Dr. Thomas P. Davis is Professor of Medical Pharmacology in the College of Medicine and Professor of Pharmacology and Toxicology in the College of Pharmacy, at the University of Arizona. He received his bachelor’s degree in biology from Loyola University, his M.Sc. in exercise physiology in Dr. David Bruce Dills’ Desert Research Institute (Founder of the Harvard Fatigue Laboratory) , University of Nevada and his Ph.D. in physiology/biochemistry in Dr. Charles Gehrke’s Experiment Station Labs at the University of Missouri-Columbia. He was hired by the late Dr. George Rathmann (Founder of Amgen and Genentech) to carry out award winning, postdoctoral training at Abbott Laboratories as a development chemist and founder of the FDA analytical confirmation laboratory in the therapy monitoring (TDX) group before joining the University of Arizona in November 1980 as a member of the UA Cancer Center . Dr. Davis’ research interests today include novel and award-winning studies of the molecular, biochemical, and pathophysiological mechanisms associated with maintenance and disruption of the blood-brain barrier and neurovascular unit that leads to CNS drug delivery challenges, in several disease states associated with hypoxia, stroke, drug abuse and pain states. He has studied the challenges of drug delivery across the blood-brain barrier with 40 continuous years of basic science, translational RO1 research grant awards, as a PI, from the N.I.H. from 1985 to 2025. His pioneering, award winning program of research has published 260 well cited, high impact, peer-reviewed research articles with a H index of 75, a i10 index of 200 and 22,000 citations. He has served as an invited chartered member on five different N.I.H., brain disorders clinical neurosciences study sections, including BINP,ANIE, N.S.F., MRC and V.A. study sections. Dr. Davis was awarded a special citation from the University of Arizona Chair of the Faculty for his extraordinary and expert service to the University in 2001, a distinguished award citation and invited lecture from Loyola-Marymount University College of Science and Engineering for inclusion on the Alumni Wall of Fame in 2003 and awarded The Founders Day Award and lecture from The University of Arizona College of Medicine in 2011. Dr. Davis continues his research program today as the P.I. of a NIH/NIDA RO1 drug delivery grant awarded to 2025. His lab was the frst to discover that the over the counter acetominophen analgesic used by millions of people every day can decrease the drug of abuse, ketamine, uptake to the brain. . His lab also discovered specific BBB drug transporters such as Pgp and OATP altered by stroke and acute pain states which can be targeted to control CNS drug delivery in stroke. Today, he continues his work on the effect of hypoxia, stroke, and acute pain on endothelial cell tight junction protein integrity, leak, permeability and Pgp transporter trafficking at the CNS.. Recently, he demonstrated that short-term hypoxia and MCAO/Stroke leads to alterations in brain permeability and OATP / PgP / BCRP transporter expression. The brain is not merely “open and closed” in stroke, but can be altered by transporter drug delivery to treat hypoxia/stroke. This work has impact for treatments of stroke where the OATP1a2 transporter is central to neuroprotectant atorvastatin delivery.
. Dr. Davis CV . cvtpd2023.docx
Research Interests :
Our Brain Barriers Reserach laboratory continues its long-term blood brain barrier / neurovascular unit (BBB/NVU) research program, continuously funded by N.I.H. since 1985, by studying the mechanisms involved in delivering drugs across the blood-brain barrier to the central nervous system (CNS) in neuropathological disease states. We were the first group to discover specific BBB drug transporters such as Pgp and OATP altered by stroke and acute pain which can be targeted to enhance drug delivery. We are also actively studying the effect of neuropathologies such as hypoxia, stroke, and acute pain on endothelial cell tight junction protein integrity , leak, permeability and Pgp transporter trafficking from the nucleus to the vascular lumen of the BBB. We have recently shown that short-term hypoxia and MCAO leads to significant alterations in permeability and OATP / PgP transporter expression that can be reversed by specific transporter antagonists, antioxidants and OTC drugs. This work has significant consequences to the treatment of stroke. Additionally, we have shown that peripheral inflammatory pain and drug-drug interactions have significant effects on BBB Pgp transporter trafficking leading to limitations in the delivery of analgesics such as codeine and morphine, to the brain. We are in the exciting position of coupling our program in CNS drug delivery by BBB transporters with our program in stroke neuropathology and pain at the neurovascular unit by recently demonstrating that the transporter OATP1a2 is central to neuroprotectant atorvastatin drug delivery in stroke. cvtpd2023.docx
