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Thomas E. Prisinzano

Researcher at University of Kentucky

Publications -  190
Citations -  5968

Thomas E. Prisinzano is an academic researcher from University of Kentucky. The author has contributed to research in topics: Salvinorin A & Agonist. The author has an hindex of 46, co-authored 178 publications receiving 5353 citations. Previous affiliations of Thomas E. Prisinzano include Scripps Research Institute & Rockefeller University.

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An Opioid Agonist that Does Not Induce μ-Opioid Receptor—Arrestin Interactions or Receptor Internalization

TL;DR: Evaluating μOR trafficking in response to activation by a novel μ-selective agonist derived from the naturally occurring plant product, salvinorin A, finds that this compound, termed herkinorin, does not promote the recruitment of β-arrestin-2 to the μOR and does not lead to receptor internalization.
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Evidence for the Involvement of Dopamine Transporters in Behavioral Stimulant Effects of Modafinil

TL;DR: The data show that modafinil interacts with DAT sites in rat brain, a property shared with agonist medications under investigation for treating cocaine dependence, and suggest that modAFinil should be tested as an adjunct for treating METH addiction.
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Neoclerodane Diterpenes as a Novel Scaffold for μ Opioid Receptor Ligands

TL;DR: A nonnitrogenous neoclerodane diterpene with mu opioid receptor affinity that is an agonist at mu opioid receptors is reported, which represents the identification of a novel structural class of mu opioids receptor agonists.
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Gedunin, a Novel Hsp90 Inhibitor: Semisynthesis of Derivatives and Preliminary Structure–Activity Relationships

TL;DR: In an effort to further probe the mechanism of action, 19 semisynthetic derivatives of gedunin were prepared and their antiproliferative activity against MCF-7 and SkBr3 breast cancer cells determined.
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Monohydroxylated metabolites of the K2 synthetic cannabinoid JWH-073 retain intermediate to high cannabinoid 1 receptor (CB1R) affinity and exhibit neutral antagonist to partial agonist activity

TL;DR: The present study indicates that further work examining the physiological effects of synthetic cannabinoid metabolism is warranted, and suggests that a complex mix of metabolically produced CB1R ligands may contribute to the adverse effect profile of JWH-073-containing products.