Vernakalant (Hydrochloride)|cas 748810-28-8|DC Chemicals
Vernakalant Hcl(RSD-1235) is an investigational mixed ion channel blocker that can terminate acute atrial fibrillation (AF) in humans at 2 to 5 mg/kg and may be more atrial-selective than available agents; in treatment of antiarrhythmic.
IC50 value:
Target:
Product Name: Vernakalant (Hydrochloride)|Cat No: DC9599|Cas: 748810-28-8|Molecule Formular: C20H32ClNO4|Molecule Weight: 385.9254|Other names: Vernakalant (Hydrochloride)
Vernakalant Hcl(RSD-1235) is an investigational mixed ion channel blocker that can terminate acute atrial fibrillation (AF) in humans at 2 to 5 mg/kg and may be more atrial-selective than available agents; in treatment of antiarrhythmic.
For research only, not for human use!
2016年6月13日星期一
TRAM-34|cas 289905-88-0|DC Chemicals
TRAM-34|cas 289905-88-0|DC Chemicals
TRAM-34 is a highly selective blocker of intermediate conductance Ca2+-activated K+ channels (KCa3.1) (Kd = 20 nM).
Product Name: TRAM-34|Cat No: DC9598|Cas: 289905-88-0|Molecule Formular: C22H17ClN2|Molecule Weight: 344.8368|Other names: TRAM-34
TRAM-34 is a highly selective blocker of intermediate conductance Ca2+-activated K+ channels (KCa3.1) (Kd = 20 nM).
in vitro: TRAM-34 inhibits the cloned and the native IKCa1 channel in human T lymphocytes with a K(d) of 20-25 nM and is 200- to 1,500-fold selective over other ion channels. Using TRAM-34, we show that blocking IKCa1 in human lymphocytes, in the absence of P450-inhibition, results in suppression of mitogen-stimulated [(3)H]thymidine incorporation of preactivated lymphocytes with EC(50)-values of 100 nM-1 microM depending on the donor. TRAM-34, a specific inhibitor of K(Ca)3.1 channels increased or decreased cell proliferation depending on the concentration. At intermediate concentrations (3-10 microM) TRAM-34 increased cell proliferation, whereas at higher concentrations (20-100 microM) TRAM-34 decreased cell proliferation.
in vivo: small molecule KCa3.1 blocker TRAM-34 effectively penetrates into the brain and achieves micromolar plasma and brain concentrations after intraperitoneal injection. Then, we subjected male Wistar rats to 90 minutes of middle cerebral artery occlusion (MCAO) and administered either vehicle or TRAM-34 (10 or 40 mg/kg intraperitoneally twice daily) for 7 days starting 12 hours after reperfusion. Both compound doses reduced infarct area by ≈ 50% as determined by hematoxylin & eosin staining on day 7 and the higher dose also significantly improved neurological deficit.
For research only, not for human use!
TRAM-34 is a highly selective blocker of intermediate conductance Ca2+-activated K+ channels (KCa3.1) (Kd = 20 nM).
Product Name: TRAM-34|Cat No: DC9598|Cas: 289905-88-0|Molecule Formular: C22H17ClN2|Molecule Weight: 344.8368|Other names: TRAM-34
TRAM-34 is a highly selective blocker of intermediate conductance Ca2+-activated K+ channels (KCa3.1) (Kd = 20 nM).
in vitro: TRAM-34 inhibits the cloned and the native IKCa1 channel in human T lymphocytes with a K(d) of 20-25 nM and is 200- to 1,500-fold selective over other ion channels. Using TRAM-34, we show that blocking IKCa1 in human lymphocytes, in the absence of P450-inhibition, results in suppression of mitogen-stimulated [(3)H]thymidine incorporation of preactivated lymphocytes with EC(50)-values of 100 nM-1 microM depending on the donor. TRAM-34, a specific inhibitor of K(Ca)3.1 channels increased or decreased cell proliferation depending on the concentration. At intermediate concentrations (3-10 microM) TRAM-34 increased cell proliferation, whereas at higher concentrations (20-100 microM) TRAM-34 decreased cell proliferation.
