Speakers
Derek Lowe
Derek Lowe received his PhD from Duke in 1988, and then did a Humboldt fellowship in Germany. Since 1989 he has worked at several different biopharma companies in a variety of therapeutic areas (CNS, metabolics, anti-infectives, oncology and more). In the last 10-15 years his research work has shifted more to chemical biology approaches to better assess target selection and other fundamental problems of drug discovery. He is the author, since 2002, of the blog "In the Pipeline", covering a variety of chemistry and biology subjects in what is now likely the longest-running site of its kind.
Michelle Arkin
Michelle Arkin is a chemical biologist, Professor and Chair of Pharmaceutical Chemistry, and Executive Director of the Small Molecule Discovery Center (SMDC) at UCSF. She is a member of the Assay Guidance Manual Editorial Board and several chemical biology journals. Michelle’s research focuses on developing methods and molecules that target currently ‘undruggable proteins,’ including protein-protein interactions and dynamic or intrinsically disordered proteins. She is a cofounder and Director of Ambagon Therapeutics, cofounder of Elgia Therapeutics, and advisor to several biotechs. Prior to UCSF, Michelle was Associate Director of Cell Biology at Sunesis Pharmaceuticals, where she helped discover inhibitors of protein-protein interactions for IL-2/IL-2R and LFA1/ICAM (lifitegrast, marketed by Novartis). She earned her PhD in Chemistry at Caltech with Jackie Barton and held a Damon Runyon postdoctoral fellowship at Genentech in the lab of Jim Wells. Michelle was named a 2024 Cope Scholar by the American Chemical Society.
2023 Speakers
Christopher P. Austin
Christopher Austin is a CEO-Partner at Flagship Pioneering in Cambridge, MA, and CEO of one of Flagship’s franchise companies, Vesalius Therapeutics, which is commercializing a novel platform to systematically develop treatments for common diseases. Before joining Flagship in 2021, Dr. Austin served for almost a decade as the founding director of the National Center for Advancing Translational Sciences at the NIH, where he formulated the strategic vision and scientific directions of the new center, and led its efforts in developing, demonstrating, and disseminating scientific and operational advances across the spectrum of translational science, from target validation to preclinical therapeutic development to clinical trials to community health implementation. Before NCATS, Austin founded and directed scientific and technology initiatives at the National Human Genome Research Institute at NIH to derive biological insights and therapeutic potential from the human genome. Austin came to NIH from Merck, where his work focused on genome-based discovery of novel targets and drugs, with a particular focus on common neuropsychiatric diseases. He received his A.B. in biology from Princeton and M.D. from Harvard Medical School, did clinical training in internal medicine and neurology at Massachusetts General Hospital, and completed a research fellowship in genetics at Harvard.
Jay Bradner
James (Jay) E. Bradner, M.D. is an American Physician-Scientist.
Recently, he served as President of the Novartis Institutes for BioMedical Research (NIBR), from January, 2015, through November, 2022. He led global internal and external Research and Early Development covering eight disease areas (hematology, oncology, immunology, neuroscience, cardiovascular disease, ophthalmology, neglected tropical diseases and musculoskeletal diseases), and five therapeutic modalities (chemistry & chemical biology, biotherapeutics, gene therapy, stem-progenitor therapy and radioligand therapy). In his seven years of leadership, NIBR innovated more than 80 development candidates, filed 75 INDs and reported out 90 positive proof-of-concept studies in human clinical investigation. Scientifically, he led a research initiative focused on molecular glues for intractable protein targets.
Prior to leading NIBR, Dr. Bradner served on the research faculty of Harvard Medical School and as an attending physician in stem cell transplantation within the Department of Medical Oncology at the Dana-Farber Cancer Institute. The research focus of the Bradner laboratory has been the study of BET bromodomain proteins and their function in gene control, innovating chemical probes and investigational drugs to study and treat cancer. Further, the Bradner laboratory pioneered a first all-chemical strategy for targeted protein degradation, which has served as a discovery platform for many academic investigators and biopharmaceutical companies. Dr. Bradner is a co-founder of five biotechnology companies and has co-authored more than 250 scientific publications and over 50 United States patent applications.
