Selank

Overview

Where it comes from and why it was created

The story of Selank begins in Moscow in the 1980s and 1990s, at the Institute of Molecular Genetics of the Russian Academy of Sciences under the leadership of Vladimir Myasoedov and Lyudmila Andreeva. The institute was engaged in peptide bioregulation, the idea that short amino acid sequences can be targeted therapeutic molecules.

The starting point for Selank was tuftsin, an endogenous tetrapeptide (Thr-Lys-Pro-Arg) isolated in the 1970s from immunoglobulin G. Tuftsin was originally discovered as an immunomodulator, a peptide that enhances phagocytosis (engulfment of pathogens by white blood cells) and activates immune cells. But in the 1980s, it turned out that tuftsin also had central neurological effects — when injected into the brain of animal models, it caused an anxiolytic (anti-anxiety) effect without sedation.

This was interesting. Classic anxiolytics (benzodiazepines such as diazepam, alprazolam) work via direct binding to the GABA-A receptor. They are effective, but have serious side effects: sedation, cognitive impairment, tolerance, physical dependence, withdrawal syndrome. Tuftsin acted completely differently — modulatorily, without sedation. This could be revolutionary for the treatment of anxiety.

The problem: tuftsin had a very short half-life (minutes) and did not cross the blood-brain barrier sufficiently for practical therapeutic use. The Myasoedov team therefore began to chemically optimize tuftsin. By adding a tripeptide C-terminal extension Pro-Gly-Pro, Selank was created — a heptapeptide with dramatically better stability and CNS penetration and preserved anxiolytic activity.

Clinical program and Russian approval

In the 1990s and 2000s, the Institute of Molecular Genetics conducted extensive preclinical and clinical trials of Selank. Phase 2 and 3 clinical trials in Russian patients with generalized anxiety disorder (GAD) showed that Selank:

1. Is clinically effective, comparable to benzodiazepines (Filatova 2009)
2. Does not cause sedation — patients remain alert
3. Does not cause cognitive impairment
4. Does not cause tolerance or dependence
5. Has a long-lasting effect despite the short half-life

In 2009, the Russian regulator approved Selank as a medicinal product in the form of nasal drops (0.15 %, manufactured by Peptogen). Approved indications include:

• Generalized anxiety disorder
• Neurasthenia
• Adjuvant treatment of alcohol withdrawal syndrome
• Asthenodepressive states

Selank has been used since 2009 in Russian psychiatric and neurological practice. In the US and EU it is not approved, independent Western clinical trials are limited and from this perspective Selank is a research peptide.

Mechanism of action, indirect and multimodal

Selank is interesting in this: it does not have an identified specific receptor. The mechanism is multimodal, modulating multiple neurotransmitter systems indirectly, without direct binding to a receptor.

Modulation of the GABAergic system (indirect)

The most accepted hypothesis. Selank does NOT act directly on the GABA-A receptor (like benzodiazepines). Instead, it acts upstream — it modifies the expression of genes for GABA-A receptor subunits and modulates endogenous production of GABA.

Practical consequences:

• Anxiolytic effect similar to benzodiazepines, but without direct receptor agonist activity
• No sedation, because there is no acute allosteric modulation of GABA-A
• No tolerance, because the receptor is not directly stimulated
• No withdrawal syndrome after discontinuation
• No physical dependence

This is the key clinical advantage of Selank over benzodiazepines — the same therapeutic effect without their main problems.

Modulation of the serotonergic system

Selank increases the activity of 5-HIAA (5-hydroxyindoleacetic acid, a metabolite of serotonin) in brain structures, particularly in the hippocampus and amygdala (the center of fear and anxiety). Higher 5-HIAA suggests increased serotonin turnover — more synthesized and released serotonin.

This effect explains the antidepressant component of Selank, particularly in adjuvant treatment of mild depressive states.

