/kg/day via intraperitoneal injection for 8 weeks. Blood glucose and 24-h urinary albumin content were measured, and kidney histopathological changes were monitored.
For research only, not for human use.
Arctiin, a plant lignan that can be extracted from the Arctium lappa (burdock) seeds, is a possible environmental endocrine disruptor compounds and have been shown to influence sex hormone metabolism as well as protein synthesis, steroid biosynthesis.
Product Name: Arctiin(NSC 315527)|Cat No: DC9659|Cas: 20362-31-6|Molecule Formular: C27H34O11|Molecule Weight: 534.55|Other names: Arctiin(NSC 315527)
Arctiin, a plant lignan that can be extracted from the Arctium lappa (burdock) seeds, is a possible environmental endocrine disruptor compounds and have been shown to influence sex hormone metabolism as well as protein synthesis, steroid biosynthesis.
in vitro: Treatment of PC-3 cells with arctiin decreased the cell number in a concentration- and time-dependent manner in serum-containing condition. Arctiin preferentially induced cell detachment, but did not have anti-proliferation or cytotoxic effects in PC-3 cells. The arctiin-induced effect was inhibited by cycloheximide, indicating that protein synthesis was required [1]. Although arctiin, the active component of AL that has been described in the literature, was not able to reduce degranulation in RBL-2H3 cells, a single high-performance liquid chromatography (HPLC) fraction from the AL extract inhibited beta-hexosaminidase release (IC(50) = 22.2 microg/ml). The growth inhibition caused by arctiin is associated with the down-regulation of cyclin D1 protein expression. Furthermore, thearctiin-induced suppression of cyclin D1 protein expression occurs in various types of human tumor cells, including osteosarcoma, lung, colorectal, cervical and breast cancer, melanoma, transformed renal cells and prostate cancer. Depletion of the cyclin D1 protein using small interfering RNA-rendered human breast cancer MCF-7 cells insensitive to the growth inhibitory effects of arctiin, implicates cyclin D1 as an important target of arctiin.
in vivo: Histopathological evaluation of prostate revealed that all the rats in any group developed adenocarcinoma in dorsolateral lobe of prostate, except two rats in 0.1% arctiin treated and one rat in 0.002% arctiin treated groups without prostate adenocarcinoma development. After oral administration of arctiin (30, 60, 120 mg/kgd) for three weeks, the levels of serum creatinine (Scr) and blood urea nitrogen (BUN) and 24-h urine protein content markedly decreased, while endogenous creatinine clearance rate (ECcr) significantly increased. STZ-induced diabetic rats were treated witharctiin at the dosage of 60 or 40 mg/kg/day via intraperitoneal injection for 8 weeks. Blood glucose and 24-h urinary albumin content were measured, and kidney histopathological changes were monitored.
For research only, not for human use.
I-BRD9|cas 1182367-47-0|DC Chemicals
I-BRD9|cas 1182367-47-0|DC Chemicals
I-BRD9 is a potent and selective BRD9 inhibitor (pIC50 = 7.3). Exhibits >70-fold selectivity for BRD9 over a panel of 34 other bromodomains and >700-fold selectivity over the BET family.
Product Name: I-BRD9|Cat No: DC9658|Cas: 1714146-59-4|Molecule Formular: C22H22F3N3O3S2|Molecule Weight: 497.55|Other names: I-BRD9
I-BRD9 is a potent and selective binder to BRD9 with a pIC50 in a Time-Resolved FRET assay of 7.3. BRD4 was used as a representative member of the BET family for initial selectivity screening, I-BRD9 displayed a pIC50 of 5.3 against this protein. I-BRD9 binds to endogenous BRD9 in a chemoproteomic assay and shows good selectivity over the BET family member BRD3.
For research only, not for human use.
I-BRD9 is a potent and selective BRD9 inhibitor (pIC50 = 7.3). Exhibits >70-fold selectivity for BRD9 over a panel of 34 other bromodomains and >700-fold selectivity over the BET family.
Product Name: I-BRD9|Cat No: DC9658|Cas: 1714146-59-4|Molecule Formular: C22H22F3N3O3S2|Molecule Weight: 497.55|Other names: I-BRD9
I-BRD9 is a potent and selective binder to BRD9 with a pIC50 in a Time-Resolved FRET assay of 7.3. BRD4 was used as a representative member of the BET family for initial selectivity screening, I-BRD9 displayed a pIC50 of 5.3 against this protein. I-BRD9 binds to endogenous BRD9 in a chemoproteomic assay and shows good selectivity over the BET family member BRD3.
For research only, not for human use.
RAD140|cas 1182367-47-0|DC Chemicals
RAD140|cas 1182367-47-0|DC Chemicals
RAD140 is a potent, orally bioavailable, nonsteroidal selective androgen receptor modulator (SARM).
Product Name: RAD140|Cat No: DC9657|Cas: 1182367-47-0|Molecule Formular: C20H16ClN5O2|Molecule Weight: 393.83|Other names: RAD140
RAD140 is a potent, orally bioavailable, nonsteroidal selective androgen receptor modulator (SARM).
IC50 value: 7 nM (Ki, fot androgen receptor)
in vitro: RAD140 demonstrates excellent affinity for the androgen receptor (Ki = 7 nM) as well as good selectivity over other steroid hormone nuclear receptors, with the closest off target receptor being the progesterone receptor (IC50 = 750 nM). [1] RAD140 is a novel SARM with high affinity and specificity for AR, is orally available, and exhibits potent anabolic effects in rodents and nonhuman primates.[
in vivo: The stability of RAD140 is high (t1/2 > 2 h) in incubations with rat, monkey, and human microsomes, and it also had good bioavailability in rats and monkeys. [1] RAD140 is also neuroprotective using the rat kainate lesion model. RAD140 is shown to exhibit peripheral tissue-specific androgen action that largely spared prostate, neural efficacy by activation of androgenic gene regulation effects, and neuroprotection of hippocampal neurons against cell death caused by systemic administration of the excitotoxin kainate.
For research only, not for human use.
RAD140 is a potent, orally bioavailable, nonsteroidal selective androgen receptor modulator (SARM).
Product Name: RAD140|Cat No: DC9657|Cas: 1182367-47-0|Molecule Formular: C20H16ClN5O2|Molecule Weight: 393.83|Other names: RAD140
RAD140 is a potent, orally bioavailable, nonsteroidal selective androgen receptor modulator (SARM).
IC50 value: 7 nM (Ki, fot androgen receptor)
in vitro: RAD140 demonstrates excellent affinity for the androgen receptor (Ki = 7 nM) as well as good selectivity over other steroid hormone nuclear receptors, with the closest off target receptor being the progesterone receptor (IC50 = 750 nM). [1] RAD140 is a novel SARM with high affinity and specificity for AR, is orally available, and exhibits potent anabolic effects in rodents and nonhuman primates.[
in vivo: The stability of RAD140 is high (t1/2 > 2 h) in incubations with rat, monkey, and human microsomes, and it also had good bioavailability in rats and monkeys. [1] RAD140 is also neuroprotective using the rat kainate lesion model. RAD140 is shown to exhibit peripheral tissue-specific androgen action that largely spared prostate, neural efficacy by activation of androgenic gene regulation effects, and neuroprotection of hippocampal neurons against cell death caused by systemic administration of the excitotoxin kainate.
For research only, not for human use.
Pristinamycin|cas 11006-76-1|DC Chemicals
Pristinamycin|cas 11006-76-1|DC Chemicals
Pristinamycin is an antibiotic used primarily in the treatment of staphylococcal infections, and to a lesser extent streptococcal infections.
Product Name: Pristinamycin|Cat No: DC9656|Cas: 11006-76-1|Molecule Formular: C71H84N10O17|Molecule Weight: 1349.48|Other names: Pristinamycin
For research only, not for human use.
Pristinamycin is an antibiotic used primarily in the treatment of staphylococcal infections, and to a lesser extent streptococcal infections.
Product Name: Pristinamycin|Cat No: DC9656|Cas: 11006-76-1|Molecule Formular: C71H84N10O17|Molecule Weight: 1349.48|Other names: Pristinamycin
For research only, not for human use.
20-O-Acetylingenol-3-angelate (cas 82425-35-2)
20-O-Acetylingenol-3-angelate (cas 82425-35-2)
20-O-Acetylingenol-3-angelate is a natural compound.
Product Name: 20-O-Acetylingenol-3-angelate|Cat No: DC9655|Cas: 82425-35-2|Molecule Formular: C27H36O7|Molecule Weight: 472.57|Other names: 20-O-Acetylingenol-3-angelate
20-O-Acetylingenol-3-angelate is a natural compound.
For research only, not for human use.
20-O-Acetylingenol-3-angelate is a natural compound.
Product Name: 20-O-Acetylingenol-3-angelate|Cat No: DC9655|Cas: 82425-35-2|Molecule Formular: C27H36O7|Molecule Weight: 472.57|Other names: 20-O-Acetylingenol-3-angelate
20-O-Acetylingenol-3-angelate is a natural compound.
For research only, not for human use.
Ingenol 5,20-Acetonide-3-O-angelate (CAS 87980-68-5)
Ingenol 5,20-Acetonide-3-O-angelate (CAS 87980-68-5)
Ingenol 5,20-Acetonide-3-O-angelate (CAS 87980-68-5)
Product Name: Ingenol 5,20-Acetonide-3-O-angelate|Cat No: DC9654|Cas: 87980-68-5|Molecule Formular: C28H38O6|Molecule Weight: 470.6|Other names: Ingenol 5,20-Acetonide-3-O-angelate
For research only, not for human use.
Ingenol 5,20-Acetonide-3-O-angelate (CAS 87980-68-5)
Product Name: Ingenol 5,20-Acetonide-3-O-angelate|Cat No: DC9654|Cas: 87980-68-5|Molecule Formular: C28H38O6|Molecule Weight: 470.6|Other names: Ingenol 5,20-Acetonide-3-O-angelate
For research only, not for human use.
Ingenol 5,20-Acetonide (CAS 77573-43-4)
Ingenol 5,20-Acetonide (CAS 77573-43-4)
Ingenol 5,20-Acetonide (CAS 77573-43-4)
Product Name: Ingenol 5,20-Acetonide|Cat No: DC9653|Cas: 77573-43-4|Molecule Formular: C23H32O5|Molecule Weight: 388.5|Other names: Ingenol 5,20-Acetonide
For research only, not for human use.
Ingenol 5,20-Acetonide (CAS 77573-43-4)
Product Name: Ingenol 5,20-Acetonide|Cat No: DC9653|Cas: 77573-43-4|Molecule Formular: C23H32O5|Molecule Weight: 388.5|Other names: Ingenol 5,20-Acetonide
For research only, not for human use.
Ingenol-3,4:5,20-diacetonide (CAS 77573-44-5)
Ingenol-3,4:5,20-diacetonide (CAS 77573-44-5)
Ingenol-3,4:5,20-diacetonide (CAS 77573-44-5)
Product Name: Ingenol-3,4:5,20-diacetonide|Cat No: DC9652|Cas: 77573-44-5|Molecule Formular: C26H36O5|Molecule Weight: 428.56|Other names: Ingenol-3,4:5,20-diacetonide
For research only, not for human use.
Ingenol-3,4:5,20-diacetonide (CAS 77573-44-5)
Product Name: Ingenol-3,4:5,20-diacetonide|Cat No: DC9652|Cas: 77573-44-5|Molecule Formular: C26H36O5|Molecule Weight: 428.56|Other names: Ingenol-3,4:5,20-diacetonide
For research only, not for human use.
Ingenol 3-angelate|cas 75567-37-2
Ingenol 3-angelate|cas 75567-37-2
Ingenol 3-Angelate is a PKC(protein kinase C)activator; anti-cancer drug and an active ingredient in Euphorbia peplus.
Product Name: Ingenol 3-angelate|Cat No: DC9651|Cas: 75567-37-2|Molecule Formular: C25H34O6|Molecule Weight: 430.53|Other names: Ingenol 3-angelate
Ingenol 3-Angelate is a PKC(protein kinase C)activator; anti-cancer drug and an active ingredient in Euphorbia peplus.
For research only, not for human use.
Ingenol 3-Angelate is a PKC(protein kinase C)activator; anti-cancer drug and an active ingredient in Euphorbia peplus.
Product Name: Ingenol 3-angelate|Cat No: DC9651|Cas: 75567-37-2|Molecule Formular: C25H34O6|Molecule Weight: 430.53|Other names: Ingenol 3-angelate
Ingenol 3-Angelate is a PKC(protein kinase C)activator; anti-cancer drug and an active ingredient in Euphorbia peplus.
For research only, not for human use.
Homoharringtonine|cas 26833-87-4|DC Chemicals
Homoharringtonine|cas 26833-87-4|DC Chemicals
Homoharringtonine(HHT) is a cytotoxic alkaloid from the evergreen tree.
Product Name: Homoharringtonine|Cat No: DC9650|Cas: 26833-87-4|Molecule Formular: C29H39NO9|Molecule Weight: 545.62|Other names: Homoharringtonine
For the detailed information of Homoharringtonine, the solubility of Homoharringtonine in water, the solubility of Homoharringtonine in DMSO, the solubility of Homoharringtonine in PBS buffer, the animal experiment（test） (test) of Homoharringtonine, the cell expriment (test) of Homoharringtonine, the in vivo, in vitro and clinical trial test of Homoharringtonine, the EC50, IC50,and Affinity of Homoharringtonine,, please contact DC Chemicals.
For research only, not for human use.
Homoharringtonine(HHT) is a cytotoxic alkaloid from the evergreen tree.
Product Name: Homoharringtonine|Cat No: DC9650|Cas: 26833-87-4|Molecule Formular: C29H39NO9|Molecule Weight: 545.62|Other names: Homoharringtonine
For the detailed information of Homoharringtonine, the solubility of Homoharringtonine in water, the solubility of Homoharringtonine in DMSO, the solubility of Homoharringtonine in PBS buffer, the animal experiment（test） (test) of Homoharringtonine, the cell expriment (test) of Homoharringtonine, the in vivo, in vitro and clinical trial test of Homoharringtonine, the EC50, IC50,and Affinity of Homoharringtonine,, please contact DC Chemicals.
For research only, not for human use.
Cephalotaxlen|cas 24316-19-6|Supplied by DC Chem
Cephalotaxlen|cas 24316-19-6|Supplied by DC Chemicals
Cephalotaxine is an antiviral as well as antitumor agent.
Product Name: Cephalotaxlen|Cat No: DC9649|Cas: 24316-19-6|Molecule Formular: C18H21NO4|Molecule Weight: 315.36|Other names: Cephalotaxlen
Cephalotaxine is an antiviral as well as antitumor agent.
For research only, not for human use.
Cephalotaxine is an antiviral as well as antitumor agent.
Product Name: Cephalotaxlen|Cat No: DC9649|Cas: 24316-19-6|Molecule Formular: C18H21NO4|Molecule Weight: 315.36|Other names: Cephalotaxlen
Cephalotaxine is an antiviral as well as antitumor agent.
For research only, not for human use.
Dodecanoic acid ingenol ester|cas 54706-70-6
Dodecanoic acid ingenol ester|cas 54706-70-6
Dodecanoic acid ingenol ester is a natural compound.
Product Name: Dodecanoic acid ingenol ester|Cat No: DC9648|Cas: 54706-70-6|Molecule Formular: C32H50O7|Molecule Weight: 546.74|Other names: Dodecanoic acid ingenol ester
For the detailed information of Dodecanoic acid ingenol ester, the solubility of Dodecanoic acid ingenol ester in water, the solubility of Dodecanoic acid ingenol ester in DMSO, the solubility of Dodecanoic acid ingenol ester in PBS buffer, the animal experiment（test） (test) of Dodecanoic acid ingenol ester, the cell expriment (test) of Dodecanoic acid ingenol ester, the in vivo, in vitro and clinical trial test of Dodecanoic acid ingenol ester, the EC50, IC50,and Affinity of Dodecanoic acid ingenol ester,, please contact DC Chemicals.
