Selank Dosage: Chart, Intranasal vs SubQ - Dosage Peptide

Selank Dosage: Chart, Intranasal vs SubQ - Dosage Peptide Selank dosage by route: the 0.15% nasal solution math, 5mg and 10mg reconstitution charts, and what the small Russian trial evidence actually establishes. Anyone searching for a selank dosage chart is usually holding a lyophilised 5 mg or 10 mg vial and trying to work out two separate things: how much bacteriostatic water to add, and what amount the published literature and the registered foreign labelling actually describe. Those are different questions with very different answer qualities — the first is arithmetic that can be verified exactly, the second is a thin, mostly Russian-language evidence base built around a nasal spray rather than an injection. This page separates them cleanly: the reconstitution mathematics is laid out so every row can be checked, and the reported research amounts are described as what investigators used and what a registered foreign product’s labelling states, not as instructions for any person. Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP). It was developed in the 1990s at the Institute of Molecular Genetics of the Russian Academy of Sciences. Structurally, it is a stabilised analogue of tuftsin — an endogenous tetrapeptide (Thr-Lys-Pro-Arg) that is enzymatically cleaved from the heavy chain of immunoglobulin G and that stimulates phagocytosis in macrophages and neutrophils[1]. Tuftsin signals at least in part through the receptor neuropilin-1[2]. Selank takes that tetrapeptide and appends the tripeptide Pro-Gly-Pro (PGP) at the C-terminus. The PGP tail is not decorative — it is a well-known stabilising motif in this family of Russian regulatory peptides, intended to slow peptidase cleavage of the parent sequence. The regulatory position matters more than almost anything else on this page, and it is routinely misstated by vendors: Selank is not FDA-approved. There is no US-approved Selank drug product, no FDA-recognised indication, and no FDA-approved labelling that states a human amount, route or frequency. Selank is not EMA-approved. There is no European centrally authorised Selank medicine. Selank is registered in the Russian Federation as an anxiolytic, marketed as a 0.15% intranasal solution (nasal drops) under registration number ЛП-№(010951)-(РГ-RU), held by the Peptogen Innovative Scientific-Production Centre[3]. That registration is a real regulatory fact, but a Russian registration is not an FDA or EMA approval, and it does not import the same evidentiary standard. In US compounding terms, Selank has no permissive status. Selank acetate (TP-7) was nominated for the FDA’s Section 503A Bulks List and placed in Category 2 — substances that “may present significant safety risks” and that compounders are not permitted to use while under evaluation[4]. It was later removed from that Category 2 list following withdrawal of the nomination by the nominator — FDA now lists selank acetate under “bulk drug substances nominated but withdrawn”, a table of substances previously in Category 2[4] — a procedural removal, not an authorisation[5]. Removal from a “do not compound” list because nobody is still asking for it is the opposite of approval. Selank is not on the 503A Bulks List. The clinical evidence base is small and geographically concentrated. The controlled human work is largely Russian-language, conducted by or near the institutes that developed the compound, with limited independent replication. A ClinicalTrials.gov search for the intervention “Selank”, accessed 17 July 2026, returned no studies with Selank as an intervention — only unrelated records surfaced by fuzzy matching[6]. That is the honest tier. If you want the compound’s background before the numbers, the overview at what Selank is as a nootropic peptide studied for anxiety and cognition covers the discovery history in more depth. This page is the dosage and reconstitution reference. Unfamiliar terms used below — lyophilisatio Because this distinction carries so much weight on this page, it is worth spelling out rather than gesturing at. A national registration means a national regulator reviewed a dossier submitted by a sponsor and permitted marketing in that country. It is a real administrative act with real requirements. What it does not automatically mean is that the underlying evidence would satisfy a different regulator applying a different standard. The differences that matter most for a reader trying to calibrate confidence are these: Dossier transparency. The FDA publishes review documents — the medical, statistical, clinical pharmacology and chemistry reviews — through Drugs@FDA, and the EMA publishes a European Public Assessment Report. Those documents let an outsider read the regulator’s own reasoning, including the objections. There is no equivalent public assessment report for Selank that an English-reading outsider can audit. What is publicly available is the labelling