Selank
Tuftsin analog
Selank (Tuftsin analog) is a cognitive & mood research compound. Anxiolytic/nootropic peptide modulating GABA and serotonin systems and raising BDNF — calm focus without sedation.
Selank quick facts
| Reported research dosing | 200mcg-800mcg |
| Route | Subq |
| Cycle length | 4-8 Weeks |
| Frequency | 1-2x Daily Am/Mid Day · 5 On 2 Off or Daily |
| Half-life | Minutes to hours (route-dependent) |
| Forms | Injectable, Nasal |
| Evidence level | Russian human studies + animal |
The anti-anxiety counterpart to Semax. Great stacked with it.
How Selank works
Anxiolytic/nootropic peptide modulating GABA and serotonin systems and raising BDNF — calm focus without sedation.
Proposed benefits
Calm focus, anxiolysis and BDNF support without sedation.
Where to get Selank
Selank is sold in 2 forms. They are not interchangeable — the dose and the route differ, so pick the one this page describes unless you know why you want another.
Selank reconstitution calculator
Research reconstitution calculator
Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Selank
Graded by what exists behind each claim.
Human clinical evidence
- The human record is Soviet and post-Soviet clinical work — real patients and real endpoints, published in Russian and rarely replicated to Western standards.
📊 Correlative data
- Russian clinical work in generalized anxiety disorder reported efficacy comparable to benzodiazepines without sedation or dependence, which is the claim that made it interesting and the one most in need of independent replication.
- Used intranasally for anxiety and social ease. The consistent report is anxiolysis without cognitive dulling — the opposite of the benzodiazepine trade-off.
🧪 Theoretical / extrapolated
- A synthetic analog of tuftsin, an immunomodulatory peptide fragment. It is proposed to modulate GABA-A expression indirectly and to affect enkephalin degradation — not to bind the benzodiazepine site, which is the mechanistic basis for the no-dependence claim.
- It also raises BDNF, like Semax, which is why the two are commonly paired and why the effect is described as building rather than acute.
How to read the Soviet clinical series →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Selank actually does
Selank is Thr-Lys-Pro-Arg-Pro-Gly-Pro, printed in exactly those seven residues in the abstract of the paper that first measured what it does to human serum Kost 2001. Read it as two pieces, because that is how it was built: Thr-Lys-Pro-Arg is tuftsin, the immunomodulatory tetrapeptide, and Pro-Gly-Pro is a synthetic tail that does not occur in the parent at all.
What the Pro-Gly-Pro buys, in minutes. It is a protease-resistance device, not decoration, and the number attached to it is small and specific. In rats, the intact heptapeptide is detectable in plasma for 7 to 10 minutes, its half-life exceeds that of other oligopeptides of similar structure, and the main pharmacologically active metabolite is tuftsin itself, Thr-Lys-Pro-Arg Boiko 1998. Proline resists most aminopeptidases, so the molecule is trimmed from the C-terminal end back to the tetrapeptide rather than shredded. The honest way to read that: the tail buys single-digit minutes of the intact molecule and then hands over a second active compound. Nobody selling this states either half.
The charge, and why it is the opposite of Semax. Lysine, arginine and a free N-terminus, and not one acidic side chain: computed isoelectric point 11.65 and net charge about +1.9 at blood pH, on a 751.9 Da molecule. Semax, the peptide it is most often paired with, is about −0.9 at the same pH. Two compounds sold as a stack sit on opposite sides of neutrality, which is why they do not behave the same on nasal mucus, on an ion-exchange column, or in the same vial.
Mechanism one: allosteric modulation of GABA binding, not the benzodiazepine site. Radioligand work on isolated rat brain plasma membranes reports that Selank affects [3H]GABA binding as a positive allosteric modulator, that its joint action with benzodiazepines is not simply additive, and — the part that matters clinically — that Selank blocked the modulatory activity of diazepam and of olanzapine, with binding sites that appear to differ but may partially overlap Vyunova 2018. That is a genuinely different claim from the one on most pages: not that it avoids the benzodiazepine site, but that it interferes with what a benzodiazepine does there.
