ニモジピン

2.7

2.82

Breast Feeding; Lactation; Antihypertensive Agents; Calcium Channel Blockers; Vasodilator Agents

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Pharmaceuticals

198.78 Ų [M+Na]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

197.8 Ų [M+H]+ [CCS Type: TW; Method: Major Mix IMS/Tof Calibration Kit (Waters)]

This chemical does not meet GHS hazard criteria for 1.5% (1 of 67) of reports.

Warning

H315 (35.8%): Causes skin irritation [Warning Skin corrosion/irritation]

P203, P260, P264, P280, P302+P352, P318, P319, P321, P332+P317, P362+P364, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 67 reports by companies from 7 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Nimodipine is usually well-tolerated orally, but its use correlates with some side effects related to its use as a vasodilator. The most common adverse effects of this medication include headache, vertigo, flushing, nausea, diarrhea, pedal edema, rash, and palpitations.

Drug Induced Liver Injury Rank (DILIrank 2.0)

Nimodipine

Ambiguous-DILI-concern

3

Adverse reactions

DOI:10.1016/j.drudis.2016.02.015

C08CA06

C - Cardiovascular system

QC - Cardiovascular system

Nimodipine belongs to the class of pharmacological agents known as calcium channel blockers. Nimodipine is indicated for the improvement of neurological outcome by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage from ruptured congenital aneurysms who are in good neurological condition post-ictus (e.g., Hunt and Hess Grades I-III). The contractile processes of smooth muscle cells are dependent upon calcium ions, which enter these cells during depolarization as slow ionic transmembrane currents. Nimodipine inhibits calcium ion transfer into these cells and thus inhibits contractions of vascular smooth muscle. In animal experiments, nimodipine had a greater effect on cerebral arteries than on arteries elsewhere in the body perhaps because it is highly lipophilic, allowing it to cross the blood brain barrier.

Although the precise mechanism of action is not known, nimodipine blocks intracellular influx of calcium through voltage-dependent and receptor-operated slow calcium channels across the membranes of myocardial, vascular smooth muscle, and neuronal cells. By specifically binding to L-type voltage-gated calcium channels, nimodipine inhibits the calcium ion transfer, resulting in the inhibition of vascular smooth muscle contraction. Evidence suggests that the dilation of small cerebral resistance vessels, with a resultant increase in collateral circulation, and/or a direct effect involving the prevention of calcium overload in neurons may be responsible for nimodipine's clinical effect in patients with subarachnoid hemorrhage.

Hepatic metabolism via CYP 3A4.

Nimodipine has known human metabolites that include 2,6-Dimethyl-4-(3-nitrophenyl)-5-propan-2-yloxycarbonyl-1,4-dihydropyridine-3-carboxylic acid, Dehydro nimodipine, and Unii-96S4GG1upr.