Semax: Complete Research Guide — ACTH(4–10) Analog BDNF Upregulation, Neuroprotection Data & White-Label Pricing (2026)
- Semax (CAS: 80714-61-0; Met-Glu-His-Phe-Pro-Gly-Pro; MW: ∼887 Da) is a synthetic heptapeptide analog of ACTH(4–10) — the cognitively active fragment of adrenocorticotropic hormone — extended with Pro-Gly-Pro at the C-terminus for metabolic stability, using the same strategy as Selank. Developed at the Institute of Molecular Genetics, Russian Academy of Sciences, by Ashmarin, Myasoedov and colleagues during the 1980s–1990s.
- Primary mechanism: BDNF (brain-derived neurotrophic factor) and TrkB receptor upregulation. A single intranasal application of Semax (50 μg/kg) produced a 3-fold increase in exon III BDNF mRNA, a 2-fold increase in trkB mRNA, a 1.4-fold increase in BDNF protein, and a 1.6-fold increase in TrkB tyrosine phosphorylation in the rat hippocampus — accompanied by improved performance on conditioned avoidance tasks (Dolotov et al., Brain Res, 2006 — PMID: 16996037).
- Ischemia model research: Medvedeva (Dergunova) et al. (2014) published a genome-wide transcriptional analysis in BMC Genomics documenting that Semax affects expression of genes related to immune and vascular systems in rat brain focal ischemia, including upregulation of VEGF family genes, neurotrophins (NGF, NT-3), and their cognate Trk receptors (PMC3987924).
- Regulatory status: Approved as a research protocol compound in Russia for neurological indications (cognitive impairment, ischemic stroke rehabilitation). Not in the US. Research-grade Semax is classified for Research Use Only (RUO) in the YPB catalog.
- Research-grade Semax is available in a 10mg configuration (Research Use Only) with batch-specific COAs through the YPB catalog.
- 12,000 monthly US searches; $12.96 gross margin per unit at Premier tier (25%); positioned as the neuroprotective cognitive research companion to Selank, completing the Russian nootropic catalog pair for white-label brands in the cognitive research category. Updated April 2026.
What Is Semax and Where Does It Come From?
Approved compound in Russia
3-Fold BDNF mRNA Upregulation
Semax (CAS: 80714-61-0; MEHFPGP; Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic heptapeptide analog of ACTH(4–10) — the seven-amino acid fragment of adrenocorticotropic hormone that retains the peptide’s cognitive and neuroprotective activities without the adrenal steroidogenic effects of full-length ACTH (1–39). Updated April 2026. The compound was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences by Ashmarin, Myasoedov, Grivennikov and colleagues as part of a long-term program investigating the neuroprotective and cognitive properties of ACTH fragments. The Pro-Gly-Pro C-terminal extension — the same stability strategy employed in Selank (tuftsin analog) — protects the ACTH(4–10) core sequence from rapid peptidase degradation and extends its effective duration.
Semax occupies a prominent position in the Russian nootropic research tradition alongside Selank: where Selank addresses GABAergic anxiolytic pathways, Semax specifically addresses BDNF-mediated neuroprotective and cognitive pathways. Both compounds are approved research protocol compounds in Russia, developed by the same Institute of Molecular Genetics team, and are frequently researched in combination in cognitive research protocols. Semax is Not in the United States and is sold by YPB exclusively for laboratory and in vitro research purposes.
Key Characteristics
| Parameter | Value |
|---|---|
| Chemical Name | Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP); ACTH(4–10)-Pro-Gly-Pro hybrid |
| Common Names | Semax; Cemax (Russian: Семакс); ACTH(4–10) analog; MEHFPGP heptapeptide |
| CAS Number | 80714-61-0 |
| Molecular Formula | C37H51N9O10S |
| Molecular Weight | ∼887 Da |
| Amino Acids | 7 (heptapeptide: Met-Glu-His-Phe-Pro-Gly-Pro; Met-Glu-His-Phe = ACTH(4–10) core; Pro-Gly-Pro = stability extension) |
| Half-Life | Improved vs. ACTH(4–10) core (~minutes) due to Pro-Gly-Pro extension; formal human PK data not published in accessible literature |
| Primary Mechanism | BDNF and TrkB upregulation (hippocampus, prefrontal cortex, basal forebrain); CREB-dependent neurotrophic gene transcription; dopaminergic and serotonergic pathway modulation |
| Alternative Names | Semax; N-acetyl Semax; ACTH(4–7)-PGP (alternate designation); TP-7; Pro-Gly-Pro extended ACTH fragment |
| FDA Status | Not FDA-approved for human use. Investigational/research compound (RUO). Research Use Only (RUO) in the US. |
| Russian Status | Approved research protocol compound in Russia for cognitive and neuroprotective indications (ischemic stroke rehabilitation, cognitive impairment). |
| WADA Status | Not explicitly listed on WADA Prohibited List as of 2025; verify current WADA list prior to athletic research applications |
| Storage | Lyophilized: −20°C. Reconstituted: 2–8°C, use within 14 days |
| Developer / Origin | Ashmarin, Myasoedov, Grivennikov et al., Institute of Molecular Genetics, Russian Academy of Sciences (1980s–1990s) |
How Does Semax Work? Primary Mechanisms of Action
Semax’s pharmacological profile centers on neurotrophic pathway activation, with BDNF upregulation as the best-characterized and most rigorously documented mechanism in the published literature.
