N-Acetyl Selank Amidate: COA, Purity and the Mass That Tells It From Selank

NA-Selank Amidate at a glance

What it is

Ac-TKPRPGP-NH₂ — the synthetic heptapeptide Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) carrying an N-terminal acetyl group and a C-terminal amide. Selank itself is PubChem CID 11765600, CAS 129954-34-3, UNII TS9JR8EP1G, C33H57N11O9, and is a synthetic analogue of the immunomodulatory tetrapeptide tuftsin

Identity on a COA

Derived formula C35H60N12O9; average mass 792.94, monoisotopic 792.4606, [M+H]⁺ 793.468. That is 41.03 Da heavier than plain Selank (751.89 / 751.4341). A reported mass near 751 is not this compound

Researched for

Anxiety and stress-related research, on the parent peptide. There is no published study of the acetylated-amidated analogue itself — PubMed returns zero records for "N-acetyl selank"

Commonly reported range

~250–900 mcg per day in divided applications, intranasal, from community sources rather than from any trial. Published human studies of the parent peptide used a fixed clinical preparation, not these figures

Route reported

Intranasal spray or drops predominantly; subcutaneous also reported. Route is not a free variable: the one head-to-head comparison — intranasal against intraperitoneal in mice — produced different receptor effects, not the same effect at different strengths (PMID 29787664). Intranasal against subcutaneous has never been compared

Reported frequency

Two to three divided applications daily in community protocols; reported cycles of roughly 14–21 days

Plasma half-life

Not established; the widely repeated "20–30 minutes" is leu-enkephalin's half-life, not Selank's, and is withdrawn here. That figure describes the peptide Selank protects from degradation — lengthening it is the proposed mechanism — and nothing has ever measured the analogue. See the half-life section

Regulatory status

Verified by absence on 2026-08-19: DailyMed returned zero labels for selank against a database published 2026-08-18, openFDA's Drugs@FDA returned no match, FAERS holds no adverse-event reports, and ClinicalTrials.gov has no registered study of it. Research use only

Reported ranges from research/community — examples, not recommendations.

What it is / mechanism

The identity of this compound is the first thing to get right, because the market is loose about it in a way that matters at the point of purchase. Selank is a synthetic heptapeptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro, built by extending the immunomodulatory tetrapeptide tuftsin (TKPR, PubChem CID 156080) with a Pro-Gly-Pro tail. PubChem records it as CID 11765600, CAS 129954-34-3, UNII TS9JR8EP1G, molecular formula C33H57N11O9, average mass 751.89, monoisotopic mass 751.43407. Its C-terminus is a free proline carboxylic acid. It also appears in the Russian literature as TP-7. N-Acetyl Selank Amidate is that same sequence with two end modifications: an acetyl group on the N-terminal threonine and an amide in place of the C-terminal hydroxyl. The doubly-modified molecule has no registry entry of its own: a PubChem search by name returns no compound and no substance, there is no UNII, and there is no CAS number we can verify against a registry (checked 2026-08-19). The singly-acetylated form does exist as its own record — N-acetyl Selank, the free acid, PubChem CID 133082488, C35H59N11O10, monoisotopic 793.4446, UNII J3PM702O93 — and it is not this compound: it is missing the C-terminal amide. That record is worth knowing about twice over, because it also independently checks the arithmetic below: PubChem's 793.4446 for the acetyl-only form is the parent's 751.4341 plus exactly the +42.0106 acetylation increment used here. The formula and masses on this page are therefore derived from the parent structure rather than quoted from a registry entry, and the derivation is stated in full in the references so it can be checked: acetylation adds C₂H₂O (+42.0106 monoisotopic) and amidation replaces an oxygen with an NH (−0.9840), giving C35H60N12O9 — average 792.94, monoisotopic 792.4606. Our arithmetic was validated against PubChem's own monoisotopic mass for the parent before being applied to the analogue. Pharmacologically, what is documented belongs to the parent peptide. Selank inhibits the enzymatic hydrolysis of plasma enkephalin with an IC₅₀ of 15 µM, more potently than the peptidase inhibitors bacitracin and puromycin (Bulletin of Experimental Biology and Medicine, 2001, PMID 11550013), and a tritium-labelling study found that this inhibition is directed at carboxypeptidases and dipeptidyl carboxypeptidases rather than at the aminopeptidases that account for roughly 80% of leu-enkephalin breakdown (Bioorganicheskaia Khimiia, 2004, PMID 15344652). In that study Selank is the inhibitor and leu-enkephalin the substrate; it measured nothing about how Selank itself is broken down. At the receptor, a radioligand study characterised Selank as a positive allosteric modulator of GABA binding whose action is not cumulative with benzodiazepines and which blocks the modulatory activity of diazepam and olanzapine; the authors concluded the binding sites are apparently distinct but may partially overlap (Protein and Peptide Letters, 2018, PMID 30255741). That is a more specific and more interesting claim than the usual summary that Selank "works on GABA without touching the benzodiazepine site," and this page has been corrected to state it as the study did.