For research only, not for human use.
Dodecanoic acid ingenol ester is a natural compound.
Product Name: Dodecanoic acid ingenol ester|Cat No: DC9648|Cas: 54706-70-6|Molecule Formular: C32H50O7|Molecule Weight: 546.74|Other names: Dodecanoic acid ingenol ester
For the detailed information of Dodecanoic acid ingenol ester, the solubility of Dodecanoic acid ingenol ester in water, the solubility of Dodecanoic acid ingenol ester in DMSO, the solubility of Dodecanoic acid ingenol ester in PBS buffer, the animal experiment（test） (test) of Dodecanoic acid ingenol ester, the cell expriment (test) of Dodecanoic acid ingenol ester, the in vivo, in vitro and clinical trial test of Dodecanoic acid ingenol ester, the EC50, IC50,and Affinity of Dodecanoic acid ingenol ester,, please contact DC Chemicals.
For research only, not for human use.
20-Deoxyingenol |cas 54706-99-9|DC Chemicals
20-Deoxyingenol |cas 54706-99-9|DC Chemicals
20-Deoxyingenol is a natural compound.
Product Name: 20-Deoxyingenol|Cat No: DC9647|Cas: 54706-99-9|Molecule Formular: C20H28O4|Molecule Weight: 332.43|Other names: 20-Deoxyingenol
For research only, not for human use.
20-Deoxyingenol is a natural compound.
Product Name: 20-Deoxyingenol|Cat No: DC9647|Cas: 54706-99-9|Molecule Formular: C20H28O4|Molecule Weight: 332.43|Other names: 20-Deoxyingenol
For research only, not for human use.
Ingenol |cas 30220-46-3|supplier DC Chemicals
Ingenol |cas 30220-46-3|supplier DC Chemicals
Ingenol is an extremely weak protein kinase C (PKC) activator. Has been found to induce apoptosis and act as an anticancer agent. Ingenol derivatives have received constant and multidisciplinary attention on account of their pleiotropic pattern of biologi
Product Name: Ingenol|Cat No: DC9646|Cas: 30220-46-3|Molecule Formular: 30220-46-3|Molecule Weight: 348.4|Other names: Ingenol
Ingenol is an extremely weak PKC (protein kinase C) activator; has been found to induce apoptosis and act as an anticancer agent.
in vitro: ingenol indeed binds to protein kinase C with a Ki of 30 microM and activates the enzyme. In addition, ingenol was biologically active in 3 separate cell systems, showing effects similar to the phorbol esters on morphological change, cell-cell communication, epidermal growth factor binding, arachidonic acid metabolite release, and ornithine decarboxylase activity.
For research only, not for human use.
Ingenol is an extremely weak protein kinase C (PKC) activator. Has been found to induce apoptosis and act as an anticancer agent. Ingenol derivatives have received constant and multidisciplinary attention on account of their pleiotropic pattern of biologi
Product Name: Ingenol|Cat No: DC9646|Cas: 30220-46-3|Molecule Formular: 30220-46-3|Molecule Weight: 348.4|Other names: Ingenol
Ingenol is an extremely weak PKC (protein kinase C) activator; has been found to induce apoptosis and act as an anticancer agent.
in vitro: ingenol indeed binds to protein kinase C with a Ki of 30 microM and activates the enzyme. In addition, ingenol was biologically active in 3 separate cell systems, showing effects similar to the phorbol esters on morphological change, cell-cell communication, epidermal growth factor binding, arachidonic acid metabolite release, and ornithine decarboxylase activity.
For research only, not for human use.
(+)-Arglabin|cas 84692-91-1|DC Chemicals
(+)-Arglabin|cas 84692-91-1|DC Chemicals
Arglabin is a sesquiterpene gamma-lactone is isolated from Artemisia glabella; anticancer natural compound.
Product Name: (+)-Arglabin|Cat No: DC9645|Cas: 84692-91-1|Molecule Formular: C15H18O3|Molecule Weight: 246.3|Other names: (+)-Arglabin
Arglabin is a sesquiterpene gamma-lactone is isolated from Artemisia glabella; anticancer natural compound.
in vitro: Arglabin-stimulated macrophages displayed a strong cytotoxic activity and the lowest doses (1.25 micrograms/mL and 0.125 micrograms/mL) induced a significant stimulation of cell mitochondrial metabolism, which correlated with [3H]TdR uptake by J774.1 cells under the same experimental conditions. Arglabin triggered the production of the three cytokines from J774-1 cells. However, the pattern of cytokine secretion differed to some extent, according to the methodology used for cytokine measurement: either traditional bioassay or specific immunoassay (ELISA). Arglabin exhibits antiexudative and antiproliferative properties on the models of acute aseptic inflammation caused by formalin, carrageenan, and histamine, and on the model of proliferative inflammation accompanying cotton-pellet granuloma. Arglabin is able to reduce the proportion of AML stem cells (CD34+CD38-) in primary AML cells.
For research only, not for human use!
Arglabin is a sesquiterpene gamma-lactone is isolated from Artemisia glabella; anticancer natural compound.
Product Name: (+)-Arglabin|Cat No: DC9645|Cas: 84692-91-1|Molecule Formular: C15H18O3|Molecule Weight: 246.3|Other names: (+)-Arglabin
Arglabin is a sesquiterpene gamma-lactone is isolated from Artemisia glabella; anticancer natural compound.
in vitro: Arglabin-stimulated macrophages displayed a strong cytotoxic activity and the lowest doses (1.25 micrograms/mL and 0.125 micrograms/mL) induced a significant stimulation of cell mitochondrial metabolism, which correlated with [3H]TdR uptake by J774.1 cells under the same experimental conditions. Arglabin triggered the production of the three cytokines from J774-1 cells. However, the pattern of cytokine secretion differed to some extent, according to the methodology used for cytokine measurement: either traditional bioassay or specific immunoassay (ELISA). Arglabin exhibits antiexudative and antiproliferative properties on the models of acute aseptic inflammation caused by formalin, carrageenan, and histamine, and on the model of proliferative inflammation accompanying cotton-pellet granuloma. Arglabin is able to reduce the proportion of AML stem cells (CD34+CD38-) in primary AML cells.
For research only, not for human use!
Bevirimat(PA-457,MPC-4326; FH11327; YK FH312)
Bevirimat(PA-457,MPC-4326; FH11327; YK FH312)
Bevirimat(YK FH312; FH11327; MPC-4326) is an anti-HIV drug derived from a betulinic acid-like compound; is believed to inhibit HIV by a novel mechanism, so-called maturation inhibition.
Product Name: Bevirimat(PA-457) |Cat No: DC9643|Cas: 174022-42-5|Molecule Formular: C36H56O6|Molecule Weight: 584.83|Other names: Bevirimat(PA-457)
Bevirimat(YK FH312; FH11327; MPC-4326) is an anti-HIV drug derived from a betulinic acid-like compound; is believed to inhibit HIV by a novel mechanism, so-called maturation inhibition.
Like protease inhibitors, bevirimat and other maturation inhibitors interfere with protease processing of newly translated HIV polyprotein precursor, called gag. Bevirimat prevents this viral replication by specifically inhibiting cleavage of the capsid protein (CA) from the SP1 spacer protein.
For research only, not for human use!
Bevirimat(YK FH312; FH11327; MPC-4326) is an anti-HIV drug derived from a betulinic acid-like compound; is believed to inhibit HIV by a novel mechanism, so-called maturation inhibition.
Product Name: Bevirimat(PA-457) |Cat No: DC9643|Cas: 174022-42-5|Molecule Formular: C36H56O6|Molecule Weight: 584.83|Other names: Bevirimat(PA-457)
Bevirimat(YK FH312; FH11327; MPC-4326) is an anti-HIV drug derived from a betulinic acid-like compound; is believed to inhibit HIV by a novel mechanism, so-called maturation inhibition.
Like protease inhibitors, bevirimat and other maturation inhibitors interfere with protease processing of newly translated HIV polyprotein precursor, called gag. Bevirimat prevents this viral replication by specifically inhibiting cleavage of the capsid protein (CA) from the SP1 spacer protein.
For research only, not for human use!
FIIN-3，FIIN3|CAS 1637735-84-2
FIIN-3，FIIN3|CAS 1637735-84-2
FIIN-3 is a potent, selective, irreversible and the next-generation covalent FGFR inhibitor.
Product Name: FIIN-3|Cat No: DC9642|Cas: 1637735-84-2 |Molecule Formular: C34H36Cl2N8O4 |Molecule Weight: 690.22|Other names: FIIN-3
FIIN-3 is a potent, selective, irreversible and the next-generation covalent FGFR inhibitor. FIIN-3 is the first inhibitor that can potently inhibit the proliferation of cells dependent upon the gatekeeper mutants of FGFR1 or FGFR2, which confer resistance to first-generation clinical FGFR inhibitors such as NVP-BGJ398 and AZD4547. FIIN-3 has the unprecedented ability to inhibit both the EGF receptor (EGFR) and FGFR covalently by targeting two distinct cysteine residues. FIIN-3 bound with FGFR4 V550L and EGFR L858R.
For research only, not for human use!
FIIN-3 is a potent, selective, irreversible and the next-generation covalent FGFR inhibitor.
Product Name: FIIN-3|Cat No: DC9642|Cas: 1637735-84-2 |Molecule Formular: C34H36Cl2N8O4 |Molecule Weight: 690.22|Other names: FIIN-3
FIIN-3 is a potent, selective, irreversible and the next-generation covalent FGFR inhibitor. FIIN-3 is the first inhibitor that can potently inhibit the proliferation of cells dependent upon the gatekeeper mutants of FGFR1 or FGFR2, which confer resistance to first-generation clinical FGFR inhibitors such as NVP-BGJ398 and AZD4547. FIIN-3 has the unprecedented ability to inhibit both the EGF receptor (EGFR) and FGFR covalently by targeting two distinct cysteine residues. FIIN-3 bound with FGFR4 V550L and EGFR L858R.
For research only, not for human use!
NSC348884,NSC-348884|CAS 81624-55-7
NSC348884,NSC-348884|CAS 81624-55-7
NSC348884 is a nucleolar phosphoprotein that displays several biological activities in ribosome biogenesis, cell proliferation, cytoplasmic/nuclear shuttle transportation, nucleic acid binding, ribonucleic cleavage, and centrosome duplication.
Product Name: NSC348884|Cat No: DC9641|Cas: 81624-55-7 |Molecule Formular: C38H40N10|Molecule Weight: 636.79|Other names: NSC348884
NSC348884 is a nucleolar phosphoprotein that displays several biological activities in ribosome biogenesis, cell proliferation, cytoplasmic/nuclear shuttle transportation, nucleic acid binding, ribonucleic cleavage, and centrosome duplication. NSC 348884 is a putative inhibitor of nucleophosmin (nucleolar phosphoprotein B23). NSC 348884 inhibits NPM oligomer formation, up-regulates p53 and induces apoptosis.
For research only, not for human use!
NSC348884 is a nucleolar phosphoprotein that displays several biological activities in ribosome biogenesis, cell proliferation, cytoplasmic/nuclear shuttle transportation, nucleic acid binding, ribonucleic cleavage, and centrosome duplication.
Product Name: NSC348884|Cat No: DC9641|Cas: 81624-55-7 |Molecule Formular: C38H40N10|Molecule Weight: 636.79|Other names: NSC348884
NSC348884 is a nucleolar phosphoprotein that displays several biological activities in ribosome biogenesis, cell proliferation, cytoplasmic/nuclear shuttle transportation, nucleic acid binding, ribonucleic cleavage, and centrosome duplication. NSC 348884 is a putative inhibitor of nucleophosmin (nucleolar phosphoprotein B23). NSC 348884 inhibits NPM oligomer formation, up-regulates p53 and induces apoptosis.
For research only, not for human use!
gamma-secretase modulator 3|cas 1431697-84-5|DC Chemicals
gamma-secretase modulator 3|cas 1431697-84-5|DC Chemicals
gamma-secretase modulator 3 is a gamma-secretase modulator.
Product Name: gamma-secretase modulator 3|Cat No: DC9640|Cas: 1431697-84-5|Molecule Formular: C24H23FN4OS|Molecule Weight: 434.529|Other names: gamma-secretase modulator 3
gamma-secretase modulator 3 is a gamma-secretase modulator.
For research only, not for human use!
gamma-secretase modulator 3 is a gamma-secretase modulator.
Product Name: gamma-secretase modulator 3|Cat No: DC9640|Cas: 1431697-84-5|Molecule Formular: C24H23FN4OS|Molecule Weight: 434.529|Other names: gamma-secretase modulator 3
gamma-secretase modulator 3 is a gamma-secretase modulator.
For research only, not for human use!
iCRT 14|cas 677331-12-3|DC Chemicals
iCRT 14|cas 677331-12-3|DC Chemicals
iCRT 14 is a novel potent inhibitor of β-catenin-responsive transcription (CRT) (IC50 = 40.3 nM in assays of Wnt pathway activity).
IC50 value: 40.3 nM
Target: Wnt inhibitor
Thought to directly influence the interaction between β-catenin and TCF4.
Product Name: iCRT 14|Cat No: DC9639|Cas: 677331-12-3|Molecule Formular: C21H17N3O2S|Molecule Weight: 375.4436|Other names: iCRT 14
iCRT 14 is a novel potent inhibitor of β-catenin-responsive transcription (CRT) (IC50 = 40.3 nM in assays of Wnt pathway activity).
Thought to directly influence the interaction between β-catenin and TCF4. Induces marked G0/G1 cell cycle arrest in HCT-116 and HT29 cell lines.
For research only, not for human use!
iCRT 14 is a novel potent inhibitor of β-catenin-responsive transcription (CRT) (IC50 = 40.3 nM in assays of Wnt pathway activity).
IC50 value: 40.3 nM
Target: Wnt inhibitor
Thought to directly influence the interaction between β-catenin and TCF4.
Product Name: iCRT 14|Cat No: DC9639|Cas: 677331-12-3|Molecule Formular: C21H17N3O2S|Molecule Weight: 375.4436|Other names: iCRT 14
iCRT 14 is a novel potent inhibitor of β-catenin-responsive transcription (CRT) (IC50 = 40.3 nM in assays of Wnt pathway activity).
Thought to directly influence the interaction between β-catenin and TCF4. Induces marked G0/G1 cell cycle arrest in HCT-116 and HT29 cell lines.
For research only, not for human use!
BMS-794833|cas 1174046-72-0|DC Chemicals
BMS-794833|cas 1174046-72-0|DC Chemicals
BMS-794833 is a potent ATP competitive inhibitor of Met/VEGFR2 with IC50 of 1.7/15 nM; also inhibits Ron, Axl and Flt3 with IC50 of <3 nM; a prodrug of BMS-817378.
IC50 value: 1.7/15 nM [1]
Target: Met/VEGFR2
BMS794833 also inhibits Met receptor activated gastric carcinoma cell line, GTL-16, with IC50 of 39 nM.
Product Name: BMS-794833|Cat No: DC9638|Cas: 1174046-72-0|Molecule Formular: C23H15ClF2N4O3|Molecule Weight: 468.84|Other names: BMS-794833
BMS-794833 is a potent ATP competitive inhibitor of Met/VEGFR2 with IC50 of 1.7/15 nM; also inhibits Ron, Axl and Flt3 with IC50 of <3 nM; a prodrug of BMS-817378.
BMS794833 also inhibits Met receptor activated gastric carcinoma cell line, GTL-16, with IC50 of 39 nM. In GTL-16 human gastric tumor xenografts model, BMS798433 shows greater than 50% TGI for at least one tumor doubling time with no overt toxicity observed during 14 days. BMS798433 also shows complete tumor stasis at a dose of 25 mg/kg against U87 glioblastoma model.
For research only, not for human use!
BMS-794833 is a potent ATP competitive inhibitor of Met/VEGFR2 with IC50 of 1.7/15 nM; also inhibits Ron, Axl and Flt3 with IC50 of <3 nM; a prodrug of BMS-817378.