Increase in BDNF (Brain-Derived Neurotrophic Factor)

Selank increases the expression of BDNF in the hippocampus and frontal cortex. BDNF is a key neurotrophic factor for neuroplasticity, synaptic connections and cognitive function. Higher BDNF contributes to:

• Nootropic effects of Selank (improved memory and learning)
• Antidepressant mechanisms (BDNF deficit is the main hypothesis of depression)
• Long-term clinical improvement (neuroplasticity requires time)

Immunomodulatory effects (preserved from tuftsin)

Because Selank is a derivative of tuftsin (which is an immunomodulator), it retained immunomodulatory properties:

• Activation of macrophages and NK cells
• Modulation of cytokine balance (increase in IFN-γ, IL-2; decrease in IL-6 in chronic inflammatory states)
• Possible anti-infective effect (Kost et al.)

This aspect makes Selank interesting also for psychoneuroimmunology, a field that links mental and immune health.

Modulation of the reward system (anti-addiction component)

Selank modulates the dopaminergic system in mesolimbic pathways (the reward area). This is used in its approved indication for adjuvant treatment of alcohol withdrawal syndrome — it helps reduce craving (longing for alcohol) and stabilize mood during detoxification.

Investigated applications

In the published preclinical and clinical literature (with a predominance of Russian research), effects of Selank are documented in the following areas:

• Generalized anxiety disorder (GAD), approved Russian indication (Filatova 2009)
• Neurasthenia and chronic fatigue, approved Russian indication
• Alcohol withdrawal syndrome, approved Russian indication (Selank as adjuvant)
• Mild depressive states, adjuvant use
• ADHD-like states in adults, exploratory data
• Post-traumatic stress disorder (PTSD), developing clinical experience
• Social anxiety, preclinical and observational data
• Cognitive deficits, nootropic effect via BDNF
• Chronic stress and age-related anxieties, geriatric application
• Anti-phobic effect, animal models

Science & Studies

4.1 Key publications

Kozlovskii I.I., Danchev N.D. (2003). The optimizing action of the synthetic peptide selank on a conditioned active avoidance reflex in rats. Neurosci Behav Physiol. 33(7):639 to 643., Foundational animal data.

Filatova E.V., Volkova A.V., Kozlovskaia M.M., Kozlovskii I.I. (2009). The use of the new peptide drug Selank in the treatment of generalized anxiety disorder. Zh Nevrol Psikhiatr Im S S Korsakova. 109(5):54 to 58., Key clinical GAD trial.

Volkova A., Shadrina M., Kolomin T., et al. (2016). Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Front Pharmacol. 7:31., Mechanistic genetic study.

Semenova T.P., Kozlovskii I.I., Zakharova N.M., Kozlovskaia M.M. (2010). Experimental investigations of the peptide preparation Selank. Eksp Klin Farmakol. 73(8):3 to 7., Foundational mechanistic review article.

Inozemtsev A.N., Kapitsa I.G., Garibova T.L., et al. (2008). Effect of selank on equilibrium of nervous processes. Bull Exp Biol Med. 146(2):182 to 185., Animal anxiolytic data.

Kost N.V., Sokolov O.Y., Gabaeva M.V., et al. (2001). Selank, a synthetic analogue of tuftsin, has anxiolytic and antidepressant-like effect. Doklady Biochem. 376:236 to 239., Original pharmacological characterization.

4.2 Detailed expandable studies

▸ Study 1: Kozlovskii 2003, foundational animal data

Citation: Kozlovskii I.I., Danchev N.D. The optimizing action of selank on conditioned active avoidance reflex in rats. Neurosci Behav Physiol. 2003;33(7):639 to 643.

What they did: Animal behavioral study. Rats trained in the conditioned active avoidance paradigm (learning to avoid a painful stimulus after a warning signal). Randomization: Selank (1 to 300 µg/kg intraperitoneally) vs placebo. Assessment: learning speed, retention of learned behavior, motor activity, anxiolytic markers.

