Fig. 6.

Model of OM’s effect on cardiac myosin. (1) OM increases the rate of entry into strong binding as previously measured by phosphate release rates, but the force generating power stroke is inhibited. (2) Myosin remains strongly bound to actin (red bar), contributing to increased thin-filament activation at intermediate calcium concentrations. (3) OM disrupts the typical pathway of myosin, causing it to pass through an ADP or apo (nucleotide-free) state with its lever arm still in the pre-power stroke position. (4) Myosin detaches from actin without needing to bind ATP. ATP binding must occur before the cycle can start again