IC50 value: 1.7/15 nM [1]
Target: Met/VEGFR2
BMS794833 also inhibits Met receptor activated gastric carcinoma cell line, GTL-16, with IC50 of 39 nM.
Product Name: BMS-794833|Cat No: DC9638|Cas: 1174046-72-0|Molecule Formular: C23H15ClF2N4O3|Molecule Weight: 468.84|Other names: BMS-794833
BMS-794833 is a potent ATP competitive inhibitor of Met/VEGFR2 with IC50 of 1.7/15 nM; also inhibits Ron, Axl and Flt3 with IC50 of <3 nM; a prodrug of BMS-817378.
BMS794833 also inhibits Met receptor activated gastric carcinoma cell line, GTL-16, with IC50 of 39 nM. In GTL-16 human gastric tumor xenografts model, BMS798433 shows greater than 50% TGI for at least one tumor doubling time with no overt toxicity observed during 14 days. BMS798433 also shows complete tumor stasis at a dose of 25 mg/kg against U87 glioblastoma model.
For research only, not for human use!
Desmopressin (Acetate)|cas 62288-83-9|DC Chemicals
Desmopressin (Acetate)|cas 62288-83-9|DC Chemicals
Desmopressin(DDAVP) acetate is the synthetic analogue of the antidiuretic hormone arginine vasopressin.
Product Name: Desmopressin (Acetate)|Cat No: DC9637|Cas: 62288-83-9|Molecule Formular: C48H68N14O14S2|Molecule Weight: 1129.269|Other names: Desmopressin (Acetate)
Desmopressin(DDAVP) acetate is the synthetic analogue of the antidiuretic hormone arginine vasopressin.
The antidiuretic properties of desmopressin have led to its use in polyuric conditions including primary nocturnal enuresis, nocturia, and diabetes insipidus. Desmopressin works by limiting the amount of water that is eliminated in the urine. Desmopressin binds to V2 receptors in renal collecting ducts, increasing water reabsorption. It also stimulates release of von Willebrand factor from endothelial cells by acting on the V2 receptor.
For research only, not for human use!
Desmopressin(DDAVP) acetate is the synthetic analogue of the antidiuretic hormone arginine vasopressin.
Product Name: Desmopressin (Acetate)|Cat No: DC9637|Cas: 62288-83-9|Molecule Formular: C48H68N14O14S2|Molecule Weight: 1129.269|Other names: Desmopressin (Acetate)
Desmopressin(DDAVP) acetate is the synthetic analogue of the antidiuretic hormone arginine vasopressin.
The antidiuretic properties of desmopressin have led to its use in polyuric conditions including primary nocturnal enuresis, nocturia, and diabetes insipidus. Desmopressin works by limiting the amount of water that is eliminated in the urine. Desmopressin binds to V2 receptors in renal collecting ducts, increasing water reabsorption. It also stimulates release of von Willebrand factor from endothelial cells by acting on the V2 receptor.
For research only, not for human use!
Pyr6|cas 245747-08-4|DC Chemicals
Pyr6|cas 245747-08-4|DC Chemicals
Pyr6 is a selective inhibitor of TRPC3 with IC50 of 0.49 uM(Ca2+ influx inhibition in thapsigargin depleted native RBL-2H3 cells).
IC50 value: 0.49 uM
Target: TRPC3 inhibitor
Pyr6 is a selective SOCE inhibitor (Yonetoku et al., 2008; Sweeney et al., 2009), Pyr6 displayed 37-fold (1.58 OM) higher potency for RBL SOCE than for TRPC3 ROCE, with an IC50 comparable to that of Pyr2 and Pyr3.
Product Name: Pyr6|Cat No: DC9636|Cas: 245747-08-4|Molecule Formular: C17H9F7N4O|Molecule Weight: 418.2684|Other names: Pyr6
Pyr6 is a selective inhibitor of TRPC3 with IC50 of 0.49 uM(Ca2+ influx inhibition in thapsigargin depleted native RBL-2H3 cells).
Pyr6 is a selective SOCE inhibitor (Yonetoku et al., 2008; Sweeney et al., 2009), Pyr6 displayed 37-fold (1.58 OM) higher potency for RBL SOCE than for TRPC3 ROCE, with an IC50 comparable to that of Pyr2 and Pyr3. Pyr6 at 3 uM diminished TRPC3 currents to only 52%. Consistent with inhibition of Orai channel activity Pyr2, Pyr3 or Pyr6 substantially inhibited typical Orai downstream signalling events in RBL mast cells (NFAT activation and degranulation) activated by passive store depletion.
For research only, not for human use!
Pyr6 is a selective inhibitor of TRPC3 with IC50 of 0.49 uM(Ca2+ influx inhibition in thapsigargin depleted native RBL-2H3 cells).
IC50 value: 0.49 uM
Target: TRPC3 inhibitor
Pyr6 is a selective SOCE inhibitor (Yonetoku et al., 2008; Sweeney et al., 2009), Pyr6 displayed 37-fold (1.58 OM) higher potency for RBL SOCE than for TRPC3 ROCE, with an IC50 comparable to that of Pyr2 and Pyr3.
Product Name: Pyr6|Cat No: DC9636|Cas: 245747-08-4|Molecule Formular: C17H9F7N4O|Molecule Weight: 418.2684|Other names: Pyr6
Pyr6 is a selective inhibitor of TRPC3 with IC50 of 0.49 uM(Ca2+ influx inhibition in thapsigargin depleted native RBL-2H3 cells).
Pyr6 is a selective SOCE inhibitor (Yonetoku et al., 2008; Sweeney et al., 2009), Pyr6 displayed 37-fold (1.58 OM) higher potency for RBL SOCE than for TRPC3 ROCE, with an IC50 comparable to that of Pyr2 and Pyr3. Pyr6 at 3 uM diminished TRPC3 currents to only 52%. Consistent with inhibition of Orai channel activity Pyr2, Pyr3 or Pyr6 substantially inhibited typical Orai downstream signalling events in RBL mast cells (NFAT activation and degranulation) activated by passive store depletion.
For research only, not for human use!
SB-705498|cas 501951-42-4|DC Chemicals
SB-705498|cas 501951-42-4|DC Chemicals
SB-705498 is a potent, selective and orally bioavailable transient receptor potential vanilloid 1 (TRPV1) receptor antagonist with a pIC50 of 7.1.
Product Name: SB-705498|Cat No: DC9635|Cas: 501951-42-4|Molecule Formular: C17H16BrF3N4O|Molecule Weight: 429.2343|Other names: SB-705498
SB-705498 is a potent, selective and orally bioavailable transient receptor potential vanilloid 1 (TRPV1) receptor antagonist with a pIC50 of 7.1.
SB-705498 potently inhibits capsaicin-induced activation of human TRPV1 expressed in 1321N1 cells or HEK293 cells with apparent pKi of 7.5 or 7.6, respectively. Coapplication of 100 nM SB-705498 rapidly, completely and reversibly inhibits hTRPV1 expressed in HEK293 cells. Compared with placebo, SB-705498 reduced the area of capsaicin-evoked flare (P=0.0047). The heat pain threshold on non-sensitised skin was elevated following SB-705498 (estimated difference from placebo [95% confidence intervals]: 1.3 degrees C [0.07,2.53], P=0.019). Following capsaicin sensitisation, the heat pain threshold and tolerance were similar between SB-705498 and placebo. However, SB-705498 increased heat pain tolerance at the site of UVB-evoked inflammation (estimated difference from placebo: 0.93 degrees C [0.25,1.6], P=0.0054). The magnitude of the pharmacodynamic effects of SB-705498 appeared to be related to plasma concentration. These results indicate that SB-705498, at a clinically safe and well-tolerated dose, has target-specific pharmacodynamic activity in humans. These data provide the first clinical evidence that a TRPV1 antagonist may alleviate pain and hyperalgesia associated with inflammation and tissue injury.
For research only, not for human use!
SB-705498 is a potent, selective and orally bioavailable transient receptor potential vanilloid 1 (TRPV1) receptor antagonist with a pIC50 of 7.1.
Product Name: SB-705498|Cat No: DC9635|Cas: 501951-42-4|Molecule Formular: C17H16BrF3N4O|Molecule Weight: 429.2343|Other names: SB-705498
SB-705498 is a potent, selective and orally bioavailable transient receptor potential vanilloid 1 (TRPV1) receptor antagonist with a pIC50 of 7.1.
SB-705498 potently inhibits capsaicin-induced activation of human TRPV1 expressed in 1321N1 cells or HEK293 cells with apparent pKi of 7.5 or 7.6, respectively. Coapplication of 100 nM SB-705498 rapidly, completely and reversibly inhibits hTRPV1 expressed in HEK293 cells. Compared with placebo, SB-705498 reduced the area of capsaicin-evoked flare (P=0.0047). The heat pain threshold on non-sensitised skin was elevated following SB-705498 (estimated difference from placebo [95% confidence intervals]: 1.3 degrees C [0.07,2.53], P=0.019). Following capsaicin sensitisation, the heat pain threshold and tolerance were similar between SB-705498 and placebo. However, SB-705498 increased heat pain tolerance at the site of UVB-evoked inflammation (estimated difference from placebo: 0.93 degrees C [0.25,1.6], P=0.0054). The magnitude of the pharmacodynamic effects of SB-705498 appeared to be related to plasma concentration. These results indicate that SB-705498, at a clinically safe and well-tolerated dose, has target-specific pharmacodynamic activity in humans. These data provide the first clinical evidence that a TRPV1 antagonist may alleviate pain and hyperalgesia associated with inflammation and tissue injury.
For research only, not for human use!
Amsacrine|cas 51264-14-3|DC Chemicals
Amsacrine|cas 51264-14-3|DC Chemicals
Amsacrine (mAMSA) an antineoplastic agent which can intercalate into the DNA of tumor cells.
Product Name: Amsacrine|Cat No: DC9634|Cas: 51264-14-3|Molecule Formular: C21H19N3O3S|Molecule Weight: 393.4589|Other names: Amsacrine
Amsacrine (mAMSA) an antineoplastic agent which can intercalate into the DNA of tumor cells. Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II.
in vitro: Amsacrine attenuated cell invasion with decreased MMP-2/MMP-9 protein expression and mRNA levels in U937, Jurkat, HL-60, K562, KU812 and MEG-01 cells. Moreover, amsacrine reduced both MMP-2/MMP-9 promoter luciferase activity and MMP-2/MMP-9 mRNA stability in leukemia cells.Studies on amsacrine-treated U937 cells revealed that amsacrine-elicited ROS generation induced JNK and p38 MAPK activation but reduced the phospho-ERK level. Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively. Amsacrine blocked HERG currents in HEK 293 cells and Xenopus oocytes in a concentration-dependent manner, with IC50 values of 209.4 nm and 2.0 microm, respectively.
in vivo: In animals treated with different doses of amsacrine (0.5-12 mg kg(-1) ), the frequencies of micronucleated polychromatic erythrocytes increased significantly after treatment with 9 and 12 mg kg(-1) . In the in vivo studies, eight patients receiving 30 mg/m2/day of m-AMSA by continuous infusion showed increased levels of chromosomal aberrations, up to a maximum of 14% (median; range, 10%-24%) at 96 hours compared to 1% (median; range, 0%-4%) in the control group; no increase was noted in SCE frequencies.
For research only, not for human use!
Amsacrine (mAMSA) an antineoplastic agent which can intercalate into the DNA of tumor cells.
Product Name: Amsacrine|Cat No: DC9634|Cas: 51264-14-3|Molecule Formular: C21H19N3O3S|Molecule Weight: 393.4589|Other names: Amsacrine
Amsacrine (mAMSA) an antineoplastic agent which can intercalate into the DNA of tumor cells. Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II.
in vitro: Amsacrine attenuated cell invasion with decreased MMP-2/MMP-9 protein expression and mRNA levels in U937, Jurkat, HL-60, K562, KU812 and MEG-01 cells. Moreover, amsacrine reduced both MMP-2/MMP-9 promoter luciferase activity and MMP-2/MMP-9 mRNA stability in leukemia cells.Studies on amsacrine-treated U937 cells revealed that amsacrine-elicited ROS generation induced JNK and p38 MAPK activation but reduced the phospho-ERK level. Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively. Amsacrine blocked HERG currents in HEK 293 cells and Xenopus oocytes in a concentration-dependent manner, with IC50 values of 209.4 nm and 2.0 microm, respectively.
in vivo: In animals treated with different doses of amsacrine (0.5-12 mg kg(-1) ), the frequencies of micronucleated polychromatic erythrocytes increased significantly after treatment with 9 and 12 mg kg(-1) . In the in vivo studies, eight patients receiving 30 mg/m2/day of m-AMSA by continuous infusion showed increased levels of chromosomal aberrations, up to a maximum of 14% (median; range, 10%-24%) at 96 hours compared to 1% (median; range, 0%-4%) in the control group; no increase was noted in SCE frequencies.
For research only, not for human use!
Toll-like receptor modulator|cas 926927-42-6|DC Chemicals
Toll-like receptor modulator|cas 926927-42-6|DC Chemicals
A Toll-like receptor modulator.
Product Name: Toll-like receptor modulator|Cat No: DC9633|Cas: 926927-42-6|Molecule Formular: C15H13F5N2O2|Molecule Weight: 348.2679|Other names: Toll-like receptor modulator
A Toll-like receptor modulator.
For research only, not for human use!
A Toll-like receptor modulator.
Product Name: Toll-like receptor modulator|Cat No: DC9633|Cas: 926927-42-6|Molecule Formular: C15H13F5N2O2|Molecule Weight: 348.2679|Other names: Toll-like receptor modulator
A Toll-like receptor modulator.
For research only, not for human use!
BAY 61-3606 (dihydrochloride)|cas 648903-57-5|DC Chemicals
BAY 61-3606 (dihydrochloride)|cas 648903-57-5|DC Chemicals
BAY 61-3606 (dihydrochloride)|cas 648903-57-5|DC Chemicals
BAY 61-3606 2Hcl is a potent, ATP-competitive, reversible, and highly selective inhibitor of Syk tyrosine kinase activity (Ki= 7.5 nM) with no inhibitory effect against Btk, Fyn, Itk, Lyn, and Src.
IC50 value: 7.5 nM (Ki) [1]
Target: Syk
in vitro: BAY 61-3606 inhibited not only degranulation (IC50 values between 5 and 46 nM) but also lipid mediator and cytokine synthesis in mast cells.
Product Name: BAY 61-3606 (dihydrochloride)|Cat No: DC9632|Cas: 648903-57-5|Molecule Formular: C20H20Cl2N6O3|Molecule Weight: 463.3172|Other names: BAY 61-3606 (dihydrochloride)
BAY 61-3606 is a potent, ATP-competitive, reversible, and highly selective inhibitor of Syk tyrosine kinase activity (Ki= 7.5 nM) with no inhibitory effect against Btk, Fyn, Itk, Lyn, and Src.
in vitro: BAY 61-3606 inhibited not only degranulation (IC50 values between 5 and 46 nM) but also lipid mediator and cytokine synthesis in mast cells. BAY 61-3606 was highly efficacious in basophils obtained from healthy human subjects (IC50 = 10 nM) and seems to be at least as potent in basophils obtained from atopic (high serum IgE) subjects (IC50 = 8.1 nM). B cell receptor activation and receptors for Fc portion of IgG signaling in eosinophils and monocytes were also potently suppressed by BAY 61-3606. We identified BAY61-3606 as an inhibitor of proliferation in colorectal cancer cells expressing mutant forms of K-RAS, but not in isogenic cells expressing wild-type K-RAS. In addition to its anti-proliferative effects in mutant cells, BAY61-3606 exhibited a distinct biological property in wild-type cells in that it conferred sensitivity to inhibition of RAF. In this context, BAY61-3606 acted by inhibiting MAP4K2 (GCK), which normally activates NFκβ signaling in wild-type cells in response to inhibition of RAF.
in vivo: Oral administration of BAY 61-3606 to rats significantly suppressed antigen-induced passive cutaneous anaphylactic reaction, bronchoconstriction, and bronchial edema at 3 mg/kg. Furthermore, BAY 61-3606 attenuated antigen-induced airway inflammation in rats.
