Timothy Richardson, PhD, has 20 years of experience in the fields of medicinal chemistry and drug discovery. He joined the Indiana University School of Medicine in early 2020 as a Senior Research Professor of Medicine in the Division of Clinical Pharmacology.
Before joining IUSM, Dr. Richardson was a Research Fellow at Lilly Research Laboratories, where he made substantial contributions to drug discovery programs that delivered clinical candidates for endocrine, musculoskeletal, and autoimmune diseases. He led technology platform teams focused on Gene Regulation, Epigenetics, and Nuclear Receptors. He also served as a Group Leader in Discovery Chemistry, helping to build a portfolio of small molecule clinical candidates for the Immunology Therapeutic Area. Dr. Richardson finished his career at Lilly as a founding member of the RNA Therapeutics Team facilitating the establishment of internal capabilities as well as an external ecosystem of partnerships, capabilities, and assets for oligonucleotide-based medicines.
Dr. Richardson leads the Medicinal Chemistry and Chemical Biology Core of the IUSM-Purdue TREAT-AD Center, an academic drug discovery center funded by the National Institute for Aging with the goal of diversifying and reinvigorating the Alzheimer’s disease (AD) drug development pipeline. The Center is developing high-quality research tools and drug-like molecules to validate and advance the next generation of drug targets for the treatment of AD. Current efforts are focused on the neuroinflammatory components of neurodegeneration driven by microglia, the non-neuronal, macrophage-like cells that serve as resident immune cells in the brain. We have discovered potent and selective inhibitors of SHIP1, a phosphatidylinositol phosphatase that plays a key role regulating pathways downstream from TREM2 and the Fcγ receptor FCγRIIB. We are also developing activators of PLCG2, a phospholipase involved in TREM2 and Fcγ receptor mediated signaling. Our hypothesis is that inhibition of SHIP1 or activation of PLCG2 early in disease will increase microglial protective functions and result in a reduced rate of disease progression and cognitive decline in AD patients.