BDNF and TrkB Upregulation via CREB Pathway
The foundational published mechanism for Semax’s cognitive research profile is upregulation of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor TrkB in the hippocampus. Dolotov et al. (2006) published the key quantitative data in Brain Research: a single intranasal application of Semax at 50 μg/kg produced the following responses in rat hippocampus versus controls — BDNF exon III mRNA: 3-fold increase; TrkB mRNA: 2-fold increase; BDNF protein: 1.4-fold increase; TrkB tyrosine phosphorylation: 1.6-fold increase. The BDNF response was CREB (cAMP response element-binding protein)-dependent, implicating a G-protein-coupled receptor pathway as the upstream initiating event (Dolotov et al., Brain Res, 2006 — PMID: 16996037).
The same group also published evidence that Semax specifically binds to sites in rat basal forebrain membranes with a measured KD of 2.4 ± 1.0 nM and a BMAX of 33.5 ± 7.9 fmol/mg protein in a calcium-dependent, reversible manner — establishing receptor-mediated binding at specific brain region targets rather than nonspecific membrane interaction. The BDNF response was region-specific (basal forebrain and hippocampus responsive; cerebellum not responsive), consistent with targeted receptor engagement rather than diffuse peptide effects.
ACTH(4–10) Core Activity Without Adrenal Effects
Full-length ACTH (adrenocorticotropic hormone, 1–39) stimulates cortisol secretion from the adrenal glands through the melanocortin-2 receptor (MC2R/ACTHR) expressed in adrenal tissue. The ACTH(4–10) fragment — which Semax’s MEHFPGP core sequence is based on — does not contain the MC2R adrenal-binding domain present in the ACTH(1–3) N-terminal sequence. Published data confirms that Semax does not stimulate cortisol secretion or adrenal activity at studied doses, specifically retaining the central cognitive and neuroprotective activities of ACTH fragments while eliminating the adrenal steroidogenic pathway engagement. This dissociation of cognitive activity from adrenal effects is the primary design rationale for Semax as a research tool.
Dopaminergic and Serotonergic Pathway Modulation
Eremin et al. published data demonstrating that Semax, as an ACTH(4–10) analog with nootropic properties, activates dopaminergic and serotonergic brain systems in rodents. Dopamine and serotonin pathway engagement provides a complementary mechanism to the BDNF/TrkB neurotrophic axis, potentially contributing to the compound’s documented effects on attention, motivation, and learning in preclinical behavioral models.
Neuroprotection in Ischemia Models
Medvedeva (Dergunova) et al. (2014) published a genome-wide transcriptional analysis in BMC Genomics examining Semax effects in the permanent middle cerebral artery occlusion (pMCAO) model of focal brain ischemia in rats. The analysis documented that Semax affects expression of genes related to the immune and vascular systems, including upregulation of VEGF family genes and their receptors, upregulation of neurotrophins NGF and NT-3 (alongside BDNF) and their cognate Trk receptors, and modulation of immune response gene networks. The breadth of the transcriptional response supported Semax’s classification as a compound with pleiotropic neuroprotective activity in ischemia research models (Medvedeva/Dergunova et al., BMC Genomics, 2014 — PMC3987924).
What Systems Has Semax Been Investigated For?
Semax’s published research applications span cognitive function, neuroprotection in ischemia models, neurotrophic biology, and immune-vascular interaction in CNS tissue — reflecting both its BDNF mechanism and the breadth of the ischemia transcriptomics program.
