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SEMAX

Research peptides

SEMAX

Available documentary data and items still to verify are detailed below.

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02 — Information to verify

Product details

Overview

Semax is a synthetic heptapeptide with sequence Met-Glu-His-Phe-Pro-Gly-Pro. Its structure is described as the ACTH(4–7) fragment followed by Pro-Gly-Pro; it is not full-length ACTH.

Structure and technical data

Technical data

Format: 10 mg. Sequence: MEHFPGP. PubChem CID 9811102 lists formula C37H51N9O10S and mass 813.9 g/mol. The reference describes non-acetylated Semax without assigning modified variants.

SEMAX: 2D molecular structure
2D molecular structure — PubChem. PubChem CID 9811102
Sequence
MEHFPGP
Molecular formula
C37H51N9O10S
Reported molecular mass
813.9 g/mol
CAS number
80714-61-0
PubChem CID
9811102
Reported synonyms
Semax; ACTH(4–7)-Pro-Gly-Pro

Reference molecular data.

View the PubChem record — PubChem CID 9811102

Research context

The cited papers analyse immune-response gene expression and protein profiles in rat models of cerebral ischaemia.

From ACTH to the MEHFPGP peptide

Met-Glu-His-Phe corresponds to ACTH(4–7), followed by Pro-Gly-Pro. This construction distinguishes Semax from full ACTH and analogues with acetylation or terminal changes. The nootropic designation describes a research area, not proven cognitive improvement from every material bearing the name.

10.1007/s00438-017-1297-1

Cerebral ischaemia: transcripts and proteins

Rat models compare immune-gene expression, proinflammatory transcripts, and protein profiles after ischaemia and reperfusion. Transcriptomics and proteomics observe different response levels. Agreement between some signals supports mechanistic hypotheses without turning the model into clinical evidence for the product.

10.1007/s00438-017-1297-1 10.1134/S0026893321010040 10.3390/ijms22126179

Immune pathways and tissue-stress responses

Research analyses inflammatory mediators and cellular programmes activated after brain injury. Changes in immunoglobulin-related or immune-cell pathways are molecular model readouts. They do not demonstrate general immune enhancement or independently establish which cells generate each signal.

10.1007/s00438-017-1297-1

Seizure models and oxidative markers

The bibliography includes a conference paper on rat malondialdehyde and protein profiles and a study of audiogenic-seizure susceptibility across mouse strains. Observed effects depend on strain and exposure timing. These models do not establish clinical efficacy in human epilepsy.

10.2991/icoh-17.2018.59 10.1007/s10517-008-0212-5

Brain networks and functional imaging

The default-mode-network paper uses resting-state functional imaging in a small healthy-volunteer sample. It reports a difference in the rostral network component versus control. A change in connectivity or functional volume is not itself a measurement of memory, attention, or cognitive performance.

10.1007/s10517-018-4234-3

Acute stress, behaviour, and early-life models

Other papers examine acute rat stress and consequences of early-life drug exposure. Neurochemical markers, pain sensitivity, and behaviour are separate outcomes. Findings in one model do not establish treatment of depression or anxiety, and absence of a behavioural effect should not be rewritten as improvement.

10.1016/j.npep.2020.102114 10.1134/S0022093023010179

References

Catalog of products presented for research activities. Not for human or veterinary use. This notice does not replace verification of applicable rules.