Semax
Semax is a Russian-developed heptapeptide ACTH 4-7 + PGP fragment that upregulates BDNF and NGF in the hippocampus; a large Russian RCT (Gusev et al. 2005, PMID 16042170, n=187) showed significant functional recovery improvement in ischemic stroke, though Western replication is essentially absent.
Semax scored 6.8 / 10 (👍 Worth trying) on the BioHarmony scale as a Substance → Peptide.
What It Is
Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro; MEHFPGP) derived from the 4-7 fragment of adrenocorticotropic hormone (ACTH) with an appended Pro-Gly-Pro (PGP) tripeptide. It was developed in the Soviet Union in the 1980s-90s by Igor Ashmarin and colleagues at Moscow State University, with the PGP extension added specifically to enhance metabolic stability and prolong receptor interaction relative to the parent ACTH 4-10 molecule.
Type: Peptide (ACTH-derived heptapeptide; gray-market research compound outside Russia).
Current status: Haven't tried.
The peptide exerts its primary effects through several converging mechanisms. First, it robustly upregulates BDNF (brain-derived neurotrophic factor) and NGF (nerve growth factor) in the hippocampus, as demonstrated in rodent models by Dolotov et al. (2006). This BDNF upregulation is the mechanistic pillar most cited in discussions of Semax's nootropic and neuroprotective properties. Second, it inhibits enkephalin-degrading enzymes, principally prolyl endopeptidase, thereby prolonging endogenous enkephalin activity and modulating opioidergic tone. Third, it shows low-affinity binding activity at melanocortin receptors (MC4R, MC5R), the same receptor class targeted by the broader ACTH family, though Semax's affinity is substantially lower than parent ACTH. Fourth, it enhances cholinergic neurotransmission, relevant to its observed cognitive and attentional effects.
Semax is administered primarily as an intranasal spray. The nasal route is not incidental: the olfactory epithelium provides a direct conduit to the CNS via axonal transport and cerebrospinal fluid circulation, bypassing the blood-brain barrier that would otherwise limit peptide CNS penetration. The 0.1% concentration is the community-standard nootropic formulation; the 1% concentration is used in Russian clinical stroke protocols and was the dose studied in the Gusev 2005 RCT.
In Russia, Semax is a registered pharmaceutical available OTC and by prescription for ischemic stroke recovery, transient ischemic attack, and optic nerve disorders. Outside Russia, it occupies a regulatory gray zone: not scheduled or banned in most Western countries but not approved, sold as a research compound, and subject to variable import restrictions.
Terminology
- ACTH: Adrenocorticotropic hormone. A 39-amino-acid pituitary hormone. Semax derives from its 4-7 fragment plus PGP extension.
- BDNF: Brain-derived neurotrophic factor. A protein that supports neuron survival, growth, and synaptic plasticity. Key driver of Semax's proposed cognitive and neuroprotective effects.
- NGF: Nerve growth factor. A neurotrophin supporting cholinergic neuron survival and peripheral nerve regeneration; upregulated by Semax in hippocampal tissue.
- BBB: Blood-brain barrier. The selective barrier limiting what crosses from blood into brain tissue; intranasal delivery partially circumvents this for peptides.
- PGP: Pro-Gly-Pro tripeptide. The C-terminal extension added to ACTH 4-7 to create Semax; improves stability and receptor residence time.
- MC4R / MC5R: Melanocortin receptor subtypes 4 and 5. Semax shows low-affinity activity here, contributing to some CNS arousal and mood effects.
- Prolyl endopeptidase: An enzyme that degrades enkephalins and other neuropeptides. Semax inhibits this enzyme, prolonging enkephalin availability.
- RCT: Randomized controlled trial. The gold-standard human evidence design; most Semax RCTs are Russian-language and not indexed on PubMed.
- TrkB: The primary receptor for BDNF. Upregulated alongside BDNF by Semax in rodent hippocampus (Dolotov 2006); mediates downstream neuroprotective signaling.
Dosing & Protocols
Dosing information is summarized from published research and community reports. This is not a prescribing guide. Consult a healthcare provider before starting any protocol.
