DR. JOHN E. NESTLER, M.D.
Osteopathic Medicine at Marshall St, Richmond, VA

5162198, Nov 10, 1992

Sep 25, 1991

7/765368

David M. Eich - Richmond VA
Robert Jesse - Richmond VA
John Nestler - Richmond VA

Virginia Commonwealth University - Richmond VA

A01N 102, A61K 3156

435 2

Treating human beings with pharmacological quantities of DHEA results in their blood having increased serum DHEA and DHEA-S and lower rates of platelet aggregation. Reducing the rate of platelet aggregation can significantly reduce the incidence of morbidity and mortality from vascular events such as myocardial infarction and stroke, as well as reduce the occurrence of restenosis following vascular interventions. The concentration of DHEA and DHEA-S in the blood and the pre-incubation time of DHEA and DHEA-S with the blood will affect its impact on platelet aggregation. Hence, prior treatment of patients who are at risk with DHEA may produce the most beneficial affects. In addition, treatment of blood with DHEA-S reduces thromboxane production. Thromboxane is produced after platelets are subjected to many different types of agonists and is responsible for recruiting other platelets to aggregate and form a thrombus; therefore, blocking the production of thromboxane will reduce or prevent platelet aggregation.

5110810, May 5, 1992

Feb 8, 1991

7/652518

David M. Eich - Suffolk VA
Robert Jesse - Richmond VA
John Nestler - Richmond VA

Virginia Commonwealth University - Richmond VA

A61K 3156

514178

Treating human beings with pharmacological quantities of DHEA results in their blood having increased serum DHEA and DHEA-S and lower rates of platelet aggregation. Reducing the rate of platelet aggregation can significantly reduce the incidence or morbidity and mortality from vascular events such as myocardial infarction and stroke, as well as reduce the occurrence of restenosis following vascular interventions. The concentration of DHEA and DHEA-S in the blood and the pre-incubation time of DHEA and DHEA-S with the blood will affect its impact on platelet aggregation. Hence, prior treatment of patients who are at risk with DHEA may produce the most beneficial affects. In addition, treatment of blood with DHEA-S reduces thromboxane production. Thromboxane is produced after platelets are subjected to many different types of agonists and is responsible for recruiting other platelets to aggregate and form a thrombus; therefore, blocking the production of thromboxane will reduce or prevent platelet aggregation.

4920115, Apr 24, 1990

Dec 28, 1988

7/291149

John E. Nestler - Richmond VA
Cornelius O. Barlascini - Columbus GA
John N. Clore - Richmond VA
William G. Blackard - Richmond VA

Virginia Commonwealth University - Richmond VA

A61K 3156

514178

Therapeutic amounts of DHEA are administered to human patients for the treatment and prevention of such disorders as atherosclerosis, angina, diabetes, obesity and congestive heart failure. Administering therapeutic quantities of DHEA to human patients has been found to reduce body fat mass and increase muscle mass, lower serum LDL cholesterol levels, lower serum apoB levels, and not affect tissue sensitivity to insulin.