Cognitive Function and Learning Research Models
Preclinical behavioral data from multiple published studies documents Semax effects in learning and memory research paradigms. The Dolotov et al. (2006) study documented improved performance on conditioned avoidance tasks in Semax-treated animals alongside the BDNF/TrkB molecular changes. Earlier work by Ashmarin, Kozlovskaya, and colleagues established Semax’s cognitive research profile in a range of behavioral models, forming the foundational preclinical evidence that supported Russian compound approval. The BDNF mechanism is considered particularly relevant to spatial memory formation, pattern recognition, and long-term potentiation in hippocampal circuits.
Ischemia and Neuroprotection Research
Semax is one of the best-characterized research peptides for cerebrovascular ischemia model research in the Russian scientific literature. Published data spans the pMCAO permanent occlusion model (Medvedeva et al. 2014, genome-wide transcriptomics) and reperfusion/ischemia models (Filippenkov et al. 2020 in Genes). Collectively, published data documents that Semax modulates expression of hundreds of genes in ischemic brain tissue, with particular enrichment in immune response, vascular biology (VEGF pathways), and neurotrophic (BDNF, NGF, NT-3) categories. The approved Russian wellness support for post-ischemic stroke rehabilitation provides regulatory validation for this research direction.
Neurotrophin Biology Research
Beyond BDNF specifically, Semax upregulates multiple members of the neurotrophin family. Published data in ischemia models documents simultaneous upregulation of BDNF (exon III CREB-dependent), NGF (nerve growth factor), NT-3 (neurotrophin-3), and their corresponding Trk receptors (TrkA, TrkB, TrkC). This broad neurotrophic profile makes Semax a useful research tool for studying neurotrophin system interactions in cognitive and neuroprotective research contexts.
What Does the Human Research Data Show So Far?
Similar to Selank, Semax has a human evidence base grounded in Russian clinical trial data collected as part of its compound approval program, with the primary registration trial data not fully published in English-language peer-reviewed journals accessible on PubMed.
Human Safety Summary
| Study | Route | N | Indication | Adverse Events | Year |
|---|---|---|---|---|---|
| Russian compound registration trials (ischemic stroke rehabilitation) | Intranasal (approved formulation) | Not fully disclosed in English-language literature | Post-ischemic stroke rehabilitation; cognitive impairment | Well tolerated in compound registration trials; no safety concerns that prevented approval. Full safety data in Russian regulatory submission. Intranasal route is the approved administration route. | 1990s–2000s |
| Clinical studies (cognitive impairment indications) | Intranasal | Not fully disclosed in English-language literature | Cognitive impairment; neurological rehabilitation | Published Russian-language clinical data documents tolerability consistent with approved intranasal formulation. No serious adverse events reported in accessible literature. | Various |
| Published pharmacokinetic / PK data in humans | N/A | N/A | N/A | Formal human pharmacokinetic data for Semax is not published in accessible English-language peer-reviewed literature as of April 2026. | N/A |
The primary clinical data supporting Semax’s Russian compound approval for ischemic stroke rehabilitation and cognitive indications exists within the Russian regulatory submission and in Russian-language clinical journals, but is not fully accessible via PubMed in English. Researchers should treat this as a regulatory fact (the approval exists and is legitimate) but should account for the limited accessibility of the underlying human trial data when evaluating the evidence base relative to Western-developed compounds with published Phase 2/3 trial data. All YPB Semax is Research Use Only and is not equivalent to the approved Russian intranasal compound formulation.
How Does Semax Compare to Other Cognitive Research Peptides?
Semax’s BDNF/TrkB neurotrophic mechanism occupies a distinct niche within the YPB cognitive category: no other catalog compound directly upregulates BDNF and TrkB at the gene and protein level through a CREB-dependent pathway.