View 3 routes and 2 protocols
Routes & Forms
| Route | Form | Clinical Range | Community Range |
|---|---|---|---|
| Intranasal spray (0.1% - nootropic) | Nasal spray solution | Not established in Western RCTs; Russian community studies reference 300-600 mcg/day | 300-1000 mcg/day (1-3 sprays per nostril, 1-2x daily) |
| Intranasal spray (1% - clinical stroke) | Nasal spray solution | 3 mg per dose, multiple doses per day; used in Gusev 2005 stroke protocol | Rarely used outside clinical setting at this concentration |
| Subcutaneous injection | Lyophilized powder reconstituted in bacteriostatic water | Used in some Russian research protocols; dose varies by indication | Less common in community use; typically 200-600 mcg per injection |
Protocols
Standard Nootropic Anecdotal
- Dose
- 300-600 mcg total
- Frequency
- Once or twice daily
- Cycling
- 1-2 weeks on / 1 week off (community-derived)
- Duration
- 1-2 week cycles
Community pattern: 1-2 weeks on, 1 week off. No clinical basis for cycle length.
Russian Stroke Protocol (clinical) Clinical
- Dose
- 3 mg per dose (1% spray)
- Frequency
- Multiple times daily under medical supervision
- Duration
- 10-14 day inpatient course
Matches Gusev 2005 trial protocol; requires physician oversight
Use-Case Specific Dosing
| Use Case | Dose | Notes |
|---|---|---|
How this score is calculated →
Upside (2.05 / 5.00)
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Efficacy | 25% | 3.3 | 0.825 | |
| Breadth of Benefits | 15% | 3.5 | 0.525 | |
| Evidence Quality | 25% | 2.5 | 0.625 | |
| Speed of Onset | 10% | 4.0 | 0.400 | |
| Durability | 10% | 2.5 | 0.250 | |
| Bioindividuality Upside | 15% | 2.8 | 0.420 | |
| Total | 3.045 |
Upside Rationale
Efficacy (3.3/5.0): The strongest efficacy signal in humans comes from Gusev et al. (2005, PMID 16042170), a Russian RCT of 187 ischemic stroke patients in which Semax 1% intranasal significantly improved functional recovery scores versus control. In healthy cognitive enhancement contexts, Russian volunteer studies report improved attention, information processing speed, and working memory, but these studies are not indexed in PubMed and have not been replicated outside Russia. Animal models consistently show memory consolidation enhancement and cognitive protection under hypoxic stress, with effect sizes suggesting a moderate-to-strong preclinical signal. In the absence of a Western cognitive RCT with formal effect size metrics (Cohen's d), the human efficacy score is calibrated at 3.3 rather than higher: meaningful, but geographically unverified.
Breadth of Benefits (3.5/5.0): Semax touches multiple systems: cognitive function and focus (primary nootropic claim), neuroprotection and stroke recovery (Russian clinical indication), optic nerve health (separate Russian indication), hypoxia and metabolic stress resilience (animal models), possible mild anxiolytic effect (inconsistent animal data), and pediatric ADHD (Russian clinical use). The range is genuinely multi-system, but the evidence strength varies considerably by endpoint. The neuroprotective and cognitive endpoints are the most supported; mood and anxiety claims rest largely on animal models and anecdote.
Evidence Quality (2.5/5.0): Animal mechanistic evidence is robust and independently replicated: BDNF upregulation (Dolotov 2006), enkephalin inhibition (Kost 2001), hypoxia models (Agapova 2007), gene expression arrays (Limborska 2002). The Gusev 2005 stroke RCT is a genuine randomized controlled trial, not a case series. However, the overwhelming majority of human evidence is in Russian-language journals with limited PubMed visibility, and Western replication is essentially absent. A -1.0 evidence integrity adjustment is applied: this is not industry-funding burial but rather geopolitical research siloing and the complete absence of independent Western replication. Without that adjustment, the mechanistic coherence alone would score this closer to 3.5. The -1.0 adjustment yields 2.5, which is honest given that a US or EU clinician cannot independently access and verify most of the evidence base.
Speed of Onset (4.0/5.0): Acute cognitive and focus effects are reported within 30-60 minutes of intranasal administration, consistent with the rapid CNS delivery via olfactory/trigeminal pathways and the enkephalin-inhibiting mechanism that operates without requiring protein synthesis. Peak functional effect is observed at 1-3 hours. This is faster onset than most oral nootropics and faster than any strategy requiring transcription-level changes. The BDNF upregulation mechanism, by contrast, requires hours to days and cumulative dosing for measurable neuroplasticity changes.
Durability (2.5/5.0): Acute effects clear within hours of a single dose. Cumulative BDNF upregulation in rodent hippocampus (Dolotov 2006, Zhuravin 2016) suggests that repeated dosing may produce lasting neuroplastic changes that outlast plasma half-life, but this has not been demonstrated in humans. Without human longitudinal data, the durability score cannot exceed 2.5: benefits are primarily present when dosing is maintained. This positions Semax closer to caffeine (acute, reversible) than to interventions with lasting structural changes (e.g., tDCS-induced plasticity windows).
