Mechanistic research dossiers with linked tools for reconstitution, mg/kg ranges and half-life curves. For investigative and educational use only.

Semax

Intranasal heptapeptide (Met‑Glu‑His‑Phe‑Pro‑Gly‑Pro), an ACTH(4‑10) analogue with nootropic and neuroprotective properties linked to BDNF signalling and post-ischemic recovery.
Evidence: Human + Preclinical Function: Nootropic & Neuroprotection Class: ACTH fragment analogue
Explore calculators for this peptide
Use the Peptide Research Tools to experiment with intranasal µg/kg exposure curves for Semax in cognitive and ischemia-recovery models. All values are placeholders and must be aligned with your own research protocol.
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Research frame & potential applications
Semax is used as a “neurotrophic nootropic”, combining pro-cognitive effects with protection against ischemic and hypoxic injury in animal and human studies. It consistently upregulates BDNF and trkB in key brain areas, and modulates inflammatory and vascular responses, making it a tool for stroke recovery, cerebrovascular insufficiency and attention-related dysfunctions.

Research areas & putative benefits

Typical Semax use-cases in CNS and vascular-brain research.

  • Cognitive enhancement in healthy subjects and those with mild cognitive impairment or attention deficits.
  • Adjunct therapy after ischemic stroke to improve neurological and functional recovery trajectories.
  • Protection against hypoxic and ischemic brain damage in experimental models.
  • Modulation of neuroinflammation, vascular tone and stress responses in brain tissue.

Mechanism stack

Key mechanisms driving Semax’s neurotrophic and cognitive profile.

Neurotrophins
BDNF/trkB axis
Single intranasal doses of Semax increase BDNF protein and trkB activation in hippocampus and basal forebrain, with parallel rises in BDNF and trkB mRNA, supporting synaptic plasticity and learning.
Ischemia response
Gene regulation & vascular support
In cerebral ischemia models, Semax shifts expression of neurotrophic, vascular and inflammatory genes, reduces neuronal loss and improves indices of cerebral circulation and tissue oxygenation.
Synaptic plasticity
Learning & memory enhancement
Behavioural studies show enhanced acquisition and retention in learning tasks, consistent with BDNF-driven strengthening of hippocampal and cortical synaptic networks.
ACTH heritage
CNS-specific fragment
As an ACTH(4–10) analogue lacking full endocrine ACTH activity, Semax emphasises central neurotrophic and behavioural effects without strong direct activation of systemic cortisol pathways.

Evidence snapshot

Highlights from Semax cognitive and stroke-related research.

Model / context Observation Relevance
Rodent learning tasks
Behavioural
Intranasal Semax improves performance in standard learning and memory paradigms, in parallel with increased BDNF/trkB signalling in associated brain regions. Supports classification as a nootropic peptide rather than purely neuroprotective agent.
Ischemic stroke models
Neuroprotection
Semax reduces infarct size, preserves neuronal structure and modulates inflammatory markers and vascular factors in experimental stroke. Basis for its use as a post-ischemic recovery adjunct in clinical protocols.
Patients with cerebrovascular disease
Clinical
Clinical courses of Semax have been associated with improved cognitive scores, attention and functional outcomes in several small-to-medium studies. Evidence is promising but mainly derived from specific regional practice patterns and trial designs.
Attention and behavioural models
Translational
In attention-related models, Semax enhances performance and can augment effects of dopaminergic stimulants, suggesting overlap with attention and motivation circuits. Provides rationale for exploring Semax in attention and executive-function contexts.

Risk frame & unknowns

Uncertainties around long-term and off-label use of Semax.

Important research caveats
  • Long-term daily use outside post-stroke or cerebrovascular indications has limited systematic safety data.
  • Most clinical work comes from a relatively narrow geographic and institutional base; broader replication is needed.
  • Combinations with other nootropics, stimulants or CNS-active peptides have not been rigorously studied.
  • Consumer and biohacking use often extrapolates beyond the modest effect sizes observed in controlled trials.
This dossier summarizes mechanistic, preclinical and clinical findings on Semax for scientific and educational purposes only. It does not provide medical advice, treatment guidance or dosing recommendations.