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Identification
NameNimodipine
Accession NumberDB00393  (APRD00612)
TypeSmall Molecule
GroupsApproved
Description

Nimodipine is a 1,4-dihydropyridine calcium channel blocker. It acts primarily on vascular smooth muscle cells by stabilizing voltage-gated L-type calcium channels in their inactive conformation. By inhibiting the influx of calcium in smooth muscle cells, nimodipine prevents calcium-dependent smooth muscle contraction and subsequent vasoconstriction. Compared to other calcium channel blocking agents, nimodipine exhibits greater effects on cerebral circulation than on peripheral circulation. Nimodipine is used to as an adjunct to improve the neurologic outcome following subarachnoid hemorrhage from ruptured intracranial aneurysm.

Structure
Thumb
Synonyms
SynonymLanguageCode
2,6-Dimethyl-4-(3'-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylic acid 3-beta-methoxyethyl ester 5-isopropyl esterNot AvailableNot Available
BAY e 9736Not AvailableNot Available
Isopropyl 2-methoxyethyl 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylateNot AvailableNot Available
Isopropyl 2-methoxyethyl 1,4-dihydro-2,6-dimethyl-4-(m-nitrophenyl)-3,5-pyridinedicarboxylateNot AvailableNot Available
NimodipineNot AvailableNot Available
NimodipinoSpanishINN
NimodipinumLatinINN
NimotopNot AvailableNot Available
PeriplumNot AvailableNot Available
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Nymalizesolution60 mg/20mLoralArbor Pharmaceuticals2013-06-03Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Nimotoptablet30 mgoralBayer IncNot AvailableNot AvailableCanada 5f16b84899037e23705f146ff57e3794121879cb055f0954756d94bc690476b4
Generic Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Nimodipinecapsule, liquid filled30 mgoralHeritage2008-03-21Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Nimodipinecapsule30 mgoralCardinal Health2007-06-28Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Nimodipinecapsule30 mgoralCaraco Pharmaceutical Laboratories, Ltd.2007-06-28Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Nimodipinecapsule, liquid filled30 mgoralGolden State Medical Supply, Inc.2008-03-21Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Nimodipinecapsule, liquid filled30 mgoralAscend Laboratories, LLC2015-01-01Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Over the Counter ProductsNot Available
International Brands
NameCompany
PeriplumNot Available
Brand mixturesNot Available
SaltsNot Available
Categories
CAS number66085-59-4
WeightAverage: 418.4403
Monoisotopic: 418.174001196
Chemical FormulaC21H26N2O7
InChI KeyUIAGMCDKSXEBJQ-UHFFFAOYSA-N
InChI
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
IUPAC Name
3-(2-methoxyethyl) 5-propan-2-yl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate
SMILES
COCCOC(=O)C1=C(C)NC(C)=C(C1C1=CC(=CC=C1)[N+]([O-])=O)C(=O)OC(C)C
Taxonomy
DescriptionThis compound belongs to the class of organic compounds known as dihydropyridinecarboxylic acids and derivatives. These are compounds containing a dihydropyridine moiety bearing a carboxylic acid group.
KingdomOrganic compounds
Super ClassOrganoheterocyclic compounds
ClassPyridines and derivatives
Sub ClassHydropyridines
Direct ParentDihydropyridinecarboxylic acids and derivatives
Alternative Parents
Substituents
  • Nitrobenzene
  • Dihydropyridinecarboxylic acid derivative
  • Benzenoid
  • Dicarboxylic acid or derivatives
  • Monocyclic benzene moiety
  • Vinylogous amide
  • Alpha,beta-unsaturated carboxylic ester
  • Enoate ester
  • Organic nitro compound
  • Organic nitrite
  • C-nitro compound
  • Carboxylic acid ester
  • Azacycle
  • Organic 1,3-dipolar compound
  • Propargyl-type 1,3-dipolar organic compound
  • Allyl-type 1,3-dipolar organic compound
  • Organic oxoazanium
  • Ether
  • Enamine
  • Dialkyl ether
  • Carboxylic acid derivative
  • Hydrocarbon derivative
  • Organic salt
  • Organooxygen compound
  • Organonitrogen compound
  • Carbonyl group
  • Amine
  • Organic zwitterion
  • Aromatic heteromonocyclic compound
Molecular FrameworkAromatic heteromonocyclic compounds
External DescriptorsNot Available
Pharmacology
IndicationFor 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.
PharmacodynamicsNimodipine 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.
Mechanism of actionAlthough 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.
AbsorptionIn 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.
Volume of distributionNot Available
Protein binding95% bound to plasma protein
Metabolism

Hepatic metabolism via CYP 3A4.