For research only, not for human use!
BAY 61-3606 (dihydrochloride)|cas 648903-57-5|DC Chemicals
BAY 61-3606 2Hcl is a potent, ATP-competitive, reversible, and highly selective inhibitor of Syk tyrosine kinase activity (Ki= 7.5 nM) with no inhibitory effect against Btk, Fyn, Itk, Lyn, and Src.
IC50 value: 7.5 nM (Ki) [1]
Target: Syk
in vitro: BAY 61-3606 inhibited not only degranulation (IC50 values between 5 and 46 nM) but also lipid mediator and cytokine synthesis in mast cells.
Product Name: BAY 61-3606 (dihydrochloride)|Cat No: DC9632|Cas: 648903-57-5|Molecule Formular: C20H20Cl2N6O3|Molecule Weight: 463.3172|Other names: BAY 61-3606 (dihydrochloride)
BAY 61-3606 is a potent, ATP-competitive, reversible, and highly selective inhibitor of Syk tyrosine kinase activity (Ki= 7.5 nM) with no inhibitory effect against Btk, Fyn, Itk, Lyn, and Src.
in vitro: BAY 61-3606 inhibited not only degranulation (IC50 values between 5 and 46 nM) but also lipid mediator and cytokine synthesis in mast cells. BAY 61-3606 was highly efficacious in basophils obtained from healthy human subjects (IC50 = 10 nM) and seems to be at least as potent in basophils obtained from atopic (high serum IgE) subjects (IC50 = 8.1 nM). B cell receptor activation and receptors for Fc portion of IgG signaling in eosinophils and monocytes were also potently suppressed by BAY 61-3606. We identified BAY61-3606 as an inhibitor of proliferation in colorectal cancer cells expressing mutant forms of K-RAS, but not in isogenic cells expressing wild-type K-RAS. In addition to its anti-proliferative effects in mutant cells, BAY61-3606 exhibited a distinct biological property in wild-type cells in that it conferred sensitivity to inhibition of RAF. In this context, BAY61-3606 acted by inhibiting MAP4K2 (GCK), which normally activates NFκβ signaling in wild-type cells in response to inhibition of RAF.
in vivo: Oral administration of BAY 61-3606 to rats significantly suppressed antigen-induced passive cutaneous anaphylactic reaction, bronchoconstriction, and bronchial edema at 3 mg/kg. Furthermore, BAY 61-3606 attenuated antigen-induced airway inflammation in rats.
For research only, not for human use!
Desvenlafaxine (succinate hydrate)|cas 386750-22-7|DC Chemicals
Desvenlafaxine (succinate hydrate)|cas 386750-22-7|DC Chemicals
Desvenlafaxine succinate hydrate is an antidepressant of the serotonin-norepinephrine reuptake inhibitor (SNRI).
Product Name: Desvenlafaxine (succinate hydrate)|Cat No: DC9631|Cas: 386750-22-7|Molecule Formular: C20H33NO7|Molecule Weight: 399.4785|Other names: Desvenlafaxine (succinate hydrate)
Desvenlafaxine succinate hydrate is an antidepressant of the serotonin-norepinephrine reuptake inhibitor (SNRI).
For research only, not for human use!
Desvenlafaxine succinate hydrate is an antidepressant of the serotonin-norepinephrine reuptake inhibitor (SNRI).
Product Name: Desvenlafaxine (succinate hydrate)|Cat No: DC9631|Cas: 386750-22-7|Molecule Formular: C20H33NO7|Molecule Weight: 399.4785|Other names: Desvenlafaxine (succinate hydrate)
Desvenlafaxine succinate hydrate is an antidepressant of the serotonin-norepinephrine reuptake inhibitor (SNRI).
For research only, not for human use!
Dapoxetine (hydrochloride)|cas 129938-20-1|DC Chemicals
Dapoxetine (hydrochloride)|cas 129938-20-1|DC Chemicals
Dapoxetine HCl is a short-acting novel selective serotonin reuptake inhibitor(SSRI).
Target: SSRI
Dapoxetine hydrochloride is a short-acting novel selective serotonin reuptake inhibitor marketed for the treatment of premature ejaculation in men.
Product Name: Dapoxetine (hydrochloride)|Cat No: DC9630|Cas: 129938-20-1|Molecule Formular: C21H24ClNO|Molecule Weight: 341.8744|Other names: Dapoxetine (hydrochloride)
Dapoxetine HCl is a short-acting novel selective serotonin reuptake inhibitor(SSRI).
Dapoxetine hydrochloride is a short-acting novel selective serotonin reuptake inhibitor marketed for the treatment of premature ejaculation in men. Premature ejaculation (PE) is the most common male sexual disorder, estimated to affect up to 30% of men. Dapoxetine is the only drug with regulatory approval for such an indication. The treatment of PE consists of primarily off-label use of oral selective serotonin reuptake inhibitors (SSRIs) via either on-demand or daily delivery.
For research only, not for human use!
Dapoxetine HCl is a short-acting novel selective serotonin reuptake inhibitor(SSRI).
Target: SSRI
Dapoxetine hydrochloride is a short-acting novel selective serotonin reuptake inhibitor marketed for the treatment of premature ejaculation in men.
Product Name: Dapoxetine (hydrochloride)|Cat No: DC9630|Cas: 129938-20-1|Molecule Formular: C21H24ClNO|Molecule Weight: 341.8744|Other names: Dapoxetine (hydrochloride)
Dapoxetine HCl is a short-acting novel selective serotonin reuptake inhibitor(SSRI).
Dapoxetine hydrochloride is a short-acting novel selective serotonin reuptake inhibitor marketed for the treatment of premature ejaculation in men. Premature ejaculation (PE) is the most common male sexual disorder, estimated to affect up to 30% of men. Dapoxetine is the only drug with regulatory approval for such an indication. The treatment of PE consists of primarily off-label use of oral selective serotonin reuptake inhibitors (SSRIs) via either on-demand or daily delivery.
For research only, not for human use!
Azaphen (dihydrochloride monohydrate)|cas 63302-99-8|DC Chemicals
Azaphen (dihydrochloride monohydrate)|cas 63302-99-8|DC Chemicals
Pipofezine(Azafen or Azaphen) is a potent inhibitor of the reuptake of serotonin.
Product Name: Azaphen (dihydrochloride monohydrate)|Cat No: DC9629|Cas: 63302-99-8|Molecule Formular: C16H23Cl2N5O2|Molecule Weight: 388.2921|Other names: Azaphen (dihydrochloride monohydrate)
Pipofezine(Azafen or Azaphen) is a potent inhibitor of the reuptake of serotonin.
Pipofezine is a tricyclic antidepressant (TCA) approved in Russia for the treatment ofdepression. In addition to its antidepressant action, pipofezine has sedative effects as well, indicating antihistamine activity.
For research only, not for human use!
Pipofezine(Azafen or Azaphen) is a potent inhibitor of the reuptake of serotonin.
Product Name: Azaphen (dihydrochloride monohydrate)|Cat No: DC9629|Cas: 63302-99-8|Molecule Formular: C16H23Cl2N5O2|Molecule Weight: 388.2921|Other names: Azaphen (dihydrochloride monohydrate)
Pipofezine(Azafen or Azaphen) is a potent inhibitor of the reuptake of serotonin.
Pipofezine is a tricyclic antidepressant (TCA) approved in Russia for the treatment ofdepression. In addition to its antidepressant action, pipofezine has sedative effects as well, indicating antihistamine activity.
For research only, not for human use!
A 419259 (trihydrochloride)|cas 1435934-25-0|DC Chemicals
A 419259 (trihydrochloride)|cas 1435934-25-0|DC Chemicals
A 419259 3Hcl is an apoptosis inducing agent that inhibits Src family kinases (c-Src).
Product Name: A 419259 (trihydrochloride)|Cat No: DC9628|Cas: 1435934-25-0|Molecule Formular: C29H37Cl3N6O|Molecule Weight: 592.0027|Other names: A 419259 (trihydrochloride)
A 419259 3Hcl is an apoptosis inducing agent that inhibits Src family kinases (c-Src). A 419259 also induces apoptosis in CML cell ines and blocks Stat5 and Erk activation.
in vitro: Treatment of the Ph+ CML cell lines K-562 and Meg-01 with A-419259 resulted in growth arrest and induction of apoptosis, while the Ph- leukemia cell lines TF-1 and HEL were unaffected over the same concentration ranges. Suppression of Ph+ cell growth by A-419259 correlated with a decrease in Src kinase autophosphorylation. A-419259 blocked Stat5 and Erk activation, consistent with the suppressive effects of the compounds on survival and proliferation. A-419259 treatment blocks all Src-family kinase activity in ES cells, preventing differentiation while maintaining pluripotency. Expression of inhibitor-resistant c-Src but not c-Yes rescued the A-419259 differentiation block, resulting in a cell population with properties of both primitive ectoderm and endoderm. Blockade of Src family kinases using an Src-specific tyrosine kinase inhibitor A-419259 decreased GRP-induced EGFR phosphorylation and MAPK activation in HNSCC.
For research only, not for human use!
A 419259 3Hcl is an apoptosis inducing agent that inhibits Src family kinases (c-Src).
Product Name: A 419259 (trihydrochloride)|Cat No: DC9628|Cas: 1435934-25-0|Molecule Formular: C29H37Cl3N6O|Molecule Weight: 592.0027|Other names: A 419259 (trihydrochloride)
A 419259 3Hcl is an apoptosis inducing agent that inhibits Src family kinases (c-Src). A 419259 also induces apoptosis in CML cell ines and blocks Stat5 and Erk activation.
in vitro: Treatment of the Ph+ CML cell lines K-562 and Meg-01 with A-419259 resulted in growth arrest and induction of apoptosis, while the Ph- leukemia cell lines TF-1 and HEL were unaffected over the same concentration ranges. Suppression of Ph+ cell growth by A-419259 correlated with a decrease in Src kinase autophosphorylation. A-419259 blocked Stat5 and Erk activation, consistent with the suppressive effects of the compounds on survival and proliferation. A-419259 treatment blocks all Src-family kinase activity in ES cells, preventing differentiation while maintaining pluripotency. Expression of inhibitor-resistant c-Src but not c-Yes rescued the A-419259 differentiation block, resulting in a cell population with properties of both primitive ectoderm and endoderm. Blockade of Src family kinases using an Src-specific tyrosine kinase inhibitor A-419259 decreased GRP-induced EGFR phosphorylation and MAPK activation in HNSCC.
For research only, not for human use!
AZM475271|cas 476159-98-5|DC Chemicals
AZM475271|cas 476159-98-5|DC Chemicals
AZM475271 is a potent and selective Src kinase inhibitor with IC50 of 5 nM; no inhibitory activity on Flt3, KDR, Tie-2.
IC50 value: 5 nM [1]
Target: Src inhibitor
in vitro: AZM475271 demonstrated strong dose-dependent inhibition of Src tyrosine kinase activity in the L3.6pl human pancreatic carcinoma cell line.
Product Name: AZM475271|Cat No: DC9627|Cas: 476159-98-5|Molecule Formular: C23H27ClN4O3|Molecule Weight: 442.9385|Other names: AZM475271
AZM475271 is a potent and selective Src kinase inhibitor with IC50 of 5 nM; no inhibitory activity on Flt3, KDR, Tie-2.
in vitro: AZM475271 demonstrated strong dose-dependent inhibition of Src tyrosine kinase activity in the L3.6pl human pancreatic carcinoma cell line. Maximum reduction of Src kinase activity was observed after incubation for 4 hours with ≥5 μmol/L. The IC50 concentration of AZM475271 to inhibit the phosphorylation of c-src, lck, and c-yes was 0.01, 0.03, and 0.08 μmol/L, respectively, in comparison with an IC50 of 0.7 μmol/L AZM475271 to inhibit KDR.
in vivo: Tumors appeared to be palpable at day 14 after tumor cell injection in all animals except mice treated with both AZM475271 and gemcitabine, in which the earliest possible palpation of the tumors was at day 17 after tumor cell injection. Treatment with gemcitabine or AZM475271 alone did not significantly change animal weight.
For research only, not for human use!
AZM475271 is a potent and selective Src kinase inhibitor with IC50 of 5 nM; no inhibitory activity on Flt3, KDR, Tie-2.
IC50 value: 5 nM [1]
Target: Src inhibitor
in vitro: AZM475271 demonstrated strong dose-dependent inhibition of Src tyrosine kinase activity in the L3.6pl human pancreatic carcinoma cell line.
Product Name: AZM475271|Cat No: DC9627|Cas: 476159-98-5|Molecule Formular: C23H27ClN4O3|Molecule Weight: 442.9385|Other names: AZM475271
AZM475271 is a potent and selective Src kinase inhibitor with IC50 of 5 nM; no inhibitory activity on Flt3, KDR, Tie-2.
in vitro: AZM475271 demonstrated strong dose-dependent inhibition of Src tyrosine kinase activity in the L3.6pl human pancreatic carcinoma cell line. Maximum reduction of Src kinase activity was observed after incubation for 4 hours with ≥5 μmol/L. The IC50 concentration of AZM475271 to inhibit the phosphorylation of c-src, lck, and c-yes was 0.01, 0.03, and 0.08 μmol/L, respectively, in comparison with an IC50 of 0.7 μmol/L AZM475271 to inhibit KDR.
in vivo: Tumors appeared to be palpable at day 14 after tumor cell injection in all animals except mice treated with both AZM475271 and gemcitabine, in which the earliest possible palpation of the tumors was at day 17 after tumor cell injection. Treatment with gemcitabine or AZM475271 alone did not significantly change animal weight.
For research only, not for human use!
Lck Inhibitor|cas 847950-09-8|DC Chemicals
Lck Inhibitor|cas 847950-09-8|DC Chemicals
Lck Inhibitor is a new class of compounds that are potent inhibitors of Lck with an IC50 value of 7 nM.
IC50 Value: 7 nM [1]
Target: Lck
in vitro: Lck Inhibitor (compound 25) exhibited good potency in the T-cell receptor-induced IL-2 secretion assay (IL- 2) and also inhibited subsequent T-cell proliferation (T-cell prolif.) in the same human T -cells.
in vivo: A once daily dose of 25was administered orally at 10, 30, and 60 mg/kg from day 9 today 17.
Product Name: Lck Inhibitor|Cat No: DC9626|Cas: 847950-09-8|Molecule Formular: C31H30N8O|Molecule Weight: 530.6229|Other names: Lck Inhibitor
Lck Inhibitor is a new class of compounds that are potent inhibitors of Lck with an IC50 value of 7 nM.
in vitro: Lck Inhibitor (compound 25) exhibited good potency in the T-cell receptor-induced IL-2 secretion assay (IL- 2) and also inhibited subsequent T-cell proliferation (T-cell prolif.) in the same human T -cells.
in vivo: A once daily dose of 25was administered orally at 10, 30, and 60 mg/kg from day 9 today 17. Paw volume was measured daily from day 9 through day 18. The compound showed a dose-dependent inhibition of arthritis, with an ED50 estimated at 24 mg/kg (Figure 6). Based on the measured plasma levels from the three dose groups, the exposure of 25 at the ED50 was estimated to be 2.7 μM·h (Cmax≈ 0.7 μM).
For research only, not for human use!
Lck Inhibitor is a new class of compounds that are potent inhibitors of Lck with an IC50 value of 7 nM.
IC50 Value: 7 nM [1]
Target: Lck
in vitro: Lck Inhibitor (compound 25) exhibited good potency in the T-cell receptor-induced IL-2 secretion assay (IL- 2) and also inhibited subsequent T-cell proliferation (T-cell prolif.) in the same human T -cells.
in vivo: A once daily dose of 25was administered orally at 10, 30, and 60 mg/kg from day 9 today 17.
