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GPCR Desensitization

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G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
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Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
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Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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Drug-receptor interaction describes the binding of receptors by drugs, but not all drug-receptor interactions result in activation and tissue response. For instance, the binding of agonists activates the receptor to generate a cellular reaction, while antagonists bind to receptors without causing their activation.
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An antagonist is a drug that binds strongly to a receptor without activating it. An antagonist prevents other molecules, such as neurotransmitters or hormones, from binding to the receptor and triggering a cellular response. Such interaction effectively hinders the normal physiological processes mediated by the receptor, resulting in various pharmacological effects depending on the specific receptor targeted.
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Controlled-deactivation cannabinergic ligands.

Rishi Sharma1, Spyros P Nikas, Carol A Paronis

  • 1Center for Drug Discovery and Departments of Chemistry and Chemical Biology and Pharmaceutical Sciences, Northeastern University , Boston, Massachusetts 02115, United States.

Journal of Medicinal Chemistry
|November 30, 2013
PubMed
Summary
This summary is machine-generated.

Researchers developed new cannabinoid analogues by adding a special ester group. These compounds offer controllable deactivation, improved druggability, and high affinity for CB1 and CB2 receptors, showing potential therapeutic benefits.

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Area of Science:

  • Medicinal Chemistry
  • Pharmacology
  • Organic Synthesis

Background:

  • Cannabinoids, such as (-)-Δ(8)-THC, interact with CB1 and CB2 receptors.
  • Developing cannabinoid analogues with controlled pharmacokinetic properties is crucial for therapeutic applications.
  • Improving druggability and managing metabolic deactivation are key challenges in cannabinoid drug design.

Purpose of the Study:

  • To synthesize novel cannabinoid analogues with enhanced druggability and controllable deactivation.
  • To investigate the structure-activity relationships of modified (-)-Δ(8)-THC analogues at CB1 and CB2 receptors.
  • To evaluate the in vitro and in vivo pharmacological effects of these novel compounds.

Main Methods:

  • Incorporation of a metabolically labile ester group at the 2'-position of (-)-Δ(8)-THC analogues.
  • Introduction of benzylic substituents α to the ester group to modulate deactivation half-lives.
  • Assessment of ligand affinities and efficacies for CB1 and CB2 receptors using in vitro assays.
  • Evaluation of enzymatic hydrolysis by plasma esterases and metabolite activity.
  • In vivo studies to assess CB1 receptor-mediated hypothermic and analgesic effects.

Main Results:

  • Novel cannabinoid analogues with a 2'-ester modification were successfully synthesized.
  • Analogues with 1'-(S)-methyl, 1'-gem-dimethyl, and 1'-cyclobutyl substituents demonstrated high affinities for both CB1 and CB2 receptors.
  • The novel ligands underwent controllable enzymatic hydrolysis by plasma esterases, yielding inactive metabolites.
  • Key analogues acted as potent CB1 receptor agonists, inducing CB1-mediated hypothermic and analgesic effects in vivo.

Conclusions:

  • The designed cannabinoid analogues possess controllable deactivation pathways and improved druggability.
  • These novel compounds exhibit high affinity and efficacy at CB1 and CB2 receptors.
  • The findings suggest potential therapeutic applications for these analogues in managing pain and temperature regulation.