Independent · non-commercial · publishes on a quarterly cycle|Current cycle 2026 Q3
Compound Evidence InstituteEvidence synthesis · established 2023Graded assessments of compounds, trials, methods and supply
Document set current to 30 July 2026
Compound monograph · §2

Semax — pharmacology

Molecular targets, mechanism of action, pharmacokinetics and interactions as characterised in humans.

Document identifier
CEI-MN-036/2
Series
Compound monograph
Version
1.0
Published
19 Apr 2026
Last reviewed
19 Apr 2026
Next review
19 Apr 2028
Identifier
10.71829/cei.mono.36
Certainty
Low
Cycle
2026 Q2

§2Pharmacology

§2.1Molecular targets

Table 2. Molecular targets recorded for Semax, with the character of the interaction and the potency where the Institute holds it.

TargetInteractionNote
Mechanism partially characterisedMelanocortin-independentReported effects on brain-derived neurotrophic factor and nerve growth factor expression, and on dopaminergic and serotonergic transmission. No primary receptor has been identified

§2.2Mechanism of action

Semax is reported to increase expression of brain-derived neurotrophic factor and its receptor TrkB in rodent hippocampus, and to modulate monoaminergic transmission. Its approved Russian indications are ischaemic stroke and cognitive disorders. The Institute assesses the underlying evidence as predominantly published in Russian-language journals with methodology and reporting that do not permit the risk-of-bias assessment its framework requires, and grades accordingly — this is a statement about assessability, not an assertion that the compound is ineffective.[1,2]

§2.3Pharmacokinetics

Terminal half-life
reported as under 30 min in plasma after intranasal administration
Time to maximum concentration
rapid
Volume of distribution
not published
Plasma protein binding
not published
Clearance
not published
Bioavailability
intranasal administration is used on the premise of direct nose-to-brain transport; the extent of that transport in humans is not established

Peptidase degradation. The Pro-Gly-Pro extension slows but does not prevent it.

Reconstructed plasma concentration–time profilePlasma concentration plotted against time after dosing, reconstructed from published pharmacokinetic parameters.0.00.20.40.60.801122Time after first dose (hours)Relative concentrationt max ≈ 0 ht½ ≈ 1 h
Modelled profileSimulated observationsDose administration
Figure 2. Illustrative. Plasma concentration–time profile reconstructed by the Institute from the published half-life and time-to-maximum-concentration parameters using a one-compartment model with first-order absorption. The curve is not digitised from a published figure and its vertical scale is relative. It is published to convey the shape of the profile and the approach to steady state, not to supply a concentration at any time point.

§2.4Interactions

  • Not characterised

References cited on this page

References are numbered in order of first citation in this document. Each superscript in the text links to its entry below.

  1. D’Hondt M, Bracke N, Taevernier L, Gevaert B, Verbeke F, Wynendaele E, De Spiegeleer B. Related impurities in peptide medicines. Journal of Pharmaceutical and Biomedical Analysis 2014;101:2–30. doi:10.1016/j.jpba.2014.06.012 · PMID 25044089
  2. Manning MC, Chou DK, Murphy BM, Payne RW, Katayama DS. Stability of protein pharmaceuticals: an update. Pharmaceutical Research 2010;27(4):544–575. doi:10.1007/s11095-009-0045-6 · PMID 20143256

Identifiers are reproduced only where the Institute holds them. Where a digital object identifier or PubMed identifier is not shown, the Institute has recorded the journal and year and has not constructed an identifier.

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