Bioindividuality Upside (2.8/5.0): Data on responder predictors are nearly absent. Community reports show wide variance: some users report dramatic focus enhancement, others report nothing or mild anxiety. The cholinergic and BDNF mechanisms predict that individuals with lower baseline BDNF (stress, depression, aging) or suboptimal cholinergic tone may respond more robustly. The intranasal delivery route introduces individual variability in absorption depending on nasal anatomy, mucus clearance rate, and mucosal health. The 2.8 score reflects the absence of responder stratification data rather than confirmed low response rates.
Downside (0.90 / 5.00)
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Safety Risk | 30% | 2.0 | 0.600 | |
| Side Effect Profile | 15% | 1.8 | 0.270 | |
| Financial Cost | 5% | 2.0 | 0.100 | |
| Time/Effort Burden | 5% | 2.0 | 0.100 | |
| Opportunity Cost | 5% | 1.8 | 0.090 | |
| Dependency / Withdrawal | 15% | 1.5 | 0.225 | |
| Reversibility | 25% | 1.2 | 0.300 | |
| Total | 1.685 | |||
| Harm subtotal × 1.4 | 1.953 | |||
| Opportunity subtotal × 1.0 | 0.290 | |||
| Combined downside | 2.243 | |||
| Baseline offset (constant) | −1.340 | |||
| Effective downside penalty | 0.903 |
Downside Rationale
Safety Risk (2.0/5.0): Published Russian trials, including the 187-patient Gusev 2005 RCT, reported no serious adverse events attributable to Semax. No catastrophic adverse event floor is triggered: no case reports of intrinsic life-threatening harm from Semax alone exist in the indexed literature. The safety concern that warrants a score above 1.0 is the thin long-term human safety dataset and the gray-market sourcing context (purity unverified by FDA or EMA). Theoretical concerns include possible seizure threshold modulation from ACTH-fragment activity, but this is not documented in clinical use. Safety risk of 2.0 reflects "low known risk with incomplete long-term data," not confirmed safety at 1.0.
Side Effect Profile (1.8/5.0): Nasal irritation is the most commonly reported side effect in Russian trials, consistent with intranasal peptide administration generally. Occasional transient headache and, at higher doses or frequencies, mild restlessness or sleep disruption have been noted anecdotally. The side effect burden is among the lowest of any active nootropic peptide class. Gastrointestinal effects are absent (intranasal delivery). No significant hormonal, hepatic, or renal signals have emerged even in the community use literature.
Financial Cost (2.0/5.0): Research-grade 0.1% Semax nasal spray from established peptide vendors costs approximately $30-60 per vial (typically 3 mL), lasting 2-4 weeks at standard dosing. This translates to roughly $30-80 per month, making it moderately accessible relative to prescription peptides but more expensive than most oral supplements. Quality variance between vendors is a practical issue that affects effective cost (inferior product = wasted spend).
Time/Effort Burden (2.0/5.0): Administration is 1-3 nasal sprays per nostril, one to two times daily: a sub-2-minute ritual. Reconstitution from lyophilized powder (for injection-grade preparations) adds 5-10 minutes per batch. Refrigeration of the solution after preparation is required. Cycling protocols add scheduling overhead but are self-managed. The burden is low compared to any device-based intervention.
Opportunity Cost (1.8/5.0): Semax stacks well with the most common nootropic compounds (racetams, cholinergics, adaptogens) given its distinct mechanism. It does not meaningfully crowd out higher-evidence cognitive interventions; a user doing Semax and exercise + sleep optimization is not substituting one for the other. The 1.8 score (below neutral) reflects that its use does not produce meaningful trade-offs in either time or stack compatibility.
Dependency/Withdrawal (1.5/5.0): No withdrawal syndrome, rebound, or receptor downregulation has been documented. Community reports do not describe tolerance development over typical cycle lengths. The cycling pattern (1-2 weeks on, 1 week off) used in the community appears precautionary rather than pharmacologically necessary. This is among the cleanest dependency profiles of any active nootropic peptide.
Reversibility (1.2/5.0): Cessation results in return to baseline cognitive function within days. No permanent changes, no taper requirement, no rebound below baseline. The reversibility profile is near-ideal. BDNF effects, if they accumulate with chronic use, would represent a positive rather than a negative persistent effect, and even these would normalize over weeks to months after stopping.
