|Systematic (IUPAC) name|
|O3-(2-methoxyethyl) O5-[(E)-3-phenylprop-2-enyl] 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine- 3,5-dicarboxylate|
|Mol. mass||492.52 g/mol|
Cilnidipine (INN) is a calcium channel blocker. Cilnidipine is the novel calcium antagonist accompanied with L-type and N-type calcium channel blocking function. It was jointly developed by Fuji Viscera Pharmaceutical Company, Japan and Ajinomoto, Japan and approved to come into market for the first time and used for high blood pressure treatment in 1995. Compared with other calcium antagonists, cilnidipine can act on the N-type calcium-channel that existing sympathetic nerve end besides acting on L-type calcium-channel that similar to most of the calcium antagonists.
Cilnidipine is yet to be approved by US FDA with Extensive studies and patient data still needing to be published on this molecule.
CILNIDIPINE due to its blocking action at N-type calcium channel dilates both arteriole & venules as a result the pressure in the capillary bed is reduced. It is used for hypertension management.
Cilnidipine has enhanced lipophilicity leading to prolonged antihypertensive effect correlated with occupancy of the binding site. In 24-hour clinical assessment, once-daily administration of cilnidipine (5–20 mg) produced BP reduction for 24-hour period. The inhibitory effect on the N-type Ca2+channel may bestow an additional clinical advantage for the treatment of hypertension, such as suppression of reflex tachycardia.
As catecholamines induce platelet activation via alpha 2-receptors on platelet membrane, decrease in norepinephrine level by cilnidipine causes attenuation of platelet activation.
- http://www.mcyy.com.cn/e-product2.asp[dead link]
- Löhn M, Muzzulini U, Essin K, et al. (May 2002). "Cilnidipine is a novel slow-acting blocker of vascular L-type calcium channels that does not target protein kinase C". J. Hypertens. 20 (5): 885–93. doi:10.1097/00004872-200205000-00023. PMID 12011649.
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