in vivo: small molecule KCa3.1 blocker TRAM-34 effectively penetrates into the brain and achieves micromolar plasma and brain concentrations after intraperitoneal injection. Then, we subjected male Wistar rats to 90 minutes of middle cerebral artery occlusion (MCAO) and administered either vehicle or TRAM-34 (10 or 40 mg/kg intraperitoneally twice daily) for 7 days starting 12 hours after reperfusion. Both compound doses reduced infarct area by ≈ 50% as determined by hematoxylin & eosin staining on day 7 and the higher dose also significantly improved neurological deficit.
For research only, not for human use!
Doxapram (hydrochloride hydrate)|cas 7081-53-0|DC Chemicals
Doxapram (hydrochloride hydrate)|cas 7081-53-0|DC Chemicals
Doxapram hydrochloride hydrate inhibits TASK-1, TASK-3, TASK-1/TASK-3 heterodimeric channel function with EC50 of 410 nM, 37 μM, 9 μM, respectively.
Target: Potassium Channel
Doxapram is a respiratory stimulant.
Product Name: Doxapram (hydrochloride hydrate)|Cat No: DC9597|Cas: 7081-53-0|Molecule Formular: C24H33ClN2O3|Molecule Weight: 432.9834|Other names: Doxapram (hydrochloride hydrate)
Doxapram hydrochloride hydrate inhibits TASK-1, TASK-3, TASK-1/TASK-3 heterodimeric channel function with EC50 of 410 nM, 37 μM, 9 μM, respectively.
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. 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 hydrochloride hydrate inhibits TASK-1, TASK-3, TASK-1/TASK-3 heterodimeric channel function with EC50 of 410 nM, 37 μM, 9 μM, respectively.
Target: Potassium Channel
Doxapram is a respiratory stimulant.
Product Name: Doxapram (hydrochloride hydrate)|Cat No: DC9597|Cas: 7081-53-0|Molecule Formular: C24H33ClN2O3|Molecule Weight: 432.9834|Other names: Doxapram (hydrochloride hydrate)
Doxapram hydrochloride hydrate inhibits TASK-1, TASK-3, TASK-1/TASK-3 heterodimeric channel function with EC50 of 410 nM, 37 μM, 9 μM, respectively.
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. 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!
2016年6月12日星期日
Azimilide (Dihydrochloride)|cas 149888-94-8|DC Chemicals
Azimilide (Dihydrochloride)|cas 149888-94-8|DC Chemicals.
Azimilide 2Hcl(NE-10064 2Hcl) is a class III antiarrhythmic compound, inhibits I(Ks) and I(Kr) in guinea-pig cardiac myocytes and I(Ks) (minK) channels expressed in Xenopus oocytes.
IC50 value:
Target:
in vitro: Azimilide blocked HERG channels at 0.1 and 1 Hz with IC50s of 1.4 microM and 5.2 microM respectively.
Product Name: Azimilide (Dihydrochloride)|Cat No: DC9596|Cas: 149888-94-8|Molecule Formular: C23H30Cl3N5O3|Molecule Weight: 530.875|Other names: Azimilide (Dihydrochloride)
Azimilide 2Hcl(NE-10064 2Hcl) is a class III antiarrhythmic compound, inhibits I(Ks) and I(Kr) in guinea-pig cardiac myocytes and I(Ks) (minK) channels expressed in Xenopus oocytes.
