With oral administration at doses of 3 mg/kg and 10 mg/kg once daily for 21 days, Vericiguat preserves heart and kidney function in a model of hypertension-induced end-organ damage in L-NAME-treated renin transgenic rats. Importantly, the Vericiguat-treated group exhibits a significant reduction in overall mortality compared to the control group^[1].

Vericiguat enhances the activity of recombinant soluble guanylate cyclase (sGC) in a concentration-dependent manner, ranging from a 1.7-fold to a 57.6-fold increase. In combination with the nitric oxide donor diethylamine/nitric oxide complex (DEA/NO), Vericiguat and DEA/NO exhibit a synergistic effect on sGC activity across various concentrations. At the highest concentrations tested (100 μM for Vericiguat and 100 nM for DEA/NO), sGC activity is elevated 341.6-fold above the baseline. Vericiguat also concentration-dependently activates an sGC reporter cell line, with an EC50 of 1005±145 nM. It concentration-dependently inhibits phenylephrine-induced contractions in rabbit saphenous artery rings, rabbit aortic rings, and canine femoral vein rings, with IC50 values of 798, 692, and 3072 nM, respectively. Moreover, Vericiguat concentration-dependently inhibits U46619-induced contractions in porcine coronary artery rings, with an IC50 of 956 nM^[1].