Researched effects

There is a real human literature here, which distinguishes this compound from most of the research market — and there is a consistent qualification attached to all of it. Three controlled clinical studies in Russian psychiatric journals report on the parent peptide in patients: 60 patients with phobic-anxiety and somatoform disorders compared against phenazepam (PMID 25176261), 62 patients with generalised anxiety disorder and neurasthenia compared against medazepam (PMID 18454096), and 70 patients in which Selank was added to phenazepam rather than replacing it (PMID 26356395). The first two report efficacy results only: the medazepam study found the anxiolytic effects of the two drugs similar, with antiasthenic and psychostimulant effects for Selank on top, and the phenazepam study reports pronounced anxiolytic and mild nootropic effects plus an anxiolytic effect still present about a week after the last administration. Neither publishes a side-effect comparison. The claim repeated across the research market — that Selank matched its benzodiazepine comparator with a milder side-effect profile — is withdrawn from this page as unsourced (28 August 2026): it appears in neither abstract, and the only tolerability result anywhere in the set belongs to the third study, scored on the UKU scale, in which both arms received phenazepam. The third is not a comparison of Selank against a benzodiazepine at all — it added Selank to phenazepam and measured against phenazepam alone — so it speaks to what Selank adds, not to how it performs in place of one. None of the three is placebo-controlled: two are active-comparator designs and one is an add-on design. That is not a small caveat in anxiety research, where placebo response is large. The one placebo-controlled human study we located measured something other than symptoms. Fifty-two healthy participants received Selank, Semax or placebo and underwent resting-state functional MRI before and at 5 and 20 minutes afterwards; the authors reported changes in connectivity between the right amygdala and right temporal cortex (Doklady Biological Sciences, 2020, PMID 32342318). It establishes that a measurable brain-level effect occurs. It does not establish a clinical benefit. The animal literature adds a qualification the marketing copy never carries: the effect appears to depend on baseline anxiety. The behavioural and nootropic response was seen in high-anxiety BALB/c mice and not in C57BL/6 mice (PMID 29787664), and the anxiolytic effect plus enkephalinase change was likewise BALB/c-only (PMID 12432865). A monoamine study is often cited alongside these and does not say the same thing: it measured neurochemistry rather than behaviour, and found Selank effects in C57Bl/6 mice as well — noradrenaline rose in the hypothalamus of both strains (PMID 19093364). Selank also attenuated aversive signs of morphine withdrawal in rats, though it remained inferior to diazepam on the same measure (PMID 36322304), and reduced ethanol-withdrawal anxiety without changing ethanol consumption (PMID 24913576). The outside view is worth stating plainly because it is the assessment least likely to reach a product page. A 2021 review in the Journal of Clinical Pharmacology, surveying GABA-receptor-active sedative-hypnotics, describes phenibut and selank as poorly studied Russian drugs with GABAergic mechanisms that are inexplicably sold to US consumers as dietary supplements (PMID 34396551). That is a judgement about the evidence base and the sales channel rather than a finding of harm, and no adverse-event reports for it exist in FAERS — but a peer-reviewed clinical pharmacology journal calling the evidence thin belongs on the same page as the studies that call it promising. None of this is a guaranteed outcome and none of it is medical advice.

