Semax — ACTH-Derived Nootropic & Neuroprotective Research Heptapeptide | Klene Peptides
For Research Use Only | Not for Human or Veterinary Administration
Semax is a synthetic heptapeptide derived from the 4–10 amino acid fragment of adrenocorticotropic hormone (ACTH): Met-Glu-His-Phe-Pro-Gly-Pro. Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences and registered as a pharmaceutical in Russia for ischemic stroke, optic nerve damage, and cognitive disorders, Semax retains the cognitive-enhancing and neuroprotective properties attributed to ACTH(4-10) while eliminating the HPA axis steroidogenic activity of the full ACTH sequence. Its most significant research mechanisms — robust and sustained upregulation of BDNF and NGF, dopaminergic modulation, melanocortin receptor interaction, and vascular neuroprotection — have positioned it as one of the most studied CNS research peptides in cognitive enhancement, ischemic neuroprotection, and neurological recovery. Klene Peptides supplies Semax to USA research institutions with verified purity and same-day fulfillment.
Every vial from Klene Peptides includes:
- ≥99%+ purity — verified by HPLC (High-Performance Liquid Chromatography)
- HPLC-MS (High-Performance Liquid Chromatography - Mass Spectrometry)
- Same-day shipping for all USA orders
Chemical Identity & Structural Profile
| Parameter | Value |
|---|---|
Full Name | Semax |
Sequence | Met-Glu-His-Phe-Pro-Gly-Pro |
Parent Molecule | ACTH(4-10) fragment |
Molecular Formula | C₃₇H₅₁N₉O₁₀S |
Molecular Weight | ~813.9 g/mol |
CAS Number | 80714-61-0 |
Origin | Institute of Molecular Genetics, Russian Academy of Sciences |
Registration | Approved pharmaceutical in Russia (stroke, optic nerve disease, cognitive disorders) |
Appearance | White lyophilized powder |
Solubility | Water, 0.9% saline |
Storage | Lyophilized: −20°C; Reconstituted: 4°C, use within 14 days |
Primary Research Delivery | Intranasal, SC, IP |
Mechanism of Action
Primary Neurochemical Mechanisms
| Mechanism | Target | Research Implication |
|---|---|---|
BDNF upregulation | Hippocampus, cortex, striatum | Neuroplasticity, learning/memory, neuroprotection |
NGF upregulation | Basal forebrain, peripheral nervous system | Cholinergic neuron support; neurodegenerative models |
Melanocortin receptor agonism (MC4R, MC5R) | CNS-expressed MCRs | Cognitive, motivational, and behavioral modulation |
Dopamine release enhancement | Prefrontal cortex, striatum | Attention, motivation, executive function research |
Serotonergic modulation | Raphe nuclei projection targets | Mood and anxiety research |
VEGF upregulation | CNS vasculature | Neuroprotective angiogenesis in ischemia models |
Oxidative stress reduction | Mitochondrial ROS; catalase/SOD upregulation | Neuronal survival under metabolic stress |
NO regulation | eNOS; cerebrovascular tone | Cerebral blood flow and ischemia protection research |
Key Distinction from Full ACTH
| Parameter | ACTH (full 39aa) | Semax (ACTH 4-10 derived) |
|---|---|---|
Cortisol elevation | Major effect | None — complete HPA axis neutrality |
Nootropic activity | Present in 4-10 fragment | Retained and enhanced |
Neuroprotective activity | Partial | Significantly enhanced |
Adrenocortical activation | Yes | No |
Dependence risk | HPA suppression risk | None observed in research |
Pharmacokinetic & ADME Profile
| Parameter | Value | Notes |
|---|---|---|
Molecular Weight | ~813.9 g/mol | CNS penetration confirmed |
BBB Penetration | Yes (demonstrated) | BDNF elevation in brain confirms active CNS penetration |
Routes (Research) | SC, IP, intranasal | Intranasal enables direct olfactory-to-CNS delivery |
Plasma Half-Life | ~5–7 minutes | Rapid plasma clearance; CNS effects persist via BDNF expression |
Bioavailability (intranasal) | Moderate | Olfactory pathway to CNS; olfactory nerve transport |
Metabolism | Endopeptidase, aminopeptidase | Pro-Gly-Pro C-terminal resists carboxypeptidase degradation |
Excretion | Renal | Metabolite clearance |
Research Applications