and a small number of indexed abstracts. Evidence volume expectation. A US or EU approval for an anxiety indication would ordinarily rest on multiple adequate and well-controlled trials, typically placebo-controlled, typically with several hundred to several thousand participants across the programme, with a formal safety database and a defined exposure requirement. The publicly indexed Selank clinical literature is orders of magnitude smaller than that. Independence. Western approval processes assume the sponsor’s data will be re-analysed by a regulator with access to patient-level datasets. Where a compound’s clinical literature comes predominantly from the institutes that created it and has not been re-analysed independently, the ordinary error-correcting machinery has not run. None of this is an accusation that the Russian registration is unfounded, and none of it demonstrates that Selank does not work. It is a statement about what a reader is entitled to conclude. “Registered in Russia” supports the sentence a national regulator permitted marketing of a 0.15% nasal solution. It does not support the sentence Selank is a proven anxiolytic, and vendors routinely make the second sentence do work the first sentence earns. A dosage chart for a compound like this is doing two jobs at once, and conflating them is where most online charts go wrong. Job one is concentration arithmetic. If you dissolve X mg of powder in Y mL of liquid, the concentration is X/Y mg per mL. That is arithmetic. It is true regardless of what the compound is, whether it works, or whether anyone should use it. It can be verified with a calculator and it has no evidentiary tier at all. Every reconstitution table below falls into this category. Job two is reporting what published work and registered labelling used. That is a claim about the literature, and it inherits the literature’s weaknesses. For Selank there is essentially one indexed human trial worth quoting, in 62 patients, plus the posology printed on the registered Russian label. Everything else circulating as a “Selank protocol” — 200 mcg twice daily, 300 mcg three times daily, 500 mcg subcutaneously, cycles of five days on and two days off — traces back to vendor pages and forum convention, not to a citable trial. So the table below is a concentration map, not a prescription. It says what a given vial and volume produces. What anyone does with that number is not addressed here, and no human protocol is recommended anywhere on this page. The broader logic of reading any dosage table is set out in the peptide dosage chart guide. Selank is unusual among peptides sold as research chemicals in that its canonical route is intranasal, not injection. The registered Russian product is a nasal drop solution[3]. The pivotal comparative clinical trial is reported to have used intranasal administration — although, as detailed below, the indexed English abstract does not itself state the route[7]. The rodent work on brain-derived neurotrophic factor used intranasal administration[8]. Subcutaneous Selank exists in vendor literature, but it has nothing resembling the same precedent in human research. This is the reverse of the situation for most peptides discussed on this site, where injection is the studied route and everything else is speculative. With Selank, the vial you have — a lyophilised powder in a glass vial with a rubber stopper — is packaged like an injectable simply because that is how peptide manufacturers package everything. The packaging is not evidence about the route. A U-100 insulin syringe is graduated in units, where 100 units = 1 mL. Therefore: 1 unit = 0.01 mL 10 units = 0.1 mL 50 units = 0.5 mL (half a syringe on a 100-unit barrel) 100 units = 1.0 mL (a full 1 mL barrel) The general relationship: for a vial of X mg reconstituted in Y mL, concentration = X/Y mg per mL. Per insulin unit, that is (X/Y) ÷ 100 mg, which — because 1 mg = 1,000 mcg — equals (X/Y) × 10 mcg per unit. That single formula generates every row in every table below, and you can re-derive any of them yourself. If you want it done interactively rather than by hand, the peptide dosage calculator runs the same arithmetic, and the insulin syringe units guide explains the unit-to-millilitre mapping in detail. Selank is supplied as a white lyophilised (freeze-dried) powder, most commonly in 5 mg and 10 mg vials. Reconstitution means adding a diluent — usually bacteriostatic water, which is sterile water containing 0.9% benzyl alcohol as a preservative — to dissolve the powder into a liquid of known concentration. Neither table below is a recommendation. Each is a map from a diluent volume to the concentration it produces. For a 5 mg vial, applying concentration = 5 ÷ Y: 1.0 mL 5 ÷ 1.0 5.0 mg/mL 50 mcg 500 mcg 1.5 mL 5 ÷ 1.5 3.33 mg/mL 33.3 mcg 333 mcg 2.0 mL 5 ÷ 2.0 2.5 mg/mL 25 mcg 250 mcg 2.5 mL 5 ÷ 2.5 2.0 mg/mL 20 mcg 200 mcg 3.0 mL 5 ÷ 3.0 1.67 mg/mL 16.7 mcg 167 mcg 3.33 mL 5 ÷ 3.33 1.5 mg/mL (= 0.15%) 15 mcg 150 mcg 5.0 mL 5 ÷ 5.0 1.0 mg/mL 10 mcg 100 mcg Check one row by hand: 5 mg ÷ 2 mL = 2.5 mg/mL. Per unit, 2.5 ÷ 100 = 0.025 mg = 25 mcg. Per 0.1 mL, 2.5 × 0.1 = 0.25 mg = 250 mcg. The row is consistent. Note the 3.33 mL row. That is the volume that reproduces the concentration of the registered Russian 0.15% nasal solution from a 5 mg vial — the arithmetic behind it is worked through in the intranasal section below. A vial-specific walkthrough sits on the Selank 5 mg vial dosage protocol page. For a 10 mg vial, concentration = 10 ÷ Y. Every value is exactly double the 5 mg row at the same volume — that is the only difference, and it is worth internalising because it removes the need to memorise two tables. 