Research information only. PrecisePep is an educational library. It is not medical advice and is not intended to assist, encourage or enable self-administration. The compounds documented here are research chemicals — most are not approved for human use. Read the full disclaimer.
PrecisePep/Blends & Stacks/Semax + Selank
Neuro-Cognitive Blend
the Russian nootropic stack · Semax/Selank · Adamax + Selank
Drive and calm from two peptides out of the same Moscow research programme — the only pairing on this site where both components are registered medicines somewhere, and neither is registered here.
These two are almost never used apart, and the reason is practical rather than pharmacological. Semax is activating. Used alone, at higher doses or late in the day, it reliably produces irritability, agitation and disrupted sleep. Selank is calming without being sedating. Together, the community position is that the pair delivers Semax's drive with Selank's floor under it.
Both come from the same Moscow research programme, both are Pro-Gly-Pro-stabilised heptapeptides, and both are registered medicines in Russia — Semax for ischaemic stroke and cognitive disorders, Selank as an anxiolytic for generalised anxiety disorder and neurasthenia.[1][2] That is a real regulatory status in a real jurisdiction, backed by a real clinical literature that is largely Russian-language, often small, and thinly replicated by independent Western groups.
Independent work has examined the two together at a systems level, describing complementary rather than overlapping effects on regulatory gene networks — the closest thing to combination evidence that exists for any stack documented on this site.[3]
Circulating protocols specify "never after 2pm" for both. That rule comes from consistent community reports of insomnia and overstimulation from late Semax dosing, and it is one of the more reliably reproduced practical observations in this space — even though the sleep effect has never been formally measured.
Shared substrate: BDNF. Both peptides upregulate brain-derived neurotrophic factor, Semax particularly in hippocampus and frontal cortex. This is the common neurotrophic floor beneath both the cognitive and the stress-resilience claims.
Shared substrate: enkephalinase inhibition. Both inhibit enzymes that degrade endogenous enkephalins, prolonging endogenous opioid signalling. This contributes to mood stabilisation and to the analgesic effects reported for the Semax family.
Divergent arm — Semax: dopaminergic activation. Enhanced dopaminergic transmission plus melanocortin-related neuroprotection. This is the drive and focus arm, and it is where the overstimulation comes from.
Divergent arm — Selank: GABAergic modulation. Alteration of GABAergic gene expression and allosteric enhancement of GABA_A-mediated inhibition — without binding the benzodiazepine site, which is the proposed reason for the absence of sedation, tolerance and withdrawal.
The combination argument. Push dopaminergic drive and simultaneously raise inhibitory tone, on a shared neurotrophic substrate. The claim is that the calm is not achieved by dulling the activation but by raising the threshold at which activation becomes agitation. Coherent; never trialled as a fixed combination.
A blend is not a compound. It is several compounds sharing a vial, and each one carries its own evidence base, dose-response curve and risk profile. Study them individually before studying them together.
| Component | Share of blend | Role in the blend | Monograph link |
|---|---|---|---|
| Semax Met-Glu-His-Phe-Pro-Gly-Pro |
Typically equal microgram dose | Activation. BDNF/TrkB and NGF upregulation, dopaminergic enhancement, enkephalinase inhibition. Supplies focus, drive and the reported clearing of brain fog — and, at higher doses or late timing, the overstimulation. | Monograph |
| Selank Thr-Lys-Pro-Arg-Pro-Gly-Pro |
Typically equal microgram dose | Regulation. GABAergic modulation without benzodiazepine-site agonism, serotonergic effects, BDNF upregulation, plus residual tuftsin-derived immune activity. Supplies the calm that keeps Semax usable. | Monograph |
The equal-microgram convention is exactly that — a convention. No dose-equivalence study exists between these two peptides, and there is no reason to assume 500 mcg of one is equipotent to 500 mcg of the other.
Both are conventionally administered intranasally, which is the route the Russian clinical data was generated on. Subcutaneous administration — common in the research community — has no supporting pharmacokinetic data for either compound.