Mechanism two: enzyme inhibition, with a structure-activity ladder nobody quotes. Selank inhibits the enzymes that hydrolyze enkephalin in human serum, dose-dependently, with an IC50 near 20 µM in one assay Kost 2001 and 15 µM in another Zozulya 2001, more potent in both than bacitracin or puromycin. The ladder is the interesting part: pentapeptide fragments kept the inhibitory activity; the tri-, tetra- and hexapeptide fragments did not Kost 2001. So the enzyme effect is not simply tuftsin acting through a longer molecule, and it is not a property of length. What is missing is the enzyme's name: these papers measure total serum enkephalin-degrading activity, not a purified aminopeptidase or neprilysin, so no single target protein has ever been named for this compound.
Cell, rodent, human — and where it stops
In cells, and this is where honesty starts. In human IMR-32 neuroblastoma cells, 84 genes of the GABAergic system were read by qPCR after GABA, Selank, olanzapine and their combinations. Selank on its own produced no change in mRNA levels at all. Combined with GABA it almost completely suppressed the changes GABA alone produced; combined with olanzapine it amplified them Filatova 2017. A compound that does nothing alone in a dish and changes what another ligand does is a modulator, and that is exactly what the membrane binding work says it is Vyunova 2018.
In rodents, with the doses stated. Rats, single administration at 300 µg/kg: 45 of 84 neurotransmission genes changed in frontal cortex at 1 hour and 22 at 3 hours, correlating with the pattern GABA itself produced Volkova 2016. Mice, 300 µg/kg/day for 5 days, intranasal against intraperitoneal: anxiolytic and nootropic effects appeared only in BALB/c, the high-anxiety freezing strain, and not in C57BL/6 — and the route changed the receptor. Intraperitoneal dosing raised [3H]SR 95531 binding to GABA receptors in frontal cortex by 38% and left hippocampal NMDA receptors alone; intranasal dosing raised [3H]MK-801 NMDA binding by 23% and left GABA receptors alone Vasil'eva 2016. At 100 µg/kg, Selank was anxiolytic in BALB/c and raised the plasma leu-enkephalin half-life in BALB/c, with no effect on either in C57Bl/6 Sokolov 2002. At 0.3 mg/kg/day for 7 days intraperitoneally in rats given 10% ethanol as their only fluid for 30 weeks, it protected object-recognition memory and prevented the ethanol-induced rise in hippocampal and frontal cortex BDNF Kolik 2019. A single 0.3 mg/kg injection cut the naloxone-precipitated morphine withdrawal index by 39.6% and raised the tactile threshold 9-fold, against 49.3% and 13-fold for diazepam at 2 mg/kg Konstantinopolsky 2022.
In humans, and there is more here than in most of this catalog. 62 patients with generalized anxiety disorder and neurasthenia, 30 on selank against 32 on medazepam, rated on Hamilton, Zung and CGI: comparable anxiolysis plus an antiasthenic effect the benzodiazepine did not have, and serum enkephalin half-life — shortened in these patients at baseline — rose on treatment Zozulia 2008. 60 patients with phobic-anxiety and somatoform disorders against phenazepam, where the anxiolytic effect persisted for one week after the last dose Medvedev 2014. 30 patients on phenazepam alone against 40 on phenazepam plus selank, where the combination reduced the benzodiazepine's attention and memory impairment, sedation, sexual disturbance and withdrawal effects Medvedev 2015. And 52 healthy volunteers scanned with resting-state fMRI before injection and at 5 and 20 minutes after Selank, Semax or placebo, with changes in connectivity between the right amygdala and right temporal cortex Panikratova 2020.
The obstacles, and none of them is ‘more research is needed’.
- The dose does not scale. Every rodent effect above sits at 100–300 µg/kg. This site's protocol is 200–800 µg in total, which for a 70 kg adult is roughly 3–11 µg/kg — between 10 and 100 times lower per kilogram. Even after body-surface-area scaling, which divides a rat dose by about 6, the 300 µg/kg rodent dose lands near 3.4 mg for a 70 kg adult: four to seventeen times the protocol. And the human trials' abstracts do not state milligrams per day, so the comparison that can actually be made is rodent-to-protocol, not clinic-to-protocol.
