Kun Ping Lu, MD, PhD

Dr. Lu joined Harvard Medical School as an Assistant Professor and Beth Israel Deaconess Medical Center as an Associate Physician in 1996. He rose through the ranks as a Professor at Harvard in 2008, the Founding Division Chief and Founding Program Director, Translational Therapeutics at Beth Israel Deaconess Medical Center in 2014, and an Associate Member at the Broad Institute of MIT and Harvard in 2017, prior to joining Western in 2022. He, along with his long-term collaborator Dr. Xiao Zhen Zhou and their team, has been largely responsible for the discoveries of Pin1-catalyzed conformational regulation as a unique signaling mechanism in health and disease and as a new paradigm for improving therapeutic efficacy and specificity for cancer, dementia, and autoimmune disease. Dr. Lu has earned many awards, including a member of the American Society for Clinical Investigation and the Association of American Physicians, and an AAAS Fellow of American Association for the Advancement of Science. Dr. Lu received his MD from Fujian Medical University, PhD from Duke University, and Postdoctoral training from Salk Institute.

Dr. Zhou received her MD from Suzhou University Medical College and postdoctoral training from Scripps Research Institute and Harvard Medical School, followed by being appointed as a faculty member at Harvard in 2001. Dr. Zhou is well recognized for her discoveries of Pin1 substrates and function, and her innovation of novel technologies enabling to study Pin1-catalyzed cis-trans conformational changes in health and disease, often in collaboration with Dr. Kun Ping Lu. Notably, she has personally developed the first mechanism-based high throughput Pin1 drug screens, leading to the unexpected discoveries that the approved drugs, all trans retinoic acid (ATRA) and ATO (arsenic trioxide), are synergistic Pin1 inhibitors, as well as the first conformation-specific antibody technology, leading to the discoveries of cis P-tau as an early driver and biomarker of neurodegeneration in Alzheimer’s disease and after brain injury or stroke, which can effectively be neutralized by stereo-specific antibody.