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Semax for ischaemic stroke, TIA, cognitive disorders and optic nerve conditions; Selank for generalised anxiety disorder and neurasthenia. Genuine regulatory approvals with domestic clinical literature behind them.
Russian clinical work in GAD and neurasthenia reports efficacy comparable to classical benzodiazepine treatment, without sedation, cognitive impairment, tolerance or withdrawal.
The best-corroborated mechanistic finding for Semax, with associated reductions in infarct volume and improved functional recovery in rodent models.
Functional connectomic and gene-network analysis has examined Semax and Selank in parallel, describing distinct but complementary effects on regulatory networks.
Direct evidence of interaction with the benzodiazepine class — relevant as both a mechanistic finding and an interaction warning.
The pairing has never been trialled as a combination product in any population.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The dominant community use case, extrapolated from cognitive-impairment and stroke populations to healthy cognition — the leap that fails routinely across the entire nootropic field.
The core reason the pair exists. Mechanistically complementary, universally reported, never measured.
Both components raise BDNF. Whether intermittent intranasal dosing produces durable structural change is unknown.
From the anti-stress and melanocortin literature. Notably, neither compound raises cortisol — the ACTH-derived Semax was specifically designed without corticotropic activity.
Fibromyalgia is a central disorder and the approved drugs for it — duloxetine, milnacipran — are monoaminergic. A centrally-acting monoaminergic pair is therefore aimed at the right target rather than a peripheral proxy, which is unusual in this library. Untested in the condition, and the interaction burden with existing fibromyalgia medication is the real issue.
BDNF elevation, dopaminergic modulation and enkephalinase inhibition all plausibly contribute. Neither compound has been trialled as an antidepressant to Western standards.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The characteristic Semax-driven report, described as clarity rather than stimulation.
The Selank contribution — users describe the combination as productive without the edge Semax alone produces.
A consistent report: many users cannot perceive Selank at all and notice its absence only when they stop taking it alongside Semax.
The origin of the "never after 2pm" rule and the most reproducible practical observation about this stack.
The amidated Semax analogue is reported as substantially more potent and longer-acting. Evidence for the analogue is thinner than for the parent, and conversion ratios are guesswork.
Diminishing effect over weeks is commonly reported and is the practical basis for the equal-time-on/off convention.
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Both compounds report benign profiles with nasal irritation as the principal issue. Registration-supported, but reflecting the reporting standards of that jurisdiction and era.
The ACTH fragment was chosen precisely to retain neurotropic effect without adrenal axis stimulation.
No FDA or EMA assessment, no independent pharmacovigilance, no long-term data in healthy adults.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The diazepam-potentiation finding means additive effect with benzodiazepines, alcohol, gabapentinoids and z-drugs should be assumed. This is the most concrete interaction risk on this page and it has direct evidence behind it.
Dopaminergic and serotonergic modulation layered on SSRIs, SNRIs, stimulants or antipsychotics is an entirely uncharacterised space, and the most plausible route to a serious adverse interaction with this stack.
Pregabalin, benzodiazepines and z-drugs are common in this population, and Selank has direct experimental evidence of potentiating diazepam. Duloxetine and milnacipran add uncharacterised serotonergic layering. This is the population most likely to be on those drugs and least likely to be told about the interaction.
BDNF signalling is regionally specific and context-dependent; more is not uniformly better, and sustained pharmacological elevation in healthy brains has never been characterised.
Brain fog and anxiety both have causes — sleep debt, thyroid dysfunction, anaemia, sleep apnoea, depression. Suppressing the symptom removes the prompt to find them.
Selank retains immune-modulating activity that community use ignores entirely.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most common complaint with intranasal use of either.
Consistently reported and easily avoided.
Reported at higher doses or with continuous use without breaks.
Occasionally reported, generally transient.
Reported by some users as the Semax effect wears off.
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Semax as 0.1% and 1% intranasal drops; Selank as 0.15% intranasal solution, both with defined dosing over defined treatment courses. Neither is registered as a combination.
