Consultant and Advisor
L. Jackson  Roberts, MD

My experience in free radical catalyzed lipid peroxidation is fundamental to the success of the VDDI projects. 
Since my original discovery of F2-isoprostanes and subsequently related other products of free radical catalyzed lipid peroxidation, my entire research has focused entirely on oxidative stress with an emphasis on the role of oxidative stress in the pathogenesis of human disease.  This has led to my being an author on more than 200 original scientific publications in this area of research. 

Positions and Honors

Positions and Employment

1969 -1970     Internship (rotating), Denver General Hospital, Denver, Colorado
1973        Internship, Internal Medicine, Washington University, St. Louis, Missouri
1973 -1975             Assistant Resident, Washington University, St. Louis, Missouri
1975 - 1977            Post-doctorate fellowship, Vanderbilt University, Nashville, TN
1977 - 1978        Instructor of Pharmacology and Medicine, Vanderbilt University    
1978 - 1983   Assistant Professor of Pharmacology and Medicine, Vanderbilt University     
1983 - 1986            Associate Professor of Pharmacology and Medicine, Vanderbilt University 
1987-present   Professor of Pharmacology and Medicine, Vanderbilt University        
2006 - 2010            T.  Edwin Rogers Professor of Pharmacology    
2010 - present     William Stokes Professor of Experimental Therapeutics
2010 - present     Director, Research Center for Pharmacology and Experimental Therapeutics
2014 - present Member, Scientific Advisory Board and Consultant VDDI Pharmaceuticals

Product Development

Lipid Oxidation Inhibitors  (Meg This is a new product development area)
The oxidation of lipids by hemeproteins contributes to a number of diseases and physiologic functions.  Lipid peroxidation catalyzed by myoglobin is a major contributor to the pathophysiology of the renal failure caused by rhabdomyolysis.  A body of evidence supports the hypothesis that lipid peroxidation catalyzed by hemoglobin contributes to the neurological injury resulting from the delayed vasospasm in subarachnoid hemorrhage (SAH).  We have discovered that acetaminophen inhibits the lipid peroxidation catalyzed by these two hemeproteins, both in vitro and in vivo.  This occurs by a similar mechanism to that by which acetaminophen inhibits the cyclooxygenase enzymes, a mechanism that accounts for its widespread use as an antipyretic and analgesic drug.  More recently, we found that acetaminophen blocks the oxidation of cardiolipins by cytochrome c, thereby preventing the release of cytochrome c from mitochondria. 

 Despite the known useful and potentially beneficial effects of inhibiting lipid oxidation by these hemeproteins, acetaminophen has major drawbacks as a drug; it can produce severe and fatal hepatotoxicity, and its very short half-life leads to marked oscillations in the plasma concentrations of drug and presumably its pharmacological effect.  Accordingly, it is the aim of this proposal to synthesize and evaluate agents that inhibit oxidation of lipids by these hemeproteins with efficacy equivalent to or greater than acetaminophen, but with absence of hepatotoxicity and with greater metabolic stability.


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