Felodipine (CGH-869) is a longlasting 1, 4-dihydropyridine calcium channel repressor.

Ca2+ channel, L-type:0.15 nM

Felodipine acts on the aortic wall by inhibiting NF-κB activation and effectively reduces serum insulin levels within macrophages, as well as intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), thereby significantly lowering systolic blood pressure and modulating vascular inflammatory responses. Oral administration of Felodipine in rats with 5/6 nephrectomy markedly decreases the mean arterial blood pressure.

In primary human VSMCs and lung fibroblasts, Felodipine significantly induced transcription and secretion of IL-6 (ED50: 5.8 nM) and IL-8 (ED50: 5.3 nM), with no effect observed from the administration of either propranolol or fenbufen on the expression of these IL genes. In guinea pig ileum longitudinal smooth muscle, Felodipine inhibited carbachol-regulated Ca2+-dependent contraction (IC50: 1.45 nM). At a concentration of 0.1 μM in rat endothelial cells, Felodipine increased NOx production and the activity of Ca2+-dependent NOS and eNOS proteins. At 10 μM, it suppressed human SMC proliferation by inhibiting PDGF-BB-induced Elk-1 activation and reducing the nuclear translocation of p42/44 mitogen-activated protein kinase. Felodipine moderately inhibited Cav3.2 T-type Ca2+ channels (IC50: 6.8 μM). In porcine coronary artery segments contracted with KCl, Felodipine significantly induced relaxation (IC50: 0.15 nM), suggesting it is 50 times more potent than nifedipine (IC50: ~8 nM) and 430 times more potent than verapamil (IC50: ~65 nM) due to its Ca2+ channel blocking action.