Both peptides have been compared head-to-head by route in animals, and neither result supports treating injection as the spray delivered more reliably. Semax: intraperitoneal was nootropic and analgesic, intranasal was more effective for learning and had no analgesic effect at all. Selank: at a matched 300 mcg/kg, intraperitoneal raised frontal-cortex GABA-receptor binding 38% with no NMDA change, while intranasal raised NMDA-receptor binding 23% with no GABA change. Put those together and the injected pair is not the sprayed pair by another route — it is a different combination. Injecting costs some of the Semax cognitive effect and swaps Selank from an NMDA profile to a GABA one, which is the arm of its pharmacology that the diazepam-comparison work sits on. Neither finding is a reason it cannot work; both are reasons the intranasal dose figures do not carry across.
The pairing has no studied dosing at all.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
All Russian clinical data was generated intranasally, exploiting nose-to-brain transport. Subcutaneous administration is a different pharmacokinetic proposition with no supporting data for either compound.
Follows from the activating profile of Semax and the several-hour duration of both. The most consistently justified practical rule for this stack.
No dose-equivalence study exists between the two peptides.
Matches the registered clinical structure for both compounds and limits total exposure in the absence of long-term data.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The dosing in the Gold Standard protocol: 500 mcg Semax (or Adamax for a stronger effect) and 500 mcg Selank, mornings only, one vial (about 20 days) then cycle off for an equal period. The protocol states plainly that the two should always be taken together.
The general community range for the plain peptides.
Commonly reported, usually as two separate subcutaneous injections at the same 250—750 mcg each used intranasally, and commonly recommended by vendor dosing guides on the grounds that injection absorbs more predictably than a spray. That much is fair. What does not follow is the dose: no human study of either compound has used injection, and the animal work found the routes producing different pharmacology rather than the same pharmacology more reliably.
The amidated analogues are reported as more potent, so community doses are lower.
Some protocols divide the daily amount. Reasonable given reported duration; still bound by the afternoon cutoff.
| Form | Semax side | Selank side | Timing & cycle |
|---|---|---|---|
| Gold Standard Protocol | 500 mcg | 500 mcg | Morning · 1 vial on, equal time off |
| Standard | 300 – 600 mcg | 250 – 750 mcg | Morning, never after 2pm |
| Amidated analogues | 100 – 300 mcg | 100 – 300 mcg | Morning |
| Split dosing | 250 mcg × 2 | 250 mcg × 2 | Morning + early afternoon |
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Functional connectomic analysis describing complementary rather than overlapping network effects — the strongest combination-level characterisation among the stacks here that have never been trialled as a combination. It is a systems-biology description rather than an outcome trial, and CagriSema is the only blend on this site with the latter. That so little combination evidence exists anywhere is the real point.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Dopaminergic drive plus raised inhibitory tone on a shared BDNF substrate.
Community stacks pair nootropic and GH peptides on a general recovery-and-neuroplasticity premise. No interaction data, and the timing rules conflict — this stack is morning-only, the GH stack is pre-sleep.
Proposed on the premise that neuronal energy availability limits cognitive benefit. Speculative.
Morning activation and evening circadian signalling as bookends. Narrative rather than mechanism.
Caffeine stacking is the most common source of overstimulation reports; the GABAergic interaction is the one with direct experimental evidence.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The near-universal community convention, and the explicit instruction in the circulating protocol.
Common, and the usual source of the jitteriness complaints.
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Given reported tolerance and the absence of long-term data, matched on/off periods limit total exposure while preserving the reported effect.
The lowest-complexity approach consistent with both the registered route and the reported activation profile.
Persistent brain fog and anxiety have common medical causes that are cheap to rule out. This is the single most useful thing anyone reaching for this stack could do first.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
500 mcg Semax (or Adamax) and 500 mcg Selank, mornings only, never after 2pm, always taken together. One vial (about 20 days) on, then off for an equal period.
Grouped in the neuro-cognitive and endocrine axis category, introduced after the metabolic, mitochondrial and regenerative phases.
This pairing is a community construct rather than a formulated product — two separately supplied compounds used together on a stimulating-plus-calming rationale. That rationale is more coherent than most stacking arguments in this library, and it has still never been studied as a combination.
