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Semax | CAS: 80714-61-0

CAS Number:
80714-61-0
Chemical Classification:
Research peptide

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Semax (CAS 80714-61-0) is a synthetic ACTH(4-10) analogue investigated for neuroprotective and nootropic mechanism research, particularly where BDNF upregulation and dopaminergic signaling are hypothesized mediators. Stroke, hypoxia, and toxin-challenge models each impose different temporal windows for peptide administration, which strongly influences observed neurochemical outcomes. Common experimental routes include intranasal dosing before middle-cerebral-artery occlusion, primary cortical neuron survival assays after glutamate excitotoxicity, and open-field locomotion paired with striatal neurotransmitter analysis. Supplied at research grade with COA, LC-MS, HPLC, and NMR data—not for cognitive enhancement outside controlled studies.

CAS
80714-61-0
Molecular Formula
C37H51N9O10
Molecular Weight
813.9 g/mol
Purity
≥98%
Appearance
White lyophilized powder
Storage
Store at -20°C

Analytical Documentation

COA✓ Available
LC-MS✓ Available
HPLC✓ Available
NMR✓ Available

Research Inquiry

Overview

Semax is a synthetic heptapeptide analog of adrenocorticotropic hormone fragment ACTH(4-10), sequence Met-Glu-His-Phe-Pro-Gly-Pro, developed for neuroprotective mechanism research in academic neuroscience programs. Unlike full ACTH, semax lacks melanocortin receptor agonism at pharmacologically relevant research doses while retaining neurotrophic and nootropic phenotypes in rodent learning models. The Pro-Gly-Pro extension enhances stability and facilitates nasal delivery research in animal studies. Semax serves as a tool peptide for investigating BDNF upregulation, dopamine metabolism, and ischemic stroke recovery endpoints in controlled preclinical experiments without pituitary adrenal axis stimulation typical of native ACTH. Supplied at ≥98% purity (C37H51N9O10; 813.9 g/mol), this material supports controlled laboratory investigation under research-use-only conditions.

Mechanism of Action

Semax increases BDNF and NGF expression in hippocampus and cortex in rodent research following intranasal or systemic administration routes approved in animal protocols. Tyrosine hydroxylase activity and dopamine turnover modulate in striatal tissue extracts, linking semax to catecholamine pathway research. Semax reduces infarct volume in middle cerebral artery occlusion models through anti-apoptotic and angiogenic mechanisms studied histologically. The peptide does not elevate corticosterone at standard research doses unlike ACTH(1-39). Gene expression profiling reveals neuroplasticity and antioxidant pathway induction in brain tissue.

Receptor Binding & Signaling

Semax shows minimal melanocortin MC1-MC5 receptor activation compared with ACTH in cAMP assays at equivalent research concentrations. Mechanism is predominantly neurotrophic gene regulation rather than classical MC receptor agonism. No significant benzodiazepine or NMDA receptor direct binding in standard panels.

Research Applications

Learning and memory behavioral research

Morris water maze, passive avoidance, and novel object recognition tests in rodents quantify semax effects on acquisition and retention with appropriate blinding and counterbalancing. Dose-response curves establish research-effective ranges. Studies contribute to cognitive enhancement neuroscience without human nootropic claims.

Stroke and ischemia neuroprotection models

Transient MCAO and photothrombotic stroke models administer semax per research protocols measuring infarct volume, neurological scores, and BDNF immunostaining. Time-window experiments test administration delays post-occlusion. Research focuses on stroke pathology biochemistry in animals.

Neurotrophin signaling biochemistry

Primary cortical neuron cultures and organotypic slices expose tissue to semax to measure BDNF secretion, TrkB phosphorylation, and CREB activation. TrkB antagonists confirm pathway dependency. Platforms support neurotrophin pharmacology research.

Optic nerve and retinal injury research

Semax originates from ophthalmic research contexts; rodent optic nerve crush models use peptide to quantify retinal ganglion cell survival and axonal regeneration markers histologically. Electroretinography provides functional readouts in specialized neuroscience laboratories.

Molecular Information

Sequence & Chain Summary

Met-Glu-His-Phe-Pro-Gly-Pro (ACTH(4-10)-Pro-Gly-Pro).

Modification Type

Pro-Gly-Pro C-terminal extension for stability.

Structural Notes

Semax is 813.9 g/mol with N-terminal methionine susceptible to oxidation forming sulfoxide impurities detectable by HPLC. SPPS and preparative chromatography yield ≥98% purity material. Intranasal delivery research requires sterile aqueous formulation preparation fresh before animal dosing. Batch-specific molecular characterization—including mass confirmation and purity profiling—is available through COA, LC-MS, HPLC, and NMR documentation supplied with Semax.

Molecular Formula
C37H51N9O10
Molecular Weight
813.9 g/mol
Purity Specification
≥98%

Experimental Notes

Stability

Lyophilized semax at −20°C resists long-term degradation when desiccated. Oxidized methionine reduces neurotrophic activity in some assays; minimize light and ambient exposure after reconstitution. Aliquot frozen stocks for multi-day study consistency. Lyophilized Semax should be protected from repeated freeze-thaw cycles, moisture, and prolonged exposure to ambient light where applicable. Analytical integrity is best preserved when material is stored under the conditions specified on the certificate of analysis.

Storage Conditions

Store at -20°C. Semax is supplied as white lyophilized powder. For long-term archival storage in research inventories, maintain sealed containers with desiccant where recommended and document lot numbers for traceability across experimental runs.

Laboratory Handling

Reconstitute in sterile saline for approved research routes. Avoid oxidizing conditions during preparation. Verify peptide integrity by HPLC if behavioral results diverge across batches. Reconstitute only with appropriate research-grade solvents compatible with your assay format. Allow vials to reach equilibrium before opening, work under clean bench conditions, and label all working solutions with concentration, date, and researcher ID per institutional SOPs.

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Frequently Asked Questions

Research-focused answers about Semax. For laboratory use only — not medical advice.

What is Semax used for in research?
Semax is for neuroprotective mechanism and cognitive neuroscience research in animal and cell models. Not for human cognitive enhancement, clinical stroke treatment, or ophthalmic therapy.
How does Semax work biologically?
Semax upregulates BDNF and modulates dopamine metabolism in brain research models, producing neuroprotective and learning-associated phenotypes without ACTH-level melanocortin or cortisol stimulation at standard research doses.
What receptors does Semax interact with?
Minimal melanocortin receptor agonism relative to ACTH; primary effects driven by neurotrophin and catecholamine pathway modulation. No established single dominant GPCR target.
Is Semax stable at room temperature?
Lyophilized semax at −20°C resists long-term degradation when desiccated. Oxidized methionine reduces neurotrophic activity in some assays; minimize light and ambient exposure after reconstitution. Aliquot frozen stocks for multi-day study consistency. For short-term laboratory workflows, minimize time at room temperature and return unused material to recommended storage promptly. Semax is not formulated for ambient long-term storage.
What is the recommended storage condition for Semax?
Store at -20°C. Store lyophilized material in a dedicated −20°C freezer, protect from moisture ingress, and avoid repeated temperature cycling. Reconstituted solutions should be aliquoted and frozen if not used within the validated window of your internal stability study.