Dr. Bradner is a graduate of Harvard College and the University of Chicago Medical School. He completed residency in Medicine at Brigham & Women's Hospital, fellowship in Medical Oncology and Hematology at the Dana-Farber Cancer Institute and postdoctoral training in chemistry and chemical biology at Harvard University (Prof. Stuart Schreiber).
David Hackos
David Hackos is currently a Senior Principal Scientist at Genentech, where he heads pain research. He obtained his B.A. in Physics from Johns Hopkins University, his PhD from the University of California, San Francisco, and did his postdoctoral work at the National Institutes of Health where he worked with Kenton Swartz on the mechanism of gating in voltage-gated ion channels. He entered the world of pain research in 2001 when he joined Renovis, a small biotech company in San Francisco. At Renovis, his group developed a series of TRPV1 antagonists, one of which entered early clinical trials as a potential neuropathic pain drug. In 2006, he left Renovis to join Roche in Palo Alto, where he worked on pain and inflammation targets such as P2X3, TRPA1, and Kv1.3. At Genentech, his research focuses on the development of novel pain drugs, in particular by selectively targeting the Nav1.7 sodium channel. Two such selective Nav1.7 inhibitors developed by his group have been tested in early clinical trials. In addition to pain research, his lab studies the genetics and biology of peripheral neuropathies such as diabetic neuropathy and chemotherapy-induced peripheral neuropathy.
William G. Kaelin, Jr., M.D.
William Kaelin is the Sidney Farber Professor of Medicine at Harvard Medical School and Dana-Farber Cancer Institute, Senior Physician in Medicine at Brigham and Women's Hospital and Howard Hughes Medical Institute Investigator. He obtained his undergraduate and M.D. degrees from Duke University and completed his training in Internal Medicine at the Johns Hopkins Hospital, where he served as chief medical resident. He was a clinical fellow in Medical Oncology at the Dana-Farber Cancer Institute and later a postdoctoral fellow in David Livingston’s laboratory, during which time he was a McDonnell Scholar.
A Nobel Laureate, Dr. Kaelin received the 2019 Nobel Prize in Physiology or Medicine. He is a member of the National Academy of Sciences, the American Academy of Arts and Sciences, the National Academy of Medicine, the American Society of Clinical Investigation, and the American College of Physicians. He previously served on the National Cancer Institute Board of Scientific Advisors, the AACR Board of Trustees, and the Institute of Medicine National Cancer Policy Board. He is a recipient of the Paul Marks Prize for cancer research from the Memorial Sloan-Kettering Cancer Center; the Richard and Hinda Rosenthal Prize from the AACR; the Doris Duke Distinguished Clinical Scientist award; the 2010 Canada International Gairdner Award; ASCI’s Stanley J. Korsmeyer Award; the Scientific Grand Prix of the Foundation Lefoulon-Delalande; the Wiley Prize in Biomedical Sciences; the Steven C. Beering Award; the AACR Princess Takamatsu Award; the ASCO Science of Oncology Award; the Helis Award; the Albert Lasker Basic Medical Research Prize; the Massry Prize; the Harriet P. Dustan Award for Science as Related to Medicine from the American College of Physicians.
Dr. Kaelin’s research seeks to understand how, mechanistically, mutations affecting tumor-suppressor genes cause cancer. His laboratory is currently focused on studies of the VHL, RB-1, and p53 tumor suppressor genes. His long-term goal is to lay the foundation for new anticancer therapies based on the biochemical functions of such proteins. His work on the VHL protein helped to motivate the eventual successful clinical testing of VEGF inhibitors for the treatment of kidney cancer. Moreover, this line of investigation led to new insights into how cells sense and respond to changes in oxygen, and thus has implications for diseases beyond cancer, such as anemia, myocardial infarction, and stroke. His group also showed that leukemic transformation by mutant IDH was reversible, setting the stage for the development and approval of mutant IDH inhibitors, and discovered how thalidomide-like drugs kill myeloma cells by degrading two otherwise undruggable transcription factors.