Neither compound is approved outside Russia, and the combination has never been studied in anything. Semax is a registered Russian medicine for stroke, cognitive impairment and optic nerve disease; Selank has Russian clinical work in generalised anxiety. Both literatures are small, largely untranslated and unreplicated outside the region. These are supplied as two separate vials — the calculator sends this entry to the individual presets for that reason.
Pathophysiology
Anxiety disorders frequently present with fatigue and reduced capacity for effort rather than with agitation, and that presentation is poorly served by sedating anxiolytics, which worsen the fatigue.
Mechanistic rationale
Selank’s reported profile is anxiolytic and mildly activating rather than sedating; Semax is reported as stimulating and pro-cognitive. The combination targets a real clinical gap — anxiety in someone who cannot afford to be slowed down. That is a more thoughtful rationale than most stacks here, and it is still an inference about two compounds neither of which has Western trial evidence.
Community reports
The most common reason for the pairing and the most consistently positive reporting. Also the most placebo-susceptible combination of endpoints in this library: subjective anxiety and subjective focus, self-assessed, days after starting.
Components carrying the argument: Selank anxiolysis + Semax activation
Pathophysiology
Attention depends on prefrontal catecholamine signalling; anxiety independently degrades working memory by consuming attentional capacity.
Mechanistic rationale
There is a genuine two-route argument here: Semax acting on plasticity and monoaminergic signalling, Selank removing the anxiety that was occupying working memory. The second route is arguably the more plausible of the two, and it is the one nobody makes.
Community reports
Reports emphasise verbal fluency and mental stamina. Cognitive self-assessment is unreliable in both directions and particularly so in people who expected an effect.
Components carrying the argument: Semax BDNF + reduced anxiety load
Pathophysiology
Reduced BDNF signalling is among the more durable findings in depression research, and anxiety and depression are comorbid far more often than not.
Mechanistic rationale
Both compounds have reported effects on BDNF and serotonergic signalling in preclinical work, so the pairing has a coherent story. No controlled trial of either compound in depression exists, and rapid subjective mood lift — which is what gets reported — arrives faster than any BDNF-mediated mechanism plausibly acts.
Community reports
Widely used for mood. If symptoms include thoughts of self-harm, that is an emergency and belongs with a person rather than a vial.
Components carrying the argument: BDNF and serotonergic effects, both inferential
Pathophysiology
Recovery after ischaemic stroke depends on neuroplasticity, and post-stroke anxiety and depression are common and independently impair rehabilitation engagement.
Mechanistic rationale
Semax holds a Russian registration for ischaemic stroke on a small, largely non-randomised local literature. Selank contributes nothing to the neurological recovery and might contribute to the mood and anxiety burden that accompanies it. The distinction matters: one component has a registered indication, the other is along for the ride.
Community reports
Not a self-directed use in any responsible sense — acute stroke is an emergency with interventions measured in hours, and rehabilitation is the highest-yield recovery-phase intervention by a wide margin.
Components carrying the argument: Semax — registered indication; Selank — adjunct at best
Pathophysiology
Fibromyalgia is a disorder of central pain processing, and the cognitive complaint patients describe as "fibro fog" is a genuine and disabling part of it.
Mechanistic rationale
This is the only entry in the fibromyalgia sections of this library whose mechanism is in the right compartment. Both compounds act centrally, on BDNF and on anxiolytic signalling, and the approved fibromyalgia drugs — duloxetine and milnacipran — are also centrally acting. Being in the right compartment is not the same as working, and no study has looked. But it is a better starting point than a tissue-repair peptide in a condition with no tissue lesion.
Community reports
Reports emphasise the cognitive and mood components more than the pain, which is consistent with what these compounds plausibly do.
Components carrying the argument: Central action — the correct compartment
Pathophysiology
People with these conditions are frequently already on serotonergic medication — SSRIs, SNRIs, tricyclics — and fibromyalgia specifically is treated with duloxetine and milnacipran.
Mechanistic rationale
Both compounds have reported serotonergic effects. Adding an uncharacterised serotonergic agent to an established serotonergic regimen has no dosing data and no interaction studies behind it, and serotonin toxicity is a real if uncommon outcome of stacked serotonergic drugs. Nobody has studied this combination against anything, let alone alongside an antidepressant.