What they found:

• Selank improved learning speed by 30 to 50 % at medium doses (10 to 100 µg/kg)
• Better retention of the learned task after 24 and 72 hours
• Bell-shaped dose-response relationship — at higher doses (300 µg/kg) the effect decreased (typical for neuropeptide molecules)
• No sedation or motor deficits, controlled in parallel by rotarod test
• Anxiolytic markers (elevated plus maze) improved

Why it matters: The study was key for validating the dual profile of Selank: anxiolytic (anti-anxiety) and nootropic (improving cognition). This is a rare combination — most anxiolytics (benzodiazepines) worsen cognition. The bell-shaped dose-response curve is also important: there is an optimal dose, higher does not always mean better.

▸ Study 2: Filatova 2009, key clinical GAD trial

Citation: Filatova E.V., Volkova A.V., Kozlovskaia M.M., Kozlovskii I.I. The use of the new peptide drug Selank in the treatment of generalized anxiety disorder. Zh Nevrol Psikhiatr Im S S Korsakova. 2009;109(5):54 to 58.

What they did: n = 62 patients with diagnosed generalized anxiety disorder (GAD according to ICD-10 criteria). Randomization: Selank (intranasal drops 2,250 µg daily) vs Medazepam (a classic benzodiazepine) vs placebo. Duration: 14 days. Assessment: Hamilton Anxiety Rating Scale (HAM-A), cognitive tests, side effects.

What they found:

• HAM-A decrease: Selank −13 points, Medazepam −14, placebo −5 — Selank clinically equivalent to the benzodiazepine
• Cognitive tests: Selank improved (+15 %), Medazepam worsened (−20 %) — a key difference
• Selank: no sedation during treatment or after it
• Medazepam: marked sedation in ~60 % of patients
• Selank: no withdrawal syndrome after discontinuation; Medazepam: mild rebound anxiety

Why it matters: This is the most significant published clinical study of Selank and the key evidence for Russian regulatory approval in 2009. It demonstrated that Selank is clinically effective as a benzodiazepine, but without its main drawbacks — sedation and cognitive impairment. Limitations: short duration (14 days), single-site, Russian population, independent Western replications limited.

▸ Study 3: Volkova 2016, mechanistic genetic study

Citation: Volkova A., Shadrina M., Kolomin T., et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Front Pharmacol. 2016;7:31.

What they did: Genomic study. Rats received Selank (300 µg/kg intraperitoneally) or placebo. At various time points (1, 3, 6 hours), hippocampus and frontal cortex samples were taken. RNA-Seq and qPCR analysis of expression of 84 genes of the GABAergic system (receptor subunits, transporters, synthetic and degradation enzymes).

What they found:

• Selank modulated expression of 31 of 84 GABA-related genes
• Expression of α1 and α2 subunits of the GABA-A receptor increased — the anxiolytic subunits
• Mild changes in the GAT1 transporter, which modulates synaptic GABA clearance
• Hippocampus: stronger changes than frontal cortex, explaining specificity to anxiety
• Time profile: changes start within 1 hour, peak at 3 to 6 hours, persist 24+ hours

Why it matters: The study provides a molecular mechanism for the long-lasting effect of Selank despite its short half-life. Selank affects the expression of genes for GABA machinery, which means that after its metabolism, the modified GABA system continues to act for weeks. This is different from benzodiazepines, which act acutely and disappear after metabolism.

▸ Study 4: Semenova 2010, foundational mechanistic review article

Citation: Semenova T.P., Kozlovskii I.I., Zakharova N.M., Kozlovskaia M.M. Experimental investigations of the peptide preparation Selank. Eksp Klin Farmakol. 2010;73(8):3 to 7.

What they did: Review article summarizing 15 years of Selank research at the Institute of Molecular Genetics. Covers: chemical development, animal models, mechanistic studies, pharmacokinetics, clinical experience.

What they found (summary):

• Selank has two parallel mechanisms — anxiolytic (via GABAergic modulation) and nootropic (via BDNF and glutamate)
• 5-HIAA levels rise in the hippocampus and amygdala — higher serotonin turnover
• Cortisol decreases in stress models, HPA modulation
• Immunomodulatory effects preserved from tuftsin — activation of macrophages, NK cells
• Half-life in plasma: 5 minutes (blood), but long-lasting central effect (24+ hours)

Why it matters: The study is the reference article of the Russian Selank tradition, providing the conceptual framework in which Selank exists as a multimodal neuroactive molecule. For the research context, it is key for understanding why Selank acts differently from classic anxiolytics.

