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Related Experiment Video

Updated: Apr 5, 2026

Simultaneous Photothrombosis and Fiber Photometry to Induce and Monitor Ischemic Stroke in Behaving Mice
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Rationally designed peptides relieve ischemic stroke by targeting TRPM2 intramolecular interactions.

Jing Yao1, Qing You2, Xingyu Liu1

  • 1Department of Neurology, Center for Membrane Receptor and Brain Medicine, the Fourth Affiliated Hospital of School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University, Yiwu, 322000, China.

Pharmacological Research
|April 3, 2026
PubMed
Summary
This summary is machine-generated.

A novel peptide inhibitor, M2IP, effectively blocks the TRPM2 channel, reducing brain injury in ischemic stroke models. This offers a promising new therapeutic strategy for ion channel-related diseases.

Keywords:
Ion channelIschemic strokeOxidative stressPeptide inhibitorTRPM2

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Area of Science:

  • Molecular biology
  • Neuroscience
  • Pharmacology

Background:

  • TRPM2 channels are calcium-permeable cation channels involved in oxidative stress sensing and pathologies like ischemic stroke.
  • Current TRPM2 inhibitors lack specificity and efficacy due to targeting conserved regions.
  • Targeting unique interfaces offers a novel strategy for developing selective ion channel inhibitors.

Purpose of the Study:

  • To design and characterize a novel peptide inhibitor (M2IP) targeting the unique inter-subunit interface (interface III) of TRPM2.
  • To evaluate the inhibitory potency, selectivity, and functional effects of M2IP on TRPM2.
  • To assess the therapeutic potential of M2IP in a mouse model of ischemic stroke.

Main Methods:

  • Peptide inhibitor design targeting TRPM2 interface III.
  • In vitro assays for inhibitory potency and selectivity against TRP channels.
  • Electrophysiology and calcium imaging to assess TRPM2 channel activity.
  • In vivo evaluation in a mouse model of ischemic stroke.

Main Results:

  • M2IP demonstrated sub-micromolar inhibitory potency and high selectivity for TRPM2 over other TRP channels.
  • M2IP effectively suppressed TRPM2-mediated currents and calcium influx.
  • M2IP treatment significantly alleviated brain injury in a mouse model of ischemic stroke.

Conclusions:

  • M2IP is a potent and selective TRPM2 peptide inhibitor.
  • Targeting unique inter-subunit interfaces is a viable strategy for developing specific ion channel therapeutics.
  • M2IP shows therapeutic potential for treating ischemic stroke and other TRPM2-related pathologies.