Cilnidipine

Cilnidipine is a long-acting, second-generation dihydropyridine Ca²⁺-channel blocker on L and N-type Ca²⁺ channel^[1][2][3][4]. Antihypertensive effects^[5]. In Vitro: Cilnidipine inhibits the L-type current with an IC₅₀ of 100 nM in neurons pretreated with omegaCgTx plus omegaAgTx^[1].
The IC₅₀ for Cilnidipine in respect of the N-type current is 200 nM^[1].
Cilnidipine dose- and time-dependently inhibits Ba²⁺ currents in A7r5 cells with the IC₅₀ at 10 nM after 10 min^[2].
Cilnidipine dose-dependently inhibits depolarization- and Ca²⁺-induced contractions of rat aortic rings, with an IC₅₀ of 10 nM at 10 min^[2].
The viability of nPC12 cells show no significant change up to 150?μM Cilnidipine, but it decreases slightly in the cells treated with greater than 200?μM Cilnidipine^[3].
Cilnidipine (100 μM, 2 hours) treatment increases the expression of p85aPI3K p-Akt, p-GSK-3β, and heat shock transcription factor (HSTF-1), and decreases levels of cytosolic cytochrome c, activated caspase 3, and cleaved PARP^[3]. In Vivo: Cilnidipine has potent inhibitory actions on N-type as well as L-type voltage-dependent Ca²⁺-channel in rat dorsal root ganglion neurons^[1].
Administration of Cilnidipine (10 mg/kg) and Nimodipine (10 mg/kg) significantly attenuates the immobilized stress-induced behavioral changes and restored memory deficits along with normalization of the corticosterone levels^[4].
Cilnidipine and Nimodipine produce comparable beneficial effects in restoring immobilization stress subjected mice^[4].
Oral administration of Cilnidipine (3 mg/kg) markedly lowers both systolic and diastolic blood pressure 1 hr after administration in 2K1C renal hypertensive dogs^[5].