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Ravil R. Petrov

Researcher at University of Montana

Publications -  8
Citations -  244

Ravil R. Petrov is an academic researcher from University of Montana. The author has contributed to research in topics: Cannabinoid receptor & Cannabinoid receptor type 2. The author has an hindex of 8, co-authored 8 publications receiving 176 citations.

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Characterization of novel cannabinoid based T-type calcium channel blockers with analgesic effects

TL;DR: A novel class of compounds whose physiological and therapeutic actions are mediated through block of Cav3.2 calcium channels is revealed, which was efficacious in mediating analgesia in mouse models of acute inflammatory pain and in reducing tactile allodynia in the partial nerve ligation model.
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Analgesic effect of a mixed T-type channel inhibitor/CB2 receptor agonist

TL;DR: This work shows that both T-type channels as well as CB2 receptors play a role in the antinociceptive action of NMP-181, and also provides a novel avenue for suppressing chronic pain through novel mixed T- type/cannabinoid receptor ligands.
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Mastering tricyclic ring systems for desirable functional cannabinoid activity

TL;DR: The present study provides novel tricyclic series as a starting point for further investigations of CB2 pharmacology and pain treatment and identified the CB2 ligand 35 which failed to promote CB2 receptor internalization and inhibited compound CP55,940-induced CB2 internalization.
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Functional characterization and analgesic effects of mixed cannabinoid receptor/T-type channel ligands

TL;DR: The results reveal that a set of novel cannabinioid receptor ligands potently inhibit T- type calcium channels and show analgesic effects in vivo, and suggest possible novel means of mediating pain relief through mixed T-type/cannabinoid receptor ligANDs.
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NMP-7 inhibits chronic inflammatory and neuropathic pain via block of Cav3.2 T-type calcium channels and activation of CB2 receptors.

TL;DR: This work shows that NMP-7 mediates a significant analgesic effect in a model of persistent inflammatory and chronic neuropathic pain by way of T-type channel modulation and CB2 receptor activation, and provides a novel therapeutic avenue for managing chronic pain conditions via mixed CB ligands/T-type channels.