ANN ARBOR, Mich., October 9, 2009 — Lycera Corp., which is developing novel small-molecule pharmaceuticals to treat autoimmune diseases, today announced the appointments of Paul S. Changelian, Ph.D. and Peter L. Toogood, Ph.D. to the company’s drug development team. Dr. Changelian, previously director of inflammation biology at Pfizer, will serve as vice president of biology. Dr. Toogood, who was an associate director and research fellow at Parke-Davis and Pfizer, will be Lycera’s vice president of chemistry and chemical biology. Both are distinguished researchers and scientists who will play important roles in Lycera’s efforts to develop novel small molecule treatments for patients with autoimmune diseases including psoriasis, rheumatoid arthritis, lupus erythematosis, inflammatory bowel disease and transplant rejection.
Together Drs. Changelian and Toogood have more than 30 years of experience in drug discovery and development. Dr. Changelian’s research focuses on autoimmune diseases, organ transplantation and kinase biology. Dr. Toogood’s research is in immunology, inflammation, infectious diseases and cancer.
“Paul and Peter bring a wealth of experience in autoimmune drug discovery and development that will be essential to Lycera’s success,” said Dr. Gary Glick, the company’s co-founder and chief scientific officer. “Their track records of successfully developing promising compounds in this area will be crucial as we continue to advance our development initiatives for small-molecule immunomodulators.”
Prior to joining Lycera, Dr. Changelian worked for nearly twenty years as a researcher for Pfizer, in several roles, including director of inflammation biology. His lab’s chief concern was the identification of molecular targets that would lead to drugs preventing renal transplant rejection. That research culminated in 2000 with the discovery of CP-690,550, a compound that has since shown efficacy in Phase II trials for renal transplantation and is currently in Phase III trials for rheumatoid arthritis and Phase II trials for multiple sclerosis, inflammatory bowel disease, psoriasis, and dry eye. Most recently, Dr. Changelian led his own pharmaceutical consulting company. His work has been published in nearly 30 peer-reviewed publications including Science. He is also currently an adjunct assistant professor of internal medicine at the University of Michigan Medical School on the faculty at the University of Michigan Medical School.
Dr. Changelian received his doctorate in immunology from Harvard University and completed his postdoctoral studies at Washington University at St. Louis.
Dr. Toogood joined Lycera after working as a research scientist and manager at Parke-Davis and Pfizer. He has led teams in cancer and infectious disease drug discovery and was an inventor of the first selective cyclin-dependent kinase 4 inhibitor to enter human clinical trials. Prior to that, he was a faculty member in the Department of Chemistry at the University of Michigan. There he established a research program in natural products total synthesis and chemical biology, funded by the National Institutes of Health and the National Science Foundation. He is the author of more than 40 peer-reviewed publications and holds several patents and pending patent applications. In addition to his work at Lycera, Dr. Toogood is an adjunct professor in the University of Michigan College of Pharmacy.
Dr. Toogood completed his doctoral work at Imperial College in London and was a NATO postdoctoral fellow at Harvard University.
Lycera Corp. is focused on the discovery and development of small-molecule immunomodulators for the treatment of patients with autoimmune diseases including psoriasis, rheumatoid arthritis, lupus erythematosis, inflammatory bowel disease and transplant rejection. Lycera is developing drug candidates that target two novel therapeutic pathways and have the potential for first-in-class oral efficacy without the adverse effects of current standard-of-care antiproliferative and immunosuppressive agents. Visit www.lycera.com for more information.