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DPreclinical / mechanistic only
No human data

N-Acetyl Semax Amidate

NA-Semax-Amidate

N-Acetyl Semax Amidate (NASA) is a synthetically modified analog of Semax, itself a heptapeptide derived from ACTH(4-10) (Met-Glu-His-Phe-Pro-Gly-Pro), carrying an N-terminal acetyl group and a C-terminal amide intended to slow enzymatic degradation and prolong action versus plain Semax. It is marketed to consumers as an intranasal nootropic/neuroprotective peptide. A critical limitation is that there is no published human or animal study of N-Acetyl Semax Amidate specifically; it does not appear in PubMed. Every claim below is extrapolated from the parent compound Semax, and even that evidence is weak: the human data are almost entirely small, Russian-language, largely open-label or non-blinded trials in stroke and cerebrovascular disease, not modern placebo-controlled RCTs, and none address healthy nootropic users or the acetylated-amidated analog sold online. Semax is a registered drug only in Russia and has never been evaluated or approved by the FDA/EMA. The true safety profile of the modified analog is unknown; product identity, purity, sterility, and dose of gray-market research peptides are unverified, and long-term effects, immunogenicity, and endocrine effects of this ACTH-derived molecule in chronic recreational use have not been studied. Treat as an experimental substance with essentially no direct safety data.

Clinical readoutPeptide · neuropeptide-nootropic
Hepatic strainNone
CardiovascularNone
HPTA suppressionNone
Half-life
Not established f…
Route
Marketed and used intra…
Evidence
D
Active
Unknown/unstudied for t…
1·t½2·t½3·t½4·t½5·t½
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Not established for N-Acetyl Semax Amidate. Native Semax is extremely short-lived in plasma (order of minutes) due to rapid peptidase cleavage; the acetyl/amide modifications are claimed by vendors to extend this, but no published human PK data exist for the analog.
Pharmacology

Mechanism of action

Semax is a fragment analog of ACTH(4-10) reported to lack corticotropic (steroidogenic) activity while retaining neurotropic effects. Proposed mechanisms, derived from preclinical parent-Semax work, include: upregulation of brain-derived neurotrophic factor (BDNF) and its TrkB receptor and of nerve growth factor (NGF) signaling; modulation of expression of neurotrophins and their receptors in cortex and hippocampus following ischemia; antioxidant/anti-inflammatory effects with reduction of nitric-oxide overproduction in hypoperfused brain; and modulation of monoaminergic (dopamine/serotonin) systems. In one human stroke trial, Semax administration was associated with increased plasma BDNF levels. The N-acetylation and C-amidation of the analog are chemical modifications intended to increase proteolytic stability, but their effect on potency, receptor engagement, distribution and safety in humans is entirely uncharacterized. Overall the mechanism for the marketed analog is hypothetical/extrapolated, not demonstrated.
Kinetics

Pharmacokinetics

Half-life

Not established for N-Acetyl Semax Amidate. Native Semax is extremely short-lived in plasma (order of minutes) due to rapid peptidase cleavage; the acetyl/amide modifications are claimed by vendors to extend this, but no published human PK data exist for the analog.

Active duration

Unknown/unstudied for the analog. Central effects of parent Semax are described as lasting hours after a single intranasal dose in preclinical/clinical reports, but no validated PK/PD data support any specific duration for NASA.

Route

Marketed and used intranasally (nasal drops/spray); parenteral use also described for Semax in Russian clinical settings. Intranasal delivery is intended for partial nose-to-brain transport but bioavailability in humans is not quantified for the analog. Route framing here is for understanding exposure/washout only, not for evasion of any testing.

Metabolism & clearance

Presumed cleared by ubiquitous plasma and tissue peptidases into constituent amino acids/fragments (e.g., the C-terminal Pro-Gly-Pro tripeptide, which is itself bioactive in preclinical models); renal handling of fragments assumed. No human ADME study exists for NASA. Washout is likely rapid for parent Semax but is unconfirmed for the modified analog.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • No verified effects are documented for N-Acetyl Semax Amidate itself; the following are reported for parent Semax and are of low evidentiary quality.
  • In Russian clinical trials of acute ischemic stroke, Semax added to standard therapy was reported to accelerate regression of neurological deficit and improve motor recovery (small, non-double-blind studies).
  • In post-stroke rehabilitation, Semax was associated with increased plasma BDNF and improved Barthel index (functional independence) and motor performance.
  • In chronic cerebrovascular insufficiency, Semax was reported to stabilize disease course and reduce risk of stroke/transient ischemic attacks over follow-up.
  • Users anecdotally report increased alertness, focus, and mood/motivation ('nootropic' effects); these subjective effects are not supported by controlled human trials in healthy people and no PubMed-indexed study substantiates cognitive enhancement in healthy adults.
  • Preclinical models suggest neuroprotective, antioxidant and neurotrophic actions, but preclinical findings do not establish human benefit.
Safety

