Key result
Mavacamten fails to significantly improve symptoms or peak VO2 over placebo in non-obstructive HCM.
Why the study?
Does mavacamten improve functional capacity and patient-reported health outcomes in patients with symptomatic nHCM?
Does mavacamten improve functional capacity and patient-reported health outcomes in patients with symptomatic nHCM?
Mean Difference: 2.7
p-value: p=0.056
Despite missing dual functional primary endpoints, mavacamten successfully engaged its biological target by profoundly reducing NT-proBNP in nHCM, suggesting that future trials should utilize mechanism-aligned endpoints and strict genetic phenotyping.
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Prajapathi et al. (2026) conducted an editorial in Symptomatic non-obstructive hypertrophic cardiomyopathy (nHCM). Mavacamten vs. Placebo was evaluated on Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS) at 48 weeks (MD 2.7 points, p=0.056). Mavacamten did not achieve statistical significance for improving the Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (MD 2.7 points, p=0.056) or peak oxygen consumption (MD 0.47 ml/kg/min, p=0.066) compared to placebo in patients with symptomatic non-obstructive hypertrophic cardiomyopathy.
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