| Parameter | Semax | Selank | NAD+ | GHK-Cu |
|---|---|---|---|---|
| Origin | ACTH(4–10) fragment + Pro-Gly-Pro; Ashmarin et al., Russia | Tuftsin + Pro-Gly-Pro; Ashmarin et al., Russia | Endogenous coenzyme; nuclear genome | Endogenous plasma tripeptide-copper; Pickart, 1973 |
| Molecular Size | 7 AA, ~887 Da (heptapeptide) | 7 AA, 751.86 Da (heptapeptide) | Small molecule, 663.4 Da | 3 AA + Cu(II), 403.93 Da |
| Primary Mechanism | BDNF/TrkB upregulation (CREB-dependent) + neuroprotection (VEGF, NGF, NT-3) + monoamine modulation | GABA-A gene expression modulation + enkephalin prolongation + BDNF normalization | NAD+ repletion → sirtuin/PARP; mitochondrial function | Gene expression reprogramming (4,000+ genes); collagen synthesis; neuroprotection |
| BDNF Activity | Direct upregulation: 3-fold mRNA, 1.4-fold protein (hippocampus); documented in multiple regions | BDNF normalization (prevents pathological elevation); modulation rather than primary upregulation | BDNF not primary mechanism | BDNF not primary mechanism |
| Regulatory Status | Approved compound in Russia (ischemia rehabilitation, cognitive indications); Not; RUO | Approved compound in Russia and Ukraine; Not; RUO | Not approved as compound | Not approved as compound; INCI cosmeceutical |
| Ischemia Research Data | Yes — genome-wide transcriptomics in pMCAO model (Medvedeva 2014, PMC3987924); Filippenkov 2020 | Neuroimmune modulation; not primarily ischemia-focused | NAD+ and mitochondrial protection; not primarily ischemia-focused | Wound healing, tissue repair; minimal ischemia data |
| Human Data | compound registration trials (Russian); full data not in English-language PubMed | Comparative trial n=62 Zozulya 2008, PMID 18454096; compound registration trials (Russian) | Phase 2 data (NMN/NR precursors) | Phase 3 ophthalmic (RGN-259) |
| PubMed Publications | 100+ (Semax / ACTH 4-10 analog) | 100+ (selank / TKPRPGP) | 1,000+ (NAD+ biology) | 300+ (GHK-Cu) |
Semax and Selank together constitute the complete Russian nootropic research compound pair: Semax (BDNF/neuroprotective) and Selank (GABAergic/neuroimmune). Both share the same Pro-Gly-Pro stability strategy, the same Russian institutional origin, and the same national compound approval. For white-label brands targeting cognitive research buyers, offering both SKUs addresses the full GABAergic + neuroprotective research spectrum from a single search audience. The NAD+ Research Guide covers the metabolic aging pathway complementary to CNS neuroprotection. The GHK-Cu Research Guide covers neuroprotection via gene expression reprogramming that complements Semax’s neurotrophic mechanism.
What Should Researchers Know About Semax Stability and Handling?
Semax at ~887 Da is a mid-weight heptapeptide. The Pro-Gly-Pro extension improves enzymatic stability over ACTH(4–10), and the methionine at position 1 requires attention to oxidation status in storage and quality verification.
Storage and Reconstitution Protocol
Lyophilized Semax is stable at −20°C for up to 24 months when protected from moisture and light. The N-terminal methionine (position 1 of MEHFPGP) is susceptible to oxidation, which can alter biological activity; lyophilized storage minimizes this risk. The approved Russian formulation is intranasal — the most extensively studied administration route for Semax, bypassing hepatic first-pass metabolism and delivering the peptide directly to the olfactory epithelium. Reconstituted solutions for in vitro research should be held at 2–8°C and used within 14 days. Avoid repeated freeze-thaw cycles.
COA Verification
At ~887 Da, HPLC purity (≥98%) combined with mass spectrometry is the standard verification protocol. MS should confirm the seven-residue MEHFPGP sequence at MW ~887 Da. Methionine oxidation status at position 1 should be confirmed, as Met-oxide impurities can alter the compound’s activity profile. L-amino acid configuration at all residues should be specified. All YPB Semax batches include lot-traceable COA documentation accessible through the COA Library.
Key Research Findings: Semax in 2026
Key Research Findings
- 3-fold hippocampal BDNF exon III mRNA increase from single application: Dolotov et al. (2006) documented single-dose intranasal Semax (50 μg/kg) producing 3-fold BDNF mRNA, 2-fold TrkB mRNA, 1.4-fold BDNF protein, and 1.6-fold TrkB phosphorylation increases in rat hippocampus (PMID: 16996037).
- CREB-dependent pathway identified: BDNF exon III is specifically CREB-dependent, implicating G-protein-coupled receptor activation as the upstream signal; calcium-dependent binding to basal forebrain membranes confirmed (KD 2.4 nM).