Ischemic Stroke & Cerebrovascular Research
Semax has been studied most extensively in stroke and ischemia, where it is approved in Russia:
| Model / Parameter | Observed Effect |
|---|---|
MCAO rodent model (ischemia-reperfusion) | Reduced infarct volume; improved neurological deficit scoring |
BDNF elevation post-ischemia | 2–7× increase in peri-infarct penumbra zone |
Inflammatory cytokine reduction | IL-1β, TNF-α suppression post-ischemia |
Cerebral blood flow | VEGF-mediated microvascular improvement |
Neurological deficit scores | Statistically significant improvement vs. vehicle |
Cognitive Enhancement & Nootropic Research
| Parameter | Research Finding |
|---|---|
Spatial learning (Morris water maze) | Significant improvement in latency to platform |
Passive avoidance retention | Enhanced memory consolidation parameters |
Attention and working memory | Improvement in human cognitive battery assessments (Russian clinical data) |
BDNF/NGF sustained elevation | 24+ hours post-administration; neuroplasticity basis |
Neuroprotection & Neurodegeneration Research
| Disease Model | Research Application |
|---|---|
Alzheimer’s-like models | NGF support for cholinergic neurons; BDNF-driven neuroplasticity |
Parkinson’s-like models | Dopaminergic protection; oxidative stress reduction |
Optic nerve damage | Registered therapeutic use in Russia; retinal ganglion cell protection |
Traumatic brain injury | Reduced secondary neuronal death in preclinical models |
ADHD & Attention Research
- Dopaminergic enhancement in prefrontal cortex pathways
- Attention and impulse control improvement in hyperkinetic behavioral models
- Complementary dopaminergic mechanism to catecholamine-based pharmacological paradigms
Research Dosing Reference
For scientific reference only — not prescriptive recommendations
| Research Model | Reported Dose | Route | Duration |
|---|---|---|---|
Ischemia/stroke (rodent) | 50–250 mcg/kg | SC, IP, intranasal | 3–14 days post-event |
Cognitive enhancement | 50–100 mcg/kg | SC, intranasal | 5–14 days |
Neuroprotection | 100–250 mcg/kg | SC, IP | Acute/subacute |
In vitro assays | 0.01–10 µM | Cell culture media | Per experiment |
Clinical reference (intranasal) | 200–600 mcg (flat dose) | Intranasal | Per approved protocol |
Data from Russian clinical trial publications and PMC-indexed preclinical research.
Reconstitution Reference
| Lyophilized Amount | Sterile/Bacteriostatic Water | Concentration |
|---|---|---|
5 mg | 2.5 mL | 2.0 mg/mL |
10 mg | 5.0 mL | 2.0 mg/mL |
Klene Peptides Quality Standards
Certificate of Analysis — Standard Parameters
Every batch supplied by Klene Peptides is verified against the following analytical benchmarks:
| Test | Specification | Method |
|---|---|---|
Purity | ≥99% | HPLC (High-Performance Liquid Chromatography) |
Molecular Identification | Confirmed | HPLC-MS (High-Performance Liquid Chromatography – Mass Spectrometry) |
Water Content | <1.5% | — |
What Every Klene Peptides Order Includes
- Lot-specific Certificate of Analysis traceable to synthesis batch
- Verified cold-chain shipping — all orders dispatched with appropriate cold-pack packaging
- Same-day fulfillment — orders placed before cutoff ship the same business day
Ordering Semax for Your Research Program
Important Research Compliance Notice
Scientific References
- Myasoedov NF, et al. "Semax: a nootropic peptide drug." Eksp Klin Farmakol. 1999;62(5):74-78.
- Dolotov OV, et al. "Semax, an analogue of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus." Brain Res. 2006;1117(1):54-60.
- Grivennikov IA, et al. "Semax: neurotrophic and anti-ischemic brain protection effects." Mol Biol. 2008.
- Kolomin T, et al. "Semax regulates gene expression in the hippocampus and frontal cortex." PLoS One. 2013.
- Shram NF, et al. "Neuroprotection by Semax in transient focal cerebral ischemia." Ross Fiziol Zh Im I M Sechenova. 2007.
- Agapova TY, et al. "Semax effect on BDNF and NGF expression in rat brain." Dokl Biol Sci. 2007.
- PubChem. Semax. CID: 122070. https://pubchem.ncbi.nlm.nih.gov