Semax

Nine peptides were identified targeting diverse aging mechanisms including metabolic restoration, telomere biology, tissue repair, and neuroprotection.; FDA-approved peptides demonstrated robust safety profiles from large-scale trials, whereas non-approved peptides lack long-term safety data.; Significant knowledge gaps exist in optimal dosing regimens, combination therapy effects, and biomarkers for monitoring efficacy.

Bioactive peptides and proteins/polypeptides, such as NGF, BDNF, GDNF, Semax, and Exendin-4, modulate critical mechanisms including reduction of oxidative stress, inhibition of neuroinflammation, preservation of mitochondria, and enhancement of synaptic plasticity.; These peptides have demonstrated efficacy in preclinical and early-phase clinical trials across a spectrum of neurodegenerative disorders, including Alzheimer's, Parkinson's, and Huntington's diseases.; Delivery challenges, including blood-brain barrier permeability and enzymatic degradation, are being addressed through innovations in peptide engineering, nanoparticle-based delivery systems, CRISPR-assisted design, and AI-driven screening.; Peptide-based therapeutics present a rational and innovative approach to NDD management by targeting multiple pathogenic mechanisms simultaneously, highlighting their potential as next-generation neuroprotective agents.

Semax improved functional recovery and inhibited LMP-related pyroptosis in SCI mice and neuroinflammation models.; Semax targeted the μ-opioid receptor (Oprm1) to regulate USP18 and deubiquitination of FTO.; USP18 knockdown confirmed its role in Semax-mediated SCI recovery.; Semax reduced oxidative stress in SCI models.

Semax and its derivative improved cognitive functions in transgenic Alzheimer's model mice, as shown by open field, novel object recognition, and Barnes maze tests.; Histological examination revealed that both peptides reduced the number of amyloid inclusions in the cortex and hippocampus of the animals' brains.; The findings suggest high potential of Semax and its derivatives for developing therapeutic and corrective strategies for Alzheimer's disease.

ACTH-like peptides generated fewer differentially expressed genes in the striatum compared to the frontal cortex.; Both peptides tended to normalize ischemia-induced gene expression disturbances for hundreds of genes in the striatum.; ACTH(6-9)PGP action worsened the expression profile of 152 striatal genes, predominantly associated with inflammation.; Approximately one hundred genes overlapped between both peptides in both tissues, linked mainly to neuroactive ligand-receptor interaction.

3774 DEGs were identified under ischemia conditions, while 1539 and 2066 DEGs were found under Semax and ACTH(6-9)PGP, respectively, at 24 hours post-tMCAO.; Both peptides significantly reduced expression distortions for 1171 genes associated with immune and neurosignaling pathways.; Only 32 DEGs differed between ACTH(6-9)PGP and Semax administration at 24 hours post-tMCAO, indicating similar effects.; The pattern of peptide action on the transcriptome depended on the time elapsed after tMCAO, as shown by comparison with 4.5-hour data.

PGP and PGPL showed Semax-unlike effects, mostly without changing gene expression 24 h after tMCAO.; PGP significantly changed expression of inflammatory genes iL1b, iL6, and Socs3 compared to Semax.; PGPL significantly changed expression of inflammatory genes iL6, Ccl3, Socs3, and Fos, and neurotransmitter genes Cplx2, Neurod6, and Ptk2b compared to Semax.; Gene enrichment analysis and a regulatory gene network distinguished common and unique effects of PGP, PGPL, and Semax under ischemia-reperfusion.

Semax prevents the formation of A:Cu2+ complexes; Semax has anti-aggregating properties against amyloid beta; Semax shows protective effects especially in the presence of Cu2+; Semax inhibits fiber formation by interfering with fibrillogenesis of A:Cu2+ complexes

What is Semax?

Semax (ACTH(4-7) Pro-Gly-Pro, N-Acetyl Semax) is a synthetic heptapeptide derived from the adrenocorticotropic hormone fragment ACTH(4-10). Its primary mechanism involves upregulation of brain-derived neurotrophic factor (BDNF) and modulation of the melanocortin system, particularly through MC1 and MC4 receptor interac

How does Semax work?

ACTH(4-10)-derived heptapeptide that elevates BDNF and modulates the melanocortin system; used clinically in Russia for stroke and cognition.

What is the research status of Semax?

Semax is currently classified as clinical trials, with 207 research references on record. This is for research purposes only and is not medical advice.

What is the molecular weight of Semax?

Semax has a molecular weight of approximately 813.9 g/mol (formula C37H51N9O10S).