- The strain is the finding. Two independent experiments report the effect in BALB/c and its absence in C57BL/6 Sokolov 2002 Vasil'eva 2016. The rodent literature is therefore about a phenotype, not about a species, and no human study has stratified people on baseline trait anxiety in the way the mouse work demands.
- The route is not a delivery detail. The same dose, in the same strain, moved GABA-receptor binding by one route and NMDA-receptor binding by the other Vasil'eva 2016. An injectable protocol and a nasal protocol are not two ways of taking one compound.
- The comparator is a benzodiazepine, in unblinded-to-Western-review trials. Both comparative trials are Russian-language, single-country, and the largest is 62 people Zozulia 2008 Medvedev 2014.
Selank pharmacokinetics — how much of it actually gets in
What degrades it, and how fast. Serum peptidases. In rats the intact heptapeptide is present in plasma for 7–10 minutes, the principal metabolite is the tuftsin tetrapeptide, and the distribution is into well-vascularized organs, liver > kidneys > heart Boiko 1998. The Pro-Gly-Pro tail is why the number is minutes rather than seconds.
The gap that is the most interesting fact on this page. Plasma residence is minutes. The clinical anxiolytic effect was reported to persist a full week after the last dose Medvedev 2014, and the rodent gene-expression response was still visible at 3 hours from one injection Volkova 2016. A molecule that is gone in ten minutes and whose effect outlasts it by four orders of magnitude is not occupying a receptor for the duration — it is triggering something that then runs on its own. Almost no page selling this compound mentions the mismatch, and it is the single strongest argument that the effect is transcriptional rather than occupancy-based.
The oral barrier. There is no oral form and no published oral bioavailability figure in any species. A 7-residue peptide swallowed meets gastric acid, then pancreatic proteases, then brush-border peptidases; the enterocyte's named peptide carrier, PepT1, handles di- and tripeptides, so a heptapeptide is outside its substrate range, and anything crossing would still face hepatic first-pass extraction. The nasal route exists to avoid all of that.
The injectable comparator, and what it does not fix. Subcutaneous injection removes the gut and the first-pass liver. It does not remove plasma peptidases — the 7–10 minute number above is a plasma number — and, per the route experiment, it does not produce the same receptor changes as the nasal route Vasil'eva 2016. A strongly cationic peptide (pI 11.65) also binds anionic mucin, which is an argument for nasal retention and against assuming that a nasal microgram equals an injected microgram.
What would have to be true, and how you would know it was not
Four predictions. Two of them say nothing will happen, which on this compound is the informative direction.
1. Morning cortisol will not move. Selank is a tuftsin analog, not a corticotropin fragment, and nothing in its published mechanism touches the HPA axis. Draw AM cortisol at baseline and at 4 weeks and expect a flat line. If it moves, the change is coming from something else in the stack or from the sleep the course changed.
2. A CBC, high-sensitivity CRP and fibrinogen will be unchanged, and this is the prediction that argues against the product. The only published work that looked at hemostasis, lipids and blood sugar under Selank is a 2014 Doklady paper whose PubMed record carries a title and no abstract Mjasoedov 2014 — so nobody can tell you what it found, including this page. At 3–11 µg/kg, ten to a hundred times below every rodent dose, the mechanistic expectation is no measurable movement in anything on a standard panel. A course that moves none of these has not failed; it has confirmed that whatever a user feels is not showing up in blood, which is a conclusion worth being able to state.
3. Plasma enkephalin degradation is the one marker the mechanism actually predicts, and you cannot order it. Both human mechanistic papers used the half-life of leu-enkephalin in plasma as their readout and both reported it rising on treatment Zozulya 2001 Zozulia 2008. No commercial laboratory offers that assay. That mismatch — a compound with a real human biomarker that no consumer can measure — is worth naming rather than substituting a marker that has nothing to do with it.
