A treatment that may attenuate the mechanistic hallmarks of oHCM1:
Excess cross-bridge formation and dysregulation of the super-relaxed state of myosin
Excess cross-bridge formation and dysregulation of the super-relaxed state of myosin are mechanistic hallmarks of HCM, which can result in hypercontractility, impaired relaxation, excess energy consumption, and myocardial wall stress.1
Heart muscle structure
Myosin-actin cross-bridge
Actin thin filament
Myosin thick filament
HCM sarcomere
Excess cross-bridge formation
Hypercontractility
Impaired relaxation
Excess energy consumption
Adapted from the Product Monograph.1 Illustrations adapted from Maron, Lancet 2013.2
CAMZYOS modulates the number of myosin heads that can enter power-generating states, which reduces the number of myosin-actin cross-bridges that form.1
Myosin inhibition with CAMZYOS1*:
- may attenuate myocardial hypercontractility
- can:
- improve myocardial relaxation
- reduce dynamic LVOT obstruction
- improve cardiac filling pressures and cardiac structure
- improve cardiac biomarkers including NT-proBNP
- improve exercise capacity (as measured by pVO2)
HCM=hypertrophic cardiomyopathy; LVOT=left ventricular outflow tract; oHCM=obstructive hypertrophic cardiomyopathy; NT-proBNP=Nterminal-proBtype natriuretic peptide; pVO2=peak oxygen consumption.
* Clinical significance is unknown.
References: 1. CAMZYOS (mavacamten capsules) Product Monograph. Bristol Myers Squibb Canada, February 14, 2024. 2. Maron BJ, Maron MS. Hypertrophic cardiomyopathy. Lancet 2013;381:242-55.