- Ischemia transcriptomics: genome-wide analysis published: Medvedeva/Dergunova et al. (2014) documented VEGF pathway, neurotrophin, and immune gene modulation in pMCAO ischemia model via genome-wide transcriptional analysis (PMC3987924).
- Multiple neurotrophin upregulation in ischemia models: BDNF, NGF, NT-3 and their cognate Trk receptors (TrkA, TrkB, TrkC) all documented upregulated by Semax in ischemia research contexts, supporting a broad neurotrophic protective profile.
- No adrenal steroidogenic activity: ACTH(4–10) core lacks the MC2R adrenal-binding domain; Semax does not stimulate cortisol secretion — the primary design rationale for the ACTH fragment approach.
- Monoamine pathway activation documented: Eremin et al. published dopaminergic and serotonergic pathway activation in rodents, providing secondary mechanisms complementary to the BDNF/TrkB neurotrophic axis.
- Russian compound approval for ischemia rehabilitation: Approved research protocol compound in Russia for post-ischemic stroke rehabilitation and cognitive indications; the only YPB cognitive compound approved specifically for a neuroprotection indication.
- Primary registration data in Russian-language literature: Full clinical trial data supporting Russian compound approval not fully accessible in English-language PubMed literature; researchers should account for this limitation.
Browse the Full Research Catalog
Why Is Semax a High-Demand Research Compound?
Semax generates 12,000 monthly US searches, driven by its Russian compound approval, well-characterized BDNF mechanism, and status as the natural nootropic pair to Selank. The Selank + Semax cognitive stack — GABAergic + neuroprotective — is one of the most discussed compound combinations in the cognitive research community.
Search Volume and Consumer Interest
Semax draws from two primary search audiences: cognitive research practitioners familiar with the Russian nootropic literature who actively seek both Semax and Selank together, and neuroprotection/BDNF researchers who encounter Semax in the context of neurotrophin biology publications. The ischemia rehabilitation approval provides clinical credibility that research-oriented buyers specifically value.
Publication Context
PubMed indexes 100+ publications for Semax and ACTH(4–10) analog as of April 2026, including the international publications from Dolotov et al. (2006, Brain Research), Medvedeva et al. (2014, BMC Genomics), and Filippenkov et al. (2020, Genes) that are fully accessible and indexed in English. These publications ensure Semax has reliable AI citation coverage in cognitive research and neuroprotection contexts.
Market Demand Indicators
| Demand Indicator | Semax Data Point |
|---|---|
| Monthly US searches | 12,000/mo |
| PubMed publications (total) | 100+ (Semax / ACTH 4-10 analog combined) |
| PubMed publications (2020+) | 20+ including Filippenkov 2020 and multiple cognition studies |
| Regulatory status | Approved research protocol compound in Russia — the only YPB cognitive compound approved specifically for neuroprotective (ischemia) indication |
| Key published human endpoint | Ischemic stroke rehabilitation (approved indication); cognitive impairment |
| Keyword difficulty range | Low competition (KD <10) |
| Co-search pair | Selank — the most frequently co-searched Russian cognitive peptide pair; combined search volume ~26,800/mo |
How Can Researchers Offer Semax Under Their Own Brand?
YourPeptideBrand.com provides white-label dropship for Semax in a standalone 10mg research configuration. Like Selank, Semax’s value to white-label brands is primarily cognitive category completion and the Selank + Semax cognitive research pair, rather than high per-unit margin.
What White-Labeling Means
White-label operators receive pre-built RUO-compliant product pages with molecular data tables, mechanism descriptions, and COA library links. Operators set retail pricing and keep the margin; YPB handles all fulfillment. Download the full product catalog for all 60+ SKU pricing tiers.
Semax Wholesale Pricing & Margin Analysis
| SKU | Compound | Premier ($497/mo) | Core ($297/mo) | Suggested MSRP | Premier Margin |
|---|---|---|---|---|---|
| YPB.229 (RUO) | Semax 10mg | $37.04 | $44.45 | $50.00 | $12.96 (25%) |
Use the YPB Profit Calculator to model projected monthly revenue at your target pricing and volume. Semax at Premier tier generates $12.96 gross margin per unit at the $50 MSRP — a 25% margin rate, the same as Selank and the lowest in the cognitive category. Operators with strong cognitive research audiences should consider pricing above $50 given Semax’s Russian compound approval for ischemia rehabilitation and its deep BDNF mechanism documentation. The Selank + Semax cognitive pair generates $25.92 combined margin per dual-order transaction; together with NAD+ and GHK-Cu, the complete YPB cognitive research catalog generates well over $350 combined margin per comprehensive order. 250+ white-label brands are already live on the platform.