Product Name: Lck Inhibitor|Cat No: DC9626|Cas: 847950-09-8|Molecule Formular: C31H30N8O|Molecule Weight: 530.6229|Other names: Lck Inhibitor
Lck Inhibitor is a new class of compounds that are potent inhibitors of Lck with an IC50 value of 7 nM.
in vitro: Lck Inhibitor (compound 25) exhibited good potency in the T-cell receptor-induced IL-2 secretion assay (IL- 2) and also inhibited subsequent T-cell proliferation (T-cell prolif.) in the same human T -cells.
in vivo: A once daily dose of 25was administered orally at 10, 30, and 60 mg/kg from day 9 today 17. Paw volume was measured daily from day 9 through day 18. The compound showed a dose-dependent inhibition of arthritis, with an ED50 estimated at 24 mg/kg (Figure 6). Based on the measured plasma levels from the three dose groups, the exposure of 25 at the ED50 was estimated to be 2.7 μM·h (Cmax≈ 0.7 μM).
For research only, not for human use!
K145 (hydrochloride)|cas 1449240-68-9|DC Chemicals
K145 (hydrochloride)|cas 1449240-68-9|DC Chemicals
K145 is a selective SphK2 inhibitor with an IC50 of 4.30±0.06 μM , while no inhibition of SphK1 at concentrations up to 10 μM.
IC50 value: 4.3 uM
Target: SphK2
in vitro: K145 inhibited the activity of SphK2 in a dose-dependent manner with an IC50 of 4.30±0.06 uM , while no inhibition of SphK1 at concentrations up to 10 uM was observed.
Product Name: K145 (hydrochloride)|Cat No: DC9625|Cas: 1449240-68-9|Molecule Formular: C18H25ClN2O3S|Molecule Weight: 384.9207|Other names: K145 (hydrochloride)
K145 is a selective SphK2 inhibitor with an IC50 of 4.30±0.06 μM , while no inhibition of SphK1 at concentrations up to 10 μM.
in vitro: K145 inhibited the activity of SphK2 in a dose-dependent manner with an IC50 of 4.30±0.06 uM , while no inhibition of SphK1 at concentrations up to 10 uM was observed. Lineweaver-Burk analysis revealed a Ki of 6.4±0.7 uM for SphK2 and indicated that K145 is a substrate competitive inhibitor (with sphingosine). K145 accumulates in U937 cells, suppresses the S1P level, and inhibits SphK2. K145 also exhibited inhibitory effects on the growth of U937 cells as well as apoptotic effects in U937 cells, and that these effects may be through the inhibition of down-stream ERK and Akt signaling pathways.
in vivo: K145 also significantly inhibited the growth of U937 tumors in nude mice by both intraperitoneal and oral administration, thus demonstrating its in vivo efficacy as a potential lead anticancer agent.
For research only, not for human use!
K145 is a selective SphK2 inhibitor with an IC50 of 4.30±0.06 μM , while no inhibition of SphK1 at concentrations up to 10 μM.
IC50 value: 4.3 uM
Target: SphK2
in vitro: K145 inhibited the activity of SphK2 in a dose-dependent manner with an IC50 of 4.30±0.06 uM , while no inhibition of SphK1 at concentrations up to 10 uM was observed.
Product Name: K145 (hydrochloride)|Cat No: DC9625|Cas: 1449240-68-9|Molecule Formular: C18H25ClN2O3S|Molecule Weight: 384.9207|Other names: K145 (hydrochloride)
K145 is a selective SphK2 inhibitor with an IC50 of 4.30±0.06 μM , while no inhibition of SphK1 at concentrations up to 10 μM.
in vitro: K145 inhibited the activity of SphK2 in a dose-dependent manner with an IC50 of 4.30±0.06 uM , while no inhibition of SphK1 at concentrations up to 10 uM was observed. Lineweaver-Burk analysis revealed a Ki of 6.4±0.7 uM for SphK2 and indicated that K145 is a substrate competitive inhibitor (with sphingosine). K145 accumulates in U937 cells, suppresses the S1P level, and inhibits SphK2. K145 also exhibited inhibitory effects on the growth of U937 cells as well as apoptotic effects in U937 cells, and that these effects may be through the inhibition of down-stream ERK and Akt signaling pathways.
in vivo: K145 also significantly inhibited the growth of U937 tumors in nude mice by both intraperitoneal and oral administration, thus demonstrating its in vivo efficacy as a potential lead anticancer agent.
For research only, not for human use!
(-)-Sparteine (sulfate pentahydrate)|cas 6160-12-9|DC Chemicals
(-)-Sparteine (sulfate pentahydrate)|cas 6160-12-9|DC Chemicals
(-)-Sparteine sulfate pentahydrate is a class 1a antiarrhythmic agent and a sodium channel blocker.
Product Name: (-)-Sparteine (sulfate pentahydrate)|Cat No: DC9624|Cas: 6160-12-9|Molecule Formular: C15H28N2O4S|Molecule Weight: 332.4588|Other names: (-)-Sparteine (sulfate pentahydrate)
(-)-Sparteine sulfate pentahydrate is a class 1a antiarrhythmic agent and a sodium channel blocker. It is an alkaloid, can chelate the bivalents calcium and magnesium.
For research only, not for human use!
(-)-Sparteine sulfate pentahydrate is a class 1a antiarrhythmic agent and a sodium channel blocker.
Product Name: (-)-Sparteine (sulfate pentahydrate)|Cat No: DC9624|Cas: 6160-12-9|Molecule Formular: C15H28N2O4S|Molecule Weight: 332.4588|Other names: (-)-Sparteine (sulfate pentahydrate)
(-)-Sparteine sulfate pentahydrate is a class 1a antiarrhythmic agent and a sodium channel blocker. It is an alkaloid, can chelate the bivalents calcium and magnesium.
For research only, not for human use!
Flecainide (acetate)|cas 54143-56-5|DC Chemicals
Flecainide (acetate)|cas 54143-56-5|DC Chemicals
Flecainide(Tambocor) is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia; works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.
IC50 Value:
Target: Nav1.5 channel
Flecainide is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia.
Product Name: Flecainide (acetate)|Cat No: DC9623|Cas: 54143-56-5|Molecule Formular: C19H24F6N2O5|Molecule Weight: 474.3947|Other names: Flecainide (acetate)
Flecainide(Tambocor) is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia; works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.
Flecainide is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia. Flecainide works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.
in vitro: Under the current-clamp condition, flecainide (1-100 microM) prolonged the action potential duration at both the early and the late phases of repolarization in a concentration-dependent manner without affecting the resting membrane potential. At a holding potential (HP) of -120 mV, flecainide use-dependently blocked WT and G1306E I(Na) equally but was more potent on R1448C channels. For WT, the extent of block depended on a holding voltage more negative than the activation threshold, being greater at -90 mV as compared to -120 and -180 mV.
in vivo: Flecainide (80-130 mg/m(2) orally) resulted in termination of the tachycardia in all 8 patients. Acute pharmacological termination of arrhythmia occurred with oral flecainide loading in 1 and temporarily with intravenous esmolol loading in 1 patient. Adjuvant therapy in form of propranolol was used in 5 and digoxin in 2.
For research only, not for human use!
Flecainide(Tambocor) is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia; works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.
IC50 Value:
Target: Nav1.5 channel
Flecainide is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia.
Product Name: Flecainide (acetate)|Cat No: DC9623|Cas: 54143-56-5|Molecule Formular: C19H24F6N2O5|Molecule Weight: 474.3947|Other names: Flecainide (acetate)
Flecainide(Tambocor) is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia; works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.
Flecainide is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia. Flecainide works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.
in vitro: Under the current-clamp condition, flecainide (1-100 microM) prolonged the action potential duration at both the early and the late phases of repolarization in a concentration-dependent manner without affecting the resting membrane potential. At a holding potential (HP) of -120 mV, flecainide use-dependently blocked WT and G1306E I(Na) equally but was more potent on R1448C channels. For WT, the extent of block depended on a holding voltage more negative than the activation threshold, being greater at -90 mV as compared to -120 and -180 mV.
in vivo: Flecainide (80-130 mg/m(2) orally) resulted in termination of the tachycardia in all 8 patients. Acute pharmacological termination of arrhythmia occurred with oral flecainide loading in 1 and temporarily with intravenous esmolol loading in 1 patient. Adjuvant therapy in form of propranolol was used in 5 and digoxin in 2.
For research only, not for human use!
SN 2|cas 823218-99-1|DC Chemicals
SN 2|cas 823218-99-1|DC Chemicals
SN 2 is a novel and potent small molecule activator of TRPML3 with EC50 of 1.13 uM.
IC50 value: 1.13 uM (EC50)
Target: TRPML3 activator
Compounds SF21, SF-41, and SN-2 elicited a much more rapid increase than the other compounds, with SF-33 and SF 51 displaying the slowest kinetics.
Product Name: SN 2|Cat No: DC9622|Cas: 823218-99-1|Molecule Formular: C17H21NO|Molecule Weight: 255.3547|Other names: SN 2
SN 2 is a novel and potent small molecule activator of TRPML3 with EC50 of 1.13 uM.
Compounds SF21, SF-41, and SN-2 elicited a much more rapid increase than the other compounds, with SF-33 and SF 51 displaying the slowest kinetics. SN-2 had a similar synergistic effect, also reaching up-to 10-fold enhancement of the combined response when compared with the individual responses, reaching average current densities of up to 3 nA/pF at -80 mV.
For research only, not for human use!
SN 2 is a novel and potent small molecule activator of TRPML3 with EC50 of 1.13 uM.
IC50 value: 1.13 uM (EC50)
Target: TRPML3 activator
Compounds SF21, SF-41, and SN-2 elicited a much more rapid increase than the other compounds, with SF-33 and SF 51 displaying the slowest kinetics.
Product Name: SN 2|Cat No: DC9622|Cas: 823218-99-1|Molecule Formular: C17H21NO|Molecule Weight: 255.3547|Other names: SN 2
SN 2 is a novel and potent small molecule activator of TRPML3 with EC50 of 1.13 uM.
Compounds SF21, SF-41, and SN-2 elicited a much more rapid increase than the other compounds, with SF-33 and SF 51 displaying the slowest kinetics. SN-2 had a similar synergistic effect, also reaching up-to 10-fold enhancement of the combined response when compared with the individual responses, reaching average current densities of up to 3 nA/pF at -80 mV.
For research only, not for human use!
Jervine|cas 469-59-0|DC Chemicals
Jervine|cas 469-59-0|DC Chemicals
Jervine(11-Ketocyclopamine) is a naturally occuring steroidal alkaloid that causes cyclopia by blocking sonic hedgehog(Shh) signaling; Jervine is an inhibitor of Smo.
IC50 value:
Target: sonic hedgehog
is derived from the Veratrum plant species.
Product Name: Jervine|Cat No: DC9621|Cas: 469-59-0|Molecule Formular: C27H39NO3|Molecule Weight: 425.6035|Other names: Jervine
Jervine(11-Ketocyclopamine) is a naturally occuring steroidal alkaloid that causes cyclopia by blocking sonic hedgehog(Shh) signaling; Jervine is an inhibitor of Smo.
is derived from the Veratrum plant species. It is a close structural analog of cyclopamine which specifically inhibits the hedgehog (Hh) pathway by interaction with the hedgehog signaling protein Smo. Jervine can be used to induce abnormal morphogenesis in a number of experimental models. Jervine is an inhibitor of Smo.
For research only, not for human use!
Jervine(11-Ketocyclopamine) is a naturally occuring steroidal alkaloid that causes cyclopia by blocking sonic hedgehog(Shh) signaling; Jervine is an inhibitor of Smo.
IC50 value:
Target: sonic hedgehog
is derived from the Veratrum plant species.
Product Name: Jervine|Cat No: DC9621|Cas: 469-59-0|Molecule Formular: C27H39NO3|Molecule Weight: 425.6035|Other names: Jervine
Jervine(11-Ketocyclopamine) is a naturally occuring steroidal alkaloid that causes cyclopia by blocking sonic hedgehog(Shh) signaling; Jervine is an inhibitor of Smo.
is derived from the Veratrum plant species. It is a close structural analog of cyclopamine which specifically inhibits the hedgehog (Hh) pathway by interaction with the hedgehog signaling protein Smo. Jervine can be used to induce abnormal morphogenesis in a number of experimental models. Jervine is an inhibitor of Smo.
For research only, not for human use!
EMD638683|cas 1181770-72-8|DC Chemicals
EMD638683|cas 1181770-72-8|DC Chemicals
EMD638683 is a potent SGK1 inhibitor with an IC50 of 3 uM.
IC50 Value: 3 uM
Target: SGK1
The serum- and glucocorticoid-inducible kinase 1 (SGK1) is transcriptionally upregulated by mineralocorticoids and activated by insulin.
Product Name: EMD638683|Cat No: DC9620|Cas: 1181770-72-8|Molecule Formular: C18H18F2N2O4|Molecule Weight: 364.3433|Other names: EMD638683
EMD638683 is a potent SGK1 inhibitor with an IC50 of 3 uM.
The serum- and glucocorticoid-inducible kinase 1 (SGK1) is transcriptionally upregulated by mineralocorticoids and activated by insulin. EMD638683 could serve as a template for drugs counteracting hypertension in individuals with type II diabetes and metabolic syndrome.
in vitro: EMD638683 was tested in vitro by determination of SGK1-dependent phosphorylation of NDRG1 (N-Myc downstream-regulated gene 1) in human cervical carcinoma HeLa-cells. EMD638683 was a SGK1 inhibitor with an IC50 of 3 μM.
in vivo: Within 24 hours in vivo EMD638683 treatment significantly decreased blood pressure in fructose/saline-treated mice but not in control animals or in SGK1 knockout mice. EMD638683 failed to alter the blood pressure in SGK1 knockout mice. Following chronic (4 weeks) fructose/high salt treatment, additional EMD638683 treatment again decreased blood pressure. EMD638683 thus abrogates the salt sensitivity of blood pressure in hyperinsulinism without appreciably affecting blood pressure in the absence of hyperinsulinism. EMD638683 tended to increase fluid intake and urinary excretion of Na(+), significantly increased urinary flow rate and significantly decreased body weight.
For research only, not for human use!
EMD638683 is a potent SGK1 inhibitor with an IC50 of 3 uM.
IC50 Value: 3 uM
Target: SGK1
The serum- and glucocorticoid-inducible kinase 1 (SGK1) is transcriptionally upregulated by mineralocorticoids and activated by insulin.
Product Name: EMD638683|Cat No: DC9620|Cas: 1181770-72-8|Molecule Formular: C18H18F2N2O4|Molecule Weight: 364.3433|Other names: EMD638683
EMD638683 is a potent SGK1 inhibitor with an IC50 of 3 uM.
The serum- and glucocorticoid-inducible kinase 1 (SGK1) is transcriptionally upregulated by mineralocorticoids and activated by insulin. EMD638683 could serve as a template for drugs counteracting hypertension in individuals with type II diabetes and metabolic syndrome.
in vitro: EMD638683 was tested in vitro by determination of SGK1-dependent phosphorylation of NDRG1 (N-Myc downstream-regulated gene 1) in human cervical carcinoma HeLa-cells. EMD638683 was a SGK1 inhibitor with an IC50 of 3 μM.
in vivo: Within 24 hours in vivo EMD638683 treatment significantly decreased blood pressure in fructose/saline-treated mice but not in control animals or in SGK1 knockout mice. EMD638683 failed to alter the blood pressure in SGK1 knockout mice. Following chronic (4 weeks) fructose/high salt treatment, additional EMD638683 treatment again decreased blood pressure. EMD638683 thus abrogates the salt sensitivity of blood pressure in hyperinsulinism without appreciably affecting blood pressure in the absence of hyperinsulinism. EMD638683 tended to increase fluid intake and urinary excretion of Na(+), significantly increased urinary flow rate and significantly decreased body weight.
For research only, not for human use!
Nafamostat (mesylate)|cas 82956-11-4|DC Chemicals
Nafamostat (mesylate)|cas 82956-11-4|DC Chemicals
Nafamostat mesylate, a synthetic serine protease inhibitor, is an anticoagulant.
