James Spudich, Ph.D., is the Douglass M. and Nola Leishman Professor of Cardiovascular Disease in the Department of Biochemistry at the Stanford University School of Medicine. Over the last five decades, the Spudich laboratory studied the structure and function of the myosin family of molecular motors in vitro and in vivo, and they developed multiple new tools, including in vitro motility assays taken to the single molecule level using laser traps. That work led to his laboratory’s current focus at Stanford on the human cardiac sarcomere and the molecular basis of hypertrophic and dilated cardiomyopathy. Dr. Spudich postulated in 2015 that a majority of hypertrophic cardiomyopathy mutations are likely to be shifting beta-cardiac myosin heads from a sequestered off-state to an active on-state for interaction with actin, resulting in the hyper-contractility seen clinically in hypertrophic cardiomyopathy (HMC) patients. This unifying hypothesis is different from earlier prevailing views, and this viewing an old disease in a new light has become the favored view in the field of the molecular basis of hypercontractility caused by HCM mutations. Dr. Spudich has given more than 50 named lectureships and keynote addresses, and has received many honors, including election to the National Academy of Sciences and recipient of the Albert Lasker Basic Medical Research Award. He is credited with co-founding MyoKardia Inc, which was acquired by Bristol Myers Squibb for $13.1 billion in 2020, and Cytokinetics, Inc., a late-stage, specialty cardiovascular biopharmaceutical company. Dr. Spudich received a Ph.D. in Biochemistry from Stanford University, in addition to completing his postdoctoral work in Genetics at Stanford University and in Structural Biology at the MRC Laboratory at Cambridge University. He is a fellow of the American Academy of Arts and Sciences and a member of the National Academy of Sciences.