in vitro: Azimilide blocked HERG channels at 0.1 and 1 Hz with IC50s of 1.4 microM and 5.2 microM respectively. Azimilide blockade of HERG channels expressed in Xenopus oocytes and I(Kr) in mouse AT-1 cells was decreased under conditions of high [K+]e, whereas block of slowly activating I(Ks) channels was not affected by changes in [K+]e. Azimilide suppressed the following currents (Kd in parenthesis): IKr (< 1 microM at -20 mV), IKs (1.8 microM at +30 mV), L-type Ca current (17.8 microM at +10 mV), and Na current (19 microM at -40 mV). Azimilide was a weak blocker of the transient outward and inward rectifier currents (Kd > or = 50 microM at +50 and -140 mV, respectively). Azimilide blocked IKr, IKs, and INa in a use-dependent manner. Furthermore, azimilide reduced a slowly inactivating component of Na current that might be important for maintaining the action potential plateau in canine ventricular myocytes. In guinea pig ventricular myocytes, NE-10064 (0.3-3 microM) significantly prolonged action potential duration (APD) at 1 Hz. At 3 Hz, NE-10064 (0.3-1 microM) increased APD only slightly, and at 10 microM decreased APD and the plateau potential. NE-10064 potently blocked the rapidly activating component of the delayed rectifier, IKr (IC50 0.4 microM), and inhibited IKs (IC50 3 microM) with nearly 10-fold less potency.
in vivo: NE-10064 (10 mg/kg intravenously, i.v.) reduced (p < 0.05) the incidence (8 of 12) of PES-induced ventricular tachycardia (VT). The cycle length of induced VT was not prolonged by NE-10064 (0.245 +/- 0.046 s predrug vs. 0.301 +/- 0.060 s postdrug). NE-10064 increased ventricular effective refractory period (VERP 166 +/- 5 ms predrug vs. 194 +/- 13 ms postdrug, p = 0.013), prolonged QTc interval (310 +/- 12 ms predrug vs. 350 +/- 16 ms postdrug, p = 0.004) and prolonged the effective refractory period (ERP) of noninfarcted myocardium (p = 0.045).
For research only, not for human use!
Azimilide 2Hcl(NE-10064 2Hcl) is a class III antiarrhythmic compound, inhibits I(Ks) and I(Kr) in guinea-pig cardiac myocytes and I(Ks) (minK) channels expressed in Xenopus oocytes.
IC50 value:
Target:
in vitro: Azimilide blocked HERG channels at 0.1 and 1 Hz with IC50s of 1.4 microM and 5.2 microM respectively.
Product Name: Azimilide (Dihydrochloride)|Cat No: DC9596|Cas: 149888-94-8|Molecule Formular: C23H30Cl3N5O3|Molecule Weight: 530.875|Other names: Azimilide (Dihydrochloride)
Azimilide 2Hcl(NE-10064 2Hcl) is a class III antiarrhythmic compound, inhibits I(Ks) and I(Kr) in guinea-pig cardiac myocytes and I(Ks) (minK) channels expressed in Xenopus oocytes.
in vitro: Azimilide blocked HERG channels at 0.1 and 1 Hz with IC50s of 1.4 microM and 5.2 microM respectively. Azimilide blockade of HERG channels expressed in Xenopus oocytes and I(Kr) in mouse AT-1 cells was decreased under conditions of high [K+]e, whereas block of slowly activating I(Ks) channels was not affected by changes in [K+]e. Azimilide suppressed the following currents (Kd in parenthesis): IKr (< 1 microM at -20 mV), IKs (1.8 microM at +30 mV), L-type Ca current (17.8 microM at +10 mV), and Na current (19 microM at -40 mV). Azimilide was a weak blocker of the transient outward and inward rectifier currents (Kd > or = 50 microM at +50 and -140 mV, respectively). Azimilide blocked IKr, IKs, and INa in a use-dependent manner. Furthermore, azimilide reduced a slowly inactivating component of Na current that might be important for maintaining the action potential plateau in canine ventricular myocytes. In guinea pig ventricular myocytes, NE-10064 (0.3-3 microM) significantly prolonged action potential duration (APD) at 1 Hz. At 3 Hz, NE-10064 (0.3-1 microM) increased APD only slightly, and at 10 microM decreased APD and the plateau potential. NE-10064 potently blocked the rapidly activating component of the delayed rectifier, IKr (IC50 0.4 microM), and inhibited IKs (IC50 3 microM) with nearly 10-fold less potency.
in vivo: NE-10064 (10 mg/kg intravenously, i.v.) reduced (p < 0.05) the incidence (8 of 12) of PES-induced ventricular tachycardia (VT). The cycle length of induced VT was not prolonged by NE-10064 (0.245 +/- 0.046 s predrug vs. 0.301 +/- 0.060 s postdrug). NE-10064 increased ventricular effective refractory period (VERP 166 +/- 5 ms predrug vs. 194 +/- 13 ms postdrug, p = 0.013), prolonged QTc interval (310 +/- 12 ms predrug vs. 350 +/- 16 ms postdrug, p = 0.004) and prolonged the effective refractory period (ERP) of noninfarcted myocardium (p = 0.045).
