CV-159 is a distinctive dihydropyridine Ca2+ antagonist exhibiting anti-inflammatory properties and possessing anti-calmodulin (CaM) activity.

CV-159, in concentrations ranging from 0.1 to 10 μM, significantly suppresses the induction of VCAM-1 by TNF-α (10 ng/ml for 24 hours) in SMCs in a concentration-dependent manner. At a concentration of 10 μM, CV-159 blocks the TNF-induced expression of e-selectin after 24 hours but does not affect the levels of vascular cell adhesion molecule-1 or intercellular adhesion molecule-1. Additionally, CV-159 significantly reduces TNF-induced ROS production when administered at 10 μM for 30 minutes [1]. Furthermore, CV-159 at 10 μM inhibits the TNF-induced phosphorylation of JNK, p38, and NF-κB p65 (Ser536) after 20 minutes of treatment [2].

CV-159 has been shown to significantly reduce brain infarct size following permanent middle cerebral artery (MCA) occlusion. Moreover, at doses of 5 and 10 mg/kg (administered orally), it markedly protects against delayed neuronal death in the hippocampal CA1 region in rats after a 15-minute transient forebrain ischemia. Additionally, CV-159 effectively mitigates the increase in water content within the infarcted cortex resulting from MCA occlusion [3].