10 ÷ 1.0 10.0 mg/mL 1,000 mcg 100 10 ÷ 2.0 200 10 ÷ 2.5 4.0 mg/mL 40 mcg 400 mcg 250 10 ÷ 3.0 300 4.0 mL 10 ÷ 4.0 400 10 ÷ 5.0 500 6.67 mL 10 ÷ 6.67 667 10.0 mL 10 ÷ 10.0 1,000 Verify the 4 mL row: 10 ÷ 4 = 2.5 mg/mL. Per unit = 2.5 × 10 = 25 mcg. Total units = 4 mL × 100 units/mL = 400 units. Total peptide check: 400 units × 25 mcg = 10,000 mcg = 10 mg. The row closes. That closure check — total units × mcg per unit should equal the vial’s stated mass — is the single most useful sanity test for any reconstitution table. If it does not close, a number is wrong. Run it on any chart you find online; a surprising number fail. The Selank 10 mg vial dosage protocol page carries the vial-specific version of this table with the same closure checks. Suppose the target is a solution where one 0.1 mL nasal actuation contains 250 mcg, starting from a 10 mg vial. Work backwards: 250 mcg per 0.1 mL means 2,500 mcg per mL = 2.5 mg/mL. Volume needed = mass ÷ concentration = 10 mg ÷ 2.5 mg/mL = 4 mL. Check against the table: the 4.0 mL row reads 2.5 mg/mL and 250 mcg per 0.1 mL. Confirmed. Check vial capacity: 4 mL requires at least a 5 mL vial, or a transfer to a larger container. The same backwards method works for any target: volume = vial mass ÷ desired concentration. This is not a recommendation of 250 mcg — it is a demonstration of the arithmetic, and it would be equally valid for any target number. This is the step most charts skip and the one that causes the most failures at the bench. A standard 2 mL peptide vial does not hold 5 mL of diluent. Selank vials are commonly 2 mL or 3 mL glass; a 5 mg vial in a 2 mL vial cannot take 3.33 mL. Any chosen volume must be within the vial’s physical capacity, which is a property of the glass and not of the label. The guide to how much bacteriostatic water to use in reconstitution covers the capacity constraint in detail. Selank makes this constraint unusually binding, and the reason is arithmetic rather than chemistry. Because the registered concentration is dilute — 1.5 mg/mL is low compared with most peptide working concentrations — reaching it from a 10 mg vial requires 6.67 mL of diluent. No standard 2 mL or 3 mL peptide vial holds that. The constraint is structural: the vial format was chosen by a manufacturer packaging an injectable powder, and the target concentration comes from a nasal product with a completely different container. They were never designed to meet. That leaves three arithmetic responses, each with a cost: Accept a higher concentration. Reconstituting a 10 mg vial in 3 mL gives 3.33 mg/mL — roughly 2.2× the registered 0.15%. The mass in any given delivered volume scales with it. The concentration is fine as arithmetic; it simply is not the registered concentration, and any comparison to the labelled posology no longer holds without a corresponding volume adjustment. Split the vial. Reconstitute in a volume the vial holds, then draw a portion into a second container and dilute further. Every additional transfer step multiplies the opportunities for volumetric error and for contamination, and each partial withdrawal loses residual volume to the syringe hub and needle. Transfer to a larger container. Dissolve in a small volume, withdraw completely, and expel into a container sized for the final volume — adding the remaining diluent there. This reaches the target concentration in one step but moves the solution out of a stoppered, single-piercing-point vial into something with a different closure and a different microbiological profile. The transfer route deserves a specific caution because it is the one most often glossed over. A lyophilised powder does not dissolve into a vacuum: displacing 6.67 mL of liquid into a 3 mL vial is not a technique problem, it is a physical impossibility. Any description of “reconstituting a 10 mg vial to 0.15%” that does not name a container larger than the vial has skipped a step. And transfer is not free: residual solution wets the interior of the source vial, the syringe barrel and the needle, so the mass that arrives in the destination container is always less than the mass on the label. For a small total mass like 5 or 10 mg, a residual of even 0.1–0.2 mL is a measurable fraction of the total. The registered