Adverse effects by system

Cardiovascular

No adequate human safety data for the analog. Parent Semax was described as well tolerated in cerebrovascular patients with a low rate of side effects; preclinical rat myocardial-infarction studies suggest a neutral-to-protective cardiac effect, but no controlled human cardiovascular safety data exist. Cardiovascular risk in healthy recreational users is unknown.

Hepatic

No hepatotoxicity signal has been reported, but hepatic safety has never been formally studied for Semax or the analog. Effectively no data.

Endocrine / HPTA

As an ACTH(4-10)-derived peptide, a theoretical concern for HPA-axis/steroidogenic or broader neuroendocrine modulation exists; Semax is reported to lack corticotropic activity, but this has not been rigorously characterized in humans and the acetylated/amidated analog is entirely unstudied. Direct HPTA (gonadal axis) effects are unstudied. Treat endocrine effects as unknown.

Reproductive

No data on fertility, pregnancy, or lactation for Semax or the analog. Must be assumed unsafe in pregnancy/breastfeeding due to absence of data.

Neuropsychiatric

No controlled data. Because Semax modulates BDNF and monoaminergic systems and users seek stimulant-like effects, theoretical risks include anxiety, agitation, insomnia, irritability or mood changes; these are anecdotal and not documented in PubMed-indexed trials.

Renal

No renal adverse-effect data. Peptide fragments are presumed renally handled; no human safety studies. Effectively no data.

Hematologic

No hematologic adverse-effect data. Effectively no data.

Dermatologic

Intranasal administration may cause local nasal mucosal irritation, burning, or dryness (a general property of nasal peptide preparations); not specifically quantified for NASA. No systemic dermatologic data.

Recovery

HPTA suppression & recovery

Suppression: No evidence of direct HPTA (gonadal axis) suppression, but genuinely unstudied. As an ACTH-fragment analog, neuroendocrine effects cannot be excluded a priori.

There is no human data on which to base any HPTA recovery guidance for this compound, and it is not an anabolic/androgenic agent or SERM, so post-cycle-therapy concepts do not straightforwardly apply. Anyone concerned about endocrine effects, or who experiences symptoms suggesting hormonal disturbance (libido changes, fatigue, mood changes), should stop use and consult an endocrinologist rather than self-manage. No SERM or hormonal 'recovery' protocol is indicated or endorsed here.

Bloodwork & vitals

Monitoring

Recommended labs & checks
No compound-specific monitoring is validated. General baseline and periodic bloodwork under a clinician is prudent for anyone using an unstudied peptide: complete blood count (CBC), comprehensive metabolic panel including liver enzymes (ALT/AST, bilirubin) and renal function (creatinine, eGFR).Consider baseline endocrine panel (morning cortisol, and a basic gonadal panel such as total testosterone/LH/FSH in men) given the ACTH-derived nature, to be interpreted by a physician/endocrinologist.Blood pressure and resting heart rate self-monitoring given stimulant-like anecdotal effects.

Cadence: Baseline before any use, then clinician-directed follow-up (e.g., at 8-12 weeks and if any symptoms arise). There is no evidence-based cadence for this compound; err toward physician oversight.

