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Heart failure

Cardiac myosin activator shows promise in phase II trial

Nature Reviews Cardiology volume 8, page 612 (2011)Cite this article

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A novel, small-molecule, sarcomere-directed activator of cardiac myosin, omecamtiv mecarbil, is well tolerated in healthy individuals, and significantly improves cardiac function in patients with stable heart failure (HF), according to two reports published in The Lancet. Professor John Cleland, from the University of Hull, UK, is “excited about the possibility of a new molecule that could improve cardiac function not only by a fundamentally different molecular mechanism, but also a very different physiological principle (prolongation of contraction rather than increased velocity of contraction).”

Dr Fady Malik “initiated this research ... based on the observation that motor proteins, of which myosin is one, could be activated by small molecules.” During cardiac contraction, myosin first weakly and then strongly binds actin to initiate cross-bridge cycling and force generation. By contrast with existing inotropes, omecamtiv mecarbil improves myocardial contraction by enhancing the transition rate between the bound states, and by prolonging the duration of systolic ejection without changing the rate of contraction.

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ORIGINAL RESEARCH PAPER

  1. Teerlink, J. R. et al. Dose-dependent augmentation of cardiac systolic function with the selective cardiac myosin activator, omecamtiv mecarbil: a first-in-man study. Lancet 378, 667–675 (2011)

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  2. Cleland, J. G. et al. The effects of the cardiac myosin activator, omecamtiv mecarbil, on cardiac function in systolic heart failure: a double-blind, placebo-controlled, crossover, dose-ranging phase 2 trial. Lancet 378, 676–683 (2011)

    Article  CAS  PubMed  Google Scholar 

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  1. Gregory B. Lim
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Lim, G. Cardiac myosin activator shows promise in phase II trial. Nat Rev Cardiol 8, 612 (2011). https://doi.org/10.1038/nrcardio.2011.137

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