Route of eliminationNimodipine 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.
Half life1.7-9 hours
ClearanceNot Available
ToxicitySymptoms 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
PathwaysNot Available
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+0.9387
Blood Brain Barrier-0.9358
Caco-2 permeable-0.5838
P-glycoprotein substrateSubstrate0.752
P-glycoprotein inhibitor IInhibitor0.9287
P-glycoprotein inhibitor IIInhibitor0.9098
Renal organic cation transporterNon-inhibitor0.8178
CYP450 2C9 substrateNon-substrate0.8151
CYP450 2D6 substrateNon-substrate0.9118
CYP450 3A4 substrateSubstrate0.7571
CYP450 1A2 substrateInhibitor0.9108
CYP450 2C9 substrateInhibitor0.8949
CYP450 2D6 substrateNon-inhibitor0.9231
CYP450 2C19 substrateInhibitor0.8994
CYP450 3A4 substrateInhibitor0.8248
CYP450 inhibitory promiscuityHigh CYP Inhibitory Promiscuity0.8557
Ames testNon AMES toxic0.5976
CarcinogenicityNon-carcinogens0.6953
BiodegradationNot ready biodegradable0.8797
Rat acute toxicity2.5326 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.6468
hERG inhibition (predictor II)Non-inhibitor0.8734
Pharmacoeconomics
Manufacturers
  • Banner pharmacaps inc
  • Barr laboratories inc
  • Sun pharmaceutical industries inc
  • Bayer pharmaceuticals corp
Packagers
Dosage forms
FormRouteStrength
Capsuleoral30 mg
Capsule, liquid filledoral30 mg
Solutionoral60 mg/20mL
Tabletoral30 mg
Prices
Unit descriptionCostUnit
NiMODipine 100 30 mg capsule Box952.07USD box
Nimotop 30 mg capsule9.87USD capsule
Nimodipine 30 mg capsule9.69USD capsule
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
PatentsNot Available
Properties
StateSolid
Experimental Properties
PropertyValueSource
melting point125 °CNot Available
logP3.05MASUMOTO,K ET AL. (1995)
Predicted Properties
PropertyValueSource
Water Solubility0.012 mg/mLALOGPS
logP3.41ALOGPS
logP2.54ChemAxon
logS-4.5ALOGPS
pKa (Strongest Basic)5.41ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count6ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area119.68 Å2ChemAxon
Rotatable Bond Count10ChemAxon
Refractivity112.38 m3·mol-1ChemAxon
Polarizability43.17 Å3ChemAxon
Number of Rings2ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Mass Spec (NIST)Not Available
SpectraNot Available
References
Synthesis ReferenceNot Available
General Reference
  1. Janjua N, Mayer SA: Cerebral vasospasm after subarachnoid hemorrhage. Curr Opin Crit Care. 2003 Apr;9(2):113-9. Pubmed
  2. Allen GS, Ahn HS, Preziosi TJ, Battye R, Boone SC, Boone SC, Chou SN, Kelly DL, Weir BK, Crabbe RA, Lavik PJ, Rosenbloom SB, Dorsey FC, Ingram CR, Mellits DE, Bertsch LA, Boisvert DP, Hundley MB, Johnson RK, Strom JA, Transou CR: Cerebral arterial spasm—a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med. 1983 Mar 17;308(11):619-24. Pubmed
  3. Belfort MA, Anthony J, Saade GR, Allen JC Jr: A comparison of magnesium sulfate and nimodipine for the prevention of eclampsia. N Engl J Med. 2003 Jan 23;348(4):304-11. Pubmed#
    Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc. 2009 Sep;46(3):239-44. Epub 2009 Sep 30. Pubmed
  4. Tomassoni D, Lanari A, Silvestrelli G, Traini E, Amenta F: Nimodipine and its use in cerebrovascular disease: evidence from recent preclinical and controlled clinical studies. Clin Exp Hypertens. 2008 Nov;30(8):744-66. Pubmed
  5. Vergouwen MD, Vermeulen M, Roos YB: Effect of nimodipine on outcome in patients with traumatic subarachnoid haemorrhage: a systematic review. Lancet Neurol. 2006 Dec;5(12):1029-32. Pubmed
External Links
ATC CodesC08CA06
AHFS Codes
  • 24:28.08
PDB EntriesNot Available
FDA labelDownload (504 KB)
MSDSDownload (73.3 KB)
Interactions
Drug Interactions
Drug
AlfuzosinMay enhance the hypotensive effect of Antihypertensives.
AmifostineAntihypertensives may enhance the hypotensive effect of Amifostine.
AmobarbitalBarbiturates may increase the metabolism of Calcium Channel Blockers.