For research only, not for human use!
E-4031|cas 113559-13-0|DC Chemicals
E-4031|cas 113559-13-0|DC Chemicals
E-4031 is a benzenesulfonamide antiarrhythmic agent; blocks the ATP-sensitive potassium channel.
IC50 value:
Target: K+ channel blocker
in vitro: Dofetilide and E-4031 induced EADs or TdP in all assays (50-83%), and the induction correlated with a significant increase in beat-to-beat variability of repolarization .
Product Name: E-4031|Cat No: DC9595|Cas: 113559-13-0|Molecule Formular: C21H29Cl2N3O3S|Molecule Weight: 474.4443|Other names: E-4031
E-4031 is a benzenesulfonamide antiarrhythmic agent; blocks the ATP-sensitive potassium channel.
in vitro: Dofetilide and E-4031 induced EADs or TdP in all assays (50-83%), and the induction correlated with a significant increase in beat-to-beat variability of repolarization. E-4031 (0.1 mumol/L) significantly prolonged cycle length and action potential duration, depolarized maximum diastolic potential, and reduced both the upstroke velocity of the action potential and the diastolic depolarization rate.
in vivo: E-4031 in doses of 0.01 and 0.1 mg/kg that can provide the plasma concentrations effectively to inhibit IKrin vitro significantly delayed the repolarization beyond the initiation of diastole, resulting in the inversion of electro-mechanical coupling, which provides an ideal proarrhythmic substrate, while the durations of left ventricular systole and diastole remained the same. Bepridil and E-4031 prolonged QT interval and ARI in all LV layers, though the magnitude of prolongation was greatest in Mid, increasing the transmural ARI dispersion, particularly during bradycardia.
For research only, not for human use!
E-4031 is a benzenesulfonamide antiarrhythmic agent; blocks the ATP-sensitive potassium channel.
IC50 value:
Target: K+ channel blocker
in vitro: Dofetilide and E-4031 induced EADs or TdP in all assays (50-83%), and the induction correlated with a significant increase in beat-to-beat variability of repolarization .
Product Name: E-4031|Cat No: DC9595|Cas: 113559-13-0|Molecule Formular: C21H29Cl2N3O3S|Molecule Weight: 474.4443|Other names: E-4031
E-4031 is a benzenesulfonamide antiarrhythmic agent; blocks the ATP-sensitive potassium channel.
in vitro: Dofetilide and E-4031 induced EADs or TdP in all assays (50-83%), and the induction correlated with a significant increase in beat-to-beat variability of repolarization. E-4031 (0.1 mumol/L) significantly prolonged cycle length and action potential duration, depolarized maximum diastolic potential, and reduced both the upstroke velocity of the action potential and the diastolic depolarization rate.
in vivo: E-4031 in doses of 0.01 and 0.1 mg/kg that can provide the plasma concentrations effectively to inhibit IKrin vitro significantly delayed the repolarization beyond the initiation of diastole, resulting in the inversion of electro-mechanical coupling, which provides an ideal proarrhythmic substrate, while the durations of left ventricular systole and diastole remained the same. Bepridil and E-4031 prolonged QT interval and ARI in all LV layers, though the magnitude of prolongation was greatest in Mid, increasing the transmural ARI dispersion, particularly during bradycardia.
For research only, not for human use!
Poloxin|cas 321688-88-4|DC Chemicals
Poloxin|cas 321688-88-4|DC Chemicals
Poloxin is a non-ATP competitive Polo-like Kinase 1 (PLK1) inhibitor that targets the polo-box domain.
