Semax
10mg
A synthetic peptide that mimics a natural brain hormone fragment, studied for its ability to boost BDNF — the brain's primary growth and repair protein. Research models have examined its potential role in focus, memory, neuroprotection, and mood, making it one of the most studied cognitive peptides in preclinical literature.
Transparency
Certificate of Analysis
Every batch independently verified by third-party laboratories.
Batch #TL-1902514-P
Semax Lab Certificates
All Trident Labs products are independently tested by accredited third-party laboratories. Results are batch-specific and provided for research transparency only. This product is not approved for human use.
The brain's own growth signal. In vitro research.
A synthetic peptide modelled on a fragment of ACTH — a hormone your brain already produces. Research has examined how Semax interacts with BDNF, the brain's primary growth and repair signal, as well as the dopamine and serotonin systems involved in focus, mood, and cognitive function.
Dolotov et al. Brain Res 2006 · Inozemtseva et al. Eur J Pharmacol 2024. All data from peer-reviewed literature. For Research Use Only — Not for Human Consumption.
Manufactured in US
US-formulated & filled
Endotoxin Tested
<0.05 EU/mL verified
Independently Tested
Horizon Analytical · 6-panel COA
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Semax is supplied exclusively for qualified in vitro laboratory research. Not for human administration.
This product is a research-grade synthetic heptapeptide supplied under research use only (RUO) designation. While Semax is approved as a pharmaceutical in Russia for ischemic stroke and cognitive disorders, it is not approved by the FDA for any indication in the United States. By purchasing, the buyer represents they are a qualified researcher using this compound solely for lawful in vitro laboratory research. Not a dietary supplement, food, drug, or medical device under US regulations. For Research Use Only — Not for Human Consumption.
Mechanism of Action
ACTH fragment.
Four active pathways.
Semax (MEHFPGP) is a synthetic heptapeptide built from the ACTH(4–10) fragment — the stretch of adrenocorticotropic hormone responsible for its CNS activity — with a C-terminal Pro-Gly-Pro (PGP) extension that confers metabolic stability and contributes independent pharmacological activity. Four well-characterized signaling arms have been documented in preclinical research.
BDNF & TrkB Upregulation — Hippocampal Neuroplasticity
A single intranasal dose of Semax (50 µg/kg) produced a 1.4-fold increase in BDNF protein, 1.6-fold increase in TrkB phosphorylation, and 3-fold increase in BDNF mRNA in rat hippocampus (Dolotov et al. 2006). BDNF/TrkB signaling underpins synaptic plasticity, long-term potentiation, and neuroprotection — the mechanistic basis for observed cognitive effects in learning paradigms.
Dopaminergic & Serotonergic System Activation
Semax rapidly activates both serotonergic and dopaminergic brain systems — measurable effects on monoamine metabolites in cortex and hippocampus documented in preclinical models. These pathways are implicated in the antidepressant-like and antistress effects observed in forced swim test and tail suspension test paradigms. Inozemtseva et al. (2024) characterized both Semax and its PGP fragment in chronic unpredictable stress models.
Prot
Stroke Model Neuroprotection — Transcriptome-Wide Effects
In transient middle cerebral artery occlusion (tMCAO) models, Semax suppresses inflammatory gene expression, prevents downregulation of neurotransmitter genes, and activates neurotrophin transcription (BDNF, NGF, TrkB). RNA-Seq analysis identified hundreds of differentially expressed genes modulated by Semax in ischemic tissue — including MMP-9 suppression, CREB activation, and JNK pathway modulation.
PGP Tail — Independent Neurotrophin Activation
The C-terminal Pro-Gly-Pro tripeptide is not merely a stability extension. PMC11498467 demonstrated PGP alone activates neurotrophin transcription (BDNF, NGF, TrkB, TrkC) in ischemic cortex — with some effects exceeding Semax itself for TrkB and TrkA receptor expression. PGP also produced antidepressant-like and antistress effects in behavioral models (Inozemtseva et al. 2024), confirming it as a pharmacologically active component.
Sequence & Structure
MEHFPGP.
Seven residues.
The four N-terminal residues (MEHF) encode the ACTH(4–10) nootropic activity. The C-terminal Pro-Gly-Pro tripeptide — the same stability extension shared with Selank — confers enzymatic resistance and contributes independent neuroprotective activity.