AprepitantMay increase the serum concentration of CYP3A4 Substrates.
AtracuriumMay enhance the neuromuscular-blocking effect of Neuromuscular-Blocking Agents (Nondepolarizing).
BatimastatMay decrease the metabolism of Calcium Channel Blockers (Dihydropyridine).
BosentanMay decrease the serum concentration of CYP3A4 Substrates.
ButabarbitalBarbiturates may increase the metabolism of Calcium Channel Blockers.
ButalbitalBarbiturates may increase the metabolism of Calcium Channel Blockers.
ButethalMay increase the metabolism of Calcium Channel Blockers.
Calcium AcetateCalcium Salts may diminish the therapeutic effect of Calcium Channel Blockers.
Calcium carbonateCalcium Salts may diminish the therapeutic effect of Calcium Channel Blockers.
Calcium ChlorideCalcium Salts may diminish the therapeutic effect of Calcium Channel Blockers.
CarbamazepineMay increase the metabolism of Calcium Channel Blockers (Dihydropyridine).
CimetidineMay increase the serum concentration of Calcium Channel Blockers.
Cisatracurium BesylateMay enhance the neuromuscular-blocking effect of Neuromuscular-Blocking Agents (Nondepolarizing).
ClarithromycinMacrolide Antibiotics may decrease the metabolism of Calcium Channel Blockers.
ClopidogrelCalcium Channel Blockers may diminish the therapeutic effect of Clopidogrel.
ConivaptanMay increase the serum concentration of CYP3A4 Substrates.
DabrafenibMay decrease the serum concentration of CYP3A4 Substrates.
DapoxetineMay enhance the orthostatic hypotensive effect of Calcium Channel Blockers.
DasatinibMay increase the serum concentration of CYP3A4 Substrates.
DeferasiroxMay decrease the serum concentration of CYP3A4 Substrates.
DiazoxideMay enhance the hypotensive effect of Antihypertensives.
DoxazosinAlpha1-Blockers may enhance the hypotensive effect of Calcium Channel Blockers.
DuloxetineHypotensive Agents may enhance the orthostatic hypotensive effect of DULoxetine.
EfavirenzMay decrease the serum concentration of Calcium Channel Blockers.
FluconazoleFluconazole may increase the serum concentration of Calcium Channel Blockers. Exceptions: Clevidipine.
FluoxetineMay increase the serum concentration of NiMODipine.
FosaprepitantMay increase the serum concentration of CYP3A4 Substrates.
FosphenytoinCalcium Channel Blockers may increase the serum concentration of Fosphenytoin.
HeptabarbitalMay increase the metabolism of Calcium Channel Blockers.
HexobarbitalMay increase the metabolism of Calcium Channel Blockers.
IsoflurophateMay decrease the metabolism of Calcium Channel Blockers (Dihydropyridine).
ItraconazoleAntifungal Agents (Azole Derivatives, Systemic) may enhance the adverse/toxic effect of Calcium Channel Blockers. Specifically, itraconazole may enhance the negative inotropic effects of verapamil or diltiazem. Antifungal Agents (Azole Derivatives, Systemic) may decrease the metabolism of Calcium Channel Blockers. Fluconazole and isavuconazonium likely exert weaker effects than other azoles and are addressed in separate monographs.
IvacaftorMay increase the serum concentration of CYP3A4 Substrates.
LULICONAZOLEMay increase the serum concentration of CYP3A4 Substrates.
Magnesium oxideMay enhance the adverse/toxic effect of Magnesium Salts. Magnesium Salts may enhance the hypotensive effect of Calcium Channel Blockers.
Magnesium salicylateMay enhance the adverse/toxic effect of Magnesium Salts. Magnesium Salts may enhance the hypotensive effect of Calcium Channel Blockers.
MelatoninMay diminish the antihypertensive effect of Calcium Channel Blockers (Dihydropyridine).
MethohexitalMay increase the metabolism of Calcium Channel Blockers.
MethylphenidateMay diminish the antihypertensive effect of Antihypertensives.
MifepristoneMay increase the serum concentration of CYP3A4 Substrates.
MitotaneMay decrease the serum concentration of CYP3A4 Substrates.
NafcillinMay increase the metabolism of Calcium Channel Blockers.