Russian product is described as a 0.15% solution, and its labelling states the composition directly as 1.5 mg of Selank per 1 mL, with methylparaben as preservative in purified water, supplied as 3 mL in a dropper bottle[3]. The percentage and the mg/mL figure agree, and it is worth showing why, because the same conversion recurs constantly. Percentage concentrations in pharmacy are usually weight/volume: x% w/v means x grams per 100 mL. So: 0.15% = 0.15 g per 100 mL 0.15 g = 150 mg 150 mg per 100 mL = 1.5 mg per mL 1.5 mg/mL = 1,500 mcg per mL That the label’s own stated composition (1.5 mg/mL) matches the percentage conversion is a genuine external check, and it is the one place on this page where a number can be tied to a regulatory document rather than reconstructed. It also tells us the total mass in a bottle: 3 mL × 1.5 mg/mL = 4.5 mg of Selank per 3 mL bottle. A 5 mg research vial contains slightly more peptide than one entire registered bottle. From there, the per-delivery amounts depend entirely on the delivery device, which is where most confusion enters: 0.05 mL One drop from a nasal dropper (approx.) 75 mcg 0.1 mL One actuation of a typical metered nasal pump 0.2 mL Two actuations / one per nostril 300 mcg Full millilitre 1,500 mcg Drop volume is an approximation, not a constant — it varies with dropper bore, viscosity, orientation and technique, typically landing somewhere near 0.05 mL. Any drop-based reconstruction is therefore approximate by construction, and this is one reason drop-counting is a poor basis for anything precise. Note also that the registered product is supplied as drops, not as a metered pump spray: a dropper does not meter, and the 0.1 mL actuation row above describes a different device entirely. The labelling for the registered Russian product describes a posology of 2 drops into each nostril, three times daily, for a course of 14 days, with repeat courses described as possible after an interval and on medical advice[3]. This is reproduced here as a description of what a foreign regulator permitted a manufacturer to print, in a country where the product is registered. It is not a protocol offered to any reader, it does not apply to a reconstituted research-chemical solution, and it carries no FDA or EMA standing whatsoever. Expressed in drops, that labelled posology is 2 drops × 2 nostrils × 3 administrations = 12 drops per day. Converting drops to mass requires a drop-volume assumption, and the label does not supply one — so the mass per day cannot be derived from the label alone. At an assumed 0.05 mL per drop, 12 drops is 0.6 mL, which at 1.5 mg/mL is 900 mcg per day. That figure is a calculation performed here from a labelled drop count and an assumed drop volume; it is not printed on the label. One further arithmetic consequence is worth noting for anyone comparing bottle sizes to vial sizes: at 0.6 mL per day, a 3 mL bottle covers five days, and a 14-day course at that rate consumes roughly 8.4 mL — close to three bottles. The 4.5 mg in one registered bottle is therefore not a 14-day supply under its own labelled drop count. The most-cited human study is Zozulya and colleagues (2008), published in Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova. Sixty-two patients with generalized anxiety disorder and neurasthenia were studied: 30 received Selank and 32 received medazepam, a benzodiazepine, with assessment by the Hamilton anxiety scale, Zung self-rating scale and CGI. The reported conclusion was that the anxiolytic effects of the two were similar, with Selank additionally showing antiasthenic and psychostimulant effects[7]. Now the part that most pages omit. The indexed English abstract of that paper states no dose, no route and no treatment duration. The widely circulated figures — “1,350 mcg per day” and “14 days” — are not present in the indexed abstract and could not be verified against the primary text for this page. They appear on vendor and aggregator pages, which is precisely the tier this reference library exists to avoid laundering. The 14-day figure does have independent support, but from the registered labelling[3], not from the trial abstract; the two should not be silently merged. The 1,350 mcg/day figure has no primary support that this page was able to locate. Zozulya et al. 2008, n=62[7] Anxiolytic effect similar to comparator medazepam; dose and route not stated in the indexed abstract Reported as intranasal by secondary sources; not stated in the abstract Not stated in the abstract Small comparative clinical trial, Russian-language, not independently replicated Registered Russian labelling[3] 0.15% solution (= 1.5 mg/mL); 2 drops per nostril, 3× daily Intranasal (drops) 14-day course National registration outside the US/EU; no FDA or EMA labelling exists “1,350 mcg per day” Circulated widely as the trial dose — Vendor/aggregator sources only; not verifiable from any primary source identified here Inozemtseva et al. 2008[8] BDNF expression