Cytokinetics Announces European Medicines Agency Validation of Marketing Authorization Application for Aficamten for the Treatment of Obstructive Hypertrophic Cardiomyopathy
CYTK 12.23.2024

About Gravity Analytica
“With regulatory filings foraficamtenalready under review in both the
The MAA is supported by the results from SEQUOIA-HCM (Safety,Efficacy, andQuantitativeUnderstanding ofObstructionImpact ofAficamteninHCM), the pivotal Phase 3 clinical trial ofaficamtenin patients with symptomatic obstructive HCM, which were published in the
The MAA validation follows the acceptance by the
About SEQUOIA-HCM
SEQUOIA-HCM (Safety,Efficacy, andQuantitativeUnderstanding ofObstructionImpact ofAficamteninHCM) was the pivotal Phase 3 clinical trial ofaficamtenin patients with symptomatic obstructive hypertrophic cardiomyopathy (HCM).
The results from SEQUOIA-HCM showed that treatment withaficamtenfor 24 weeks significantly improved exercise capacity compared to placebo, increasing peak oxygen uptake (pVO2) measured by cardiopulmonary exercise testing (CPET) by 1.8 ml/kg/min compared to baseline in patients treated withaficamtenversus 0.0 ml/kg/min in patients treated with placebo (least square mean (LSM) difference [95% CI] of 1.74 mL/kg/min [1.04 - 2.44]; p=0.000002). Statistically significant improvements were observed in all 10 prespecified secondary endpoints, including Valsalva left ventricular outflow tract (LVOT) gradient,
Additional analyses from SEQUOIA-HCM have demonstrated that treatment withaficamtenis associated with improvements in cardiac structure, function, and biomarkers without negatively impacting systolic function.
AboutAficamten
Aficamtenis an investigational selective, small molecule cardiac myosin inhibitor discovered following an extensive chemical optimization program that was conducted with careful attention to therapeutic index and pharmacokinetic properties and as may translate into next-in-class potential in clinical development.Aficamtenwas designed to reduce the number of active actin-myosin cross bridges during each cardiac cycle and consequently suppress the myocardial hypercontractility that is associated with HCM. In preclinical models,aficamtenreduced myocardial contractility by binding directly to cardiac myosin at a distinct and selective allosteric binding site, thereby preventing myosin from entering a force producing state.
The development program foraficamtenis assessing its potential as a treatment that improves exercise capacity and relieves symptoms in patients with HCM as well as its potential long-term effects on cardiac structure and function.Aficamtenwas evaluated in SEQUOIA-HCM, a positive pivotal Phase 3 clinical trial in patients with symptomatic obstructive hypertrophic cardiomyopathy (HCM).Aficamtenreceived Breakthrough Therapy Designation for the treatment of symptomatic obstructive HCM from the
Aficamtenis also currently being evaluated in MAPLE-HCM, a Phase 3 clinical trial ofaficamtenas monotherapy compared to metoprolol as monotherapy in patients with obstructive HCM; ACACIA-HCM, a Phase 3 clinical trial ofaficamtenin patients with non-obstructive HCM; CEDAR-HCM, a clinical trial ofaficamtenin a pediatric population with obstructive HCM; and FOREST-HCM, an open-label extension clinical study ofaficamtenin patients with HCM.
About Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is a disease in which the heart muscle (myocardium) becomes abnormally thick (hypertrophied). The thickening of cardiac muscle leads to the inside of the left ventricle becoming smaller and stiffer, and thus the ventricle becomes less able to relax and fill with blood. This ultimately limits the heart’s pumping function, resulting in reduced exercise capacity and symptoms including chest pain, dizziness, shortness of breath, or fainting during physical activity. HCM is the most common monogenic inherited cardiovascular disorder, with approximately 280,000 patients diagnosed, however, there are an estimated 400,000-800,000 additional patients who remain undiagnosed in the
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This press release contains forward-looking statements for purposes of the Private Securities Litigation Reform Act of 1995 (the “Act”).
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References:
- Maron, MS, et al. Aficamten for Symptomatic Obstructive Hypertrophic Cardiomyopathy. N Engl J Med. DOI: 10.1056/NEJMoa2401424
- CVrg: Heart Failure 2020-2029, p 44; Maron et al. 2013 DOI: 10.1016/S0140-6736(12)60397-3; Maron et al 2018 10.1056/NEJMra1710575
Symphony Health 2016-2021 Patient Claims Data DoF;- Maron MS, Hellawell JL, Lucove JC,
Farzaneh-Far R , Olivotto I. Occurrence of Clinically Diagnosed Hypertrophic Cardiomyopathy inthe United States . Am J Cardiol. 2016; 15;117(10):1651-1654. - Gersh, B.J., Maron, B.J., Bonow, R.O., Dearani, J.A., Fifer, M.A., Link, M.S., et al. 2011 ACCF/AHA guidelines for the diagnosis and treatment of hypertrophic cardiomyopathy. A report of the
American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines.Journal of the American College of Cardiology and Circulation , 58, e212-260. - Hong Y, Su WW,
Li X. Risk factors of sudden cardiac death in hypertrophic cardiomyopathy. Current Opinion in Cardiology. 2022Jan 1 ;37(1):15-21

Source: Cytokinetics, Incorporated