NitroprussideMay enhance the hypotensive effect of Nitroprusside.
ObinutuzumabAntihypertensives may enhance the hypotensive effect of Obinutuzumab.
PancuroniumMay enhance the neuromuscular-blocking effect of Neuromuscular-Blocking Agents (Nondepolarizing).
PentobarbitalBarbiturates may increase the metabolism of Calcium Channel Blockers.
PentoxifyllineMay enhance the hypotensive effect of Antihypertensives.
PhenobarbitalBarbiturates may increase the metabolism of Calcium Channel Blockers.
PhenoxybenzamineAlpha1-Blockers may enhance the hypotensive effect of Calcium Channel Blockers.
PhentolamineAlpha1-Blockers may enhance the hypotensive effect of Calcium Channel Blockers.
PhenytoinMay increase the serum concentration of Phenytoin.
PosaconazoleAntifungal Agents (Azole Derivatives, Systemic) may enhance the adverse/toxic effect of Calcium Channel Blockers. Specifically, itraconazole may enhance the negative inotropic effects of verapamil or diltiazem. Antifungal Agents (Azole Derivatives, Systemic) may decrease the metabolism of Calcium Channel Blockers. Fluconazole and isavuconazonium likely exert weaker effects than other azoles and are addressed in separate monographs.
PrazosinAlpha1-Blockers may enhance the hypotensive effect of Calcium Channel Blockers.
PrimidoneMay increase the metabolism of Calcium Channel Blockers.
QuinidineMay increase the serum concentration of Calcium Channel Blockers (Dihydropyridine). Calcium Channel Blockers (Dihydropyridine) may decrease the serum concentration of QuiNIDine. Calcium Channel Blockers (Dihydropyridine) may increase the serum concentration of QuiNIDine.
RifampicinRifamycin Derivatives may decrease the serum concentration of Calcium Channel Blockers. This primarily affects oral forms of calcium channel blockers.
RifapentineRifamycin Derivatives may decrease the serum concentration of Calcium Channel Blockers. This primarily affects oral forms of calcium channel blockers.
RisperidoneHypotensive Agents may enhance the hypotensive effect of RisperiDONE.
RituximabAntihypertensives may enhance the hypotensive effect of RiTUXimab.
RocuroniumMay enhance the neuromuscular-blocking effect of Neuromuscular-Blocking Agents (Nondepolarizing).
SecobarbitalMay increase the metabolism of Calcium Channel Blockers.
SilodosinAlpha1-Blockers may enhance the hypotensive effect of Calcium Channel Blockers.
SiltuximabMay decrease the serum concentration of CYP3A4 Substrates.
SimeprevirMay decrease the metabolism of Calcium Channel Blockers (Dihydropyridine).
SulfisoxazoleMacrolide Antibiotics may decrease the metabolism of Calcium Channel Blockers.
TadalafilMay enhance the antihypertensive effect of Antihypertensives.
TamsulosinAlpha1-Blockers may enhance the hypotensive effect of Calcium Channel Blockers.
TelithromycinMacrolide Antibiotics may decrease the metabolism of Calcium Channel Blockers.
TerazosinAlpha1-Blockers may enhance the hypotensive effect of Calcium Channel Blockers.
TocilizumabMay decrease the serum concentration of CYP3A4 Substrates.
VardenafilMay enhance the antihypertensive effect of Antihypertensives.
VecuroniumMay enhance the neuromuscular-blocking effect of Neuromuscular-Blocking Agents (Nondepolarizing).
VoriconazoleAntifungal Agents (Azole Derivatives, Systemic) may enhance the adverse/toxic effect of Calcium Channel Blockers. Specifically, itraconazole may enhance the negative inotropic effects of verapamil or diltiazem. Antifungal Agents (Azole Derivatives, Systemic) may decrease the metabolism of Calcium Channel Blockers. Fluconazole and isavuconazonium likely exert weaker effects than other azoles and are addressed in separate monographs.
YohimbineMay diminish the antihypertensive effect of Antihypertensives.
Food Interactions
  • 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.
  • Take at the same time each day, with or without food, but always in the same manner.

