Benjamin Weiss (January 26, 1937) is an American neuropharmacologist, Emeritus Professor of Pharmacology and Physiology at Drexel University College of Medicine.
He was the first to propose, based on his experimental work, that selective inhibition of phosphodiesterases which are expressed differentially in all tissues, could be used as a target for drug development.
His work is the basis for many marketed and developmental human drugs that selectively inhibit cyclic nucleotide phosphodiesterases.
Weiss was born in The Bronx in 1937 and was raised on a chicken farm in New Jersey where his immigrant parents moved in 1946.
He did further training as a research associate at Columbia University, College of Physicians and Surgeons, with Erminio Costa from 1966 to 1968.
From 1968 to 1972 Weiss worked at the National Institute of Mental Health at St Elizabeths Hospital, Washington, D.C., where he held the position of chief of the Section on Neuroendocrinology.
Weiss and co-workers did extensive work which demonstrated that certain neuropeptides [21,22], alpha adrenergic antagonists [23]and phenothiazineantipsychotic drugs were potent inhibitors of calmodulin activated enzymes [24,25,26,27,28].
Modulation of Adrenergic Receptor-Linked Adenylate Cyclase System: Using the pineal gland as a model, Weiss and his colleagues were the first to show that the beta-adrenergic receptor-linked adenylate cyclasesystem is modified chronically by a variety of physiological factors and pharmacological perturbations [reviewed in 29].
Weiss and his group, assisted by Genoveva Uzunova (Davidkova), who carried out a significant part of the antisense RNA studies in his group, used molecular biological, biochemical, pharmacological, cell biological techniques (cell cultures, fluorescence microscopy), and mouse models, to develop antisense oligonucleotides to the D1 and D2 dopamine receptors.
These studies opened up the possibility to develop a new gene therapeutic approachto treat neurologic and psychiatric conditions associated with D2 receptor hyperactivity such as chorea and addiction to alcohol [47].