Who This Is For
Semax is best positioned for white-label brands building a comprehensive cognitive research catalog that pairs Russian nootropic research tradition with modern neurotrophic biology. Brands already offering Selank should offer Semax as the mandatory companion SKU — the search audiences overlap nearly completely, and practitioners and researchers searching for one almost always search for the other. Brands with strong BPC-157 or healing content can extend into cognitive research with Selank + Semax as a two-SKU entry point at combined low keyword competition.
Methodology & Data Sources
Methodology & Data Sources
Scientific literature: PubMed and Embase searched for “Semax,” “ACTH 4-10 analog,” “MEHFPGP,” “Met-Glu-His-Phe-Pro-Gly-Pro,” and CAS 80714-61-0. Search conducted through April 2026.
Key sources: Dolotov et al. (2006) Brain Res (PMID: 16996037); Medvedeva/Dergunova et al. (2014) BMC Genomics (PMC3987924); Filippenkov et al. (2020) Genes (PMC7555804); Dolotov et al. (2006) J Neurochem (basal forebrain binding data); Eremin et al. (dopaminergic/serotonergic data). Russian compound registration data not fully accessible in English-language PubMed.
Regulatory context: Russian compound approval for Semax confirmed via institutional publications from the Institute of Molecular Genetics. Approved intranasal formulation for ischemic stroke rehabilitation and cognitive indications. Exact clinical trial registry data not fully accessible in English.
Search volume data: Google Ads keyword data via DataForSEO, April 2026. Monthly US searches for “semax,” “semax peptide,” and close variants combined.
Pricing data: YPB Full Pricing Catalog, current as of April 2026. Premier ($497/mo) and Core ($297/mo) membership tiers. Margin calculated as MSRP minus Premier wholesale price.
Limitations: Primary compound registration clinical data published primarily in Russian-language journals not fully accessible via PubMed. Formal human pharmacokinetic data not published in accessible English-language literature. This article is for educational purposes and does not constitute medical or research protocol advice.
References
- Dolotov, O. V., Karpenko, E. A., Inozemtseva, L. S., Seredenina, T. S., Levitskaya, N. G., Rozyczka, J., Dubynina, E. V., Novosadova, E. V., Andreeva, L. A., Alfeeva, L. Yu., Kamensky, A. A., Grivennikov, I. A., Myasoedov, N. F., & Engele, J. (2006). Semax, an analog of ACTH(4–10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res, 1117(1), 54–60. PMID: 16996037
- Dolotov, O. V., Karpenko, E. A., Seredenina, T. S., et al. (2006). Semax, an analogue of adrenocorticotropin (4–10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. J Neurochem, 97(Suppl 1), 82–86.
- Medvedeva, E. V. (Dergunova), Dmitrieva, V. G., Povarova, O. V., et al. (2014). The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. BMC Genomics, 15, 228. PMC3987924
- Filippenkov, I. B., Stavchansky, V. V., Denisova, A. E., et al. (2020). Novel insights into the protective properties of ACTH(4–7)PGP (Semax) peptide at the transcriptome level following cerebral ischaemia-reperfusion in rats. Genes, 11(6), 681. PMC7555804
- Eremin, K. O., Kudrin, V. S., Grivennikov, I. A., et al. Semax, an ACTH(4–10) analogue with nootropic properties, activates dopaminergic and serotonergic brain systems in rodents. Neurochem Res, 30(12), 1493–1500.
- Medvedeva, E. V., Dmitrieva, V. G., Povarova, O. V., et al. (2013). Effect of semax and its C-terminal fragment Pro-Gly-Pro on the expression of VEGF family genes and their receptors in experimental focal ischemia of the rat brain. J Mol Neurosci, 49(2), 328–333.
- Ashmarin, I. P., Nezavibatko, V. N., Myasoedov, N. F., et al. (1997). Design and investigation of a nootropic analog of adrenocorticotropin (4–10) without steroidogenic activity. Neurosci Behav Physiol, 27(2), 153–157.
- Grivennikov, I. A., Dolotov, O. V., Zolotarev, Y. A., et al. (2008). Semax and selank as neuroprotective peptides: recent advances in studying the molecular targets and cellular mechanisms. Bull Exp Biol Med, 146(4), 560–563.
