Cortagen

In a rat model of transected sciatic nerve, intramuscular administration of the tetrapeptide cortagen (Ala-Glu-Asp-Pro) accelerated axonal regeneration. The peptide increased the elongation rate of regenerating nerve fibers by 27% and the conduction velocity along the recovering fibers by 40% relative to controls. The data indicate a neurotropic action promoting peripheral nerve fiber growth and functional maturation.

Scientists cut the sciatic nerve in rats and then gave some of them cortagen injections. The treated rats' nerves grew back faster and carried electrical signals better than untreated rats. This suggested the peptide could help damaged nerves repair themselves more quickly. This is early animal research.

This study in male Wistar rats followed the longer-term (delayed) recovery of sensory nerve function after sciatic nerve injury treated with cortagen, focusing on restoration of cutaneous mechanoreceptor and touch-sensation responses. It indicates the tetrapeptide's influence extended beyond the acute regeneration phase to sensory functional recovery.

This follow-up rat study looked at whether cortagen's benefits lasted over a longer period after nerve injury by measuring how well the rats regained their sense of touch. It indicated the peptide helped restore not just nerve growth but the animals' ability to feel again. It remains a small animal study.

Using microarray profiling of 15,247 transcripts in female mouse heart tissue, the authors found Cortagen (Ala-Glu-Asp-Pro) significantly altered expression of 234 clones (1.53% of the total), corresponding to 110 known genes, with a maximum upregulation of +5.42-fold and maximum downregulation of -2.86-fold. Comparison against other short peptides and melatonin revealed both shared and Cortagen-specific transcriptional signatures, supporting the hypothesis that short peptide bioregulators exert tissue-level effects through modulation of gene expression.

Researchers gave mice the Cortagen peptide and then scanned thousands of genes in their heart tissue to see which changed activity. Cortagen switched roughly a hundred genes up or down, some of them uniquely compared with other peptides. This gave a molecular hint that these tiny peptides may work by turning genes on and off.

In a rat model of chronic cerebral ischemia, both cortexin and the tetrapeptide cortagen accelerated recovery of disturbed individual behavior in animals differing in innate hypoxia resistance. The peptides prevented excessive activation of lipid peroxidation and counteracted the decline in antioxidant activity in brain tissue. The authors concluded these bioregulators have neuroprotective, antioxidant-supporting potential in chronic ischemic brain injury.

In rats with reduced blood flow to the brain, both cortexin and cortagen helped the animals recover their normal behavior faster and protected brain tissue from oxidative damage. The authors suggested these agents could support neuroprotective treatment during ongoing poor brain circulation. It is animal research from the peptide's originating group.