Nicardipine

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Nicardipine
File:Nicardipine.svg
Systematic (IUPAC) name
2-[benzyl(methyl)amino]ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate
Pharmacokinetic data
Protein binding >95%
Biological half-life 8.6 hours
Identifiers
CAS Number 55985-32-5
ATC code C08CA04 (WHO)
PubChem CID 4474
DrugBank APRD00088
Chemical data
Formula C26H29N3O6
Molar mass 479.525 g/mol[[Script error: No such module "String".]]
Physical data
Melting point 6 °C (43 °F)
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Nicardipine hydrochloride (Cardene) is a medication used to treat high blood pressure and angina. It belongs to the class of calcium channel blockers.

Nicardipine is a dihydropyridine calcium-channel blocking agent used for the treatment of vascular disorders such as chronic stable angina, hypertension, and Raynaud's phenomenon. It is available in oral and intravenous formulations. Its mechanism of action and clinical effects closely resemble those of nifedipine and the other dihydropyridines (amlodipine, felodipine), except that nicardipine is more selective for cerebral and coronary blood vessels. Furthermore, nicardipine does not intrinsically decrease myocardial contractility and may be useful in the management of congestive heart failure. Nicardipine also has a longer half-life than nifedipine. Nicardipine was approved by the FDA in December 1988. The patent for both Cardene and Cardene SR expired in October 1995.

It has been used in percutaneous coronary intervention.[1]

Nicardipine must be used with caution in patients with renal failure because of possible kidney shutdown.

References

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Nicardipine inhibits the transmembrane influx of calcium ions into cardiac muscle and smooth muscle without changing serum calcium concentrations. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. The effects of nicardipine are more selective to vascular smooth muscle than cardiac muscle. In animal models, nicardipine produced relaxation of coronary vascular smooth muscle at drug levels which cause little or no negative inotropic effect.


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