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Pinealon

EDR peptide, Glu-Asp-Arg tripeptide

Quick Stats
Studies 19
Trials 1
Score 2
2011 pubmed 17 citations

Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes.

Khavinson. V V; Ribakova. Y Y; Kulebiakin. K K; Vladychenskaya. E E; Kozina. L L; Arutjunyan. A A; Boldyrev. A A

Key Findings

  • Pinealon reduces reactive oxygen species (ROS) in cerebellar granule cells, neutrophils, and PC12 cells in a dose‑dependent way
  • It decreases necrotic cell death as measured by propidium iodide staining
  • It delays ERK 1/2 activation and alters the cell cycle, suggesting possible direct interaction with cellular DNA

Practical Outcomes

  • For biohackers, pinealon looks like a potential antioxidant supplement, but the research is limited to cell cultures with no human dosing or safety data. Until clinical studies are done, it’s not ready for concrete dosing protocols, and any use should be experimental and cautious.

Summary

The lab study shows that the synthetic peptide pinealon can lower harmful oxidative molecules and protect cells from dying in test‑tube experiments, and it also seems to influence cell growth signals, hinting it might do more than just act as an antioxidant.

Abstract

The synthetic tripeptide pinealon (Glu-Asp-Arg) demonstrates dose-dependent restriction of reactive oxygen species (ROS) accumulation in cerebellar granule cells, neutrophils, and pheochromocytoma (PC12) cells, induced by oxidative stress stimulated by receptor-dependent or -independent processes. At the same time, pinealon decreases necrotic cell death measured by the propidium iodide test. The protective effect of pinealon is accompanied with a delayed time course of ERK 1/2 activation and modification of the cell cycle. Because restriction of ROS accumulation and cell mortality is saturated at lower concentrations, whereas cell cycle modulation continues at higher concentrations of pinealon, one can conclude that besides its known antioxidant activity, pinealon is able to interact directly with the cell genome.

Study Information

Provider

pubmed

Year

2011

Date

2011-10-06T00:00:00.000Z

DOI

10.1089/rej.2011.1172

Citations

17

References

24