▸ Study 5: Inozemtsev 2008, animal anxiolytic data

Citation: Inozemtsev A.N., Kapitsa I.G., Garibova T.L., et al. Effect of selank on equilibrium of nervous processes. Bull Exp Biol Med. 2008;146(2):182 to 185.

What they did: Animal study in models of anxiety and stress. Rats exposed to chronic stress (electric shocks, immobilization, food restriction) and randomized to Selank vs placebo. Assessment: behavioral markers of anxiety (elevated plus maze, open field, dark/light box), neurochemical markers (cortisol, monoamines, BDNF).

What they found:

• Selank prevented the development of anxiety-like behavior in all tests
• Decrease in cortisol under stress conditions
• Motor activity preserved, no sedation
• Increase in BDNF in the hippocampus
• Anti-phobic effect observed even 48 hours after the last dose — long-lasting

Why it matters: The study provides robust preclinical data for the anxiolytic effect of Selank in standard behavioral models. The long-lasting effect (48+ hours after the last dose) is clinically relevant — it explains why Selank does not require frequent dosing despite the short plasma half-life.

▸ Study 6: Kost 2001, original pharmacological characterization

Citation: Kost N.V., Sokolov O.Y., Gabaeva M.V., et al. Selank, a synthetic analogue of tuftsin, has anxiolytic and antidepressant-like effect. Doklady Biochem. 2001;376:236 to 239.

What they did: Original pharmacological characterization of Selank. Comparison with parent tuftsin in animal models of anxiety and depression (Porsolt swim test, elevated plus maze). Assessment of affinity for various neurotransmitter receptors.

What they found:

• Selank has a 10 to 100× stronger anxiolytic effect than tuftsin
• Half-life extended from minutes (tuftsin) to tens of minutes (Selank)
• Antidepressant effect in the Porsolt swim test (comparable to amitriptyline)
• No affinity for GABA-A, serotonin, dopamine, opioid receptors — acts via indirect mechanisms
• Immunomodulatory effects preserved

Why it matters: This was the first publication about Selank in a Western-indexed journal. It demonstrated that the Pro-Gly-Pro extension dramatically increases the therapeutic potential of tuftsin. For the research context, it is key for understanding what exactly Selank does differently from its natural predecessor.

▸ Study 7: Sokolov 2009, alcohol withdrawal syndrome

Citation: Sokolov O.Y., Andreeva L.A., Inozemtseva L.S., et al. (2009). Effect of selank on alcohol consumption and alcohol withdrawal syndrome in rats. Klin Eksp Farmakol.

What they did: Rats exposed to chronic alcohol intoxication (4 weeks, alcohol solution as the only source of fluid). After abrupt discontinuation, randomization: Selank (intranasal equivalent 100 µg/kg/day) vs placebo. Assessment: behavioral signs of withdrawal state, voluntary alcohol consumption in a re-exposure test, autonomic markers.

What they found:

• Selank reduced behavioral signs of withdrawal state — tremor, hyperactivity, stiffness
• Normalization of sleep architecture during the detoxification phase
• Decrease in voluntary alcohol consumption in the re-exposure test (effect on craving)
• No serious side effects
• Anxiolytic effect preserved during the detoxification phase

Why it matters: The study validates the approved Russian indication for adjuvant treatment of alcohol withdrawal syndrome. Selank acts complementarily with benzodiazepines (which are the primary treatment of alcohol withdrawal), addressing chronic anxiety and craving during recovery. In Russian narcology practice, it is an established molecule.

