MYK-224 is our second therapeutic candidate that specifically targets cardiac myosin to reduce the excess myosin-actin cross-bridge formation underlying HCM.  MYK-224 is designed to preserve the unique advantages of mavacamten’s mechanism, including the ability to reduce excess contractility and potentially address impaired relaxation while reducing pharmacokinetic variability. With a shorter half life, MYK-224 may reduce the time required to achieve steady state and thereby provide dosing flexibility. We initiated a Phase 1 clinical study of MYK-224 in healthy volunteers in August 2019 with initial data anticpated in mid-2020.