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Article

Design and engineering of μO-conotoxin MfVIA mutants to enhance NaV1.8 inhibition and analgesic efficacy in inflammatory pain.

Bioorganic & medicinal chemistry - 1 Oct 2026

Gao Xinyu, Wang Nan, Zhan Leqing, Yu Jinpeng, Jiang Hongfei, Zhangsun Dongting, Luo Sulan, Zhu Xiaopeng

Abstract excerpt

Voltage-gated sodium (NaV) channels are essential for action potential initiation and propagation and play key roles in pain signaling. NaV1.8 is predominantly expressed in nociceptors and drives persistent sodium currents that support repetitive firing, making it an attractive target for analgesic development. Venom peptides provide a valuable source of NaV1.8-targeted leads. MfVIA, a μO-conotoxin from Conus...

Topics

Animals
Conotoxins
Analgesics
Mice
NAV1.8 Voltage-Gated Sodium Channel
Pain
Drug Design
Inflammation
Structure-Activity Relationship
Voltage-Gated Sodium Channel Blockers

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Male

Dose-Response Relationship, Drug

Mutation

Source

Identifiers

PMID: 42391962
DOI: 10.1016/j.bmc.2026.118738

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026.

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