Semax reports from a 2025 spinal cord injury animal study

Catalog peptide Semax appears in a 2025 British Journal of Pharmacology paper by Liu and colleagues.

Animal model. The paper reported that Semax was linked, in female mice, to functional recovery scores after spinal cord injury and to inhibition of lysosomal membrane permeabilization-related pyroptosis in that model and in neuroinflammation models, with decreased oxidative stress measures. The same paper reported RNA-sequencing analyses in which Semax was associated with regulation of ubiquitin-specific protease USP18, and that USP18 knockdown was used to examine that reported role in the spinal cord injury model.

Analyses reported with the animal work. Network pharmacology and molecular docking were reported to identify the μ-opioid receptor as a Semax target and to connect that target with USP18 and subsequent deubiquitination of fat mass and obesity-associated protein (FTO). Those steps are computational and are not themselves an in vitro, animal-model, or clinical outcome.

Limitation. Reported experiments used female mice and the models described in the paper. The abstract does not report human outcomes or long-term safety. Knockdown and docking results do not establish findings outside those experiments.

Sources

- Semax peptide targets the μ opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice. 2025. DOI: https://doi.org/10.1111/bph.70122 — https://pubmed.ncbi.nlm.nih.gov/40692165/