Product Name: Poloxin|Cat No: DC9594|Cas: 321688-88-4|Molecule Formular: C18H19NO3|Molecule Weight: 297.3484|Other names: Poloxin
Poloxin is a non-ATP competitive Polo-like Kinase 1 (PLK1) inhibitor that targets the polo-box domain.
in vitro: Poloxin induces centrosome fragmentation and abnormal spindle and chromosome misalignment, which activate the spindle assembly checkpoint and prolong mitosis. Notably, centrosomal fragmentation induced by Poloxin is partially attributable to dysfunctional Kizuna, a key substrate of Plk1 at centrosomes. Moreover, Poloxin strongly inhibits proliferation of a panel of cancer cells by inducing mitotic arrest, followed by a surge of apoptosis.
in vivo: Poloxin inhibit tumor growth in nude mice xenografted with MDA-MB-231 or HeLa cells. A significant reduction of tumor volume after approximately 6 weeks of treatment with Poloxin or TQ in MDA-MB-231 xenograft mice compared with vehicle DMSO treatment.
For research only, not for human use!
Poloxin is a non-ATP competitive Polo-like Kinase 1 (PLK1) inhibitor that targets the polo-box domain.
Product Name: Poloxin|Cat No: DC9594|Cas: 321688-88-4|Molecule Formular: C18H19NO3|Molecule Weight: 297.3484|Other names: Poloxin
Poloxin is a non-ATP competitive Polo-like Kinase 1 (PLK1) inhibitor that targets the polo-box domain.
in vitro: Poloxin induces centrosome fragmentation and abnormal spindle and chromosome misalignment, which activate the spindle assembly checkpoint and prolong mitosis. Notably, centrosomal fragmentation induced by Poloxin is partially attributable to dysfunctional Kizuna, a key substrate of Plk1 at centrosomes. Moreover, Poloxin strongly inhibits proliferation of a panel of cancer cells by inducing mitotic arrest, followed by a surge of apoptosis.
in vivo: Poloxin inhibit tumor growth in nude mice xenografted with MDA-MB-231 or HeLa cells. A significant reduction of tumor volume after approximately 6 weeks of treatment with Poloxin or TQ in MDA-MB-231 xenograft mice compared with vehicle DMSO treatment.
For research only, not for human use!
Pim1/AKK1-IN-1|cas 1093222-27-5|DC Chemicals
Pim1/AKK1-IN-1|cas 1093222-27-5|DC Chemicals
PIM/AKK1-IN-1 is a potent multi-kinase inhibitor with Kd values of 35 nM/53 nM/75 nM/380 nM for Pim1/AKK1/MST2/LKB1 respectively; also inhibits MPSK1 and TNIK.
Product Name: Pim1/AKK1-IN-1|Cat No: DC9593|Cas: 1093222-27-5|Molecule Formular: C20H13N5O|Molecule Weight: 339.3501|Other names: Pim1/AKK1-IN-1
PIM/AKK1-IN-1 is a potent multi-kinase inhibitor with Kd values of 35 nM/53 nM/75 nM/380 nM for Pim1/AKK1/MST2/LKB1 respectively; also inhibits MPSK1 and TNIK.
For research only, not for human use!
PIM/AKK1-IN-1 is a potent multi-kinase inhibitor with Kd values of 35 nM/53 nM/75 nM/380 nM for Pim1/AKK1/MST2/LKB1 respectively; also inhibits MPSK1 and TNIK.
Product Name: Pim1/AKK1-IN-1|Cat No: DC9593|Cas: 1093222-27-5|Molecule Formular: C20H13N5O|Molecule Weight: 339.3501|Other names: Pim1/AKK1-IN-1
PIM/AKK1-IN-1 is a potent multi-kinase inhibitor with Kd values of 35 nM/53 nM/75 nM/380 nM for Pim1/AKK1/MST2/LKB1 respectively; also inhibits MPSK1 and TNIK.
For research only, not for human use!
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