Dosage — reported ranges (overview)

The figures below are what community and vendor sources report. They are not a recommendation, not a personal dose, and — importantly for this compound — not what any published study administered. Reported intranasal use of Selank and its analogues clusters around 250–900 mcg per day, split into two or three applications, with reported cycles of roughly 14–21 days. Some sources describe short courses going considerably higher. Because there is no published study of the acetylated-amidated analogue at all, every one of these numbers was arrived at by transferring a figure from the parent peptide to a molecule with different stability, which is precisely the step the modification is supposed to make invalid: if the amide genuinely slows degradation, the analogue should not be used on the parent's schedule, and nobody has measured what the correct schedule would be. The published human work is not translatable into these numbers either. The Russian clinical studies used a fixed pharmaceutical preparation administered in a clinic; the animal work is quoted in mcg/kg (100–300 mcg/kg is the range that recurs across PMID 24450168, PMID 29787664, PMID 24291245 and PMID 12432865), and reading a rodent mcg/kg figure across to a human is an allometric-scaling exercise, not a multiplication. This page does not do it. The figures above are the parent peptide's own reported numbers, and they are repeated here for one reason: to show why carrying them across to a modified molecule is unsound. Our Selank guide covers the parent's reported schedules in their own right and is the page to read for them. What this page adds — and what the queries arriving here actually ask for — is which molecule is in the vial, and the nasal-actuation and salt-form arithmetic that changes what a stated concentration delivers.

A printable protocol sheet with a reconstitution reference and an injection log comes with All-Access Lifetime.

Reconstitution — bac-water math

Reconstitution is concentration arithmetic, not a dose. Add W mL of bacteriostatic water to a vial containing V mg of peptide and the concentration is (V × 1000) ÷ W mcg/mL. On a U-100 insulin syringe 100 units is 1 mL, so units = (mcg wanted ÷ mcg/mL) × 100. Worked example on a 10 mg vial with 2 mL of bacteriostatic water: 10,000 ÷ 2 = 5,000 mcg/mL, so a 250 mcg example is 250 ÷ 5,000 × 100 = 5 units. One caution about the table's second column: reported use of this compound is DIVIDED across two or three applications a day, so the 250 mcg column is roughly one application while the 750 mcg column is closer to a whole day's reported total. It is shown as a single draw to make the arithmetic legible, not because any source describes 750 mcg being given at once. Every row in the table draws well under 100 units, so no example needs a second draw. Two corrections that the arithmetic alone will not give you, and that matter more on this compound than on most. First, the nasal pump sets the delivered amount, not the vial. This peptide is predominantly reported intranasally, and a metered nasal spray pump delivers a fixed volume per actuation — commonly 0.1 mL. Load a pump with the 2 mL preparation above at 5,000 mcg/mL and each actuation delivers 500 mcg, which is twice the entire low end of the reported daily range in a single spray. To make one 0.1 mL actuation equal roughly 125 mcg you need 1,250 mcg/mL, which for a 10 mg vial means reconstituting into 8 mL of bacteriostatic water. That is a large diluent volume for a microgram-dosed peptide and it is the practical reason a 30 mL bacteriostatic water vial suits this compound better than a 10 mL one — a single 10 mL vial does not cover two preparations. Check the stated delivery volume of your own pump before assuming 0.1 mL; it is a property of the pump, not a convention. Second, the label weight is probably not the peptide weight. Peptides of this class are supplied as salts, and PubChem carries a separate record for Selank acetate (CID 155489759, C35H61N11O11, average mass 811.9) alongside the free base at 751.89; a diacetate form is also indexed. Those figures are for the parent; for this compound (free base 792.94) a vial labelled 10 mg weighed as the monoacetate holds about 9.30 mg of peptide, and as the diacetate about 8.68 mg. Residual trifluoroacetate from reversed-phase purification has the same effect. That is up to a 14% error in every concentration figure above, in the direction of less peptide than the label says — and a purity percentage on a certificate does not reveal it, because purity and net peptide content are two different tests. If the certificate does not report content, the honest reading of the table below is that its concentrations are upper bounds. All of this is handling arithmetic for research material, not a dosing instruction. Add water slowly down the vial wall and swirl rather than shaking.

This is concentration math, not a dose recommendation.