Warning signs — seek care
  • Severe or persistent headache, visual changes, focal weakness or numbness, or speech difficulty (seek emergency care; do not assume the peptide is protective).
  • Chest pain, palpitations, syncope, or markedly elevated blood pressure.
  • New or worsening anxiety, agitation, insomnia, panic, or mood disturbance.
  • Persistent nasal bleeding, pain, or infection at the administration site.
  • Signs of allergic reaction (rash, swelling, difficulty breathing) — stop immediately and seek care.
  • Any symptom of hormonal disturbance — stop and consult an endocrinologist.
Do not use if

Contraindications

  • Pregnancy and breastfeeding (no safety data).
  • Children and adolescents (no safety data outside specific Russian pediatric neurology use of parent Semax under medical supervision).
  • Known hypersensitivity/allergy to Semax or peptide components.
  • Active or unstable neuropsychiatric illness, uncontrolled anxiety, or seizure disorder (theoretical CNS-stimulating/neuromodulatory risk, unstudied).
  • Any acute neurological event (e.g., suspected stroke) must be managed by emergency medical services and a physician, not self-treated with a research peptide.
  • Use of unverified gray-market/research-chemical product of unknown purity, dose, or sterility is strongly discouraged.
Combinations

Interaction profile

  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • Recognize that N-Acetyl Semax Amidate itself has no published human safety or efficacy data; you are self-experimenting with an uncharacterized substance.
  • This is not a treatment for stroke or any neurological emergency. If you or someone else has stroke symptoms (face droop, arm weakness, speech difficulty), call emergency services immediately — do not use a peptide.
  • Do not use in pregnancy, breastfeeding, or in minors.
  • If you choose to use it, a clinician should be involved: get baseline bloodwork (CBC, liver and kidney function) and consider baseline endocrine labs, and re-check periodically.
  • Start only after discussing with a physician; never chase higher doses for stronger effects — there is no established safe or effective dose for this analog and this monograph does not endorse one.
  • Stop immediately and seek medical care for chest pain, severe headache, neurological changes, allergic reaction, severe anxiety/agitation, or persistent nasal injury.
  • Gray-market research peptides carry risks of mislabeling, contamination, and non-sterility; unverified injectables/nasal products can cause infection. Product identity and purity cannot be assumed.
  • Do not combine with other stimulants or investigational nootropics without clinician input, given unknown interactions.
  • Anyone worried about hormonal or mood effects should stop and consult an endocrinologist or physician rather than self-treating.
Evidence

Citations (7)

Every clinical claim above is tied to a primary source. Overall evidence grade D — this compound lacks adequate human data; claims rest on preclinical or mechanistic evidence.

  1. 01

    In post-ischemic-stroke patients, Semax added to rehabilitation increased plasma BDNF levels and was associated with faster functional recovery and improved motor performance and Barthel index.

    RCTPMID 29798983 ↗

  2. 02

    In the acute period of hemispheric ischemic stroke, Semax (synthetic ACTH(4-10) derivative) included in intensive therapy increased regression of general cerebral and focal, especially motor, neurological deficits; reported daily doses were 12 mg (moderate strokes) and 18 mg (severe strokes) over 5-10 day courses.

    RCT[The efficacy of semax in the treatment of patients at different stages of ischemic stroke]DOI 10.17116/jnevro20181183261-68 ↗

  3. 03

    In patients with chronic cerebrovascular insufficiency, Semax was reported to stabilize disease progression and reduce risk of stroke/transient ischemic attacks, with a low percentage of side effects and good tolerability including in older patients.

    CohortPMID 15792140 ↗

  4. 04

    Acute ischemic stroke clinical/electrophysiological study establishing Semax dosing (12-18 mg/day) and neurological outcomes versus conventional therapy.

    RCT[Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)]PMID 11517472 ↗

  5. 05

    Semax and its C-terminal Pro-Gly-Pro tripeptide modulate expression of neurotrophins (BDNF, NGF, NT-3) and their Trk/p75 receptors in rat cortex and hippocampus after cerebral ischemia, a proposed neuroprotective mechanism.

    Preclinical[The effect of semax and its C-end peptide PGP on expression of the neurotrophins and their receptors in the rat brain during incomplete global ischemia]PMID 22295573 ↗

  6. 06

    In rat myocardial infarction models, Semax did not impair cardiac function and partially prevented adverse ventricular remodeling / ischemia-induced cardiomyocyte ultrastructural changes, suggesting a neutral-to-protective cardiac effect (preclinical only).

    PreclinicalPMID 17385423 ↗

  7. 07

    Preclinical rat data that Semax prevented ischemia-induced cardiomyocyte ultrastructural changes in acute myocardial infarction and blunted nitrate elevation, without altering cardiac function.

    Preclinical[Protective effect of peptide semax the rat heart in acute myocardial infarction]PMID 16967870 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice