Treating the deficient
NO-sGC-cGMP pathway
Treating the deficient
NO-sGC-cGMP pathway
VERQUVO is a first-in-class sGC stimulator* that targets a pathway currently unaddressed in chronic HFrEF – the deficient NO-sGC-cGMP pathway involved in HF progression.
*approved in heart failure
VERQUVO directly stimulates soluble guanylate cyclase (sGC), both independently and synergistically with nitric oxide (NO), to improve myocardial and vascular functions.
In fact, VERQUVO is the only treatment which specifically restores this deficient pathway involved in HF progression.
Current HF treatments mainly block the harmful effects of the body’s natural compensatory mechanisms (e.g. RAAS and SNS), and that’s how VERQUVO works differently.
VERQUVO targets the unaddressed NO-sGC-cGMP pathway
A new approach to managing HF patients following a worsening HF event.
VERQUVO targets the NO-sGC-cGMP pathway, which plays a critical role in the progression of HF and is unaddressed by existing therapies.
sGC is a critical signaling enzyme that produces cGMP in cardiomyocytes and vascular smooth muscle cells and is important for the healthy functioning of these cells. In healthy individuals, NO stimulates sGC, thereby facilitating cGMP production.
In patients with HF, however, NO levels are reduced due to oxidative stress, which impairs sGC activity and, in turn, leads to cGMP deficiency. This leads to a deficiency in the NO-sGC-cGMP pathway, which contributes to disease progression and worsening HF.
By directly stimulating sGC independently and synergistically with NO, VERQUVO works to improve myocardial and vascular function and slows the progression of HF.