Injection / administration basics

The most consequential handling fact about this compound is that its two reported routes are not two ways of delivering the same thing. One study administered Selank to the same mouse strains at the same 300 mcg/kg/day for five days by two routes and measured receptor binding afterwards. Intraperitoneal administration raised GABA-receptor binding sites in the frontal cortex by 38% and left NMDA receptors unchanged; intranasal administration raised NMDA-receptor binding by 23% and left GABA receptors unchanged. The authors attributed the divergence to route-specific pharmacokinetics and biotransformation (PMID 29787664). That experiment set intranasal against intraperitoneal administration; it did not test the subcutaneous route, and neither has anything else. So "intranasal or subcutaneous, whichever you prefer" — which is how this page used to describe the choice, and how the market generally describes it — rests on no comparison at all, while the one route comparison that has been run says route changes the pharmacology rather than just the amount delivered. Intranasal is the route the community protocols and the Russian research both predominantly use, and the brain-tissue distribution work was done intranasally (PMID 16637290). Practically, the reconstituted solution is transferred to a sterile metered spray bottle, and the amount delivered is fixed entirely by concentration multiplied by the pump's actuation volume — which is why the arithmetic in the section above matters more here than the injection technique does. Nasal dryness and throat irritation are the commonly reported local effects. Where subcutaneous handling is described, it follows the pattern of any microgram-dosed research peptide: a small-gauge insulin syringe, refrigerated reconstituted solution, rotated sites. It is worth being explicit that no published human study of this peptide used the subcutaneous route. None of this is instruction for human use.

Half-life & frequency rationale

This page previously stated that the parent peptide Selank has a plasma half-life of about 20–30 minutes. That figure is withdrawn, and the reason it was wrong is worth setting out, because the same number is repeated across the peptide market. A PubMed search restricted to title and abstract for Selank together with pharmacokinetics or half-life returns four records, and not one of them reports a plasma half-life for Selank. Two (PMID 11550013, PMID 12432865) report a half-life that belongs to leu-enkephalin, not to Selank. The other two concern Selank's own disposition — brain-tissue distribution and degradation products after intranasal administration (PMID 16637290) and a route comparison (PMID 29787664) — and neither states a half-life. PMID 11550013 reports that patients with generalised anxiety have a shortened plasma enkephalin half-life and that Selank inhibits enkephalin hydrolysis. PMID 12432865 reports that Selank increased the half-life of plasma leu-enkephalin in high-anxiety mice. The clinical study PMID 18454096 measures the same thing in patients. In other words, the half-life in the Selank literature is a quantity Selank acts on — lengthening it is the proposed mechanism — and at some point in transmission it was reattached to Selank itself. We can find no primary pharmacokinetic study establishing a plasma half-life for Selank in any species, and no measurement of any kind for the acetylated-amidated analogue. What is documented is the degradation pathway rather than a number. A tritium-labelling study identified the major products of Selank breakdown in blood plasma as the pentapeptide TKPRP, the tripeptide TKP, and the dipeptides RP and GP (PMID 16637290), A companion analysis is sometimes read as describing how Selank itself is cleared; it does not — there Selank is the inhibitor and leu-enkephalin the substrate, and what it establishes is that Selank's inhibition targets carboxypeptidases and dipeptidyl carboxypeptidases (PMID 15344652). TKPRPGP losing Gly-Pro to give TKPRP, and TKPRP losing Arg-Pro to give TKP, is degradation proceeding inward from the C-terminal end, with the N-terminal threonine surviving into both of the largest fragments. That is the honest case for the modification, and it is asymmetric. A C-terminal amide blocks carboxypeptidase attack, and the labelling study above is the only cited work that followed Selank itself and observed its breakdown products — so that is the one route with direct evidence behind it. An N-terminal acetyl group blocks aminopeptidase attack, which is a real degradation route for peptides generally but is not the one these products point to for this peptide. So one half of "N-Acetyl Selank Amidate" has a documented rationale and the other half has a plausible one, and neither has been shown to work because no pharmacokinetic comparison of the analogue against the parent has been published. Treat any specific half-life figure you encounter for this compound — including the one this page used to publish — as unsourced until someone names the study. One further correction in the same family: this page previously reported intranasal bioavailability for Selank of 60–80%. A PubMed search for Selank together with bioavailability returns zero records. That figure is withdrawn as well.

