86384-98-7

Basic information

• Product Name: CV 159
• Synonyms: CV 159;1,4-Dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylic acid 3-methyl 5-[6-[(5-phenyl-1H-pyrazol-3-yl)oxy]hexyl] ester
• CAS NO: 86384-98-7
• Molecular Formula: C31H34N4O7
• Molecular Weight: 574.6243
• Mol File: 86384-98-7.mol
• Article Data: 2

Chemical Properties

• Boiling Point: 755.5°Cat760mmHg
• Flash Point: 410.7°C
• Appearance: /
• Density: 1.249g/cm³
• Vapor Pressure: 1.02E-22mmHg at 25°C
• Refractive Index: 1.586
• CAS DataBase Reference: CV 159(CAS DataBase Reference)
• NIST Chemistry Reference: CV 159(86384-98-7)
• EPA Substance Registry System: CV 159(86384-98-7)

Safety Data

• Hazardous Substances Data: 86384-98-7(Hazardous Substances Data)

Usage

InChI:InChI=1/C31H34N4O7/c1-20-27(30(36)40-3)29(23-14-11-15-24(18-23)35(38)39)28(21(2)32-20)31(37)42-17-10-5-4-9-16-41-26-19-25(33-34-26)22-12-7-6-8-13-22/h6-8,11-15,18-19,29,32H,4-5,9-10,16-17H2,1-3H3,(H,33,34)

Upstream product

• 86385-48-0 3-amino-crotonic acid 6-(5-phenyl-3-pyrazolyloxy)hexyl ester 
• 39562-17-9 methyl 2-(3-nitrophenylmethylene)acetoacetate 

Relevant articles and documents

Effects of a calcium-channel blocker (CV159) on hepatic ischemia/reperfusion injury in rats: Evaluation with selective NO/pO2 electrodes and an electron paramagnetic resonance spin-trapping method

Nitric oxide (NO) and the partial pressure of oxygen (pO2) in the liver were simultaneously quantified in rats with partial hepatic ischemia/reperfusion injury (PHIRI). Real-time NO/pO2 monitoring and immunohistochemical analysis for superoxide dismutase and inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) were performed to evaluate the protective effects of a dihydropyridine-type calcium-channel blocker-CV159-on PHIRI. Serum high-mobility-group box-1 (HMGB-1) was measured to assess cellular necrosis. Moreover, we used in vitro/ex vivo electron paramagnetic resonance spin trapping to assess the hydroxyl radical ( ?OH)-scavenging activity (OHSA) of CV159 and the liver tissue. The NO levels were significantly higher in CV159-treated rats than in control rats throughout the ischemic phase. Immediately after reperfusion, the levels temporarily increased in waves and then gradually decreased in the treated rats but remained constant in the control rats. pO 2 was continually higher in the treated rats. In these rats, hepatic eNOS expression increased, whereas iNOS expression decreased. The treated rats exhibited significantly higher cytosolic and mitochondrial concentrations NOx (NO2+NO3). The serum HMGB-1 levels significantly decreased in the treated rats. Moreover, CV159 directly scavenged ·OH and both mitochondrial and cytosolic OHSA were preserved in the treated rats. Thus, CV159-mediated inhibition of intracellular Ca2+ overloading may effectively minimize organ damage and also have ·OH-scavenging activity and the cytoprotective effects of eNOS-derived NO.