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Title: Analgesic effects of Phα1β toxin : a review of mechanisms of action involving pain pathways.
Authors: Silva, Juliana Figueira da
Binda, Nancy Scardua
Pereira, Elizete Maria Rita
Lavor, Mário Sérgio Lima de
Vieira, Luciene Bruno
Souza, Alessandra Hubner de
Rigo, Flávia Karine
Ferrer, Hèlia Tenza
Castro Júnior, Célio José de
Ferreira, Juliano
Gomez, Marcus Vinicius
Keywords: Pain
Phα1β peptide
Voltage-activated calcium channels
Issue Date: 2021
Citation: SILVA, J. F. da. et al. Analgesic effects of Phα1β toxin: a review of mechanisms of action involving pain pathways. Journal of Venomous Animals and Toxins including Tropical Diseases, v. 27, 2021. Disponível em: <>. Acesso em: 11 out. 2022.
Abstract: Phα1β is a neurotoxin purified from spider venom that acts as a high-voltage-activated (HVA) calcium channel blocker. This spider peptide has shown a high selectivity for N-type HVA calcium channels (NVACC) and an analgesic effect in several animal models of pain. Its activity was associated with a reduction in calcium transients, glutamate release, and reactive oxygen species production from the spinal cord tissue and dorsal ganglia root (DRG) in rats and mice. It has been reported that intrathecal (i.t.) administration of Phα1β to treat chronic pain reverted opioid tolerance with a safer profile than ω-conotoxin MVIIA, a highly selective NVACC blocker. Following a recent development of recombinant Phα1β (CTK 01512-2), a new molecular target, TRPA1, the structural arrangement of disulphide bridges, and an effect on glial plasticity have been identified. CTK 01512-2 reproduced the antinociceptive effects of the native toxin not only after the intrathecal but also after the intravenous administration. Herein, we review the Phα1β antinociceptive activity in the most relevant pain models and its mechanisms of action, highlighting the impact of CTK 01512-2 synthesis and its potential for multimodal analgesia.
ISSN: 1678-9199
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