Primary Sequence — 7 Residues
Dolotov et al. Brain Res 2006 · Wikipedia / RU pharmacopoeia. Research use only.
Molecular Identity
7 AA
MEHFPGP sequence
887 Da
MW — C₃₈H₅₃N₉O₁₀S
ACTH
4–10 fragment analogue
1996
Russian approval
Full Sequence
Met-Glu-His-Phe-Pro-Gly-Pro
ACTH(4–10) + PGP stability extension
Institute of Molecular Genetics, Russian Academy of Sciences
Compound Profile
Full specification.
Molecular and analytical specification from peer-reviewed literature and Trident Labs batch records.
| Common Name | Semax / ACTH(4–7)PGP |
| Sequence | Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP) |
| CAS Number | 80714-61-0 |
| Molecular Formula | C₃₈H₅₃N₉O₁₀S |
| Molecular Weight | 887.97 Da |
| Structure | Synthetic heptapeptide · ACTH(4–10) core + Pro-Gly-Pro C-terminal extension |
| Parent Fragment | ACTH(4–10) — nootropic fragment of adrenocorticotropic hormone |
| Pharmacophore | His³-Phe⁴ — key residues for receptor interaction and BDNF modulation |
| Primary Targets | BDNF/TrkB axis · Dopaminergic · Serotonergic · Melanocortin receptors (proposed) |
| BDNF Response | 1.4× protein · 3× mRNA — single dose, rat hippocampus (Dolotov 2006) |
| Plasma t½ | ~minutes — rapid clearance; downstream signaling persists hours |
| Form | Lyophilized powder · sealed glass vial |
| Purity | ≥99% HPLC · Mass Spec verified · 6-panel COA · Horizon Analytical |
| Endotoxin | <0.05 EU/mL · LAL-tested · Horizon Analytical |
| Solubility | Water, saline, PBS · 1 mg/mL typical working stock |
| Regulatory | RUOIn Vitro Research Use Only — Not for Human Consumption (US) |
Signaling Profile
Four measurable
pathway outputs.
Each arm is independently quantifiable in cell-based assay formats — from ELISA-based BDNF protein measurement to monoamine metabolite profiling, gene expression assays, and inflammatory cytokine panels.
BDNF/TrkB Upregulation — Hippocampal Neuroplasticity
3-fold BDNF mRNA increase, 1.4-fold protein elevation, 1.6-fold TrkB phosphorylation — all from a single 50 µg/kg dose in rats. Measurable via ELISA, Western blot, qPCR. The primary and best-characterized mechanism. Binding studies: KD 2.4 ± 1.0 nM in rat basal forebrain.
Dopamine & Serotonin System Activation
Rapid activation of serotonergic and dopaminergic systems documented in cortical and hippocampal tissue. Semax potentiates D-amphetamine locomotor effects — consistent with dopaminergic pathway engagement. Monoamine metabolite profiling (HPLC-EC) is the standard assay endpoint for this arm.
Neuroprotection — Transcriptome-Wide Anti-Inflammatory
In tMCAO ischemia models: suppresses MMP-9, activates CREB, modulates JNK — measurable by immunohistochemistry and Western blot. RNA-Seq (tMCAO): hundreds of DEGs — inflammatory gene suppression + neurotransmitter gene preservation. Reduces infarct volume in stroke models.
PGP Tail — NGF & Neurotrophin Receptor Activation
PGP alone activates BDNF, NGF, TrkB, TrkC, and TrkA in ischemic cortex (PMC11498467) — with TrkA/TrkC effects exceeding Semax itself. Also produces antidepressant-like effects in behavioral models. Confirms the C-terminal extension is an active pharmacophore, not a passive stability modification.
Dolotov et al. Brain Res 2006 · PMC8226508 · PMC11498467. In vitro / preclinical data — research use only.
3×
BDNF mRNA Increase
Single dose · rat hippocampus
7 AA
Peptide Length
MEHFPGP sequence
1996
Russian Approval
Stroke & cognitive disorders
4
Signaling Pathways
BDNF · DA/5HT · Neuroprotection · PGP
Key Research Observations
What the literature
demonstrates.