Verdict
✅ Best for: Biohackers and nootropic users seeking acute cognitive enhancement (focus, processing speed, working memory) with low side-effect burden and mechanistic credibility beyond typical supplement stack; individuals interested in neuroprotection as a longevity-adjacent strategy given the BDNF/NGF mechanism; researchers and clinicians in countries where it is legal who want a peptide with at least one genuine RCT (versus purely anecdotal peptides); older adults with early cognitive concerns who want a lower-risk exploratory option while waiting for Western evidence; anyone who has plateaued on standard nootropics (caffeine, racetams) and wants a mechanistically distinct tool.
❌ Avoid if: Pregnant or breastfeeding (no safety data); history of seizure disorder (theoretical ACTH-fragment CNS excitability concern); baseline high anxiety (some users report exacerbation; mixed signal in animal models); taking MAOIs or psychiatric medications without physician clearance; in jurisdictions where importation is prohibited or actively enforced (verify local law before ordering); unwilling to accept the inherent quality uncertainty of gray-market research compounds; seeking an intervention with Western peer-reviewed replication: Semax currently cannot deliver that.
Use Case Breakdown
The overall BioHarmony score reflects the intervention's primary evidence profile. These subratings are independent assessments per use case.
| Use Case | Score | Summary |
|---|---|---|
| 👍 Cognition / Focus Primary | 6.5 | Russian healthy-volunteer studies + robust animal cognition data; acute focus reported widely in community. |
| 👍 Neuroprotection Primary | 6.5 | BDNF/NGF upregulation + stroke recovery RCT (Gusev 2005) support neuroprotective classification. |
| 👍 Memory Primary | 6.0 | Extensive animal memory-consolidation models; limited human RCTs (Russian); BDNF mechanism plausible. |
| ○ Stress / Resilience Primary | 4.0 | Hypoxia/metabolic stress resilience in animal models; indirect human relevance. |
| 👍 Neuroplasticity | 6.0 | BDNF + NGF upregulation in hippocampus (animal data, Dolotov 2006) directly supports neuroplasticity. |
| ⚖️ Geriatric / Aging Population | 5.0 | Stroke recovery + neuroprotection indication in elderly is the primary clinical use case in Russia. |
| ○ Nerve Regeneration | 4.5 | Optic nerve indication in Russia; animal nerve regeneration models positive; human data limited. |
| ○ Flow State / Peak Mental Performance | 4.5 | Acute focus + BDNF mechanism plausible; community reports of enhanced flow; no formal measurement. |
| ○ Traumatic Brain Injury | 4.5 | Neuroprotective mechanism + stroke RCT overlap; no dedicated TBI RCT exists but mechanism is directly relevant. |
| ○ Reaction Time / Coordination | 4.0 | Acute nootropic effect + animal psychomotor data; plausible in community use context. |
| ○ Healthspan | 4.0 | Cognitive preservation + neuroprotection = healthspan-relevant; mechanistic, not proven in humans. |
| ○ Energy / Fatigue | 4.0 | Acute mental energy is the primary community-reported benefit; no formal fatigue measurement. |
| ○ Eye / Vision Health | 3.5 | Russian clinical use for optic nerve atrophy; limited published data but registered indication. |
| ○ Mood / Emotional Regulation | 3.5 | Anecdotal mood-lift reports; no controlled human mood data. |
| ○ Anxiety | 3.5 | Mixed: some animal anxiolytic data; human evidence absent; community reports inconsistent. |
| ○ Longevity / Lifespan | 3.5 | Neuroprotective mechanism has longevity relevance; no lifespan data. |
| ○ Creativity / Divergent Thinking | 3.0 | Indirectly via cognitive enhancement; no creativity-specific data. |
| ○ Anti-Inflammatory | 3.0 | Animal neuro-inflammatory data; not a primary anti-inflammatory agent. |
| ○ Pediatric Use | 3.0 | Russian ADHD pediatric use is a registered indication; data not peer-reviewed in Western literature. |
Frequently Asked Questions
How does Semax work in the brain?
Semax upregulates BDNF and NGF in the hippocampus within hours of administration, as demonstrated in rat models by Dolotov et al. (2006). It also enhances cholinergic neurotransmission, shows low-affinity activity at melanocortin receptors (MC4/MC5), and inhibits enkephalin-degrading enzymes (prolyl endopeptidase), effectively prolonging enkephalin activity. The combined result is acute cognitive enhancement plus downstream neuroprotective signaling. Unlike its parent ACTH 4-10, Semax adds the PGP tripeptide to extend receptor interaction time.
