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.

H294264_P717027

    Referencesexpand_less
    • 1
      Mann DL et al. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 10th ed. Elsevier/Saunders; 2015.
    • 2
      Heidenreich et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;e895–e1032.
    • 3
      McDonagh TA, Metra M, Adamo M et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: Developed by the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Eur Heart J. 2021;42(36):3599–3726.
    • 4
      Triposkiadis F, Karayannis G, Giamouzis G et al. The sympathetic nervous system in heart failure physiology, pathophysiology, and clinical implications. J Am Coll Cardiol. 2009;54(19):1747–1762.
    • 5
      Matsumura K, Sugiura T. Effect of sodium glucose cotransporter 2 inhibitors on cardiac function and cardiovascular outcome: a systematic review. Cardiovasc Ultrasound. 2019;17(1):26.
    • 6
      Nightingale B. A review of the proposed mechanistic actions of sodium glucose cotransporter-2 inhibitors in the treatment of heart failure. Cardiol Res. 2021;12:60–66.
    • 7
      Armstrong PW, Pieske B, Anstrom KJ et al. VICTORIA Study Group. Vericiguat in patients with heart failure and reduced ejection fraction. N Engl J Med. 2020;382(20):1883–1893.
    • 8
      Armstrong PW, Pieske B, Anstrom KJ et al. VICTORIA Study Group. Vericiguat in patients with Heart Failure and reduced ejection fraction.
    • 9
      Hulot JS, Trochu JN, Donal E et al. Vericiguat for the treatment of heart failure: mechanism of action and pharmacological properties compared with other emerging therapeutic options. Expert Opin Pharmacother. 2021;22(14):1847-–1855.
    • 10
      Armstrong PW, Roessig L, Patel MJ et al. A multicenter, randomized, double-blind, placebo-controlled trial of the efficacy and safety of the oral soluble guanylate cyclase stimulator: the VICTORIA trial. JACC Heart Fail. 2018;6(2):96–104.
    • 11
      Gheorghiade M, et al. Soluble guanylate cyclase: a potential therapeutic target for heart failure. Heart Fail Rev. 2013; 18(2):123-134.
    • 12
      Sandner P. From molecules to patients: exploring the therapeutic role of soluble guanylate cyclase stimulators. Biol Chem. 2018; 399(7):679-690.
    • 13
      Archer SL, Huang JM, Hampl V, et al. Nitric oxide and cGMP cause vasorelaxation by activation of a charybdotoxin-sensitive K channel by cGMP-dependent protein kinase. Proc Natl Acad Sci USA. 1994; 9(16):7583-7587.
    • 14
      Ponikowski P, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2016; 37(27):2129-2200.
    • 15
      Yancy CW, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Task. Circ. 2017; 136(6): 137-161.
    • 16
      Kong Q, Blanton RM. Protein kinase G I and heart failure: Shifting focus from vascular unloading to direct myocardial anti remodeling effects. Circ Heart Fail. 2013; 6(6):1268-1283.