Target: Serine Protease
Tranilast (FUT-175) is an antiallergic drug for bronchial asthma.
Product Name: Nafamostat (mesylate)|Cat No: DC9619|Cas: 82956-11-4|Molecule Formular: C21H25N5O8S2|Molecule Weight: 539.5819|Other names: Nafamostat (mesylate)
Nafamostat mesylate, a synthetic serine protease inhibitor, is an anticoagulant.
Tranilast (FUT-175) is an antiallergic drug for bronchial asthma. It has been used for the treatment of allergic disorders such as asthma, allergic rhinitis and atopic dermatitis. It has also been investigated for use as an antiproliferative drug on drug-eluting stents.
A 20-40 mg/h dose of FUT-175 prolonged coagulation time sufficiently in the instrumental blood of the extracorporeal circuit but not in the systemic blood. Its anticoagulant activity decreased immediately after hemodialysis. Therefore, we could manage all patients without any bleeding trouble during hemodialysis with FUT-175 as an anticoagulant. Although there were side effects of FUT-175, such as nausea, vomiting, itching and eruption, they were not serious, and FUT-175 could be administered without interruption. FUT-175 seems to be useful as an anticoagulant during hemodialysis for patients susceptible to bleeding.
For research only, not for human use!
Nafamostat mesylate, a synthetic serine protease inhibitor, is an anticoagulant.
Target: Serine Protease
Tranilast (FUT-175) is an antiallergic drug for bronchial asthma.
Product Name: Nafamostat (mesylate)|Cat No: DC9619|Cas: 82956-11-4|Molecule Formular: C21H25N5O8S2|Molecule Weight: 539.5819|Other names: Nafamostat (mesylate)
Nafamostat mesylate, a synthetic serine protease inhibitor, is an anticoagulant.
Tranilast (FUT-175) is an antiallergic drug for bronchial asthma. It has been used for the treatment of allergic disorders such as asthma, allergic rhinitis and atopic dermatitis. It has also been investigated for use as an antiproliferative drug on drug-eluting stents.
A 20-40 mg/h dose of FUT-175 prolonged coagulation time sufficiently in the instrumental blood of the extracorporeal circuit but not in the systemic blood. Its anticoagulant activity decreased immediately after hemodialysis. Therefore, we could manage all patients without any bleeding trouble during hemodialysis with FUT-175 as an anticoagulant. Although there were side effects of FUT-175, such as nausea, vomiting, itching and eruption, they were not serious, and FUT-175 could be administered without interruption. FUT-175 seems to be useful as an anticoagulant during hemodialysis for patients susceptible to bleeding.
For research only, not for human use!
TMC353121|cas 857066-90-1|DC Chemicals
TMC353121|cas 857066-90-1|DC Chemicals
TMC353121 is a potent RSV fusion inhibitor with pEC50 of 9.9(t1/2 in lung = 25 h).
IC50 value: 9.9(pEC50) [1]
Target: RSV fusion inhibitor
The activity profile of 56d(TMC353121) was found to be identical to the profile of JNJ-2408068.
Product Name: TMC353121|Cat No: DC9618|Cas: 857066-90-1|Molecule Formular: C32H42N6O3|Molecule Weight: 558.7143|Other names: TMC353121
TMC353121 is a potent RSV fusion inhibitor with pEC50 of 9.9(t1/2 in lung = 25 h).
The activity profile of 56d(TMC353121) was found to be identical to the profile of JNJ-2408068. After iv administration, 56d was rapidly eliminated with a plasma clearance of 5.4 L/h/kg. The plasma concentrations dropped quickly within the first hour after dosing and then much more slowly. The plasma half-life determined between 4 and 24 h (last blood sampling time point) was about 10 h. 56d was shown to be active by intravenous, oral, and aerosol administration in the cotton rat model at doses of 10 mg/kg, 40 mg/kg, and 5 mg/mL, respectively.
For research only, not for human use!
TMC353121 is a potent RSV fusion inhibitor with pEC50 of 9.9(t1/2 in lung = 25 h).
IC50 value: 9.9(pEC50) [1]
Target: RSV fusion inhibitor
The activity profile of 56d(TMC353121) was found to be identical to the profile of JNJ-2408068.
Product Name: TMC353121|Cat No: DC9618|Cas: 857066-90-1|Molecule Formular: C32H42N6O3|Molecule Weight: 558.7143|Other names: TMC353121
TMC353121 is a potent RSV fusion inhibitor with pEC50 of 9.9(t1/2 in lung = 25 h).
The activity profile of 56d(TMC353121) was found to be identical to the profile of JNJ-2408068. After iv administration, 56d was rapidly eliminated with a plasma clearance of 5.4 L/h/kg. The plasma concentrations dropped quickly within the first hour after dosing and then much more slowly. The plasma half-life determined between 4 and 24 h (last blood sampling time point) was about 10 h. 56d was shown to be active by intravenous, oral, and aerosol administration in the cotton rat model at doses of 10 mg/kg, 40 mg/kg, and 5 mg/mL, respectively.
For research only, not for human use!
CMK|cas 821794-90-5|DC Chemicals
CMK|cas 821794-90-5|DC Chemicals
CMK is a RSK2 kinase inhibitor.
Product Name: CMK|Cat No: DC9617|Cas: 821794-90-5|Molecule Formular: C18H19ClN4O2|Molecule Weight: 358.8221|Other names: CMK
CMK is a RSK2 kinase inhibitor.
For research only, not for human use!
CMK is a RSK2 kinase inhibitor.
Product Name: CMK|Cat No: DC9617|Cas: 821794-90-5|Molecule Formular: C18H19ClN4O2|Molecule Weight: 358.8221|Other names: CMK
CMK is a RSK2 kinase inhibitor.
For research only, not for human use!
BIX 02565|cas 1311367-27-7|DC Chemicals
BIX 02565|cas 1311367-27-7|DC Chemicals
BIX 02565 is a novel ribosomal S6 kinase 2 (RSK2) inhibitor with an IC50 of 1.1 nM.
IC50 Value: 1.1 nM (RSK2)
Target: RSK2
BIX 02565 is an attractive candidate for use in vitro and in vivo to explore the role of RSK as a target for the treatment heart failure.
Product Name: BIX 02565|Cat No: DC9616|Cas: 1311367-27-7|Molecule Formular: C26H30N6O2|Molecule Weight: 458.5554|Other names: BIX 02565
BIX 02565 is a novel ribosomal S6 kinase 2 (RSK2) inhibitor with an IC50 of 1.1 nM.
BIX 02565 is an attractive candidate for use in vitro and in vivo to explore the role of RSK as a target for the treatment heart failure. Besides, BIX 02565 is a multikinase inhibitor, including LRRK2, RET, CLK2, FLT3 and PDGFR.
At this point, we returned to the panel of 20 kinases used for optimization to obtain a more accurate picture of kinase selectivity for 24. Six kinases furnished an IC50 less than 1 lM: the ?ve that had shown greater than 80% inhibition in the selectivity count, and PDGFRa which had shown 71% inhibition. Additionally, compound 24 was more than 100-fold selective relative to RSK for the kinase panel, with the exception of LRRK2 and PRKD1, for which compound 24 showed 16- and 35-fold selectivity, respectively. We then expanded the kinase panel to include over 200 additional unique kinases. We were pleased to ?nd that 24 had an IC50 of less than 1 lM for only four other family members (PRKD2, PRKD3, RET, and FLT3). These results con?rmed the power of the selectivity screening methodology developed for this program. By tracking a broader panel of potentially cross-reactive kinases at a single concentration, we were able to identify a compound with high selectivity vs. most of the readily testable portion of the kinome.
For research only, not for human use!
BIX 02565 is a novel ribosomal S6 kinase 2 (RSK2) inhibitor with an IC50 of 1.1 nM.
IC50 Value: 1.1 nM (RSK2)
Target: RSK2
BIX 02565 is an attractive candidate for use in vitro and in vivo to explore the role of RSK as a target for the treatment heart failure.
Product Name: BIX 02565|Cat No: DC9616|Cas: 1311367-27-7|Molecule Formular: C26H30N6O2|Molecule Weight: 458.5554|Other names: BIX 02565
BIX 02565 is a novel ribosomal S6 kinase 2 (RSK2) inhibitor with an IC50 of 1.1 nM.
BIX 02565 is an attractive candidate for use in vitro and in vivo to explore the role of RSK as a target for the treatment heart failure. Besides, BIX 02565 is a multikinase inhibitor, including LRRK2, RET, CLK2, FLT3 and PDGFR.
At this point, we returned to the panel of 20 kinases used for optimization to obtain a more accurate picture of kinase selectivity for 24. Six kinases furnished an IC50 less than 1 lM: the ?ve that had shown greater than 80% inhibition in the selectivity count, and PDGFRa which had shown 71% inhibition. Additionally, compound 24 was more than 100-fold selective relative to RSK for the kinase panel, with the exception of LRRK2 and PRKD1, for which compound 24 showed 16- and 35-fold selectivity, respectively. We then expanded the kinase panel to include over 200 additional unique kinases. We were pleased to ?nd that 24 had an IC50 of less than 1 lM for only four other family members (PRKD2, PRKD3, RET, and FLT3). These results con?rmed the power of the selectivity screening methodology developed for this program. By tracking a broader panel of potentially cross-reactive kinases at a single concentration, we were able to identify a compound with high selectivity vs. most of the readily testable portion of the kinome.
For research only, not for human use!
SR3335|cas 293753-05-6|DC Chemicals
SR3335|cas 293753-05-6|DC Chemicals
SR3335 (ML-176) is a selective RORα synthetic ligand, directly binds to RORα, but not other RORs, and functions as a selective partial inverse agonist of RORα in cell-based assays.
Product Name: SR3335|Cat No: DC9615|Cas: 293753-05-6|Molecule Formular: C13H9F6NO3S2|Molecule Weight: 405.3359|Other names: SR3335
SR3335 (ML-176) is a selective RORα synthetic ligand, directly binds to RORα, but not other RORs, and functions as a selective partial inverse agonist of RORα in cell-based assays.
Furthermore, SR3335 suppresses the expression of endogenous RORα target genes in HepG2 involved in hepatic gluconeogenesis including glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. The first selective synthetic RORα inverse agonists may hold utility for suppression of elevated hepatic glucose production in type 2 diabetics.
For research only, not for human use!
SR3335 (ML-176) is a selective RORα synthetic ligand, directly binds to RORα, but not other RORs, and functions as a selective partial inverse agonist of RORα in cell-based assays.
Product Name: SR3335|Cat No: DC9615|Cas: 293753-05-6|Molecule Formular: C13H9F6NO3S2|Molecule Weight: 405.3359|Other names: SR3335
SR3335 (ML-176) is a selective RORα synthetic ligand, directly binds to RORα, but not other RORs, and functions as a selective partial inverse agonist of RORα in cell-based assays.
Furthermore, SR3335 suppresses the expression of endogenous RORα target genes in HepG2 involved in hepatic gluconeogenesis including glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. The first selective synthetic RORα inverse agonists may hold utility for suppression of elevated hepatic glucose production in type 2 diabetics.
For research only, not for human use!
Hydroxyfasudil (hydrochloride)|cas 155558-32-0|DC Chemicals
Hydroxyfasudil (hydrochloride)|cas 155558-32-0|DC Chemicals
Hydroxyfasudil (hydrochloride)|cas 155558-32-0|DC Chemicals
Hydroxyfasudil Hcl(HA1100 Hcl), metabolite of Fasudil, is a potent Rho-kinase inhibitor and vasodilator.
IC50 Value: 0.12 uM (ROCK1); 0.17 uM (ROCK2) [1]
Target: ROCK1/2
in vitro: Fasudil (1-10 μM) and hydroxyfasudil (0.3-10 μM) significantly prevented endothelin-induced cardiomyocyte hypertrophy [2].
Product Name: Hydroxyfasudil (hydrochloride)|Cat No: DC9614|Cas: 155558-32-0|Molecule Formular: C14H18ClN3O3S|Molecule Weight: 343.829|Other names: Hydroxyfasudil (hydrochloride)
Hydroxyfasudil Hcl(HA1100 Hcl), metabolite of Fasudil, is a potent Rho-kinase inhibitor and vasodilator.
in vitro: Fasudil (1-10 μM) and hydroxyfasudil (0.3-10 μM) significantly prevented endothelin-induced cardiomyocyte hypertrophy [2]. Hydroxyfasudil significantly attenuated serotonin (IC)-induced vasoconstriction of SA (-7 +/- 1% vs. 2 +/- 1%, p < 0.01). Coronary I/R significantly impaired coronary vasodilation to acetylcholine after I/R (SA, p < 0.05; and A, p < 0.01 vs. before I/R) and L-NMMA further reduced the vasodilation, whereas hydroxyfasudil completely preserved the responses.
in vivo: Treatment with hydroxyfasudil significantly improved bladder intercontraction intervals. Rats treated with hydroxyfasudil also showed a significant reduction of histopathological features associated with cystitis. Twelve-week-old male SHRs were treated with hydroxyfasudil (3 or 10 mg/kg, i.p.) once a day for 6 weeks. Treatment with hydroxyfasudil significantly improved the decreased penile cGMP concentrations, the increased Rho kinase activities, the increased norepinephrine-induced contractions, and the decreased acetylcholine-induced relaxation in a dose-dependent manner.
For research only, not for human use!
Hydroxyfasudil (hydrochloride)|cas 155558-32-0|DC Chemicals
Hydroxyfasudil Hcl(HA1100 Hcl), metabolite of Fasudil, is a potent Rho-kinase inhibitor and vasodilator.
IC50 Value: 0.12 uM (ROCK1); 0.17 uM (ROCK2) [1]
Target: ROCK1/2
in vitro: Fasudil (1-10 μM) and hydroxyfasudil (0.3-10 μM) significantly prevented endothelin-induced cardiomyocyte hypertrophy [2].
Product Name: Hydroxyfasudil (hydrochloride)|Cat No: DC9614|Cas: 155558-32-0|Molecule Formular: C14H18ClN3O3S|Molecule Weight: 343.829|Other names: Hydroxyfasudil (hydrochloride)
Hydroxyfasudil Hcl(HA1100 Hcl), metabolite of Fasudil, is a potent Rho-kinase inhibitor and vasodilator.
in vitro: Fasudil (1-10 μM) and hydroxyfasudil (0.3-10 μM) significantly prevented endothelin-induced cardiomyocyte hypertrophy [2]. Hydroxyfasudil significantly attenuated serotonin (IC)-induced vasoconstriction of SA (-7 +/- 1% vs. 2 +/- 1%, p < 0.01). Coronary I/R significantly impaired coronary vasodilation to acetylcholine after I/R (SA, p < 0.05; and A, p < 0.01 vs. before I/R) and L-NMMA further reduced the vasodilation, whereas hydroxyfasudil completely preserved the responses.
in vivo: Treatment with hydroxyfasudil significantly improved bladder intercontraction intervals. Rats treated with hydroxyfasudil also showed a significant reduction of histopathological features associated with cystitis. Twelve-week-old male SHRs were treated with hydroxyfasudil (3 or 10 mg/kg, i.p.) once a day for 6 weeks. Treatment with hydroxyfasudil significantly improved the decreased penile cGMP concentrations, the increased Rho kinase activities, the increased norepinephrine-induced contractions, and the decreased acetylcholine-induced relaxation in a dose-dependent manner.
For research only, not for human use!
CCG-63808|cas 620113-73-7|DC Chemicals
CCG-63808|cas 620113-73-7|DC Chemicals
CCG-63808 is a reversible inhibitor of regulator of G-protein signaling (RGS) proteins.
Product Name: CCG-63808|Cat No: DC9613|Cas: 620113-73-7|Molecule Formular: C25H15FN4O2S|Molecule Weight: 454.4756|Other names: CCG-63808
CCG-63808 is a reversible inhibitor of regulator of G-protein signaling (RGS) proteins.
For research only, not for human use!
CCG-63808 is a reversible inhibitor of regulator of G-protein signaling (RGS) proteins.