4. The persistence claim is falsifiable at home in a week. The published clinical claim is that the anxiolytic effect lasts about seven days after the final dose Medvedev 2014. Stop, and log anxiety daily for ten days. If the effect disappears within 24 hours, the published pharmacodynamics are not reproducing at this dose, and that is a real finding about the protocol rather than about the person.
What nobody has tested yet
Six experiments that nobody has run. The first two would settle what this molecule actually is.
1. Selank against tuftsin, head to head, at equimolar dose. The main active metabolite of Selank is tuftsin Boiko 1998. So either Selank is a delivery vehicle for a tetrapeptide that has been known since the 1970s, or the heptapeptide does something the tetrapeptide cannot. One experiment — both peptides, the same anxiety model, the same molar dose — answers it, and in nearly thirty years it has not been published.
2. Which of the two mechanisms the anxiolysis needs. The fragment ladder already exists: pentapeptide fragments keep the enzyme-inhibiting activity and the tri-, tetra- and hexapeptides do not Kost 2001. Run the active pentapeptide in an anxiety model. If it is anxiolytic, the enkephalinase mechanism is carrying the effect; if it is not, the GABA modulation is. Nobody has done it.
3. The interaction that two papers contradict each other on. Membrane work reports Selank blocking the modulatory activity of diazepam Vyunova 2018; a clinical trial reports Selank added to phenazepam improving outcomes and easing withdrawal Medvedev 2015. Blocking a benzodiazepine's action and smoothing a benzodiazepine taper are not the same prediction. No study has measured benzodiazepine effect size with and without Selank in the same people.
4. Phenotype stratification in humans. The entire rodent literature says the response belongs to the high-anxiety phenotype Sokolov 2002 Vasil'eva 2016. A trial that stratified on baseline trait anxiety, or even a self-experiment group that recorded a baseline GAD-7 before starting, would be the first human test of the one variable the animal work says matters most.
5. Intranasal against subcutaneous, in people, same dose. In mice the two routes moved different receptor systems Vasil'eva 2016. In humans nobody has compared them on any endpoint, and this site sells both.
6. BDNF, in the direction the paper actually reports. The one controlled rodent measurement found Selank preventing an ethanol-induced increase in BDNF rather than raising it Kolik 2019, and the intranasal rat study is titled as regulation of BDNF expression rather than elevation of it Inozemtseva 2008. Whether Selank raises BDNF in an undamaged brain has not been established, and plasma BDNF is orderable, so a before-and-after series in healthy users would be new information rather than confirmation.
Selank — its own safety story, not its class's
The class block on this page is written for cognitive enhancers in general — cholinergics, dopaminergics, glutamatergics. Selank is none of those and carries three risks of its own.
1. The dependence claim is a mechanistic argument, not a withdrawal study. The reason to expect no dependence is that Selank does not act at the benzodiazepine site. What exists to support it in people is a 62-patient trial against medazepam Zozulia 2008 and a 60-patient trial against phenazepam Medvedev 2014. No discontinuation study has been published, and the compound demonstrably touches opioid-relevant circuitry: a single 0.3 mg/kg dose cut morphine withdrawal signs by 39.6% in dependent rats Konstantinopolsky 2022. That is evidence it acts there, not evidence it is inert there.
2. The interaction nobody warns about is with the drugs people are most likely to be on. In isolated brain membranes Selank blocked the modulatory activity of both diazepam and olanzapine on GABA binding Vyunova 2018; in cells it amplified olanzapine's effect on gene expression Filatova 2017. Anyone taking a benzodiazepine or an antipsychotic is standing exactly where the two published statements disagree, and no interaction study exists in a person.
3. The developmental datum, stated with both halves. In mouse embryonic stem cells, Selank at 100 µM reduced the proportion of cells differentiating into GABA-positive neurons by 61% — alongside thyroliberin at 58% and NGF at 87% — and the authors' own conclusion from the same experiments was that these peptides do not produce a toxic effect during the embryonic and fetal period Kobylyanskii 2017. Both sentences are true. 100 µM in a dish is not a dose in a person. What matters is that this is the only developmental datum that exists: there is no pregnancy data of any kind for this compound, and a shift in GABAergic differentiation is not a reassuring place for the record to stop.