What does the human evidence actually show for Semax?
The strongest human evidence is Gusev et al. (2005, PMID 16042170), a large Russian RCT in 187 ischemic stroke patients showing significant functional recovery improvement with Semax 1% intranasal versus control. Russian healthy-volunteer studies report cognitive and focus improvements, but these are not indexed in PubMed in English and have not been independently replicated in Western populations. Animal evidence is robust; human evidence is geographically siloed and limited.
How much Semax should I take and when?
For nootropic use, the community-standard dose is 1-3 sprays per nostril of 0.1% concentration (total 300-1000 mcg/day), taken once or twice daily. Morning dosing is preferred; late-afternoon use may disrupt sleep in some users. A common cycling pattern is 1-2 weeks on followed by 1 week off, though no clinical basis exists for this cycle length. The clinical 1% concentration (3 mg/dose) is reserved for stroke recovery under medical supervision in Russia.
Is Semax safe, and are there known side effects?
Published Russian trials report a low and mild adverse event profile: the most commonly noted effects are transient nasal irritation, occasional mild headache, and rare reports of fatigue or irritability. No serious adverse events were reported in the Gusev 2005 stroke RCT. Long-term safety in humans is unknown; there are no multi-year human studies. The absence of Western trials means post-market surveillance data is thin. No catastrophic AE floor is triggered.
Who should avoid Semax?
Semax should be avoided during pregnancy and breastfeeding (no safety data), by individuals with a history of seizure disorders (ACTH-fragment activity has theoretical CNS excitability implications), and by those with documented melanocortin sensitivity. Sourcing is a practical concern: as a gray-market research compound in the US and EU, purity is vendor-dependent. Anyone on psychiatric medications or MAOIs should consult a physician before use. Anxiety exacerbation is occasionally reported, making it a poor fit for high-baseline anxiety individuals.
What is the evidence gap between Russian and Western research on Semax?
Semax was developed in the Soviet Union and is registered as a medicine only in Russia, where it remains the primary research base. The majority of human trials are published in Russian-language journals with limited PubMed indexing; only 1-2 English-language peer-reviewed publications exist. No independent Western RCT in healthy adults has been completed as of 2026. This is not evidence of inefficacy but rather reflects geopolitical research siloing. The animal mechanistic literature (BDNF, NGF, memory consolidation) is independently replicated and credible.
How fast does Semax work, and how long do effects last?
Acute cognitive and focus effects are typically reported within 30-60 minutes of intranasal administration, with peak effect at 1-3 hours; the plasma half-life is approximately 30-60 minutes. The enkephalin-inhibiting mechanism may extend functional duration modestly beyond plasma half-life. Cumulative BDNF upregulation effects, if they occur in humans as they do in rodents (Dolotov 2006), would require 2-4 weeks of consistent dosing to manifest as measurable neuroplasticity changes. Stopping Semax results in gradual return to baseline.
What is the legal status of Semax outside Russia?
In Russia, Semax is a registered pharmaceutical (OTC and prescription formulations). In the US, EU, and UK, it is not approved as a drug or dietary supplement, placing it in a regulatory gray zone: legal to possess for research purposes in most US states but potentially subject to import restrictions. It is sold openly by peptide research vendors but carries no FDA-approved quality or purity assurance. Travelers should research import laws for their specific country; some customs agencies have seized shipments.
How This Score Could Change
BioHarmony scores are living assessments. New research, regulatory changes, or personal context can shift the score up or down. These are the most likely scenarios that would change this intervention's rating.
| Scenario | Dimension shifts | New Score |
|---|---|---|
| First Western RCT in healthy adults confirms cognitive benefit | Evidence 2.5→3.5, Bioindividuality 2.8→3.2 | 7.0 / 10 💪 Strong recommend |
| Long-term BDNF durability confirmed in humans | Durability 2.5→3.5, Efficacy 3.3→3.8 | 7.0 / 10 💪 Strong recommend |
| Serious AE or safety signal emerges in post-market surveillance | Safety 2.0→3.5 | 6.3 / 10 👍 Worth trying |
| Russian evidence base retracted or severely discredited | Evidence 2.5→1.8 | 6.6 / 10 👍 Worth trying |
| Mega-trial confirms cognitive + neuroprotective benefit with responder data | Efficacy 3.3→4.0, Breadth 3.5→4.0, Evidence 2.5→3.2, Bioindiv 2.8→3.5 | 7.2 / 10 💪 Strong recommend |
| FDA approval in US with OTC access and quality standardization | Cost 2.0→1.5, Bioindividuality 2.8→3.5 | 6.9 / 10 👍 Worth trying |
Key Evidence Sources
- Gusev EI et al. (2005). Neuroprotective effects of Semax in patients with ischemic stroke. Zh Nevrol Psikhiatr Im S S Korsakova. PMID 16042170.. Flagship Russian RCT (n=187 ischemic stroke patients); functional recovery improvement with Semax 1% vs control.
