Nimodipine

418.44

418.44

266-127-0

758476

DTXSID5023370

C08CA06|C - Cardiovascular system

29333990

120

2.7

white solid

1.3268 (rough estimate)

125 °C

526.3°C at 760 mmHg

277.3ºC

1.561

methanol: 62.5 mg/mL

Store at RT

LD50 in mice, rats (mg/kg): 3562, 6599 orally; 33, 16 i.v. (Schlüter)

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

Ⅲ

IRRITANT

2811

1

20/21/22-48/22

36

US7975500

Xn

Stable under normal temperatures and pressures.

P201, P202, P260, P264, P280, P281, P302+P352, P308+P313, P314, P321, P332+P313, P362, P405, P501

H315

|Warning|H315 (36.36%): Causes skin irritation [Warning Skin corrosion/irritation]|P201, P202, P260, P264, P280, P281, P302+P352, P308+P313, P314, P321, P332+P313, P362, P405, and P501|Aggregated GHS information provided by 67 companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Symptoms of overdosage would be expected to be related to cardiovascular effects such as excessive peripheral vasodilation with marked systemic hypotension.

95% bound to plasma protein

For use as an adjunct to improve neurologic outcome following subarachnoid hemorrhage (SAH) from ruptured intracranial berry aneurysms by reducing the incidence and severity of ischemic deficits.|FDA Label|Treatment of aneurysmal subarchnoidal haemorrhage

Nimodipine is a second generation calcium channel blocker used in the treatment of cerebral vasospasm after subarachnoid hemorrhage. Nimodipine is not widely used and has not been implicated in causing clinically apparent acute liver injury.

Cardiovascular Agents

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.

A class of drugs that act by selective inhibition of calcium influx through cellular membranes. (See all compounds classified as Calcium Channel Blockers.)|Drugs used to cause dilation of the blood vessels. (See all compounds classified as Vasodilator Agents.)|Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS. (See all compounds classified as Antihypertensive Agents.)

In humans, nimodipine is rapidly absorbed after oral administration, and peak concentrations are generally attained within one hour. Bioavailability is 100% following intravenous administration and 3-30% following oral administration due to extensive first-pass metabolism.|Nimodipine is eliminated almost exclusively in the form of metabolites and less than 1% is recovered in the urine as unchanged drug. Numerous metabolites, all of which are either inactive or considerably less active than the parent compound, have been identified.

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.

1.7-9 hours

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.

Admon

Human drugs -> Rare disease (orphan)|Human Drugs -> EU pediatric investigation plans|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Pharmaceuticals