Independent observations from preclinical models and gene expression studies. Not Trident Labs claims. All data from peer-reviewed literature.
A single intranasal application of Semax (50 µg/kg) produced a 3-fold increase in BDNF exon III mRNA, 2-fold increase in TrkB mRNA, 1.6-fold increase in TrkB phosphorylation, and 1.4-fold increase in BDNF protein — all in rat hippocampus. Semax-treated animals showed a significant increase in conditioned avoidance reactions in a learning paradigm. Binding studies identified a high-affinity binding site in rat basal forebrain (KD = 2.4 ± 1.0 nM), confirming a specific molecular target beyond diffuse receptor modulation.
Dolotov OV et al., Brain Res 2006;1117(1):54–60. PMID: 16996037
In the transient middle cerebral artery occlusion (tMCAO) model — a standard ischemic stroke paradigm — Semax suppressed expression of inflammatory genes while simultaneously preventing the massive downregulation of neurotransmitter system genes typically seen post-ischemia. RNA-Seq analysis identified hundreds of differentially expressed genes, with key proteomic effects: MMP-9 suppression, CREB activation, and JNK inhibition — three markers of neuroprotection and reduced apoptotic signaling.
PMC8226508 · PMC7350263 — tMCAO RNA-Seq and protein expression studies
The Pro-Gly-Pro C-terminal tail — shared with Selank — demonstrates independent pharmacological activity. In ischemic cortex, PGP alone upregulated BDNF, NGF, TrkB, TrkC, and TrkA mRNA — with TrkA and TrkC effects exceeding Semax itself. In behavioral models of depression and chronic stress, PGP produced antidepressant-like effects (forced swim test, tail suspension test) comparable to Semax, confirming the C-terminal extension is a pharmacophore, not a metabolic stabilizer.
PMC11498467 · Inozemtseva et al. Eur J Pharmacol 2024
Inozemtseva et al. (2024) evaluated Semax and its PGP fragment in a model of chronic unpredictable stress (CUS) using forced swim test and tail suspension test. Both Semax and PGP reduced immobility time — a standard preclinical antidepressant-like endpoint. Both also attenuated stress-induced behavioral changes, with effects measured across multiple validated anxiety and depression paradigms. These findings provide mechanistic context for the dopaminergic and serotonergic activation documented in earlier neurochemical studies.
Inozemtseva LS et al., Eur J Pharmacol 2024 — PMID indexed
Storage & Handling
Stability protocol.
Lab handling notes.
Semax is a synthetic heptapeptide containing methionine — susceptible to oxidation. Proper cold storage and light protection are essential for maintaining BDNF assay-ready activity.
Long-term
−20°C
Lyophilized, sealed. Stable 24 months. Avoid frost-free freezers — thermal cycling degrades Met residue.
In solution
4°C
Stable 7–14 days refrigerated. Aliquot for single use. Avoid multiple freeze-thaw cycles.
Solvent
PBS / H₂O
Reconstitute in sterile water or PBS pH 7.4. Typical stock: 1 mg/mL. Dilute to assay concentration in buffer.
Avoid
Oxidants
Methionine (Met¹) is vulnerable to oxidation. Use amber vials. Avoid peroxide-containing solvents or prolonged air exposure.
For Research Use Only — Not for Human Consumption. Semax is supplied exclusively for in vitro laboratory research. Not a drug, dietary supplement, food, or medical device under US regulations. For lawful in vitro research use only by qualified researchers.
Published Literature
Indexed research
on Semax.
Independent peer-reviewed studies. Not Trident Labs claims. For Research Use Only.
Semax Regulates BDNF and TrkB Expression in the Rat Hippocampus
The landmark study establishing Semax's BDNF mechanism. Single intranasal dose (50 µg/kg) produced: 3-fold increase BDNF exon III mRNA, 2-fold increase TrkB mRNA, 1.6-fold increase TrkB phosphorylation, 1.4-fold increase BDNF protein — all in rat hippocampus. Semax-treated animals showed significantly increased conditioned avoidance reactions. Tritium-labeled Semax binding confirmed KD = 2.4 ± 1.0 nM and BMAX = 33.5 ± 7.9 fmol/mg protein in rat basal forebrain — evidence for a specific high-affinity binding site. Provides mechanistic basis for cognitive effects via BDNF/TrkB system modulation. Brain Res 2006;1117(1):54–60. PMID: 16996037.