change in rat hippocampus Intranasal (rat) Acute Preclinical, animal only Volkova et al. 2016[9] 300 mcg/kg; 84-gene neurotransmission panel in rat frontal cortex at 1 h and 3 h Kasian et al. 2017[10] Selank 300 mcg/kg + diazepam in chronic mild stress, elevated plus maze Intranasal (rat); diazepam oral Chronic stress model Filatova et al. 2017[11] GABAergic gene expression in IMR-32 cells n/a In vitro, human cell line Subcutaneous human protocol None identified SubQ No published human standard exists Read the third and last rows carefully. They are the two most honest lines in the table. A widely repeated convention holds that the trial regimen was three drops per nostril, three times daily, totalling 1,350 mcg. It is worth showing how that number is generated, explicitly labelled as a reconstruction from two unverified inputs — not as evidence, and not as confirmation of anything: Assume 1.5 mg/mL and assume a drop volume of ~0.05 mL. One drop ≈ 75 mcg. 1,350 mcg ÷ 75 mcg = 18 drops per day. 18 drops ÷ 3 administrations per day = 6 drops per administration. 6 drops ÷ 2 nostrils = 3 drops per nostril, three times daily. The arithmetic closes. That closure means nothing. The 1,350 figure and the drop count were derived from each other using an assumed drop volume; demonstrating that two reconstructed numbers are mutually consistent is not independent confirmation of either. This is the exact failure mode the rest of this page objects to, and it is included here only so that a reader who encounters the “three drops” convention elsewhere can see where it comes from. Worse for the convention: the registered labelling states two drops per nostril, not three[3]. Under the same 0.05 mL drop assumption, the labelled posology yields 900 mcg per day, not 1,350. The circulating figure and the only regulatory document available disagree by 50%. Either the drop-volume assumption is wrong (1,350 mcg over 12 labelled drops would require ~0.075 mL per drop), or the trial used a regimen different from the label, or the 1,350 figure is simply wrong. This page cannot resolve which, and says so rather than picking the answer that makes the table look tidy. If a solution is transferred to a metered nasal bottle, three device facts govern everything: Actuation volume. Most fine-mist nasal pumps deliver approximately 0.1 mL per press, but this varies by pump. The actual figure should come from the device specification, not assumption. A dropper — the format the registered product actually uses — does not meter at all. Priming loss. A new pump needs several actuations before it delivers a full metered volume. That peptide is lost. Dead volume. A nasal bottle cannot draw its last fraction of a millilitre. A 10 mg vial reconstituted into 5 mL nominally gives 50 actuations at 0.1 mL; in practice priming and dead volume reduce the usable count, so the real yield is lower than the arithmetic suggests. Any per-vial “supply” calculation that ignores this overstates. This is the question the search phrase “selank intranasal vs subq” is really asking, and the answer is asymmetric enough to state bluntly. Intranasal is where the precedent lives. The registered product is a nasal drop solution[3]. The BDNF work in rat hippocampus used intranasal delivery[8], as did the frontal-cortex gene-expression work at 300 mcg/kg[9] and the chronic-mild-stress behavioural work[10]. The comparative clinical trial is reported by secondary sources to have used the nasal route, which is consistent with everything else, though the abstract does not state it[7]. The pharmacological rationale usually offered is that intranasal delivery bypasses first-pass hepatic metabolism and may permit some nose-to-brain transfer via olfactory and trigeminal pathways — a proposed mechanism, and one that is contested in its magnitude across compounds generally, not a settled quantity for Selank specifically. There is no registered subcutaneous Selank product anywhere, no identified human trial using the subcutaneous route, and no published human protocol. Subcutaneous Selank appears in vendor and forum literature. That is a genuinely different tier from “the route used in the trial that everyone cites.” Two consequences follow that are worth stating explicitly: Amounts do not transfer between routes. Bioavailability by the nasal route and by the subcutaneous route are different, unequal, and — for Selank in humans — not established with the precision that would let anyone convert one into the other. A number pulled from an intranasal source and re-labelled as a subcutaneous amount is not a conversion; it is a guess wearing a citation. Formulation is not interchangeable either. A solution prepared for nasal use and a solution prepared for parenteral use have different requirements for sterility, tonicity, pH, particulates and preservative. Note that the registered nasal product uses methylparaben as its preservative[3], not the benzyl alcohol found in bacteriostatic water. They