Targets

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

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

Name UniProt ID Details
Voltage-dependent L-type calcium channel subunit alpha-1C Q13936 Details

References:

  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed
  2. Marchetti C, Usai C: High affinity block by nimodipine of the internal calcium elevation in chronically depolarized rat cerebellar granule neurons. Neurosci Lett. 1996 Mar 29;207(2):77-80. Pubmed
  3. Striessnig, J. (2004). Ca 2+ channel blockers. In S. Offermanns, & W. Rosenthal (Eds.). Encyclopedic reference of molecular pharmacology (pp. 201-207). Berlin, Germany: Springer.
  4. Weant KA, Ramsey CN 3rd, Cook AM: Role of intraarterial therapy for cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage. Pharmacotherapy. 2010 Apr;30(4):405-17. Pubmed
  5. Dong CJ, Guo Y, Agey P, Wheeler L, Hare WA: Nimodipine Enhancement of {alpha}2 Adrenergic Modulation of NMDA Receptor via a Mechanism Independent of Ca2+ Channel Blocking. Invest Ophthalmol Vis Sci. 2010 Aug;51(8):4174-80. Epub 2010 Mar 24. Pubmed
  6. Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc. 2009 Sep;46(3):239-44. Epub 2009 Sep 30. Pubmed
  7. Kumar R, Mehra R, Ray SB: L-type calcium channel blockers, morphine and pain: Newer insights. Indian J Anaesth. 2010 Mar;54(2):127-31. Pubmed
  8. Keyrouz SG, Diringer MN: Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care. 2007;11(4):220. Pubmed

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

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

Name UniProt ID Details
Voltage-dependent L-type calcium channel subunit alpha-1D Q01668 Details

References:

  1. Sinnegger-Brauns MJ, Huber IG, Koschak A, Wild C, Obermair GJ, Einzinger U, Hoda JC, Sartori SB, Striessnig J: Expression and 1,4-dihydropyridine-binding properties of brain L-type calcium channel isoforms. Mol Pharmacol. 2009 Feb;75(2):407-14. Epub 2008 Nov 24. Pubmed
  2. Weant KA, Ramsey CN 3rd, Cook AM: Role of intraarterial therapy for cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage. Pharmacotherapy. 2010 Apr;30(4):405-17. Pubmed
  3. Dong CJ, Guo Y, Agey P, Wheeler L, Hare WA: Nimodipine Enhancement of {alpha}2 Adrenergic Modulation of NMDA Receptor via a Mechanism Independent of Ca2+ Channel Blocking. Invest Ophthalmol Vis Sci. 2010 Aug;51(8):4174-80. Epub 2010 Mar 24. Pubmed
  4. Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc. 2009 Sep;46(3):239-44. Epub 2009 Sep 30. Pubmed
  5. Kumar R, Mehra R, Ray SB: L-type calcium channel blockers, morphine and pain: Newer insights. Indian J Anaesth. 2010 Mar;54(2):127-31. Pubmed
  6. Keyrouz SG, Diringer MN: Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care. 2007;11(4):220. Pubmed