Antidepressant-like and Antistress Effects of Semax and Melanotan II in Chronic Unpredictable Stress
Evaluated Semax and its PGP fragment in a chronic unpredictable stress (CUS) model using forced swim test (FST) and tail suspension test (TST). Both Semax and PGP reduced immobility time in FST and TST — standard preclinical antidepressant-like endpoints. Both attenuated stress-induced behavioral changes across multiple validated paradigms. The finding that PGP alone produces effects comparable to full Semax confirms the C-terminal tripeptide as an active pharmacophore, not merely a metabolic stabilizer. Provides the most recent characterization of Semax's mood-modulating mechanisms. Eur J Pharmacol 2024. PMID indexed.
Brain Protein Expression Profile Confirms Protective Effect of Semax in Cerebral Ischemia–Reperfusion
In the tMCAO ischemia-reperfusion model, evaluated Semax's effect on key protein expression: MMP-9 (inflammation / ECM degradation), c-Fos (neuronal activation), JNK (apoptotic signaling), and CREB (neuroprotection / plasticity). Semax suppressed MMP-9 and JNK while activating CREB — a protein expression profile consistent with reduced inflammation and enhanced neuroprotective signaling. Confirms proteomic effects previously identified at the transcriptome level in RNA-Seq studies. Brain Res PMC8226508.
Semax and Pro-Gly-Pro Activate Neurotrophin Gene Transcription After Cerebral Ischemia
Comparative study of Semax vs PGP fragment in ischemic cortex neurotrophin gene expression. Both activated BDNF, NGF, TrkC, and TrkB mRNA. PGP treatment for 24h additionally enhanced TrkA and TrkC receptor genes — effects not seen with Semax alone. Confirms PGP as an active pharmacophore with partially distinct transcriptional targets from the ACTH(4–10) core. Provides molecular basis for PGP's independent neuroprotective and antidepressant-like profile. PMC11498467.
Transcriptome-Level Effects of Semax in tMCAO Stroke Model — Novel Insights
Genome-wide RNA-Seq analysis in tMCAO subcortical tissue identified hundreds of differentially expressed genes in ischemic tissue — with Semax treatment showing: activation of large numbers of genes in inflammation, immune response, and apoptosis pathways (tMCAO alone), versus Semax-mediated suppression of inflammatory genes and preservation of neurotransmitter system gene expression. Previously unknown compensation effects and signal pathway modulation revealed. Provides comprehensive transcriptome basis for Semax neuroprotection. PMC7350263.
Semax Peptide: Neurotrophic Research, Cognitive Studies & Laboratory Applications
2025 comprehensive research review synthesizing three decades of Semax literature. Covers BDNF/TrkB binding kinetics (KD 2.4 nM), PGP tail independent pharmacology, dopaminergic/serotonergic activation, stroke neuroprotection data, and Russian regulatory approval history (1996). Reviews all major published preclinical data and the limitations of the evidence base (predominantly Russian institutions, limited Western-standard RCT data). Positions Semax as one of the most studied nootropic peptides with the strongest evidence base of any synthetic regulatory peptide for BDNF modulation. April 2025.
Independent peer-reviewed research — not Trident Labs claims. Semax is supplied for in vitro research use only. Not for human consumption. For lawful in vitro research use only by qualified researchers.
Cited Sources
References
All scientific claims sourced from peer-reviewed literature.
Semax, an analog of ACTH(4–10) with cognitive effects, regulates BDNF and TrkB expression in the rat hippocampus
Antidepressant-like and antistress effects of the ACTH(4-10) synthetic analogs Semax and Melanotan II on male rats
Brain protein expression profile confirms the protective effect of ACTH(4–7)PGP (Semax) in cerebral ischemia–reperfusion
Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia
Novel insights into the protective properties of ACTH(4-7)PGP (Semax) at the transcriptome level following cerebral ischaemia-reperfusion
Semax Peptide: Neurotrophic Research, Cognitive Studies & Laboratory Applications
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