Community reports
Interaction with prescribed medication is rarely raised in community discussion, and prescribers are rarely told.
Components carrying the argument: Serotonergic effects of both compounds
| Use | Which compound carries it | Evidence | The thing to know |
|---|---|---|---|
| Anxiety with fatigue | Selank | Russian, small, vs medazepam | The best version of the stacking case |
| Cognition / focus | Semax | Russian, registered | Reduced anxiety may do more than BDNF |
| Depression | Both | None | Reports arrive faster than the mechanism |
| Stroke recovery | Semax | Registered in Russia | Selank contributes nothing here |
| Fibromyalgia | Both | None | Right compartment — rare in this library |
| On an SSRI or SNRI? | Both | — | Uncharacterised serotonergic stacking |
For anxiety: cognitive behavioural therapy has the strongest evidence of any intervention and its benefit outlasts the treatment. SSRIs and SNRIs are first-line pharmacotherapy; exercise has a real effect size.
For depression: CBT is comparable to medication in mild to moderate presentations, SSRIs and SNRIs are effective, and treating comorbid alcohol use and sleep disorder changes outcomes more than most people expect.
For stroke: thrombolysis and thrombectomy within their windows, stroke-unit care, secondary prevention, and early intensive rehabilitation — the highest-yield recovery-phase intervention there is.
For fibromyalgia: pregabalin, duloxetine and milnacipran are approved, and graded exercise combined with cognitive behavioural therapy has the strongest evidence of any intervention. Non-restorative sleep is close to universal and obstructive sleep apnoea is under-diagnosed in this population.
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
Supplied as two separate lyophilised vials, commonly 5 or 10 mg each, or as pre-made intranasal sprays. The 10 mg + 10 mg pairing is the common presentation, and it is a lot of peptide for this use. At 500 mcg a day, a single 10 mg vial is twenty days — so the pair is forty vial-days of Semax and forty of Selank if run together, which is well beyond the in-use window for a reconstituted solution and is the argument for reconstituting a fraction at a time or splitting into several containers. Reconstituted into 5 mL, 10 mg gives 2 mg/mL, so a 0.1 mL nasal actuation is 200 mcg and a 500 mcg dose is two and a half sprays — which is the case the calculator flags, because a pump cannot deliver half an actuation. Reconstituting 10 mg into 8 mL instead puts a 500 mcg dose at four clean sprays. For intranasal use the reconstituted solution is transferred to a nasal spray bottle — a step that introduces sterility and dose-accuracy problems the injectable route does not have. Spray bottles are typically replaced between vials.
Lyophilised: refrigerated or frozen. Reconstituted: 2–8 °C. In-use nasal bottles are a contamination risk over a 20-day course.
Commonly 5 mg and 10 mg lyophilised vials of each; registered forms are 0.1%/1% and 0.15% intranasal solutions.
Both are Pro-Gly-Pro-stabilised against enzymatic degradation, making them relatively robust compared with their unmodified parent fragments.
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Both are registered medicines in the Russian Federation — Semax for ischaemic stroke, TIA, cognitive disorders and optic nerve conditions; Selank as an anxiolytic. Neither is approved by the FDA, EMA or MHRA, and neither is registered anywhere as a combination product.
Western supply is research-chemical grade. The amidated analogues — Adamax, N-Acetyl Semax Amidate, N-Acetyl Selank Amidate — have no registration anywhere and thinner evidence than their parents.
Regulatory and trial claims re-checked against primary sources on 20 August 2026. Checked: Semax recommended by PCAC July 2026; Selank not nominated in either round; route comparisons for both components and the 10 mg + 10 mg vial arithmetic. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
Athletes subject to WADA, USADA, UKAD, NCAA or military testing should assume any peptide is prohibited unless they have verified otherwise against the current WADA Prohibited List. Several classes here (growth-hormone secretagogues, TB-4 analogues, metabolic modulators) are explicitly named. Check the current list — it is republished annually.
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.
