Efonidipine (hydrochloride monoethanolate)

Efonidipine (NZ-105) hydrochloride monoethanolate is an orally active dual L-type and T-type calcium channel blocker (CCB) with IC₅₀ values of 1.8 and 350 nM, respectively. Efonidipine hydrochloride monoethanolate inhibits SARS-CoV-2 main protease. Efonidipine hydrochloride monoethanolate modulates adrenal steroidogenesis by increasing the expression of steroidogenic acute regulatory protein (StAR), dbcAMP-or angiotensin II-induced StAR mRNA expression and DHEA-S production, while suppressing the biosynthesis of aldosterone and cortisol. Efonidipine hydrochloride monoethanolate reduces plasma aldosterone levels in vivo. Efonidipine hydrochloride monoethanolate improves cardiac function in heart failure models by inhibiting T-type calcium channels (via both tonic and use-dependent blockade), independently of blood pressure reduction. Efonidipine hydrochloride monoethanolate can be used for research in hypertension, heart failure, and disorders involving dysregulated steroid hormone synthesis^{[1][2][3][4][5]}. In Vitro:Efonidipine (10 μM, 24 h) hydrochloride monoethanolate induces an increase in StAR mRNA that is independent of extracellular Ca²⁺ in NCI-H295R human adrenocortical cells^[2].
Efonidipine (1 μM, 24 h) hydrochloride monoethanolate significantly increases the production of DHEA-S in NCI-H295R human adrenocortical cells^[2].
In Vivo:Efonidipine (0.1% in diet, p.o., 4 weeks) hydrochloride monoethanolate inhibits T type calcium channels and improves cardiac function during the progression of heart failure in UM-X7.1 hamsters and gold hamsters^[1].