What zero reported adverse events means here. The published human denominator across every trial is under two hundred people, all in one country, over weeks. That base cannot exclude an event with an incidence of one in a hundred, and the honest sentence is that tolerability looks good in small short trials and nothing longer exists.
Sources read for this page
- Kost NV, Sokolov OY, et al. Semax and selank inhibit the enkephalin-degrading enzymes from human serum. Bioorganicheskaia Khimiia 2001 · PMID 11443939
- Zozulya AA, Neznamov GG, et al. The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bulletin of Experimental Biology and Medicine 2001 · PMID 11550013
- Sokolov OY, et al. Effects of Selank on behavioral reactions and activities of plasma enkephalin-degrading enzymes in mice with different phenotypes of emotional and stress reactions. Bulletin of Experimental Biology and Medicine 2002 · PMID 12432865
- Boiko SS, et al. The pharmacokinetics and metabolism of heptapeptide--a prospective synthetic analog of tuftsin with psychostimulating action in rats. Eksperimentalnaia i Klinicheskaia Farmakologiia 1998 · PMID 9854633
- Zozulia AA, Neznamov GG, et al. Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia. Zhurnal Nevrologii i Psikhiatrii im S S Korsakova 2008 · PMID 18454096
- Medvedev VE, et al. A comparison of the anxiolytic effect and tolerability of selank and phenazepam in the treatment of anxiety disorders. Zhurnal Nevrologii i Psikhiatrii im S S Korsakova 2014 · PMID 25176261
- Medvedev VE, et al. Optimization of the treatment of anxiety disorders with selank. Zhurnal Nevrologii i Psikhiatrii im S S Korsakova 2015 · PMID 26356395
- Volkova A, Shadrina M, et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Frontiers in Pharmacology 2016 · PMID 26924987
- Filatova E, Kasian A, et al. GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells. Frontiers in Pharmacology 2017 · PMID 28293190
- Vasil'eva EV, et al. Comparison of pharmacological effects of heptapeptide Selank after intranasal and intraperitoneal administration to BALB/c and C57BL/6 mice. Eksperimentalnaia i Klinicheskaia Farmakologiia 2016 · PMID 29787664
- Vyunova TV, Andreeva LA, et al. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein and Peptide Letters 2018 · PMID 30255741
- Kolik LG, et al. Selank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating of BDNF Content in the Hippocampus and Prefrontal Cortex in Rats. Bulletin of Experimental Biology and Medicine 2019 · PMID 31625062
- Konstantinopolsky MA, et al. Selank, a Peptide Analog of Tuftsin, Attenuates Aversive Signs of Morphine Withdrawal in Rats. Bulletin of Experimental Biology and Medicine 2022 · PMID 36322304
- Panikratova YR, et al. Functional Connectomic Approach to Studying Selank and Semax Effects. Doklady Biological Sciences 2020 · PMID 32342318
- Kobylyanskii AG, et al. Studying the Toxic Effects of Some Biologically Active Peptides on the Model of Mouse Embryonic Stem Cells. Bulletin of Experimental Biology and Medicine 2017 · PMID 29063333
- Inozemtseva LS, et al. Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Doklady Biological Sciences 2008 · PMID 18841804
- Mjasoedov NF, et al. The influence of Selank on the parameters of the hemostasis system, lipid profile, and blood sugar level in the course of experimental metabolic syndrome. Doklady Biological Sciences 2014 · PMID 25371249
Selank — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- This class is broad, but the predicted problems cluster by mechanism rather than by molecule. Cholinergics (racetams, and anything raising acetylcholine) predict headache — the classic one, from choline demand outrunning supply. Dopaminergics and eugeroics predict tolerance, sleep disruption and a flat mood on the days off. Anything glutamatergic or AMPA-facing carries a theoretical excitotoxicity concern at high doses.
- The pattern worth internalizing: anything that borrows performance from tomorrow eventually presents the bill. Sleep is the most common currency it gets paid in.
What has actually been reported
- Headache is the most reported effect across the racetam family and usually responds to added choline.
