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A synthetic pentadecapeptide originally isolated from the cytoprotective fraction of human gastric juice. BPC-157 upregulates growth hormone receptor expression in tendon fibroblasts, modulates nitric oxide (NO) synthesis, and activates the FAK-paxillin pathway to accelerate cytoskeletal reorganisation. It also interacts with dopaminergic and serotonergic systems, underpinning neuroprotective outcomes observed in preclinical models.

Selank is a synthetic heptapeptide analogue of the endogenous immunomodulatory peptide Tuftsin, developed by the Institute of Molecular Genetics in Russia. It modulates expression of Brain-Derived Neurotrophic Factor (BDNF) and serotonin metabolism, with studies demonstrating upregulation of BDNF in hippocampal tissue — a mechanism studied in preclinical models of neuroplasticity, learning consolidation, and stress resilience.

Semax is a synthetic heptapeptide analogue of the adrenocorticotropic hormone (ACTH) fragment 4–7, developed at the Institute of Molecular Genetics, Moscow. It upregulates BDNF and Nerve Growth Factor (NGF) expression in the hippocampus and prefrontal cortex, and enhances activity in the serotonergic and dopaminergic systems. Its resistance to degradation by endopeptidases confers extended CNS bioavailability relative to native ACTH fragments.

NAD+ (Nicotinamide Adenine Dinucleotide) is a critical coenzyme in cellular energy metabolism, serving as an electron carrier in the mitochondrial electron transport chain. It is a required substrate for Sirtuin deacetylases (SIRT1–7) and PARP enzymes involved in DNA repair. NAD+ levels decline with age; restoration is an active area of longevity research linked to mitochondrial biogenesis, genomic stability, and metabolic regulation.

MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA type-c) is a peptide encoded within the mitochondrial genome — a rare class of mitochondria-derived peptides (MDPs). It translocates to the nucleus in response to metabolic stress and activates AMPK pathways, with insulin sensitivity, glucose uptake, and fatty acid oxidation outcomes studied in preclinical models. Considered a key regulator of the mitochondria-to-nucleus retrograde signalling pathway.