Key result
mMyh6E932del mutation boosts myofiber maximal peak force by ~44% vs controls.
Population
In vitro synthesized proximal S2 region of hMyh7 and variants, and in vivo CRISPR-Cas9-mediated knock-in…
Comparison
Amg 27119 for in vitro assays; mMyh6E932del… vs Wild-type/control mice for in vivo experiments
Design
Preclinical
Follow-up
6 to 9 months (for in vivo mouse model)
Authors
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The E932del mutation disrupts the myosin S2-cMyBP-C interaction, leading to diastolic dysfunction and hypercontractility, which may be therapeutically targeted by myopeptides like Amg 27119.
Absolute Event Rate: 29.29% vs 20.311%
p-value: p=0.0039
The E932del mutation disrupts the myosin S2-cMyBP-C interaction, leading to diastolic dysfunction and hypercontractility, which may be therapeutically targeted by myopeptides like Amg 27119.
Rzewnicki et al. (2025) studied Hypertrophic cardiomyopathy. mMyh6E932del mutation vs. Controls was evaluated on Maximal peak force production in skinned myofibers (nM/mm^2) (p=0.0039). The mMyh6E932del mutation significantly increased maximal peak force production in skinned myofibers compared to controls (29.29 vs 20.311 nM/mm^2, p=0.0039).
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