- Irritability, blunted affect and a rebound low on cessation are commonly reported with the stimulant-adjacent members.
- Most of this class has little or no controlled human safety data at the doses actually used.
How to reduce the risk
Same mechanism as the prediction.
- Take a choline source with any racetam. The headache is the mechanism running out of substrate, and it is largely preventable rather than something to push through.
- Dose in the morning. Almost everything in this class has a longer functional tail than its half-life suggests, and sleep is the first thing you lose.
- Use them for something, not as a habit. The compounds that carry tolerance genuinely reward intermittent use aimed at a task, and genuinely punish daily use aimed at feeling normal.
- One at a time, and long enough to judge it. This is the class where people stack five and cannot tell you which one is doing anything — and the effects are subjective, so attribution is already hard enough.
- If you need it to feel normal, stop. That is the line where a tool has become a dependency, and it is the one worth watching for.
What it does to your bloodwork
A fact about the assay.
- No routine marker tracks these. Sleep is the assay — if it is degrading, the compound is costing more than it is producing, and that shows up before anything else does.
Don't run this if
- A seizure history — several of these lower the threshold at least theoretically, and it is not worth establishing empirically.
- Bipolar disorder, for the dopaminergic members especially.
- Alongside prescribed psychiatric medication without knowing exactly how the mechanisms overlap.
The honest unknown
- Chronic use is essentially uncharacterized. The specific unmeasured thing is what daily cholinergic or dopaminergic pressure does to baseline function over years — not whether a few weeks is tolerable.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Food is not a factor — pick a time you will keep
Nothing you eat touches a subcutaneous injection, so there is no meal to plan around. What does matter is a fixed slot: the commonest reason an injectable protocol underperforms is missed doses, not mistimed ones.
With a short half-life, dose it near the effect you want rather than at a fixed hour.
From half-life and route, not a dosing trial.
Selank — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Selank moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Most of this class has no predicted marker movement at all, and saying so is more useful than listing markers that will not move.
What to do: A baseline liver panel is reasonable for anything taken daily and long-term. Beyond that there is nothing specific to chase.
Everything on this page, in an order
This one is free and stays free. What Skool adds is the rest of the shelf — 278 compounds and 371 supplements with the protocol, the stack order and the bloodwork to run beside it.
Join Skool — $10/mo →Bloodwork to run alongside Selank
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| TSH (Thyroid-Stimulating Hormone) | Thyroid disease imitates every cognitive complaint there is |
| Vitamin B12 | Deficiency causes fog long before it causes anemia |
| Methylmalonic Acid (MMA) | Catches the deficiency a normal B12 hides |
| Ferritin | Low iron flattens cognition at levels most labs call fine |
| Vitamin D (25-Hydroxy) | Commonly low, cheap to correct, associated with mood |
The Brain Fog & Cognition panel covers these in one order — 12 markers, $233.06 with the discount applied.
Check results you already have → · All 103 markers A–Z
Selank — frequently asked questions
What is Selank?
Selank (Tuftsin analog) is a cognitive & mood research compound. Anxiolytic/nootropic peptide modulating GABA and serotonin systems and raising BDNF — calm focus without sedation.
What dosing does the research reference for Selank?
In the research literature, Selank is referenced in the 200mcg-800mcg range, 1-2x Daily Am/Mid Day · 5 On 2 Off or Daily. It is supplied as a lyophilized powder and reconstituted with bacteriostatic water; the calculator above converts a research amount into syringe units. For research use only — not a recommendation for human use.
What is the half-life of Selank?
Selank has an approximate half-life of Minutes to hours (route-dependent), which is part of what determines how often it's dosed.
What forms does Selank come in?
Selank is available as: Injectable, Nasal.
What's the evidence behind Selank?
Current evidence level: Russian human studies + animal. Selank is offered for research purposes only and is not an approved medicine.
Selank inside a finished plan
One arm of 2 Protocol Blueprints, free to read in full.
What Selank is used for
Selank appears under 4 goals in the goal router.
Related Cognitive & Mood compounds
Where this goes next
Selank is the bdnf arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.