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Nimodipine(BAY-e 9736)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Nimodipine(BAY-e 9736)图片
CAS NO:66085-59-4
规格:≥98%
包装与价格:
包装价格(元)
250mg电议
500mg电议
1g电议
2g电议
5g电议
10g电议

产品介绍
Nimodipine (formerly BAY E 9736; BAY-E-9736, Nimotop, Periplum) is a potent dihydropyridine/DHP class of calcium channel blocker (CCB) and an autophagy inhibitor with antihypertensive effects. It has been approved for use in the treatment of high blood pressure.
理化性质和储存条件
Molecular Weight (MW)418.44
FormulaC21H26N2O7
CAS No.66085-59-4
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: 84 mg/mL (200.7 mM)
Water: < 1 mg/mL
Ethanol: 84 mg/mL (200.7 mM)
Other infoChemical Name: 3-isopropyl 5-(2-methoxyethyl) 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate
InChi Key: UIAGMCDKSXEBJQ-UHFFFAOYSA-N
InChi Code: InChI=1S/C21H26N2O7/c1-12(2)30-21(25)18-14(4)22-13(3)17(20(24)29-10-9-28-5)19(18)15-7-6-8-16(11-15)23(26)27/h6-8,11-12,19,22H,9-10H2,1-5H3
SMILES Code: CC1=C(C(OCCOC)=O)C(C2=CC([N+]([O-])=O)=CC=C2)C(C(OC(C)C)=O)=C(C)N1
SynonymsBAY E 9736; BAY-E-9736, Nimodipine, Nimotop, Periplum, BAY E 9736, BAYE9736
实验参考方法
In Vitro

In vitro activity: Nimodipine decreases both the peak amplitude and the integrated area of the AHP in an age- and concentration-dependent manner. Nimodipine (100 nM) significantly reduces the AHP in aging CA1 neurons. Nimodipine increases excitability in an age- and concentration-dependent manner by decreasing spike frequency accommodation (increasing the number of action potentials during prolonged depolarizing current injection). Nimodipine decreases accommodation only at higher concentrations in young CA1 neurons. Nimodipine decreases the plateau phase of the calcium AP at concentrations as low as 100 nM in aging neurons and 10 mM in young rat neurons.


Cell Assay: Nimodipine decreases intracellular free Ca2+,Beclin-1 and autophagy. Target: Calcium Channel Nimodipine is main use is in the prevention of cerebral vasospasm and resultant ischemia, a complication of subarachnoid hemorrhage (a form of cerebral bleed), specifically from ruptured intracranial berry aneurysms irrespective of the patient's post-ictus neurological condition. Its administration begins within 4 days of a subarachnoid hemorrhage and is continued for three weeks. If blood pressure drops by over 5%, dosage is adjusted. There is still controversy regarding the use of intravenous nimodipine on a routine basis .

In VivoNimodipine results in reversible, dose-related suppression of the compound action potential of the auditory nerve (CAP; N1-P1), a prolongation of N1 latency at suprathreshold levels, an elevated CAP threshold, a decrease in N1 latency at a constant amplitude measured at CAP threshold, a reduction in cochlear microphonics (CM), and a reduction of the negative summating potential (SP) to a point where it becomes positive. Nimodipine (10 mg/kg, SC), an L-type dihydropyridine Ca2+ channel antagonist, appears to completely block the establishment of conditioning of cocaine's effects, but only partially blocks sensitization to cocaine. Nimodipine (5-20 mg/kg, SC) inhibits in a dose-related manner self-administration both of cocaine and morphine contingent upon a nose-poke response.
Animal model N/A
Formulation & Dosage 5-20 mg/kg, SC
ReferencesJ Neurophysiol. 1992 Dec;68(6):2100-9; Hear Res. 1990 Jul;46(3):277-87.