are not the same product in a different bottle. Registered product exists? Yes — Russia, 0.15% nasal drops[3] No, anywhere Used in the cited human trial? Reported by secondary sources; route not stated in the indexed abstract[7] No Route used in the cited rodent work? Yes[9][10] Not in the studies cited here Published human amount? Labelled posology exists (2 drops/nostril, 3× daily)[3] FDA-recognised protocol? Tolerability reported in a regulatory document Labelling describes allergic reactions on individual intolerance, and an unpleasant taste when solution reaches the pharynx[3] Not characterised — no registered product and no identified human trial That tolerability row deserves a caveat rather than reassurance. The listed adverse effects come from a national labelling document, not from a published safety dataset an outsider can inspect, and the indexed abstract of the one comparative trial reports no tolerability data at all[7]. A short adverse-effect list on a label is not evidence of a benign safety profile; it is evidence of what a manufacturer was permitted to print. Selank’s proposed mechanism is genuinely interesting and genuinely unsettled. Several distinct lines of work exist, and they are at different tiers. The most-developed hypothesis is that Selank acts on GABAergic neurotransmission. Volkova and colleagues administered Selank intranasally (300 mcg/kg, in a 6 µl volume) or GABA to rats and measured an 84-gene neurotransmission panel in the frontal cortex by real-time PCR, reporting significant expression changes in a large fraction of genes at 1 hour and fewer at 3 hours[9]. Filatova and colleagues extended this into a human neuroblastoma cell line (IMR-32), but found no direct effect: Selank on its own produced no change in the mRNA levels of the genes studied. Its only measured actions were combinatorial — it suppressed the expression changes GABA produced alone, and increased the number of genes altered by olanzapine — which the authors read as partial support for the idea that the peptide affects GABA’s interaction with its receptor rather than gene expression directly[11]. Note that the paper’s title is more affirmative than its result. Vyunova and colleagues reported that Selank affects GABA binding in a manner consistent with allosteric modulation, and that its joint action with benzodiazepines is not simply additive[12]. In the behavioural arm of this literature, Kasian and colleagues gave intranasal Selank at 300 mcg/kg alongside oral diazepam at 1 mg/kg in an unpredictable chronic mild stress model, assessing anxiety on the elevated plus maze[10] — note that the two agents were given by different routes, which limits what a direct comparison between them can mean. What that body of work supports is a plausible and specific mechanistic hypothesis. What it does not support is the claim, common on vendor pages, that Selank “modulates GABA receptors like a benzodiazepine without the downsides” as an established fact in humans. Gene-expression changes in rat cortex and a neuroblastoma line are mechanistic evidence, not clinical evidence. The mechanism is unpacked further in the discussion of how Selank is proposed to modulate GABAergic activity. Kost and colleagues reported that both Semax and Selank dose-dependently inhibit the enkephalin-degrading enzymes from human serum, with a reported half-maximal inhibitory concentration of approximately 20 µM for Selank and 10 µM for Semax[13]. The proposed implication is that Selank could indirectly extend endogenous enkephalin signalling. This is an in vitro serum finding, and the micromolar potency is worth holding onto: micromolar is a relatively weak in vitro concentration, and whether it is reached in relevant tissue after a nasal dose in a human is not established. Whether the finding translates into a meaningful in vivo effect at the amounts described in the clinical literature is unknown. Inozemtseva and colleagues reported that intranasal Selank regulates BDNF expression in the rat hippocampus in vivo[8]. Later rodent work reported effects on BDNF content in hippocampus and prefrontal cortex in an ethanol-induced memory impairment model[14]. Both are animal studies. “Raises BDNF” is a frequent marketing line; the accurate version is “alters BDNF expression in rodent brain regions in specific experimental models.” Because Selank is a tuftsin analogue, and tuftsin is a phagocytosis-stimulating immunopeptide acting via neuropilin-1[1][2], an immunomodulatory profile is frequently attributed to Selank by inheritance. Structural analogy is a reason to investigate, not a result. Sharing a sequence motif with tuftsin does not establish that Selank reproduces tuftsin’s activity at any particular amount, and the extended PGP tail changes the molecule’s enzymatic fate. Note that these four mechanisms are not one mechanism. A compound described as simultaneously a GABAergic allosteric modulator, an enkephalinase inhibitor, a neurotrophin reg