Vericiguat is a soluble guanylate cyclase (sGC) stimulant that improves ejection fraction in heart failure patients by enhancing the NO sgC cGMP signaling pathway. Its mechanism of action involves multiple effects such as vasodilation, anti myocardial fibrosis, and alleviation of ventricular remodeling, especially suitable for heart failure patients with reduced ejection fraction (HFrEF).

1. Activate the NO sGC cGMP pathway

(1) Viliximab directly stimulates sGC enzyme activity and can increase the production of cyclic guanosine monophosphate (cGMP) without relying on nitric oxide (NO).

(2) CGMP acts as a second messenger and exerts cardiovascular protection by activating protein kinase G (PKG).

2. Improve vasodilation function

(1) By increasing cGMP levels, Viliximab promotes vascular smooth muscle relaxation and reduces peripheral vascular resistance.

(2) This reduces cardiac afterload, increases stroke volume, and thus improves left ventricular ejection fraction (LVEF).

3. Inhibit myocardial fibrosis

(1) The cGMP/PKG pathway can block the signal of transforming growth factor - β (TGF - β), reduce collagen deposition and myocardial fibrosis.

(2) This effect delays the process of ventricular remodeling and maintains ventricular contraction coordination.

4. Reduce ventricular remodeling

(1) Long term medication improves ventricular geometry by inhibiting myocardial cell apoptosis and pathological hypertrophy.

(2) Clinical studies have shown that it can significantly reduce NT proBNP levels, reflecting a reduction in ventricular wall stress.

5. Collaborate with existing treatments

(1) When used in combination with beta blockers, ARNI, etc., Viliximab exhibits complementary and synergistic effects through different mechanisms.

(2) Its unique sGC stimulating effect fills the pathway gap in current HFrEF treatment.