Semax 30mg

Sequence: Met-Glu-His-Phe-Pro-Gly-Pro
Molecular Formula: C37H51N9O10S
Molecular Weight: 813.92 g/mol
CAS Number: 80714-61-0
Synonyms: Pro-Gly-Pro-ACTH

Semax is a synthetic analogue of an ACTH fragment, corresponding to amino acids 4–10 of ACTH with a C-terminal Pro-Gly-Pro motif. In laboratory research, Semax is used in preclinical models to probe pathway-level regulation of:

• Neurotrophin-linked transcription: experimental readouts involving BDNF and NGF gene-expression dynamics in CNS-relevant regions.
• Systems-level brain network activity: research imaging endpoints assessing resting-state network behavior and connectivity patterns.
• Neurovascular and immune-associated gene programs: genome-wide transcriptional profiling in animal models with emphasis on vascular-system and immune-system gene sets in brain tissue.
• Learning/memory model endpoints: mechanistic comparisons using ACTH-related peptides in rodent genetic models with cognition-focused behavioral readouts .
• Monoaminergic signaling markers: studies of serotonergic pathway measures and neurotrophin-dependent behavioral paradigms in rodents.
• Oxidative stress biomarker panels: liver-associated morphofunctional and lipid peroxidation endpoints under stress-model conditions.

Pathway / Mechanistic Context

Across cited preclinical literature, Semax is evaluated as a modulator of gene-expression programs and systems-level neural network activity. Reported endpoints include transcriptomic changes in CNS tissue, neurotrophin-associated transcriptional dynamics, and network-level activity patterns measured by experimental neuroimaging approaches. In addition, publications describe Semax-associated shifts in peripheral oxidative stress biomarker panels and hepatic tissue readouts under stress-model conditions.

1. Resting-State Network Readouts

Experimental imaging work reports changes in resting-state network behavior after Semax exposure, including measured effects on the default mode network as defined within that study’s analytic framework [1]. Background literature on default mode and social-cognition network relationships is commonly used to interpret these kinds of resting-state measures in neuroscience research .

Image showing the overlap of activation between the resting mode network and parts of the brain responsible social cognition.
Source: PubMed

2. Genome-Wide Transcriptional Profiling in a Rodent Ischemia Model

In a rat model of focal brain ischemia, genome-wide transcriptional analysis reported Semax-associated changes in expression across immune- and vascular-system related gene sets in brain tissue, providing a molecular context for mechanistic investigation of neurovascular and inflammatory pathway regulation in this model [3].

3. Neurotrophin-Related Gene Expression Dynamics

Rodent studies report that Semax exposure is associated with time-dependent gene expression changes in the hippocampus and frontal cortex, including reported effects on BDNF and NGF gene-expression measures within the study design [5].

4. ACTH-Related Peptides in a Genetic Epilepsy Model

Preclinical work in a Kcna1-null mouse model reports that ACTH exposure is associated with preservation of learning and memory readouts in the experimental paradigm, providing comparative context for research on ACTH-derived peptide fragments such as Semax.

5. Serotonergic and Neurotrophin-Linked Behavioral Paradigms

Rodent studies evaluating altered hippocampal BDNF levels report behavioral and serotonergic consequences in experimental models, supporting broader mechanistic frameworks that connect neurotrophin abundance, serotonergic pathway markers, and behavioral outputs in preclinical research.

6. Peripheral Oxidative Stress and Hepatic Biomarker Readouts

Additional cited studies describe Semax-associated effects on hepatic morphofunctional endpoints and lipid peroxidation markers in rat stress-model conditions, including biochemical measures relevant to oxidative stress research workflows.