SAN MATEO, Calif. & CAMBRIDGE, Mass.--(BUSINESS WIRE)--Kronos Bio, Inc., dedicated to the development of first-in-class therapies that modulate historically undruggable targets, announced today that it has appointed Jorge F. DiMartino, M.D., Ph.D., as Chief Medical Officer and Executive Vice President, Clinical Development. In this newly created position, Dr. DiMartino will lead Kronos Bio’s clinical function and oversee the advancement of its oncology pipeline, which includes two preclinical programs discovered via the company’s Small Molecule Microarray (SMM) screening platform. Dr. DiMartino will be based in Kronos’ San Mateo office.
“As a physician-scientist focused on translational development, Jorge is ideally suited to join Kronos at this stage of our growth, as we are focused on discovering bioactive molecules against oncology targets that have historically been considered undruggable,” said Norbert Bischofberger, Ph.D., President and Chief Executive Officer of Kronos. “Jorge’s deep expertise in epigenetics and protein homeostasis will be uniquely valuable in our effort to develop drugs which interfere with transcription factors, pursue targeted protein degradation, and advance highly-differentiated products into human testing.”
Dr. DiMartino joins Kronos from Celgene Corp., where he served as Vice President, Translational Development, Protein Homeostasis and Epigenetics Thematic Center of Excellence. At Celgene, Dr. DiMartino built a discovery team with industry leading epigenetic profiling capabilities in pursuit of chromatin modifier targets. His translational team has driven BET and LSD1 inhibitor programs through Phase 1, delivering robust data packages to support proof of concept trial designs. Prior to Celgene, he was Group Medical Director, BioOncology/ Exploratory Clinical Development at Genentech Inc., where he was the Development Team Leader for the BCL2 (venetoclax, navitoclax) collaboration with Abbvie, Inc. and managed a team advancing a broad portfolio of early-stage oncology compounds.
“I look forward to leveraging my oncology drug development expertise, which spans drug discovery to Phase 3 trial design, to help Kronos build its clinical organization and progress its two lead preclinical programs toward Investigational New Drug applications,” said Dr. DiMartino. “Kronos’ mission to discover and develop novel therapies against historically undruggable cancer targets dovetails perfectly with my passion for understanding cancer biology and translating this knowledge into clinical development strategies to benefit cancer patients.”
In addition to his work in industry, since 2007 Dr. DiMartino has been an Adjunct Clinical Assistant Professor of Pediatrics in the Division of Hematology/Oncology at Stanford University School of Medicine, participating in the care of pediatric oncology patients. Earlier in his academic career, he was Assistant Professor of Pediatrics, Division of Experimental Hematology, at Cincinnati Children’s Hospital Medical Center. Prior to that, he was an Instructor in the Departments of Pathology and Pediatrics at Stanford University School of Medicine, where he studied how chimeric transcription factors mediate leukemogenesis.
Dr. DiMartino received a B.A. in genetics from the University of California, Berkeley, a Ph.D. in immunology from Cornell University Graduate School of Medical Sciences, and an M.D. from the University of California, San Diego, School of Medicine. He completed a residency in pediatrics and a fellowship in pediatric hematology/oncology at the Lucile Salter Packard Children’s Hospital at Stanford, and a post-doctoral fellowship in the Department of Pathology at Stanford.
About Kronos Bio
Kronos Bio, Inc. is dedicated to the discovery and development of first-in-class therapies that modulate historically undruggable targets. We leverage deep capabilities in high-throughput small molecule microarrays, targeted protein degradation, and cancer biology in order to identify potent and selective compounds against transcription factors and other central drivers of oncogenic signaling.