Cilnidipine

Cilnidipine

Clinical data
ATC code	C08CA14 (WHO)
Identifiers
IUPAC name O3-(2-methoxyethyl) O5-[(E)-3-phenylprop-2-enyl] 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine- 3,5-dicarboxylate
PubChem CID	5282138
E number	{{#property:P628}}
ECHA InfoCard	{{#property:P2566}}
Chemical and physical data
Formula	C27H28N2O7
Molar mass	492.52 g/mol

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Cilnidipine (INN) is a calcium channel blocker. Clinidipine 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, clinidipine 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.

Medical Uses

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 reduces. It is used for hypertension management.

Lack of Supporting Data

• Cilnidipine is not approved by US FDA.
• Cilnidipine is backed by only 51 studies, compared to 1000s on other CCBs
• Cilnidipine has only 197 studies ever done on it.
• Patient count is very low for Cilnidipine.
• Most of Cilnidipine data is based on Animal Testing.

Clinical Benifits

Cilnidipine controls hypertension for 24 hours with once daily dose. 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. This indicates that once-daily cilnidipine exerts a sufficient and prolonged reduction of BP. Cilnidipine has 50 times higher selectivity for N-type of calcium channels than amlodipine. 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.