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Richard B Westkaemper

4 papers in the library · 310 citations · publishing 2004-2009

Papers

Screening the receptorome to discover the molecular targets for plant-derived psychoactive compounds: a novel approach for CNS drug discovery.

Pharmacology & therapeutics May 1, 2004 Bryan L Roth, Estela Lopez, Scott Beischel et al. 98 citations

Psychoactive plants alter perception, emotion, and cognition, and understanding their molecular mechanisms may reveal the biological basis of consciousness and provide validated targets for central nervous system drug discovery. This review describes an unbiased, discovery-based approach that screens the main active ingredients of psychoactive plants against the 'receptorome'—the portion of the proteome encoding receptors. It overviews the receptorome, describes public-domain in silico resources, and details new tools for mining data from the National Institute of Mental Health Psychoactive Drug Screening Program's K(i) Database. Three case studies on Hypericum perforatum, Salvia divinorum, and Ephedra sinica illustrate the approach, and recommendations for future studies are offered.

Identification of the molecular mechanisms by which the diterpenoid salvinorin A binds to kappa-opioid receptors.

Biochemistry June 21, 2005 Feng Yan, Philip D Mosier, Richard B Westkaemper et al. 91 citations

Salvinorin A, a hallucinogenic compound from the plant Salvia divinorum, selectively and potently activates kappa-opioid receptors (KORs), making it the only known lipid-like molecule to do so and the only non-nitrogenous opioid receptor agonist. Key residues in KORs responsible for its high binding affinity and agonist efficacy were identified: interactions with tyrosine residues in helix 7 (Tyr313 and Tyr320) and helix 2 (Tyr119) stabilize salvinorin A in the binding pocket, while activation requires interactions with helix 7 tyrosines Tyr312, Tyr313, and Tyr320 and with Tyr139 in helix 3.

Structure-based design, synthesis, and biochemical and pharmacological characterization of novel salvinorin A analogues as active state probes of the kappa-opioid receptor.

Biochemistry July 28, 2009 Feng Yan, Ruslan V Bikbulatov, Viorel Mocanu et al. 81 citations

Salvinorin A, the most potent naturally occurring hallucinogen, targets the kappa-opioid receptor (KOR). Researchers designed and synthesized novel irreversible salvinorin A-derived ligands, RB-64 and RB-48, as active state probes of KOR. Based on molecular modeling, they targeted cysteine residue C315(7.38) for covalent binding. Both compounds were extraordinarily potent and selective KOR agonists in vitro and in vivo. RB-64 showed wash-resistant inhibition of binding requiring a free cysteine near the binding pocket. Mass spectrometry confirmed C315(7.38) as the anchoring residue and suggested a biochemical mechanism for covalent binding. These findings provide direct evidence of a free cysteine in the agonist-bound KOR state and insights into salvinorin A's binding and activation mechanism.

Differential helical orientations among related G protein-coupled receptors provide a novel mechanism for selectivity. Studies with salvinorin A and the kappa-opioid receptor.

The Journal of biological chemistry February 2, 2007 Timothy A Vortherms, Philip D Mosier, Richard B Westkaemper et al. 40 citations

Salvinorin A, the active compound in the hallucinogenic plant Salvia divinorum, binds selectively and potently to the kappa-opioid receptor (KOR). Unlike most ligands for peptide-binding receptors, it is non-nitrogenous and lipid-like. Using chimeric receptors, mutagenesis, accessibility methods, and modeling, the study found that helix 2 of KOR is essential for binding, with two valine residues (Val-108 and Val-118) conferring selectivity. Modeling suggested these residues indirectly affect binding by rotating helix 2. Accessibility experiments comparing KOR and the delta-opioid receptor, which does not bind salvinorin A, showed differential water accessibility of key residues, indicating that differences in helix 2 orientation are critical for salvinorin A's selective binding to KOR.