- Levitskaya, N. G., Sebentsova, E. A., Andreeva, L. A., Alfeeva, L. Yu., Kamenskij, A. A., & Myasoedov, N. F. (2004). Comparative characteristics of the nootropic and neuroprotective effects of Semax and its Pro-Gly-Pro C-terminal analog. Ross Fiziol Zh Im I M Sechenova, 90(8), 1041–1053.
Frequently Asked Questions
Semax (CAS: 80714-61-0; Met-Glu-His-Phe-Pro-Gly-Pro; ~887 Da) is a synthetic heptapeptide analog of ACTH(4–10), the cognitively active fragment of adrenocorticotropic hormone, extended with Pro-Gly-Pro at the C-terminus for metabolic stability. Developed at the Institute of Molecular Genetics, Russian Academy of Sciences. In research models, published data demonstrates Semax upregulates BDNF and TrkB in the hippocampus via a CREB-dependent pathway — a single intranasal dose produced a 3-fold increase in BDNF exon III mRNA, 2-fold increase in TrkB mRNA, 1.4-fold BDNF protein increase, and 1.6-fold TrkB phosphorylation increase in rat hippocampus (Dolotov et al., Brain Res, 2006 — PMID: 16996037). Genome-wide transcriptomics in ischemia models documented VEGF pathway and multi-neurotrophin gene modulation (Medvedeva et al. 2014, PMC3987924). Semax is approved in Russia for ischemia rehabilitation; it is Not and is classified for Research Use Only (RUO) in the US. Updated April 2026.
Full-length ACTH (adrenocorticotropic hormone, 1–39) stimulates cortisol secretion from the adrenal cortex via the melanocortin-2 receptor (MC2R/ACTHR), which is encoded primarily in adrenal tissue. This adrenal steroidogenic activity is the primary safety limitation of pharmacological ACTH use. The ACTH(4–10) fragment — the core of Semax — does not contain the MC2R-binding N-terminal domain (ACTH 1–3) and therefore does not stimulate adrenal cortisol secretion. Semax specifically retains the ACTH(4–10) neurotrophic and cognitive activities while eliminating adrenal engagement, making it a research tool for studying the CNS mechanisms of ACTH biology independently from the adrenal-pituitary axis (Ashmarin et al. 1997). This dissociation is the primary design rationale of Semax as a distinct research compound from ACTH.
Dolotov et al. (2006, PMID: 16996037) published the foundational BDNF quantification data: a single intranasal Semax dose (50 μg/kg in rats) produced a 3-fold increase in BDNF exon III mRNA, a 2-fold increase in TrkB mRNA, a 1.4-fold increase in BDNF protein levels, and a 1.6-fold increase in TrkB tyrosine phosphorylation in rat hippocampus versus controls, all statistically significant (p<0.05, ANOVA + Mann-Whitney). The BDNF response was CREB-dependent (exon III-specific), implicating G-protein-coupled receptor signaling as the upstream mechanism. The same group published complementary data showing that tritium-labeled Semax binds specifically to rat basal forebrain membranes at KD 2.4 nM with calcium-dependent, reversible characteristics. BDNF upregulation was also confirmed in prefrontal cortex and striatum in subsequent work, with regional specificity (hippocampus/basal forebrain responsive; cerebellum not responsive).
The Pro-Gly-Pro C-terminal extension improves proteolytic stability over the native ACTH(4–10) core sequence. Formal human pharmacokinetic data is not published in accessible English-language literature. Lyophilized Semax is stable at −20°C for up to 24 months. The N-terminal methionine (position 1 of MEHFPGP) is susceptible to oxidation, producing met-oxide impurities that can alter biological activity; lyophilized storage and protection from oxidizing conditions minimize this risk. The approved Russian formulation is intranasal — the route with the most published efficacy data; for in vitro research, reconstitution with bacteriostatic water and storage at 2–8°C (use within 14 days) applies. COA verification should include HPLC purity (≥98%), MS confirmation at ~887 Da, and methionine oxidation status.
Semax is an approved research protocol compound in Russia for ischemic stroke rehabilitation and cognitive indications, based on domestic clinical trial data conducted under Russian regulatory standards. This approval constitutes a substantive human evidence base. However, the primary clinical trial data is not fully published in English-language peer-reviewed journals accessible via PubMed, which limits independent evaluation by non-Russian researchers. Formal human pharmacokinetic data for the natural Semax sequence is not published in accessible literature. Researchers should treat the Russian approval as a legitimate regulatory fact while accounting for the limited accessibility of the underlying human data. All YPB Semax is Research Use Only and is not equivalent to the approved intranasal Russian compound formulation.
