ArticlePain2025
Small molecule targeting Na V 1.7 via inhibition of CRMP2-Ubc9 interaction reduces pain-related outcomes in a rodent osteoarthritic model.
Article in Pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Parabrachial bombesin receptor subtype 3 neurons facilitate heat hypersensitivity in persistent pain.bioRxiv : the preprint server for biology · 2026Article
- Targeting CRMP2 for Chronic Pain: From Molecular Mechanisms to Therapeutic Strategies.Biomedicines · 2026Review
- Collagen II hydrogel-mediated sustained delivery of lacosamide attenuates cartilage degeneration and pain in osteoarthritis.Bioactive materials · 2026Article
- CRMP2 inhibits metastasis formation by impairing ILF3-dependent stabilization of CXCL10 mRNA in breast cancer.Cell death & disease · 2026Article
- Single-nuclei RNA sequencing reveals distinct transcriptomic signatures of rat dorsal root ganglia in a chronic discogenic low back pain model.The journal of pain · 2026Article
- Light-aversion and cephalic allodynia in an intravenous CGRP model of migraine-like behaviour in male and female rats.The journal of headache and pain · 2026Article
- Refining the adjuvant-induced rat model of monoarthritis by optimizing the induction volume and injection site.Scientific reports · 2025Article
- Quinoline-Based Neuropilin‑1 Antagonists Exhibit a Pure Antagonist Profile and Block Vascular Endothelial Growth Factor-Induced Pain.ACS pharmacology & translational science · 2025Article
- Beyond single targets: leveraging degeneracy in sodium channels for osteoarthritis analgesia.Pain reports · 2025Article
- Ion channels as therapeutic targets in osteoarthritis.Trends in pharmacological sciences · 2025Review
- Mouse models of non-dystrophic and dystrophic myotonia exhibit nociplastic pain-like behaviors.bioRxiv : the preprint server for biology · 2025Article
- Voltage-Gated Ion Channels in Neuropathic Pain Signaling.Life (Basel, Switzerland) · 2025Review
- Preclinical Animal Models to Investigate the Role of NaLife (Basel, Switzerland) · 2025Review
- Uncoupling the CRMP2-CaThe journal of pain · 2024Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Uncoupling the CRMP2-CabioRxiv : the preprint server for biology · 2024Article
- Sodium channels NaNeurobiology of pain (Cambridge, Mass.)Article
- The contribution of clock genes BMAL1 and PER2 in osteoarthritis-associated pain.Neurobiology of pain (Cambridge, Mass.)Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
abstractOsteoarthritis (OA) is a highly prevalent and disabling joint disease, characterized by pathological progressive joint deformation and clinical symptoms of pain. Disease-modifying treatments remain unavailable, and pain-mitigation is often suboptimal, but recent studies suggest beneficial effects by inhibition of the voltage-gated sodium channel Na V 1.7. We previously identified compound 194 as an indirect inhibitor of Na V 1.7 by preventing SUMOylation of the Na V 1.7-trafficking protein, collapsin response mediator protein 2. Compound 194 reduces the functional activity of Na V 1.7 channels and produces effective analgesia in a variety of acute and neuropathic pain models. However, its effectiveness has not yet been evaluated in models of OA. Here, we explore the effects of 194 on pain-related outcomes in the OA-like monoiodoacetate model using behavioral assessment, biochemistry, novel in vivo fiber photometry, and patch clamp electrophysiology. We found that the monoiodoacetate model induced (1) increased pain-like behaviors and calcium responses of glutamatergic neurons in the parabrachial nucleus after evoked cold and mechanical stimuli, (2) conditioned place aversion to mechanical stimulation, (3) functional weight bearing asymmetry, (4) increased sodium currents in dorsal root ganglia neurons, and (5) increased calcitonin gene-related peptide-release in the spinal cord. Crucially, administration of 194 improved all these pain-related outcomes. Collectively, these findings support indirect inhibition of Na V 1.7 as an effective treatment of OA-related pain through the inhibition of collapsin response mediator protein 2-SUMOylation via compound 194.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.