QuickView for Nimodipine (compound)

Summary
General Info

PubChem

PubChem Compound 157132

Name:	Nimodipine
PubChem Compound ID:	157132
Description:	A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.
Molecular formula:	C₂₁H₂₆N₂O₇
Molecular weight:	418.44 g/mol
Synonyms:	NCGC00024675-01; Tocris-0600; NCGC00015714-01; 77940-92-2; Lopac-N-149; 3,5-Pyridinedicarboxylic acid, 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-, 2-methoxyethyl 1-methylethyl ester, (4R)-

DrugBank

Identification

Name:	Nimodipine
Name (isomeric):	DB00393
Drug Type:	small molecule
Description:	A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.
Synonyms:	Nimodipinum [INN-Latin]; Nimodipino [INN-Spanish]
Brand:	Nimotop, Periplum
Category:	Vasodilator Agents, Calcium Channel Blockers, Antihypertensive Agents
CAS number:	66085-59-4

Pharmacology

Indication:	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.
Pharmacology:	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.... show more » 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. show less «
Mechanism of Action:	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. Nimodipine binds specifically to L-type voltage-gated calcium channels. The inhibition of calci... show more » 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. Nimodipine binds specifically to L-type voltage-gated calcium channels. The inhibition of calcium ion transfer results 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. show less «
Absorption:	Bioavailability is 100% following intravenous administration and 3-30% following oral administration due to extensive first-pass metabolism.
Protein binding:	95%
Biotransformation:	Hepatic metabolism via cytochrome P450 3A4.
Half Life:	1.7-9 hours
Toxicity:	Symptoms of overdosage would be expected to be related to cardiovascular effects such as excessive peripheral vasodilation with marked systemic hypotension.
Affected organisms:	Humans and other mammals

Interactions

Food interaction:

Take at the same time each day, with or without food, but always in the same manner.

Grapefruit down regulates post-translational expression of CYP3A4, the major metabolizing enzyme of nimodipine. Grapefruit, in all forms (e.g. whole fruit, juice and rind), can significantly increase serum levels of nimodipine and may cause toxicity. Avoid grapefruit products while on this medication.

Drug interaction:

Valproic Acid	Valproic acid increases the effect of nimodipine
Divalproex sodium	Valproic acid increases the effect of nimodipine
Tipranavir	Tipranavir may decrease the metabolism and clearance of the calcium channel blocker, Nimodipine. Monitor for changes in Nimodipine therapeutic and adverse effects if Tipranavir is initiated, discontinued or dose changed.
Telithromycin	Telithromycin may reduce clearance of Nimodipine. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Nimodipine if Telithromycin is initiated, discontinued or dose changed.
Cimetidine	Cimetidine increases the effect of the calcium channel blocker, nimodipine.

Targets

Voltage-dependent L-type calcium channel subunit alpha-1C

Voltage-dependent L-type calcium channel subunit alpha-1D

Voltage-dependent L-type calcium channel subunit alpha-1F

Voltage-dependent L-type calcium channel subunit alpha-1S

Voltage-dependent L-type calcium channel subunit beta-1

Voltage-dependent L-type calcium channel subunit beta-2

Voltage-dependent L-type calcium channel subunit beta-3

Voltage-dependent L-type calcium channel subunit beta-4

Mineralocorticoid receptor

Aryl hydrocarbon receptor

Enzymes

Cytochrome P450 3A4

Cytochrome P450 3A5