Most used for Most used for Brain Health.
Semax is a synthetic peptide derived from a fragment of adrenocorticotropic hormone (ACTH). It consists of seven amino acids and was developed in Russia for research and therapeutic purposes. Semax is reported to enhance cognitive function, memory, attention, and stress resilience while providing neuroprotective effects.
Research use only (not for human use)
WADA-compliant / allowed in sports
| Protocol | Duration | Dosage | Frequency |
|---|---|---|---|
| Titration Phase 1 | Day 1 + | 50–100 µg | 1 time a day1x/day |
| Titration Phase 2 | Day 4 + | 100–150 µg | 1 time a day1x/day |
| Maintenance Phase | Day 8 + | 150–300 µg | 1 time a day1x/day |
| Cycling Phase | Day 22 + | 0 µg | —— |
| Maintenance Phase | Day 29 + | 150–300 µg | 1 time a day1x/day |
| Cycling Phase | Day 50 + | 0 µg | —— |
This peptide is cycled to reduce tolerance, prevent receptor down-regulation, support long-term effectiveness, and allow the body time to reset between active phases. The highlighted rows show the repeating cycle with 21 days on followed by 7 days off. These ranges reflect common practitioner-guided protocols, and do not reflect medical advice.
Semax is a synthetic peptide derived from the adrenocorticotropic hormone (ACTH) fragment. It consists of seven amino acids arranged in a specific sequence to enhance its activity in the nervous system. It was developed in Russia for research and therapeutic purposes.
Semax is reported to improve cognitive function, memory, and learning ability. It may also enhance focus, mental clarity, and stress resilience. Additionally, some studies suggest it has neuroprotective and mood-regulating effects.
Studies in animals and humans suggest that Semax supports cognitive and neuroprotective functions by influencing neurotrophin systems and vascular‑immune responses. In rats, Semax increased mRNA expression of brain‑derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in hippocampal and cortical tissue. In models of focal cerebral ischaemia, Semax modulated expression of genes involved in vasculogenesis and immune cell migration, which are presumed mechanisms for its protective effect on nervous tissue 1, 2. Additionally, a clinical study in stroke patients reported improved functional recovery and motor performance associated with Semax administration 3
Among its main reported benefits are improved learning, memory, attention, and stress resilience. Animal research shows Semax facilitates acquisition of tasks such as passive avoidance and Morris water maze performance under normal and stressed conditions 4. Studies also indicate neuroprotective effects including reduced neuronodegeneration after ischemic insult and prevention of amyloid β fibril formation in experimental model 5. In sum, Semax appears to enhance cognitive performance and provide neuroprotection through modulation of neurotrophic, vascular and immune pathways.
There is limited published human‑trial data on the negative side effects of Semax. One clinical report noted that the drug was “well tolerated” with a “minor percent of side‑effects” in older patients 6. In preclinical and anecdotal sources there are some reported mild adverse responses. Some user‑ and database‑derived summaries list nasal irritation, headaches, dizziness, increased anxiety and insomnia in a small number of cases 7. In summary, while Semax appears to have a low incidence of documented negative effects, the evidence base remains small and largely preliminary.
Semax works through several interrelated biological mechanisms in the brain. Research in rats shows that it increases expression of neurotrophins such as Brain‑derived neurotrophic factor (BDNF) and Nerve growth factor (NGF) and up‑regulates the BDNF receptor TrkB in the hippocampus, thereby supporting synaptic plasticity and neuron survival. It also modulates gene expression related to immune responses and blood‑vessel formation, such that in a rat model of brain ischemia it suppressed inflammatory gene expression and increased genes tied to neurotransmission and vascular processes 8, 9. In addition the peptide influences intracellular calcium dynamics in hippocampal neurons, affecting neuronal excitability and signaling 10. Together these effects support enhanced neural plasticity, improved neuronal resilience, and modulation of immune‑vascular interactions in the brain.