Product Name: CCG-63808|Cat No: DC9613|Cas: 620113-73-7|Molecule Formular: C25H15FN4O2S|Molecule Weight: 454.4756|Other names: CCG-63808
CCG-63808 is a reversible inhibitor of regulator of G-protein signaling (RGS) proteins.
For research only, not for human use!
CCG-63802|cas 620112-78-9|DC Chemicals
CCG-63802|cas 620112-78-9|DC Chemicals
CCG-63802 is a reversible inhibitor of regulator of G-protein signaling (RGS) protein; with greatest potency at RGS4.
IC50 value:
Target: RGS
CCG-63802 is selective amongst RGS proteins, with greatest potency at RGS4..
Product Name: CCG-63802|Cat No: DC9612|Cas: 620112-78-9|Molecule Formular: C26H18N4O2S|Molecule Weight: 450.5117|Other names: CCG-63802
CCG-63802 is a reversible inhibitor of regulator of G-protein signaling (RGS) protein; with greatest potency at RGS4.
CCG-63802 is selective amongst RGS proteins, with greatest potency at RGS4. CCG-63802 inhibits GTPase accelerating protein activity of RGS4 and blocks its interaction with Gαo. Retains activity under reducing conditions.
For research only, not for human use!
CCG-63802 is a reversible inhibitor of regulator of G-protein signaling (RGS) protein; with greatest potency at RGS4.
IC50 value:
Target: RGS
CCG-63802 is selective amongst RGS proteins, with greatest potency at RGS4..
Product Name: CCG-63802|Cat No: DC9612|Cas: 620112-78-9|Molecule Formular: C26H18N4O2S|Molecule Weight: 450.5117|Other names: CCG-63802
CCG-63802 is a reversible inhibitor of regulator of G-protein signaling (RGS) protein; with greatest potency at RGS4.
CCG-63802 is selective amongst RGS proteins, with greatest potency at RGS4. CCG-63802 inhibits GTPase accelerating protein activity of RGS4 and blocks its interaction with Gαo. Retains activity under reducing conditions.
For research only, not for human use!
PI-1840|cas 1401223-22-0|DC Chemicals
PI-1840|cas 1401223-22-0|DC Chemicals
PI-1840 is a potent and selective inhibitor for chymotrypsin-like (CT-L) (IC50 value = 27 ± 0.14 nM) over trypsin-like and peptidylglutamyl peptide hydrolyzing (IC50 values >100 μM) activities of the proteasome.
Product Name: PI-1840|Cat No: DC9611|Cas: 1401223-22-0|Molecule Formular: C22H26N4O3|Molecule Weight: 394.4668|Other names: PI-1840
PI-1840 is a potent and selective inhibitor for chymotrypsin-like (CT-L) (IC50 value = 27 ± 0.14 nM) over trypsin-like and peptidylglutamyl peptide hydrolyzing (IC50 values >100 μM) activities of the proteasome.
in vitro: PI-1840 is over 100-fold more selective for the constitutive proteasome over the immunoproteasome. Mass spectrometry and dialysis studies demonstrate that PI-1840 is a noncovalent and rapidly reversible CT-L inhibitor. In intact cancer cells, PI-1840 inhibits CT-L activity, induces the accumulation of proteasome substrates p27, Bax, and IκB-α, inhibits survival pathways and viability, and induces apoptosis. Furthermore, PI-1840 sensitizes human cancer cells to the mdm2/p53 disruptor, nutlin, and to the pan-Bcl-2 antagonist BH3-M6.
in vivo: PI-1840 but not bortezomib suppresses the growth in nude mice of human breast tumor xenografts.
For research only, not for human use!
PI-1840 is a potent and selective inhibitor for chymotrypsin-like (CT-L) (IC50 value = 27 ± 0.14 nM) over trypsin-like and peptidylglutamyl peptide hydrolyzing (IC50 values >100 μM) activities of the proteasome.
Product Name: PI-1840|Cat No: DC9611|Cas: 1401223-22-0|Molecule Formular: C22H26N4O3|Molecule Weight: 394.4668|Other names: PI-1840
PI-1840 is a potent and selective inhibitor for chymotrypsin-like (CT-L) (IC50 value = 27 ± 0.14 nM) over trypsin-like and peptidylglutamyl peptide hydrolyzing (IC50 values >100 μM) activities of the proteasome.
in vitro: PI-1840 is over 100-fold more selective for the constitutive proteasome over the immunoproteasome. Mass spectrometry and dialysis studies demonstrate that PI-1840 is a noncovalent and rapidly reversible CT-L inhibitor. In intact cancer cells, PI-1840 inhibits CT-L activity, induces the accumulation of proteasome substrates p27, Bax, and IκB-α, inhibits survival pathways and viability, and induces apoptosis. Furthermore, PI-1840 sensitizes human cancer cells to the mdm2/p53 disruptor, nutlin, and to the pan-Bcl-2 antagonist BH3-M6.
in vivo: PI-1840 but not bortezomib suppresses the growth in nude mice of human breast tumor xenografts.
For research only, not for human use!
ONO-AE3-208|cas 402473-54-5|DC Chemicals
ONO-AE3-208|cas 402473-54-5|DC Chemicals
ONO-AE3-208(AE 3-208) is an EP4 antagonist; suppresses cell invasion, migration, and metastasis of prostate cancer.
IC50 value:
Target: EP4
EP4 over-expressing LNCaP was established, and their cell invasiveness was compared with the control LNCaP (LNCaP/mock).
Product Name: ONO-AE3-208|Cat No: DC9610|Cas: 402473-54-5|Molecule Formular: C24H21FN2O3|Molecule Weight: 404.4335|Other names: ONO-AE3-208
ONO-AE3-208(AE 3-208) is an EP4 antagonist; suppresses cell invasion, migration, and metastasis of prostate cancer.
EP4 over-expressing LNCaP was established, and their cell invasiveness was compared with the control LNCaP (LNCaP/mock). The in vitro cell proliferation, invasion, and migration of these cells were examined under different concentrations of ONO-AE3-208. An in vivo bone metastatic mouse model was constructed by inoculating luciferase expressing PC3 cells into left ventricle of nude mice. Their bone metastasis was observed by bioluminescent imaging with or without ONO-AE3-208 administration. The EP4 mRNA expression levels were higher in PC3 than in LNCaP, and EP4 over-expression of LNCaP cells enhanced their cell invasiveness.
Arachidonic acid caused dose-dependent dilation of the attached Af-Art (from 8.6 ± 1.2 to 15.3 ± 0.7 μm; P<0.001; n=6), and this effect was blocked by ONO-AE3-208 (10(-7) mol/L).
For research only, not for human use!
ONO-AE3-208(AE 3-208) is an EP4 antagonist; suppresses cell invasion, migration, and metastasis of prostate cancer.
IC50 value:
Target: EP4
EP4 over-expressing LNCaP was established, and their cell invasiveness was compared with the control LNCaP (LNCaP/mock).
Product Name: ONO-AE3-208|Cat No: DC9610|Cas: 402473-54-5|Molecule Formular: C24H21FN2O3|Molecule Weight: 404.4335|Other names: ONO-AE3-208
ONO-AE3-208(AE 3-208) is an EP4 antagonist; suppresses cell invasion, migration, and metastasis of prostate cancer.
EP4 over-expressing LNCaP was established, and their cell invasiveness was compared with the control LNCaP (LNCaP/mock). The in vitro cell proliferation, invasion, and migration of these cells were examined under different concentrations of ONO-AE3-208. An in vivo bone metastatic mouse model was constructed by inoculating luciferase expressing PC3 cells into left ventricle of nude mice. Their bone metastasis was observed by bioluminescent imaging with or without ONO-AE3-208 administration. The EP4 mRNA expression levels were higher in PC3 than in LNCaP, and EP4 over-expression of LNCaP cells enhanced their cell invasiveness.
Arachidonic acid caused dose-dependent dilation of the attached Af-Art (from 8.6 ± 1.2 to 15.3 ± 0.7 μm; P<0.001; n=6), and this effect was blocked by ONO-AE3-208 (10(-7) mol/L).
For research only, not for human use!
Terutroban|cas 165538-40-9|DC Chemicals
Terutroban|cas 165538-40-9|DC Chemicals
Terutroban is a thromboxane/prostaglandin endoperoxide receptor antagonist.
IC50 value：
Target: TP receptor
in vivo: Terutroban is a selective antagonist of the thromboxane/prostaglandin endoperoxide receptor, in preventing retinal ischaemia in a model of diabetes in rats.
Product Name: Terutroban|Cat No: DC9609|Cas: 165538-40-9|Molecule Formular: C20H22ClNO4S|Molecule Weight: 407.911|Other names: Terutroban
Terutroban is a thromboxane/prostaglandin endoperoxide receptor antagonist.
in vivo: Terutroban is a selective antagonist of the thromboxane/prostaglandin endoperoxide receptor, in preventing retinal ischaemia in a model of diabetes in rats. Terutroban significantly protect retinal vascularity from ischaemia in experimental diabetes, and this result could be attributed not only to its antiplatelet/antithrombotic activities but also to its vascular properties.Terutroban has antiplatelet properties. In addition, Terutroban has shown to improve flow-mediated dilatation of the brachial artery after a single administration in patients with coronary artery disease.Terutroban is a potent antithrombotic agent and also possesses antiatherosclerotic and antivasoconstrictor properties.
For research only, not for human use!
Terutroban is a thromboxane/prostaglandin endoperoxide receptor antagonist.
IC50 value：
Target: TP receptor
in vivo: Terutroban is a selective antagonist of the thromboxane/prostaglandin endoperoxide receptor, in preventing retinal ischaemia in a model of diabetes in rats.
Product Name: Terutroban|Cat No: DC9609|Cas: 165538-40-9|Molecule Formular: C20H22ClNO4S|Molecule Weight: 407.911|Other names: Terutroban
Terutroban is a thromboxane/prostaglandin endoperoxide receptor antagonist.
in vivo: Terutroban is a selective antagonist of the thromboxane/prostaglandin endoperoxide receptor, in preventing retinal ischaemia in a model of diabetes in rats. Terutroban significantly protect retinal vascularity from ischaemia in experimental diabetes, and this result could be attributed not only to its antiplatelet/antithrombotic activities but also to its vascular properties.Terutroban has antiplatelet properties. In addition, Terutroban has shown to improve flow-mediated dilatation of the brachial artery after a single administration in patients with coronary artery disease.Terutroban is a potent antithrombotic agent and also possesses antiatherosclerotic and antivasoconstrictor properties.
For research only, not for human use!
NS-304|cas 475086-01-2|DC Chemicals
NS-304|cas 475086-01-2|DC Chemicals
NS-304(Selexipag; ACT-293987) is an oral, selective prostacyclin receptor agonist for the treatment of pulmonary arterial hypertension.
IC50 value:
Target:
NS-304 is an orally available and potent agonist for the PGI(2) receptor (IP receptor).
Product Name: NS-304|Cat No: DC9608|Cas: 475086-01-2|Molecule Formular: C26H32N4O4S|Molecule Weight: 496.6217|Other names: NS-304
NS-304(Selexipag; ACT-293987) is an oral, selective prostacyclin receptor agonist for the treatment of pulmonary arterial hypertension.
NS-304 is an orally available and potent agonist for the PGI(2) receptor (IP receptor). The inhibition constant (K(i)) of MRE-269 for the human IP receptor was 20 nM; in contrast, the K(i) values for other prostanoid receptors were >2.6 microM. MRE-269 was therefore a highly selective agonist for the IP receptor. The plasma concentrations of MRE-269 remained near peak levels for more than 8 h after oral administration of NS-304 to rats and dogs, and NS-304 increased femoral skin blood flow in rats in a long-lasting manner without affecting the hemodynamics. These findings indicate that NS-304 acts as a long-acting IP receptor agonist in vivo. The continuous vasodilation evoked by NS-304 was not attenuated by repeated treatment, indicating that NS-304 is unlikely to cause severe desensitization of the IP receptor in rats.
For research only, not for human use!
NS-304(Selexipag; ACT-293987) is an oral, selective prostacyclin receptor agonist for the treatment of pulmonary arterial hypertension.
IC50 value:
Target:
NS-304 is an orally available and potent agonist for the PGI(2) receptor (IP receptor).
Product Name: NS-304|Cat No: DC9608|Cas: 475086-01-2|Molecule Formular: C26H32N4O4S|Molecule Weight: 496.6217|Other names: NS-304
NS-304(Selexipag; ACT-293987) is an oral, selective prostacyclin receptor agonist for the treatment of pulmonary arterial hypertension.
NS-304 is an orally available and potent agonist for the PGI(2) receptor (IP receptor). The inhibition constant (K(i)) of MRE-269 for the human IP receptor was 20 nM; in contrast, the K(i) values for other prostanoid receptors were >2.6 microM. MRE-269 was therefore a highly selective agonist for the IP receptor. The plasma concentrations of MRE-269 remained near peak levels for more than 8 h after oral administration of NS-304 to rats and dogs, and NS-304 increased femoral skin blood flow in rats in a long-lasting manner without affecting the hemodynamics. These findings indicate that NS-304 acts as a long-acting IP receptor agonist in vivo. The continuous vasodilation evoked by NS-304 was not attenuated by repeated treatment, indicating that NS-304 is unlikely to cause severe desensitization of the IP receptor in rats.
For research only, not for human use!
MK-2894|cas 1006036-87-8|DC Chemicals
MK-2894|cas 1006036-87-8|DC Chemicals
MK-2894 is a highly potent and selective second generation EP4 antagonist.
IC50 value:
Target: EP4
MK-2894 exhibits favorable pharmacokinetic profile in a number of preclinical species and potent anti-inflammatory activity in several animal models of pain/inflammation.
Product Name: MK-2894|Cat No: DC9607|Cas: 1006036-87-8|Molecule Formular: C25H22F3NO3S|Molecule Weight: 473.5073|Other names: MK-2894
MK-2894 is a highly potent and selective second generation EP4 antagonist.
MK-2894 exhibits favorable pharmacokinetic profile in a number of preclinical species and potent anti-inflammatory activity in several animal models of pain/inflammation. MK-2894 also shows favorable GI tolerability profile in rats when compared to traditional NSAID indomethacin.
For research only, not for human use!
MK-2894 is a highly potent and selective second generation EP4 antagonist.
IC50 value:
Target: EP4
MK-2894 exhibits favorable pharmacokinetic profile in a number of preclinical species and potent anti-inflammatory activity in several animal models of pain/inflammation.
Product Name: MK-2894|Cat No: DC9607|Cas: 1006036-87-8|Molecule Formular: C25H22F3NO3S|Molecule Weight: 473.5073|Other names: MK-2894
MK-2894 is a highly potent and selective second generation EP4 antagonist.
MK-2894 exhibits favorable pharmacokinetic profile in a number of preclinical species and potent anti-inflammatory activity in several animal models of pain/inflammation. MK-2894 also shows favorable GI tolerability profile in rats when compared to traditional NSAID indomethacin.
For research only, not for human use!
Desogestrel|cas 54024-22-5|DC Chemicals
Desogestrel|cas 54024-22-5|DC Chemicals
Desogestrel(Org-2969) is a third-generation 19-nortestosterone derivative progestogen; is contained in many oral contraceptive preparations, both combined (COCs) to ethinyl-estradiol (EE) or alone in a progestin-only pill (POP)..
Product Name: Desogestrel|Cat No: DC9604|Cas: 54024-22-5|Molecule Formular: C22H30O|Molecule Weight: 310.473|Other names: Desogestrel
Desogestrel(Org-2969) is a third-generation 19-nortestosterone derivative progestogen; is contained in many oral contraceptive preparations, both combined (COCs) to ethinyl-estradiol (EE) or alone in a progestin-only pill (POP).
For research only, not for human use!
Desogestrel(Org-2969) is a third-generation 19-nortestosterone derivative progestogen; is contained in many oral contraceptive preparations, both combined (COCs) to ethinyl-estradiol (EE) or alone in a progestin-only pill (POP)..