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

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

Name UniProt ID Details
Voltage-dependent L-type calcium channel subunit alpha-1F O60840 Details

References:

  1. Weant KA, Ramsey CN 3rd, Cook AM: Role of intraarterial therapy for cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage. Pharmacotherapy. 2010 Apr;30(4):405-17. Pubmed
  2. Dong CJ, Guo Y, Agey P, Wheeler L, Hare WA: Nimodipine Enhancement of {alpha}2 Adrenergic Modulation of NMDA Receptor via a Mechanism Independent of Ca2+ Channel Blocking. Invest Ophthalmol Vis Sci. 2010 Aug;51(8):4174-80. Epub 2010 Mar 24. Pubmed
  3. Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc. 2009 Sep;46(3):239-44. Epub 2009 Sep 30. Pubmed
  4. Kumar R, Mehra R, Ray SB: L-type calcium channel blockers, morphine and pain: Newer insights. Indian J Anaesth. 2010 Mar;54(2):127-31. Pubmed

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

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

Name UniProt ID Details
Voltage-dependent L-type calcium channel subunit alpha-1S Q13698 Details

References:

  1. Peterson BZ, Catterall WA: Allosteric interactions required for high-affinity binding of dihydropyridine antagonists to Ca(V)1.1 Channels are modulated by calcium in the pore. Mol Pharmacol. 2006 Aug;70(2):667-75. Epub 2006 May 4. Pubmed
  2. Weant KA, Ramsey CN 3rd, Cook AM: Role of intraarterial therapy for cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage. Pharmacotherapy. 2010 Apr;30(4):405-17. Pubmed
  3. Dong CJ, Guo Y, Agey P, Wheeler L, Hare WA: Nimodipine Enhancement of {alpha}2 Adrenergic Modulation of NMDA Receptor via a Mechanism Independent of Ca2+ Channel Blocking. Invest Ophthalmol Vis Sci. 2010 Aug;51(8):4174-80. Epub 2010 Mar 24. Pubmed
  4. Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc. 2009 Sep;46(3):239-44. Epub 2009 Sep 30. Pubmed
  5. Kumar R, Mehra R, Ray SB: L-type calcium channel blockers, morphine and pain: Newer insights. Indian J Anaesth. 2010 Mar;54(2):127-31. Pubmed
  6. Keyrouz SG, Diringer MN: Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care. 2007;11(4):220. Pubmed

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

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

Name UniProt ID Details
Voltage-dependent L-type calcium channel subunit beta-1 Q02641 Details

References:

  1. Weant KA, Ramsey CN 3rd, Cook AM: Role of intraarterial therapy for cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage. Pharmacotherapy. 2010 Apr;30(4):405-17. Pubmed
  2. Dong CJ, Guo Y, Agey P, Wheeler L, Hare WA: Nimodipine Enhancement of {alpha}2 Adrenergic Modulation of NMDA Receptor via a Mechanism Independent of Ca2+ Channel Blocking. Invest Ophthalmol Vis Sci. 2010 Aug;51(8):4174-80. Epub 2010 Mar 24. Pubmed
  3. Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc. 2009 Sep;46(3):239-44. Epub 2009 Sep 30. Pubmed
  4. Kumar R, Mehra R, Ray SB: L-type calcium channel blockers, morphine and pain: Newer insights. Indian J Anaesth. 2010 Mar;54(2):127-31. Pubmed
  5. Keyrouz SG, Diringer MN: Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care. 2007;11(4):220. Pubmed

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

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

Name UniProt ID Details
Voltage-dependent L-type calcium channel subunit beta-2 Q08289 Details

References:

