This product is an unconjugated, non-therapeutic recombinant analog of imciromab, a monoclonal antibody directed against human cardiac myosin. It is supplied for research use only and is not the clinical imaging agent (historically formulated as imciromab pentetate). Built around the antigen-binding specificity for cardiac myosin heavy chain, this Fab-format research-grade reagent is useful as a defined anti-cardiac-myosin binder for in-vitro and preclinical work: as a positive or isotype-matched control in binding and specificity assays, as a capture or detection reagent for exposed intracellular myosin in damaged cardiomyocytes, for immunostaining and Western workflows on cardiac tissue lysates, and for antibody-engineering and format-comparison studies. Because it is a Fab fragment (G2a, kappa), it is monovalent and lacks an Fc region, making it suited to studies where avidity effects, Fc-mediated functions, or steric bulk must be minimized. Offered in bulk milligram-to-gram quantities at research-grade endotoxin levels (typically under 1 EU/mg, with ultra-low-endotoxin options under 0.5 EU/mg), it supports reproducible, scalable experimentation and assay development.
Cardiac myosin is the principal motor protein of the heart's contractile apparatus. Each myosin II molecule comprises two heavy chains (in cardiac muscle, the beta/MYH7 and alpha/MYH6 isoforms) and associated essential and regulatory light chains. The globular heavy-chain head contains the actin-binding site and the ATPase activity that powers cross-bridge cycling, converting chemical energy into the sliding of thick and thin filaments that produces sarcomere shortening and myocardial contraction. The coiled-coil tail mediates thick-filament assembly. Because myosin is an abundant intracellular structural protein, it is normally sequestered from the circulation and immune system; loss of sarcolemmal integrity during myocardial necrosis exposes cardiac myosin, which is the basis for its use as a marker of irreversible cardiomyocyte injury. Mutations in cardiac myosin genes are linked to hypertrophic and dilated cardiomyopathies, underscoring its centrality to cardiac structure and function.