Product Name: Desogestrel|Cat No: DC9604|Cas: 54024-22-5|Molecule Formular: C22H30O|Molecule Weight: 310.473|Other names: Desogestrel
Desogestrel(Org-2969) is a third-generation 19-nortestosterone derivative progestogen; is contained in many oral contraceptive preparations, both combined (COCs) to ethinyl-estradiol (EE) or alone in a progestin-only pill (POP).
For research only, not for human use!
Ciprofibrate|cas 52214-84-3|DC Chemicals
Ciprofibrate|cas 52214-84-3|DC Chemicals
Ciprofibrate is a peroxisome proliferator-activated receptor agonist.
Target: PPAR
Ciprofibrate is a hypolipidemic compound that can induce proliferation of peroxisomes in liver cells of rats.
Product Name: Ciprofibrate|Cat No: DC9603|Cas: 52214-84-3|Molecule Formular: C13H14Cl2O3|Molecule Weight: 289.1544|Other names: Ciprofibrate
Ciprofibrate is a peroxisome proliferator-activated receptor agonist.
Ciprofibrate is a hypolipidemic compound that can induce proliferation of peroxisomes in liver cells of rats. Known to be a PPARα (peroxisome proliferator-activated receptor α) agonist.
For research only, not for human use!
Ciprofibrate is a peroxisome proliferator-activated receptor agonist.
Target: PPAR
Ciprofibrate is a hypolipidemic compound that can induce proliferation of peroxisomes in liver cells of rats.
Product Name: Ciprofibrate|Cat No: DC9603|Cas: 52214-84-3|Molecule Formular: C13H14Cl2O3|Molecule Weight: 289.1544|Other names: Ciprofibrate
Ciprofibrate is a peroxisome proliferator-activated receptor agonist.
Ciprofibrate is a hypolipidemic compound that can induce proliferation of peroxisomes in liver cells of rats. Known to be a PPARα (peroxisome proliferator-activated receptor α) agonist.
For research only, not for human use!
Balaglitazone|cas 199113-98-9|DC Chemicals
Balaglitazone|cas 199113-98-9|DC Chemicals
Balaglitazone (DRF-2593; NN-2344) is a novel partial agonist of PPAR-γ.
IC50 Value:
Target: PPARγ
in vitro: The Rs for the separations were 3.5 for balaglitazone enantiomers, 3.5 for pioglitazone enantiomers, and 3.7 for rosiglitazone.
Product Name: Balaglitazone|Cat No: DC9602|Cas: 199113-98-9|Molecule Formular: C20H17N3O4S|Molecule Weight: 395.4317|Other names: Balaglitazone.
Balaglitazone (DRF-2593; NN-2344) is a novel partial agonist of PPAR-γ.
in vitro: The Rs for the separations were 3.5 for balaglitazone enantiomers, 3.5 for pioglitazone enantiomers, and 3.7 for rosiglitazone. The squared correlation coefficients (r2) were found to be 0.999 for all three compounds.
in vivo: Balaglitazone treated groups shown significantly reduce of HbA1c (%), FSG (mmol/L), postprandial glucose as comparison to pioglitazone. Balaglitazone 10 mg and 20 mg show the similar magnitudes of the effects which comparable to the effects seen in the pioglitazone 45 mg group. The incidence of fluid retention and fat accumulation fewer than those observed with pioglitazone 45 mg. Sixty male dio induced obese rats were divided into five categories: vehicle, pioglitazone 10 mg/kg, pioglitazone 30 mg/kg, balaglitazone 5 mg/kg, balaglitazone 10 mg/kg. At day -7, 21 and 42 fasting serum samples were collected and whole body tissue composition was evaluated by MR scanning.
For research only, not for human use!
Balaglitazone (DRF-2593; NN-2344) is a novel partial agonist of PPAR-γ.
IC50 Value:
Target: PPARγ
in vitro: The Rs for the separations were 3.5 for balaglitazone enantiomers, 3.5 for pioglitazone enantiomers, and 3.7 for rosiglitazone.
Product Name: Balaglitazone|Cat No: DC9602|Cas: 199113-98-9|Molecule Formular: C20H17N3O4S|Molecule Weight: 395.4317|Other names: Balaglitazone.
Balaglitazone (DRF-2593; NN-2344) is a novel partial agonist of PPAR-γ.
in vitro: The Rs for the separations were 3.5 for balaglitazone enantiomers, 3.5 for pioglitazone enantiomers, and 3.7 for rosiglitazone. The squared correlation coefficients (r2) were found to be 0.999 for all three compounds.
in vivo: Balaglitazone treated groups shown significantly reduce of HbA1c (%), FSG (mmol/L), postprandial glucose as comparison to pioglitazone. Balaglitazone 10 mg and 20 mg show the similar magnitudes of the effects which comparable to the effects seen in the pioglitazone 45 mg group. The incidence of fluid retention and fat accumulation fewer than those observed with pioglitazone 45 mg. Sixty male dio induced obese rats were divided into five categories: vehicle, pioglitazone 10 mg/kg, pioglitazone 30 mg/kg, balaglitazone 5 mg/kg, balaglitazone 10 mg/kg. At day -7, 21 and 42 fasting serum samples were collected and whole body tissue composition was evaluated by MR scanning.
For research only, not for human use!
T0070907|cas 313516-66-4|DC Chemicals
T0070907|cas 313516-66-4|DC Chemicals
T0070907 is a potent and selective PPARγ antagonist with IC50 of 1 nM; displays > 800-fold selectivity for PPARγ over PPARα and PPARδ.
Product Name: T0070907|Cat No: DC9601|Cas: 313516-66-4|Molecule Formular: C12H8ClN3O3|Molecule Weight: 277.6632|Other names: T0070907
T0070907 is a potent and selective PPARγ antagonist with IC50 of 1 nM; displays > 800-fold selectivity for PPARγ over PPARα and PPARδ.
in vitro: T0070907 blocks agonist-induced recruitment of coactivator-derived peptides to PPARγ in a homogeneous time-resolved fluorescence-based assay and promotes recruitment of the transcriptional corepressor NCoR to PPARγ in both glutathione S-transferase pull-down assays and a PPARγ/retinoid X receptor (RXR) α-dependent gel shift assay. Studies with mutant receptors suggest that T0070907 modulates the interaction of PPARγ with these cofactor proteins by affecting the conformation of helix 12 of the PPARγ ligand-binding domain. Interestingly, whereas the T0070907-induced NCoR recruitment to PPARγ/RXRα heterodimer can be almost completely reversed by the simultaneous treatment with RXRα agonist LGD1069, T0070907 treatment has only modest effects on LGD1069-induced coactivator recruitment to the PPARγ/RXRα heterodimer. T0070907 treatment inhibits proliferation, invasion and migration but does not significantly affect apoptosis. Molecular inhibition using a dominant negative (Δ462) receptor yields similar results. T007 also mediates a dose-dependent decrease in phosphorylation of PPARγ, and its ability to bind to DNA, and may directly affect mitogen-activated protein kinase signaling.
in vivo: Lipopolysaccharide preconditioning significantly attenuates the development of renal dysfunction, hepatocellular injury, and circulatory failure as well as the increase in the plasma levels of interleukin-1 [beta] caused by severe endotoxemia. T0070907 can attenuate all of these beneficial effects afforded by preconditioning with lipopolysaccharide.
For research only, not for human use!
T0070907 is a potent and selective PPARγ antagonist with IC50 of 1 nM; displays > 800-fold selectivity for PPARγ over PPARα and PPARδ.
Product Name: T0070907|Cat No: DC9601|Cas: 313516-66-4|Molecule Formular: C12H8ClN3O3|Molecule Weight: 277.6632|Other names: T0070907
T0070907 is a potent and selective PPARγ antagonist with IC50 of 1 nM; displays > 800-fold selectivity for PPARγ over PPARα and PPARδ.
in vitro: T0070907 blocks agonist-induced recruitment of coactivator-derived peptides to PPARγ in a homogeneous time-resolved fluorescence-based assay and promotes recruitment of the transcriptional corepressor NCoR to PPARγ in both glutathione S-transferase pull-down assays and a PPARγ/retinoid X receptor (RXR) α-dependent gel shift assay. Studies with mutant receptors suggest that T0070907 modulates the interaction of PPARγ with these cofactor proteins by affecting the conformation of helix 12 of the PPARγ ligand-binding domain. Interestingly, whereas the T0070907-induced NCoR recruitment to PPARγ/RXRα heterodimer can be almost completely reversed by the simultaneous treatment with RXRα agonist LGD1069, T0070907 treatment has only modest effects on LGD1069-induced coactivator recruitment to the PPARγ/RXRα heterodimer. T0070907 treatment inhibits proliferation, invasion and migration but does not significantly affect apoptosis. Molecular inhibition using a dominant negative (Δ462) receptor yields similar results. T007 also mediates a dose-dependent decrease in phosphorylation of PPARγ, and its ability to bind to DNA, and may directly affect mitogen-activated protein kinase signaling.
in vivo: Lipopolysaccharide preconditioning significantly attenuates the development of renal dysfunction, hepatocellular injury, and circulatory failure as well as the increase in the plasma levels of interleukin-1 [beta] caused by severe endotoxemia. T0070907 can attenuate all of these beneficial effects afforded by preconditioning with lipopolysaccharide.
For research only, not for human use!
Senicapoc|cas 289656-45-7|DC Chemicals
Senicapoc|cas 289656-45-7|DC Chemicals
Senicapoc(ICA17043) is a potent and selective Gardos channel blocker; blocked Ca(2+)-induced rubidium flux from human RBCs/ inhibited RBC dehydration with IC50s of 11 nM/30 nM, respectively.
IC50 value: 11/30 nM [1]
Target: Gardos channel
in vitro: ICA-17043 blocked Ca(2+)-induced rubidium flux from human RBCs with an IC(50) value of 11 +/- 2 nM (CLT IC(50) = 100 +/- 12 nM) and inhibited RBC dehydration with an IC(50) of 30 +/- 20 nM [1].
in vivo: In a transgenic mouse model of sickle cell disease (SAD), treatment with ICA-17043 (10 mg/kg orally, twice a day) for 21 days showed a marked and constant inhibition of the Gardos channel activity (with an average inhibition of 90% +/- 27%, P <.005), an increase in RBC K(+) content (from 392 +/- 19.9 to 479.2 +/- 40 mmol/kg hemoglobin [Hb], P <.005), a significant increase in hematocrit (Hct) (from 0.435 +/- 0.007 to 0.509 +/- 0.022 [43.5% +/- 0.7% to 50.9% +/- 2.2%], P <.005), a decrease in mean corpuscular hemoglobin concentration (MCHC) (from 340 +/- 9.0 to 300 +/- 15 g/L [34.0 +/- 0.9 to 30 +/- 1.5 g/dL], P <.05), and a left-shift in RBC density curves [1].
Product Name: Senicapoc|Cat No: DC9600|Cas: 289656-45-7|Molecule Formular: C20H15F2NO|Molecule Weight: 323.336|Other names: Senicapoc
Senicapoc(ICA17043) is a potent and selective Gardos channel blocker; blocked Ca(2+)-induced rubidium flux from human RBCs/ inhibited RBC dehydration with IC50s of 11 nM/30 nM, respectively.
in vitro: ICA-17043 blocked Ca(2+)-induced rubidium flux from human RBCs with an IC(50) value of 11 +/- 2 nM (CLT IC(50) = 100 +/- 12 nM) and inhibited RBC dehydration with an IC(50) of 30 +/- 20 nM.
in vivo: In a transgenic mouse model of sickle cell disease (SAD), treatment with ICA-17043 (10 mg/kg orally, twice a day) for 21 days showed a marked and constant inhibition of the Gardos channel activity (with an average inhibition of 90% +/- 27%, P <.005), an increase in RBC K(+) content (from 392 +/- 19.9 to 479.2 +/- 40 mmol/kg hemoglobin [Hb], P <.005), a significant increase in hematocrit (Hct) (from 0.435 +/- 0.007 to 0.509 +/- 0.022 [43.5% +/- 0.7% to 50.9% +/- 2.2%], P <.005), a decrease in mean corpuscular hemoglobin concentration (MCHC) (from 340 +/- 9.0 to 300 +/- 15 g/L [34.0 +/- 0.9 to 30 +/- 1.5 g/dL], P <.05), and a left-shift in RBC density curves [1]. Senicapoc is well tolerated when administered to SCD patients and produces dose-dependent increases in hemoglobin and decreases in markers of hemolysis. Atopic sheep were administered either 30 mg/kg Senicapoc (ICA-17073), a selective inhibitor of the K(Ca)3.1-channel, or vehicle alone (0.5% methylcellulose) twice daily (orally).
For research only, not for human use!
Senicapoc(ICA17043) is a potent and selective Gardos channel blocker; blocked Ca(2+)-induced rubidium flux from human RBCs/ inhibited RBC dehydration with IC50s of 11 nM/30 nM, respectively.
IC50 value: 11/30 nM [1]
Target: Gardos channel
in vitro: ICA-17043 blocked Ca(2+)-induced rubidium flux from human RBCs with an IC(50) value of 11 +/- 2 nM (CLT IC(50) = 100 +/- 12 nM) and inhibited RBC dehydration with an IC(50) of 30 +/- 20 nM [1].
in vivo: In a transgenic mouse model of sickle cell disease (SAD), treatment with ICA-17043 (10 mg/kg orally, twice a day) for 21 days showed a marked and constant inhibition of the Gardos channel activity (with an average inhibition of 90% +/- 27%, P <.005), an increase in RBC K(+) content (from 392 +/- 19.9 to 479.2 +/- 40 mmol/kg hemoglobin [Hb], P <.005), a significant increase in hematocrit (Hct) (from 0.435 +/- 0.007 to 0.509 +/- 0.022 [43.5% +/- 0.7% to 50.9% +/- 2.2%], P <.005), a decrease in mean corpuscular hemoglobin concentration (MCHC) (from 340 +/- 9.0 to 300 +/- 15 g/L [34.0 +/- 0.9 to 30 +/- 1.5 g/dL], P <.05), and a left-shift in RBC density curves [1].
Product Name: Senicapoc|Cat No: DC9600|Cas: 289656-45-7|Molecule Formular: C20H15F2NO|Molecule Weight: 323.336|Other names: Senicapoc
Senicapoc(ICA17043) is a potent and selective Gardos channel blocker; blocked Ca(2+)-induced rubidium flux from human RBCs/ inhibited RBC dehydration with IC50s of 11 nM/30 nM, respectively.
in vitro: ICA-17043 blocked Ca(2+)-induced rubidium flux from human RBCs with an IC(50) value of 11 +/- 2 nM (CLT IC(50) = 100 +/- 12 nM) and inhibited RBC dehydration with an IC(50) of 30 +/- 20 nM.
in vivo: In a transgenic mouse model of sickle cell disease (SAD), treatment with ICA-17043 (10 mg/kg orally, twice a day) for 21 days showed a marked and constant inhibition of the Gardos channel activity (with an average inhibition of 90% +/- 27%, P <.005), an increase in RBC K(+) content (from 392 +/- 19.9 to 479.2 +/- 40 mmol/kg hemoglobin [Hb], P <.005), a significant increase in hematocrit (Hct) (from 0.435 +/- 0.007 to 0.509 +/- 0.022 [43.5% +/- 0.7% to 50.9% +/- 2.2%], P <.005), a decrease in mean corpuscular hemoglobin concentration (MCHC) (from 340 +/- 9.0 to 300 +/- 15 g/L [34.0 +/- 0.9 to 30 +/- 1.5 g/dL], P <.05), and a left-shift in RBC density curves [1]. Senicapoc is well tolerated when administered to SCD patients and produces dose-dependent increases in hemoglobin and decreases in markers of hemolysis. Atopic sheep were administered either 30 mg/kg Senicapoc (ICA-17073), a selective inhibitor of the K(Ca)3.1-channel, or vehicle alone (0.5% methylcellulose) twice daily (orally).
For research only, not for human use!
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