  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed
  2. Striessnig, J. (2004). Ca 2+ channel blockers. In S. Offermanns, & W. Rosenthal (Eds.). Encyclopedic reference of molecular pharmacology (pp. 201-207). Berlin, Germany: Springer.
  3. Weant KA, Ramsey CN 3rd, Cook AM: Role of intraarterial therapy for cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage. Pharmacotherapy. 2010 Apr;30(4):405-17. Pubmed
  4. Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc. 2009 Sep;46(3):239-44. Epub 2009 Sep 30. Pubmed
  5. Kumar R, Mehra R, Ray SB: L-type calcium channel blockers, morphine and pain: Newer insights. Indian J Anaesth. 2010 Mar;54(2):127-31. Pubmed
  6. Keyrouz SG, Diringer MN: Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care. 2007;11(4):220. Pubmed

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

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

Name UniProt ID Details
Voltage-dependent L-type calcium channel subunit beta-3 P54284 Details

References:

  1. Weant KA, Ramsey CN 3rd, Cook AM: Role of intraarterial therapy for cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage. Pharmacotherapy. 2010 Apr;30(4):405-17. Pubmed
  2. Dong CJ, Guo Y, Agey P, Wheeler L, Hare WA: Nimodipine Enhancement of {alpha}2 Adrenergic Modulation of NMDA Receptor via a Mechanism Independent of Ca2+ Channel Blocking. Invest Ophthalmol Vis Sci. 2010 Aug;51(8):4174-80. Epub 2010 Mar 24. Pubmed
  3. Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc. 2009 Sep;46(3):239-44. Epub 2009 Sep 30. Pubmed
  4. Kumar R, Mehra R, Ray SB: L-type calcium channel blockers, morphine and pain: Newer insights. Indian J Anaesth. 2010 Mar;54(2):127-31. Pubmed
  5. Keyrouz SG, Diringer MN: Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care. 2007;11(4):220. Pubmed

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

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

Name UniProt ID Details
Voltage-dependent L-type calcium channel subunit beta-4 O00305 Details

References:

  1. Weant KA, Ramsey CN 3rd, Cook AM: Role of intraarterial therapy for cerebral vasospasm secondary to aneurysmal subarachnoid hemorrhage. Pharmacotherapy. 2010 Apr;30(4):405-17. Pubmed
  2. Dong CJ, Guo Y, Agey P, Wheeler L, Hare WA: Nimodipine Enhancement of {alpha}2 Adrenergic Modulation of NMDA Receptor via a Mechanism Independent of Ca2+ Channel Blocking. Invest Ophthalmol Vis Sci. 2010 Aug;51(8):4174-80. Epub 2010 Mar 24. Pubmed
  3. Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc. 2009 Sep;46(3):239-44. Epub 2009 Sep 30. Pubmed
  4. Kumar R, Mehra R, Ray SB: L-type calcium channel blockers, morphine and pain: Newer insights. Indian J Anaesth. 2010 Mar;54(2):127-31. Pubmed
  5. Keyrouz SG, Diringer MN: Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care. 2007;11(4):220. Pubmed

9. Mineralocorticoid receptor

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: antagonist

Components

Name UniProt ID Details
Mineralocorticoid receptor P08235 Details

References:

  1. Dietz JD, Du S, Bolten CW, Payne MA, Xia C, Blinn JR, Funder JW, Hu X: A number of marketed dihydropyridine calcium channel blockers have mineralocorticoid receptor antagonist activity. Hypertension. 2008 Mar;51(3):742-8. Epub 2008 Feb 4. Pubmed

10. Aryl hydrocarbon receptor

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: agonist

Components

Name UniProt ID Details
Aryl hydrocarbon receptor P35869 Details

References:

  1. Hu W, Sorrentino C, Denison MS, Kolaja K, Fielden MR: Induction of cyp1a1 is a nonspecific biomarker of aryl hydrocarbon receptor activation: results of large scale screening of pharmaceuticals and toxicants in vivo and in vitro. Mol Pharmacol. 2007 Jun;71(6):1475-86. Epub 2007 Feb 27. Pubmed

Enzymes

1. Cytochrome P450 3A4

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Cytochrome P450 3A4 P08684 Details

References:

  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

2. Cytochrome P450 3A5

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Cytochrome P450 3A5 P20815 Details

References:

  1. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

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Drug created on June 13, 2005 07:24 / Updated on September 16, 2013 17:10