- Dolotov OV et al. (2006). Semax, an analogue of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Research. PMID 16579966.. Primary mechanistic study: BDNF and trkB upregulation in hippocampus with Semax; independently published in English.
- Asmarin IP et al. (1997). A successful combination of short peptides with amino acids in the regulation of physiological functions. Biokhimiia. PMID 9353299.. Foundational Russian paper on ACTH-fragment peptide regulatory activity; early mechanistic rationale.
- Levitskaya NG et al. (2018). Intranasal administration of Semax and its effects on the central nervous system. Neuroscience and Behavioral Physiology.. Reviews intranasal Semax pharmacokinetics and CNS access via olfactory/trigeminal routes.
- Limborska SA et al. (2002). Analysis of Semax activity using oligonucleotide microchips. Molecular Biology (Mosk). PMID 12456051.. Microarray study demonstrating wide gene-expression changes with Semax in rat brain including BDNF-pathway genes.
- Manchenko DM et al. (2010). Effect of Semax on the behavior of rats in a model of depression. Eksperimental'naia i klinicheskaia farmakologiia. PMID 21323127.. Animal model: Semax shows antidepressant-like effects in forced swim test; basis for anecdotal mood claims.
- Kost NV et al. (2001). Semax inhibits the enkephalin-degrading enzymes from human blood. Neurokhimiia. PMID 11605512.. Demonstrates enkephalin-degrading enzyme (prolyl endopeptidase) inhibition; explains opioidergic modulation component.
- Agapova TY et al. (2007). Neurospecific effects of Semax on hypoxia and ischemia in animal models. Peptides.. Animal study: Semax improves outcomes in hypoxia and cerebral ischemia models; supports neuroprotection claim.
- Ashmarin IP et al. (1997). Regulatory peptides: synthesis, structures, mechanisms of action. Uspekhi Biologicheskoi Khimii.. Foundational Russian peptide pharmacology review; patent-era documentation of Semax design rationale.
- Grivennikov IA et al. (2008). Nerve growth factor and cognitive functions. Progress in Neurobiology.. Broader NGF-cognition review; contextualizes Semax NGF-upregulation findings in hippocampus.
- Kolik LG et al. (2014). Effectiveness of peptide anxiolytic Selank and antidepressant Semax in treatment of anxiety and depressive mixed states. Bulletin of Experimental Biology and Medicine. PMID 25430671.. Russian animal comparison study: Semax vs Selank in anxiety-depression mixed models.
- Zhuravin IA et al. (2016). Semax treatment during early postnatal period exerts long-lasting effects on behavior and brain-derived neurotrophic factor in rats. Developmental Psychobiology. PMID 26989837.. Demonstrates cumulative BDNF effects with developmental Semax exposure in rats; durability data.
Other interventions for Cognition & Focus
See all ratings →📊 How BioHarmony scoring works
BioHarmony translates a weighted expected-value calculation into a reader-facing 0–10 score. 5.0 is neutral (benefits and risks balance). Above 5 = benefits outweigh risks; below 5 = risks outweigh benefits.
Harm-type downsides (safety risk, side effects, reversibility, dependency) carry a 1.4× precautionary multiplier. Harm weighs more than benefit. Opportunity-type downsides (financial cost, time/effort, opportunity cost) are subtracted at face value.
Use case subratings are independent assessments of how well the intervention addresses specific health goals. They are not components of the overall score. Each subrating reflects the scorer's judgment based on use-case-specific evidence, safety, and effect sizes.
Every dimension is evaluated on a 1–5 scale, and the baseline (1) is subtracted before weighting. A perfect intervention with zero downsides contributes zero penalty rather than a residual floor, so top-tier scores are actually reachable.
EV = Upside − Downside
EV = 2.045 − 0.903 = 1.142
EV ranges from −5 to +5. Adding 7 shifts to 2–12, dividing by 12 normalizes to 0–1, then ×10 gives the 0–10 score.
Score = ((1.142 + 7) / 12) × 10 = 6.8 / 10
