A neuroprotective intervention doesn't heal an injured brain. It reduces the extent of the injury when the insult happens — smaller infarcts after stroke, less oxidative damage under metabolic stress, fewer neurons lost in excitotoxic events, better functional outcomes after traumatic brain injury. The clinical bar for a neuroprotective peptide is: does it measurably reduce the biological damage when administered before, during, or shortly after a controlled insult in a research model, and does that translate to functional-outcome improvement.

In practice, the mechanisms cluster into four families: antioxidant defence (upregulating endogenous SOD, catalase, glutathione peroxidase), anti-apoptotic signalling (preserving mitochondrial membrane potential, blocking caspase cascades), anti-neuroinflammatory action (modulating microglial activation phenotype and cytokine release), and neurotrophic support (BDNF/NGF-like effects that support stressed neurons through the acute injury window). Different peptides emphasise different combinations of these arms.

The peptides catalogued below all show at least one of these effect signatures in published research. Some — Cerebrolysin, Cortexin — are clinically approved neuroprotective preparations in Russia and adjacent jurisdictions. Others (Pinealon, Epitalon, GHK-Cu, DSIP) sit closer to the research-tool end of the spectrum. FGL and P21 add a distinctive neurogenic angle on top of the direct neuroprotection.

For acute-stroke and traumatic-brain-injury recovery research with a strong clinical-translation angle: Cerebrolysin has the deepest evidence base, including Cochrane systematic-review coverage in vascular dementia and CASTA stroke-trial data. Cortexin is the closest Russian analogue with a broader paediatric clinical positioning.

For gerontoprotective and cognitive-ageing research within the Khavinson framework: Pinealon is the neuroprotective bioregulator and Epitalon adds the pineal-directed circadian and telomerase angle. GHK-Cu provides an antioxidant / gene-expression-modulation angle from a different conceptual starting point.

For research designs that combine neuroprotection with neurogenic effects — particularly Alzheimer's-model work — FGL (FGFR1-driven) and P21 (CNTF-derived) are the research tools designed for that combined effect profile.

For sleep-architecture and stress-resilience research in cognitive-ageing contexts, DSIP provides indirect neuroprotection through HPA-axis attenuation and slow-wave-sleep support rather than through the direct injury-response mechanisms.

For BDNF-mediated neuroprotection under ischaemic stress with an established intranasal delivery pathway, N-Acetyl Semax Amidate extends the parent Semax's neuroprotective evidence base with better pharmacokinetics.