Yes. YourPeptideBrand.com provides white-label dropship for Semax in a 10mg configuration at $37.04 Premier wholesale, with a suggested MSRP of $50 generating $12.96 gross margin per unit (25% margin). This is the same margin profile as Selank and is the lowest margin percentage in the cognitive research category. Operators may consider pricing above $50 given Semax’s Russian approval for ischemia rehabilitation and the published BDNF mechanism depth. Storefronts launch within 30 days with no inventory requirements. Use the profit calculator to model different MSRP scenarios.
Every Semax batch includes a lot-specific COA from an independent third-party laboratory covering: qualitative ID (HPLC + MS confirmation of MEHFPGP sequence at ~887 Da and methionine oxidation status), HPLC purity (≥98%), L-amino acid configuration at all residues, endotoxin (<1 EU/mg), TAMC, and TYMC. Methionine oxidation status confirmation is important for Semax quality assurance, as the N-terminal Met-1 is susceptible to oxidation during storage. Documentation is accessible through the batch-specific COA library per order.
Premier tier members ($497/mo) access Semax 10mg at $37.04 wholesale. At the suggested $50 MSRP, gross margin is $12.96 per unit (25%) — the lowest percentage margin in the cognitive research category, matching Selank. Core tier ($297/mo) pricing is $44.45 per unit. The strategic positioning for Semax is the Selank + Semax cognitive pair: combined search volume across both compounds exceeds 26,800/mo, both have Russian compound approval, and both target the same cognitive research buyer. The dual-SKU Semax + Selank basket generates $25.92 combined margin per order. Adding NAD+ 500mg ($156.05 Premier margin) and GHK-Cu 100mg ($92.96) to the cognitive research catalog generates $274.93 combined margin per comprehensive cognitive order from a single research buyer.
Key Takeaways
Research Takeaways
- 3-fold hippocampal BDNF exon III mRNA from single application: Dolotov et al. (2006) published quantitative BDNF/TrkB upregulation data from a single intranasal dose — the most rigorously documented BDNF mechanism of any compound in the YPB cognitive category (PMID: 16996037).
- CREB-dependent pathway at KD 2.4 nM receptor binding: Specific, calcium-dependent, reversible binding confirmed in basal forebrain; G-protein-coupled receptor upstream mechanism implicated by CREB-dependent BDNF exon III response.
- No adrenal steroidogenic activity: ACTH(4–10) core lacks the MC2R adrenal-binding domain; Semax does not stimulate cortisol secretion — the primary design rationale separating it from full ACTH research tools.
- Genome-wide ischemia transcriptomics published: Medvedeva et al. (2014) documented VEGF pathway, NGF, NT-3, and Trk receptor modulation in pMCAO model via BMC Genomics analysis (PMC3987924).
- Russian compound approval for ischemia rehabilitation: The only YPB cognitive compound with regulatory approval for a neuroprotective indication; approval is legitimate but clinical trial data is not fully accessible in English-language PubMed.
- Pro-Gly-Pro stability strategy: Same C-terminal extension as Selank; both compounds share this metabolic stability approach, suggesting the two compounds as a deliberate research design pair from the same Russian research group.
- Primary clinical data in Russian literature: compound registration trial data not fully accessible in English; researchers should account for this in evidence evaluation.
Business Takeaways
- $12.96 gross margin at Premier tier (25%) — same as Selank; lowest in the cognitive category. Operators should consider pricing above $50 MSRP given ischemia approval and BDNF mechanism depth.
- 12,000 monthly searches at very low KD — co-search with Selank means the same content investment captures ~26,800/mo combined audience across both cognitive Russian nootropic compounds.
- Mandatory Selank companion SKU: The Selank + Semax pair is the most frequently co-researched cognitive peptide combination; brands offering one should offer both to avoid sending buyers to competitors for the other.
- Complete cognitive research catalog: Selank + Semax + NAD+ + GHK-Cu addresses GABAergic, neurotrophic, metabolic aging, and gene expression pathways — four mechanistically non-overlapping cognitive research mechanisms from a single catalog.
Ready to complete your cognitive research catalog with Semax? Book a consultation with the YPB team and discuss full cognitive category positioning.
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