Identification of a Partial and Selective TRPV1 Agonist CPIPC for Alleviation of Inflammatory Pain

Molecules. 2022 Aug 25;27(17):5428. doi: 10.3390/molecules27175428.

Abstract

Transient receptor potential vanilloid 1 (TRPV1) is a non-selective cation channel, predominantly expressed in a subset of peripheral sensory neurons for pain signaling. Topical application of agonist capsaicin for desensitizing TRPV1 currents has been approved for relief of chronic pain. However, the potent TRPV1 capsaicin is not ingestible and even topical capsaicin causes common side effects such as skin irritation, swelling, erythema and pruritus, suggesting that a mild TRPV1 agonist might be helpful for reducing side effects while reliving pain. In this study, we reported on a partial and selective TRPV1 agonist 4-(5-chloropyridin-2-yl)-N-(1H-indazol-6-yl)piperazine-1-carboxamide named CPIPC that was modified based on targeting the residue Arg557, important for conversion between the channel antagonism and agonism. Whole-cell patch clamp recordings indicated a concentration-dependent activation of TRPV1 currents by CPIPC with an EC50 of 1.56 ± 0.13 μM. The maximum efficacy of CPIPC (30 μM) was about 60% of saturated capsaicin (10 μM). Repetitive additions of CPIPC caused TRPV1 current desensitization in both TRPV1-expressing HEK293 cells and dorsal root ganglion (DRG) sensory neurons. Oral administration of CPIPC dose-dependently alleviated inflammatory pain in mice. Further site-directed mutagenesis combined with molecular docking revealed that residue Arg557 is critical for TRPV1 activation by CPIPC. Taken together, we identified a novel partial and selective TRPV1 agonist CPIPC that exhibits antinociceptive activity in mice.

Keywords: TRPV; desensitization; dorsal root ganglion and antinociception; site-directed mutagenesis; whole-cell patch clamp.

MeSH terms

  • Animals
  • Capsaicin* / pharmacology
  • Capsaicin* / therapeutic use
  • Ganglia, Spinal
  • HEK293 Cells
  • Humans
  • Mice
  • Molecular Docking Simulation
  • Pain / drug therapy
  • Sensory Receptor Cells
  • TRPV Cation Channels* / agonists

Substances

  • TRPV Cation Channels
  • TRPV1 protein, human
  • TRPV1 protein, mouse
  • Capsaicin

Grants and funding

This research was funded by the research grants from National Natural Science Foundation of China (81973299 for K.W., 81573410 and 82104149 for Y.L.), the Ministry of Science and Technology of China (2018ZX09711001-004-006 for K.W.) and Shandong Provincial Natural Science Foundation of China (No. ZR2021QH192 for Q.Z. and ZR2020QH100 for Y.L.).