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Our Science – Figg Website
William Douglas Figg Sr., Pharm.D.
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Biography
Dr. Figg received his B.S. in pharmacy from Samford University and his doctorate in pharmacy (Pharm.D.) from Auburn University. He also has a dual MBA degree from Columbia University and London Business School. Following his clinical internship at the University of Alabama at Birmingham and his fellowship training at the University of North Carolina at Chapel Hill, he joined the Clinical Pharmacology Branch of the NCI. Dr. Figg became chief of the Molecular and Clinical Pharmacology Section in 1993. More recently, the Clinical Pharmacology Research Core and the Preclinical Pharmacology Research Core were formed, which he also heads.
Dr. Figg has focused his research on utilizing pharmacological principles in anticancer drug development and evaluating novel new agents in the treatment of cancer of the prostate.
Dr. Figg was Chair of the NCI's Vascular Biology Faculty until 2006. He serves on the steering committee of the GU Faculty, Molecular Targets Faculty and Vascular Biology Faculty. He is on the editorial board of ten peer reviewed scientific journals (e.g., Clinical Cancer Research, Cancer Biology and Therapy, Journal of American Pharmaceutical Association, Molecular Cancer Therapeutics, Pharmacotherapy).
He has been licensed to practice pharmacy since 1988 and in 1991, he became board certified in Pharmacotherapy (recertified in 1999).
Dr. Figg is a Captain in the US Public Health Services' Commissioned Corps.
He holds adjunct appointments at three schools of pharmacy, Virginia Commonwealth University, University of Michigan and the University of Maryland. Within Dr. Figg's program he currently has seven graduate students working on completing their Ph.D. thesis work. These are made possible through NCI collaborations with several universities (Oxford University, George Washington University, University of Maryland, Johns Hopkins University, and Virginia Commonwealth University). In addition, four individuals have already completed their thesis work in Dr. Figg's laboratory.
Dr. Figg is also a fellow in the American College of Clinical Pharmacy and a fellow in the American College of Clinical Pharmacology. He was named the Allen J Brands Clinical Pharmacist of the Year in 2001, the Association of Military Surgeons of the United States in 2003 gave him the Clinical Pharmacist of the Year award, and he received the 2005 Leon Goldberg Young Investigator Award from the American Society of Clinical Pharmacology and Therapeutics. In addition, he received the 2008 Russell R Miller Award and the 2008 ASHP Award for Sustained Contribution to the Scientific Literature.
Dr. Figg has over 400 peer-reviewed publications, has patented over 80 novel anticancer agents and devices and given over 100 invited scientific presentations/lectures throughout the world.
Research
View Dr. Figg's Current Clinical Trials
Research Focus - Pharmacology and Experimental Therapeutics
A successful drug development program requires a complete understanding of the pharmacology of the agents being evaluated.
Molecular Pharmacology Section
The Molecular Pharmacology Section within the Medical Oncology Branch, CCR, NCI (the independent research section of Dr. Figg's) has, as its primary focus, understanding the pharmacology of new anticancer agents. In particular, this section is focused on angiogenesis, understanding its importance, as well as identifying angiogenesis inhibitors. In addition, we have a strong interest in prostate cancer, the importance of angiogenesis in prostate cancer, and genes that predict the risk of prostate cancer.
The activity of traditional cytotoxic chemotherapies in prostate cancer has historically been disappointing. Thus, the Molecular Pharmacology Section (MPS) embarked upon an evaluation of several anticancer agents that appeared to inhibit tumor growth through novel mechanisms. We conducted either phase I or phase II clinical trials of the following agents in patients with prostate cancer: somatuline (which inhibits insulin-like growth factor); pentosan (which inhibits angiogenesis); gallium (a heavy metal thought to inhibit bone metastasis); high-dose lovastatin (an inhibitor of isoprenylation); phenylacetate (a differentiating agent); phenylbutyrate (a differentiating agent); CAI (a signal transduction inhibitor), COL-3 (an MMP inhibitor), and decitabine (a hypomethylating agent). Although all of these agents showed promise in either laboratory animals with cancer or cultured human cancer cells, clinical activity in humans is still being assessed.
We have also clinically evaluating thalidomide (an angiogenesis inhibitor), thalidomide plus taxotere, and ketoconazole plus alendronate (a bisphosphanate that may inhibit MMPs) in patients with hormone-refractory prostate cancer in four separate studies. We recently completed phase I studies of 2ME and CC5013 (both antiangiogenic agents).
In addition, in collaboration with several academic universities, we have synthesized over 187 thalidomide analogs and have screened them for activity as angiogenesis inhibitors. To this end, we have identified several extremely potent compounds in four different model systems and are moving those forward through clinical testing.
Originally marketed as a sedative in Europe, thalidomide was not approved in this country because of the teratogenic effects (stunted limb growth in fetuses) associated with the drug. Thalidomide is presently being used as an experimental drug in the treatment of a variety of diseases with autoimmune characteristics. Recently, in vitro data from Harvard University has suggested that thalidomide has antiangiogenic activity. We have followed up on this initial observation to determine that a metabolite of thalidomide is responsible for the antiangiogenic properties. Thalidomide's safety in nonpregnant humans has been established most recently in a study of graft-versus-host disease. Its known side effects include sedation, constipation, and sensory peripheral neuropathy (occurring in 3 percent of subjects). Because the progression of prostate cancer is highly dependent on angiogenesis, we are completing a phase II study in patients with hormone-refractory disease. Of the first 63 patients treated, 68 percent of the patients receiving 200 mg/day had some decline in PSA. This is extremely encouraging considering that we have shown that thalidomide upregulates the expression of PSA at a molecular level.
Currently, in collaboration with several pharmaceutical/biotechnology companies, we are screening for compounds that inhibit angiogenesis. Using in vitro models optimized in our laboratory, we have identified several potential agents. We are also designing new agents to hit key targets in this pathway.
Clinical Pharmacology Program
The primary research interest of the Clinical Pharmacology Program (CPP) within the Medical Oncology Branch, CCR, NCI, is to use pharmacokinetic and pharmacodynamic concepts in the development of novel anticancer agents. We have divided this program into units: Analytical Chemistry, Clinical Pharmacokinetics, and Pharmacogenetics. Dr. Figg has headed this core for the past 14 years. The CPP is directly responsible for the pharmacokinetic/pharmacodynamic analysis of numerous phase I and II clinical trials conducted within the NCI. In addition, the CPP provides direct pharmacokinetic support for many studies performed elsewhere in the extramural community. Within the section, we utilize compartmental and noncompartmental approaches to define the disposition of agents. Also, we are often required to characterize the plasma protein-binding properties and metabolism of new agents through in vitro techniques. Furthermore, several of our clinical trials have used adaptive control with a feedback mechanism to target particular plasma concentrations.
Dr. Figg also heads the Preclinical Pharmacology Research Core within the Molecular Targets Program, as well as the Biological Specimen Processing Core within the CCR.
This page was last updated on 12/8/2008.
