Peptide Protocol

Semax: ACTH fragment — BDNF induction and cognitive clarity.

Synthetic ACTH(4-7)-Pro-Gly-Pro heptapeptide. Approved in Russia for stroke and cognitive enhancement. Intranasal or SubQ.

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200–900 mcg
Daily Dose
4–8 weeks on / 4 off
Cycle
Intranasal / SubQ
Route
1–2× daily
Frequency
Overview

What is Semax?

Semax was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences by Vladimir Ilyich Sebentsov and colleagues. The ACTH(4-7) core sequence (Met-Glu-His-Phe) is responsible for cognitive and neuroprotective effects of ACTH without any adrenocorticotropic activity — it cannot stimulate cortisol release. The Pro-Gly-Pro extension protects it from rapid enzymatic degradation.

Semax's primary mechanism is potent induction of BDNF (brain-derived neurotrophic factor) and CNTF expression in brain tissue. BDNF drives neuroplasticity, synaptic strengthening, and neurogenesis in the hippocampus — the neurobiological substrate of learning and memory. It also modulates dopaminergic, serotonergic, and cholinergic systems, and demonstrates neuroprotective effects in ischemia models.

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BDNF / NGF Induction
Potently upregulates BDNF and NGF gene expression in the frontal cortex, hippocampus, and striatum — the primary mechanism for cognitive and neuroprotective effects.
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Neuroplasticity Enhancement
BDNF-driven TRKB activation promotes synaptic plasticity, LTP enhancement, and dendritic spine growth in hippocampal and cortical neurons.
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Neuroprotection
Reduces ischemia-reperfusion injury in the brain by suppressing oxidative stress, inflammatory cytokines, and pro-apoptotic signaling in neurons.
Neurotransmitter Modulation
Modulates dopaminergic reward circuits and enhances serotonergic and cholinergic tone — contributing to mood, motivation, and cognitive clarity.
Dosing Protocol

Dosing Schedule

Parameters documented in published preclinical and clinical research.

⚠️ Research use only. The following documents parameters from published preclinical and clinical research. Not medical advice. Not for human consumption. Consult a licensed healthcare professional before any use.
PhaseDoseFrequencyDurationNotes
Intranasal200–300 mcg per nostril1–2× daily4–8 weeksPrimary research route. 2–3 drops per nostril. N-Acetyl Semax Amidate preferred.
SubQ200–500 mcgOnce daily4–8 weeksSubcutaneous administration for more consistent bioavailability than intranasal.
High dose600–900 mcgDaily SubQ2–4 weeksAcute cognitive or neuroprotective research protocols.
Off cycle4 weeksTake equal time off before repeating cycle.
Safety Profile

Safety & Side Effects

✓ Generally Well Tolerated
Clinically approved in Russia/Ukraine for stroke and cognitive disorders
No adrenocorticotropic activity — does not stimulate cortisol
Potent BDNF induction with extensive neuroscience research support
Generally well tolerated across multiple clinical applications
⚠ Potential Concerns
Not FDA-approved; evidence base primarily from Russian/CIS research
Intranasal bioavailability is variable and formulation-dependent
Potential for anxiety or overstimulation at higher doses
Limited long-term human safety data from Western RCTs
⚠️
Research use onlyThis page is an educational reference. None of this constitutes medical advice. Consult a qualified professional before any use. All compounds are for research purposes only.
Evidence Base

Academic References

  1. [1]
    Ashmarin IP, et al. (1997). Anxiolytic action of Semax on rats. Bull Exp Biol Med. 124(6):529–30. PubMed ↗
  2. [2]
    Grigoriev VV, et al. (2016). Neuroprotective and cognition-enhancing properties of ACTH(4-7)PGP (Semax). Acta Naturae. 8(1):82–91. PubMed ↗
  3. [3]
    Dolotov OV, et al. (2006). Semax, an analog of ACTH(4-7) with a prolonged action, protects against ischemic brain injury. Front Neuroenergetics. 2006. PubMed ↗
  4. [4]
    Shadrina MI, et al. (2001). Expression analysis of neuroprotective effect of Semax. J Mol Neurosci. 17(2):237–44. PubMed ↗
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