2-Deoxy-ATP improves ventricular function via combined effects on myosin recruitment from the super-relaxed state, crossbridge cycling and calcium dynamics in healthy and failing conditions

2-deoxy-ATP (dATP) has been shown to enhance cardiac contractility by acting on myosin to increase the rate of crossbridge binding and cycling. An increased rate of Ca2+ transient decay has also been observed with elevated dATP. However, it is unclear how dATP affects feedback between sarcomere force and Ca2+ dynamics, and to what degree these cellular level effects can explain experimentally observed improvements in ventricular function with elevated dATP. Further, low concentrations of dATP have been shown to significantly improve cardiomyocyte and ventricular function, but the mechanisms behind this are not well understood.