Cilnidipine ( CAS: 132203-70-4 )

Cilnidipine (INN) is a calcium channel blocker. Effects of Cilnidipine compels to rethink on hypertension management. 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,Japanand Ajinomoto,Japanand 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. Due to its N-type calcium-channel blocking properties, it has more advantages compared to conventional calcium-channel blockers. It has lower incidence of Pedal edema, one of the major adverse effects of other calcium channel blockers. Cilnidipine has similar blood pressure lowering efficacy as compared to amlodipine.

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. The accumulated fluid in the tissues flows back to veins & thus Cilnidipine minimizes the incidence of pedal edema.

Clinical benefits

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.