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Semax

ACTH(4-10) analogue, Heptapeptide SEMAX

Quick Stats
Studies 172
Trials 37
Score 2
2003 pubmed

Effect of Semax peptide on survival of cultured rat pheochromocytoma cells during oxidative stress.

Safarova. E R ER; Shram. S I SI; Zolotarev. Yu A YA; Myasoedov. N F NF

Key Findings

  • Semax reduced the number of cells damaged by oxidative stress in a dose‑dependent manner
  • The protective effect varied depending on when Semax was added to the cell culture
  • The results hint that Semax’s neuroprotective action may stem from shielding neurons from oxidative damage

Practical Outcomes

  • For biohackers, the study shows Semax has antioxidant‑like effects in cell models, but there’s no human dosage or safety data yet. It’s not ready to be turned into a self‑experiment protocol, though it supports the idea of exploring Semax for brain health under professional guidance.

Summary

A lab study found that the peptide Semax can protect rat nerve‑like cells from damage caused by hydrogen peroxide, a chemical that creates oxidative stress. The protection got stronger with higher doses and worked best when the peptide was added at the right time. This suggests Semax might help guard brain cells against oxidative injury, like what happens in a stroke, but the work was done in a dish, not in people.

Abstract

We studied the effects of Semax (antiinsulin peptide with neuroprotective effect) on the survival of cultured rat pheochromocytoma cell after oxidative stress induced by short-term incubation with hydrogen peroxide. Studies with fluorescent dyes propidium iodide and Hoechst 33258 showed that cell incubation with hydrogen peroxide led to the formation of damaged cells with characteristic signs of necrosis. Semax dose-dependently reduced the number of cells damaged by oxidative stress. The efficiency of Semax depended on the time of its addition to the culture medium. The results suggest that the neuroprotective effect of Semax in ischemic stroke can be due to its capacity to protect neurons from damage caused by oxidative stress.

Study Information

Provider

pubmed

Year

2003

DOI

10.1023/a:1024141232307