Stacking — overview

The pairing that dominates discussion is Selank with Semax — two Russian peptides from the same research programme, combined on the reasoning that one is anxiolytic and the other nootropic. The amidated forms of both are sold as a matched pair. Worth knowing before treating that as established: the only human study that administered both did so as separate arms, not as a combination, and it measured brain connectivity rather than any outcome (PMID 32342318). No controlled study of the combination exists. The interaction that does have evidence behind it is not with another research peptide but with prescription GABAergic medicines, and it is documented at the receptor: non-cumulative action with benzodiazepines, and blockade of diazepam's and olanzapine's modulatory activity (PMID 30255741). That is the interaction most likely to matter to anyone reading this page, and it is the one community stacking lists never mention. Our cross-compound stacking guide covers where pairings are redundant rather than additive; for this compound the honest summary is that the peptide pairings are unstudied and the drug interaction is not.

For how combinations are grouped by research context, the named blends, and why a pre-mixed blend vial cannot be calculated from its total milligrams, see the peptide stacks guide.

Storage & handling

• Lyophilized (powder): store sealed and refrigerated at about 2–8°C (36–46°F), protected from light and moisture; long-term storage is commonly at −20°C or below.
• Reconstituted (in bacteriostatic water): refrigerate at 2–8°C, protect from light, avoid freeze-thaw cycles and vigorous shaking; reconstituted solution has a limited stable window commonly described as a few weeks.
• Note the diluent volume this compound implies. Bringing a 10 mg vial to the ~1,250 mcg/mL needed for a 125 mcg metered nasal actuation takes 8 mL of bacteriostatic water for one vial — which is why a 30 mL vial rather than a 10 mL one is the practical size here. Bacteriostatic rather than sterile water is what makes a multi-entry vial multi-entry; the benzyl alcohol is the reason.

Evidence File

The N-Acetyl Selank Amidate Evidence File

Every published study in this literature was run on the unmodified parent peptide Selank, and PubMed returns no record for the acetylated, amidated analogue under any spelling. That much is on the free page. What this file does is read the human papers as documents rather than as citations: which had a placebo arm, which had a comparator, which reported a number at all, and which reported something other than the quantity its citation is normally used to support. It also traces several of the compound's most-repeated figures back to the individual sentence each came from, and states what that sentence was actually about.

• 6 human-subject publications reviewed, 0 of them on this analogue
• 3 clinical-outcome studies with no published dose, route or duration
• 2 published IC50 values where the market quotes one
• 0 registered trials in any registry reachable from here

Sourcing File

The N-Acetyl Selank Amidate Sourcing File

This compound has no registry record of any kind, which means the identity section of any certificate that ships with it had to be assembled from somewhere else. This file works out where each piece would have come from, what the sequence itself rules out about the tests a laboratory can run on it, and which of the confusable neighbours a given number on a document would actually describe. It recomputes the salt-form arithmetic to its structural worst case, and it documents what the reference databases themselves get wrong about this family before a vendor ever copies from them.

• 0 registry records: no CAS, no UNII, no CID for this molecule
• 0.0233 Da between this compound's protonated ion and an incomplete synthesis
• 6 reference-layer records carrying naming, sequence or stoichiometry defects
• 97 to 125 mcg per actuation from one identical preparation

Benefit & Outcome Review

The N-Acetyl Selank Amidate Benefit and Outcome Review

Every benefit claim made for this compound is inherited from a different molecule, and inheritance is not measurement. This review takes the claims one at a time and asks what was measured, in what species, in what baseline condition, and with what number attached. Several claims survive that treatment in a narrower form than the marketing states, one survives with a figure that turns out to be a losing comparison, several turn out to rest on a condition the copy drops, and one has a single adjacent datum in the literature that points the opposite way.

• 0 of these findings measured on the acetylated, amidated analogue
• 0 effect sizes published in any human study of the parent peptide
• 39.6 percent for Selank against diazepam's 49.3 on the same measure
• 3 independent papers converge: effect only where the baseline was abnormal

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