Two different nervous systems
Peripheral nerves — the ones running to your hands, feet and organs — regenerate. Schwann cells clear debris and form guidance channels, and axons regrow along them at roughly one millimetre per day. Slow, but real.
The central nervous system is different. After injury, astrocytes form a glial scar and the environment becomes actively inhibitory to axon regrowth. Myelin-associated inhibitors block extension. The CNS prioritises containing damage over regrowing through it.
So a compound with strong evidence for sciatic nerve crush recovery in rats tells you very little about spinal cord or brain injury. The claim does not transfer, however similar the language sounds.
What the compounds are actually doing
BPC-157 has the largest animal literature for peripheral nerve regeneration, with rat sciatic crush studies reporting accelerated functional recovery. The proposed mechanism runs through VEGF-mediated angiogenesis — new nerves need new blood supply.
Cerebrolysin is the outlier for CNS work, with human trials in stroke and traumatic brain injury. Its measured effects are modest, and the trials that show most benefit are the ones that combine it with rehabilitation.
GHK-Cu has animal evidence for nerve outgrowth alongside its better-established skin remodelling work. SS-31 shows neuroprotection in animal models, largely by preventing mitochondrial failure in stressed neurons — which is protection rather than regeneration.
Where the CNS does still change
The CNS may not regrow axons well, but it reorganises. Functional recovery after stroke is largely a story of surviving circuits taking over the work of lost ones.
That reorganisation is activity-driven. It happens in the circuits that get used, in proportion to how much they get used. Which is exactly why compound-plus-rehabilitation beats compound alone in the trial data.