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Nimodipine Calcium Channel inhibitor

Cat.No.S1747

Nimodipine (BAY E 9736) is a dihydropyridine calcium channel blocker and an autophagy inhibitor, used in the treatment of high blood pressure.
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Quality Control

Batch: Purity: 99.08%
99.08

Solubility

In vitro
Batch:

DMSO : 84 mg/mL (200.74 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 84 mg/mL

Water : Insoluble

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In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 418.44 Formula

C21H26N2O7

Storage (From the date of receipt)
CAS No. 66085-59-4 Download SDF Storage of Stock Solutions

Synonyms BAY E 9736 SMILES CC1=C(C(C(=C(N1)C)C(=O)OC(C)C)C2=CC(=CC=C2)[N+](=O)[O-])C(=O)OCCOC

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Mechanism of Action

Targets/IC50/Ki
Calcium channel
In vitro
Nimodipine decreases both the peak amplitude and the integrated area of the AHP in an age- and concentration-dependent manner. This compound (100 nM) significantly reduces the AHP in aging CA1 neurons. It 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). This chemical decreases accommodation only at higher concentrations in young CA1 neurons. It 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.
In vivo
Nimodipine 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. This compound (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. This chemical (5-20 mg/kg, SC) inhibits in a dose-related manner self-administration both of cocaine and morphine contingent upon a nose-poke response.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/7862852/
  • [5] https://pubmed.ncbi.nlm.nih.gov/1533936/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2026-03-17)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT06900998 NOT_YET_RECRUITING
Alcohol Use Disorder
Yale University
2026-09-01 PHASE2
NCT07681869 NOT_YET_RECRUITING
Alcohol Use Disorder
Yale University
2026-09-01 PHASE2
NCT07144956 NOT_YET_RECRUITING
Aneurysmal Subarachnoid Hemorrhage
Centre Hospitalier St Anne
2025-12-15 PHASE3
NCT06615882 NOT_YET_RECRUITING
Intracranial Vasospasm
Yonsei University
2024-09
NCT06998368 RECRUITING
Mediation of 5G Effects on Sleep
Hans-Peter Landolt
2024-10-22
NCT07048522 RECRUITING
Colectomy; Open Surgery; Pain; Pain, Postoperative; Pain, Acute
University of Ioannina
2025-05-19

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