top of page

Synthetic ACTH-Derived Neuroactive Heptapeptide

Semax

Semax is a neuroactive heptapeptide documented within Alford Molecular Research's Research Compound Library. As a research-only molecule, it is studied for its chemical characteristics and molecular signaling properties in nonclinical experimental models.

Chemical Class

Synthetic ACTH-derived heptapeptide

Evidence Classification

Preliminary

Primary Research Domain

Neuroactive Peptides

Primary Research Areas

neurotrophic signaling; cognitive biology; neuroplasticity; melanocortin-related mechanisms; stress-response models

Molecular Data Card
Compound

Semax

Aliases / Synonyms

ACTH(4-7) analogue

Chemical Class

Synthetic ACTH-derived heptapeptide

CAS Number

80714-61-0

PubChem CID

9811102

Molecular Formula

C37H51N9O10S

Avg Molecular Weight

813.92 g/mol

Sequence

Met-Glu-His-Phe-Pro-Gly-Pro

N-Terminal State

Free amino terminus

C-Terminal State

Free carboxyl terminus

Molecular Identity

The chemical identity of Semax is defined by its heptapeptide sequence: Met-Glu-His-Phe-Pro-Gly-Pro. This sequence identifies Semax as a synthetic analogue derived from the adrenocorticotropic hormone fragment ACTH(4-7), featuring a specific Pro-Gly-Pro tripeptide extension that distinguishes it from naturally occurring ACTH metabolites. Within analytical research, the presence of methionine at the N-terminus is of critical importance, as methionine can undergo oxidative modification under various experimental and storage conditions. Consequently, precise characterization of the peptide's oxidative state is required to confirm structural integrity in synthesis and research applications. Semax serves primarily as a neuroactive research tool for examining ACTH-derived peptide signaling within experimental biological systems.

Research Model

The research model for Semax involves melanocortin-derived peptide biology, neurotrophic signaling, and transcriptional and signaling changes reported in experimental systems. Investigation focuses on neuroplasticity-associated mechanisms and experimental findings from preclinical systems. Where a direct receptor mechanism is uncertain, it is explicitly noted as a subject for further research. These findings describe experimental outcomes in research models and are distinguished from established human clinical outcomes.

Intracellular Signaling

Experimental studies have examined downstream changes in neurotrophic and cellular signaling pathways associated with Semax exposure. Research focuses on intracellular signaling modulations observed within defined experimental frameworks, without establishing specific receptor affinities or constant interaction parameters.

Research & Study Data

Summarized preclinical models and cellular systems investigate Semax within neurotrophic, neuroplasticity, stress-response, and ischemia-related experimental frameworks. This information is provided for scientific research context and does not imply clinical outcomes.

Neurotrophic Signaling

Experimental investigation of pathways associated with neuronal growth, survival, and adaptive signaling.

Neuroplasticity

Research examining cellular and molecular processes associated with synaptic and neuronal adaptation.

Cognitive Biology

Experimental work involving memory, learning, attention, and related neurobiological processes.

Stress-Response Biology

Research examining neuroendocrine and cellular responses to physiological or experimental stress.

Ischemia-Related Models

Preclinical and translational research examining biological responses in ischemia-associated experimental systems.

Peptide Neurobiology

Research involving ACTH-derived peptide fragments and related signaling systems.

Semax → Peptide/Neurotrophic Signaling → Intracellular Signaling Changes → Neuronal Cellular Effects → Neural-Tissue Response → Functional Biomarkers → Cognitive/Neurological Outcomes

Each step requires independent evidence. Molecular or cellular changes do not by themselves establish meaningful human neurological outcomes.

Evidence Assessment

Evidence Classification: Preliminary

The evidence base for Semax includes both preclinical and human research; however, the strength of evidence varies substantially by specific endpoint. Route, formulation, study design, population, and outcome measures materially affect interpretation. Findings from one delivery route should not automatically be extrapolated to another, and mechanistic or preclinical findings should not be represented as established clinical benefit.

Analytical Considerations
Methionine Oxidation Control

Semax contains methionine and may be susceptible to oxidative modification during synthesis, purification, storage, and handling. Analytical characterization should distinguish intact peptide from oxidized species where relevant. Chromatographic purity, net peptide content, and oxidation state are analytically distinct quality attributes.

Example Analytical Documentation
  • Identity by MS
  • RP-HPLC or UPLC purity
  • Quantitative net peptide content
  • Exact sequence confirmation
  • N-terminal and C-terminal state
  • Counterion / salt state
  • Residual solvents
  • Water content
  • Oxidation products
  • Degradation products
  • Endotoxin where relevant
  • Sterility where relevant

Alford Molecular Research has reviewed third-party analytical documentation for Semax research material including molecular identity, quantitative content, purity, and endotoxin testing. Analytical results are lot-specific and should not be generalized to other batches.

Stability & Handling

Research-material stability is contingent upon moisture control, light exclusion, temperature maintenance, and container integrity. Repeated freeze-thaw cycles and oxidation exposure should be minimized in experimental protocols.

Research / Regulatory Context

Semax has been studied in neuroactive and neuroprotective research contexts, including clinical and translational literature outside the United States; the existence of human research does not establish that every proposed neurological, cognitive, or wellness application is clinically proven; regulatory and clinical status vary by jurisdiction and indication; and Alford Molecular Research evaluates the evidence independently from commercial marketing claims.

RESEARCH-ONLY NOTICE: This information is for scientific and research context only and not for treatment, diagnosis, or human use. Alford Molecular Research provides nonclinical documentation and evidence-level classification for compounds studied for potential biological relevance to human physiology.

bottom of page