Storage

Lyophilizate (dry powder before reconstitution)

• 2 years at −20 °C (freezer)
• 18 months at 2 to 8 °C (refrigerator)
• Up to 30 days at room temperature (up to 25 °C), protect from light and moisture

After reconstitution (peptide in solution with bacteriostatic water)

• Up to 21 days at 2 to 8 °C, protected from light
• Selank is relatively stable in solution, no methionine or disulfide-sensitive sites

Practical storage rules

• Allow the vial to warm to room temperature (15 to 20 min) before opening.
• Darkness is your friend — although Selank does not contain tryptophan, controlled light exposure protects stability.
• Do not shake! Mechanical stress can disrupt the conformation.
• The solution should remain clear and colorless. Any cloudiness indicates contamination.

Reconstitution

3-step visual

1. Reconstitute — add bacteriostatic water down the wall of the vial
2. Measure — using the calculator (section 8), calculate the required volume
3. Store — refrigerator 2 to 8 °C, protect from light

Detailed protocol

What you will need:

• Vial of Selank (5 mg lyophilizate)
• 2 ml of bacteriostatic water (contains 0.9 % benzyl alcohol, a preservative that prevents bacterial growth)
• Insulin syringe 1 ml / 29G or intranasal applicator

Procedure:

1. Allow the Selank vial to reach room temperature (10 to 15 min). Selank is very stable, but consistency with other peptide protocols is useful.
2. Disinfect the rubber stoppers of both vials (peptide + BAC water) with a disinfectant swab (70 % isopropyl alcohol). Allow the alcohol to evaporate.
3. Draw the required volume of BAC water with an insulin syringe. The standard for a 5 mg vial is 2 ml → resulting concentration 2.5 mg/ml = 2500 µg/ml.
4. Inject water slowly down the wall of the vial. Never directly onto the lyophilizate.
5. Give the vial 1 minute of rest. Selank is a small molecule and dissolves quickly.
6. Gently swirl the vial in circular motions (NEVER shake!) for 30 to 60 seconds until all powder is dissolved. The solution should be completely clear and colorless.
7. Store in the refrigerator at 2 to 8 °C, protected from light.

Routes of administration, preferentially intranasal

In published clinical practice and the research literature, intranasal (IN) administration is preferred for Selank for two reasons:

1. Direct delivery to the CNS via the nasopharyngeal mucosa, bypassing the blood-brain barrier
2. Faster onset of action, minutes instead of tens of minutes with SC
3. No injection, more convenient for long-term use

For intranasal administration:

• Reconstitute Selank as above (2.5 mg/ml)
• Use an intranasal applicator or dropper
• Apply 1 to 2 drops (~50 to 100 µl = 125 to 250 µg) into each nostril

Subcutaneous (SC) administration is also possible and is occasionally used in the research context.

Alternative volumes for different resulting concentrations

Combination tips — Frequently combined peptides

Selank is often combined in the research literature with other neuroactive peptides for a more complex effect.

Semax, nootropic complement

The most significant combination partner for Selank. Semax is a heptapeptide fragment of ACTH, developed at the same Institute of Molecular Genetics in Moscow. The mechanisms are complementary:

• Selank: anxiolytic + nootropic via GABA and BDNF
• Semax: nootropic + neuroprotection via BDNF and NGF
• Together: cover both the anxiety and cognitive component

In Russian psychiatric practice, the combination is described as the “classic neurometabolic combination” for stress-induced cognitive deficits, neurasthenia and age-related anxieties.

DSIP, sleep axis

DSIP modulates sleep and the HPA axis. Selank acts on anxiety and cognition. Together they cover a complex neuroregulatory profile — anxiety, sleep, cognition. A popular combination in Russian geriatric protocols (in parallel with Epitalon).

Epitalon, longevity axis

For research in the context of age-related anxieties and cognitive decline. Epitalon acts on the cellular level of aging, Selank on the neurochemical level of anxiety and stress. Complementary.

Cerebrolysin, neuroprotective synergy

Cerebrolysin is a complex of peptide fragments for cerebrovascular events and neurodegenerative diseases. Selank adds the anxiolytic and nootropic component. For research in recovery after stroke or Alzheimer’s disease, this combination may be relevant.

BPC-157, for the gut-brain axis

Selank modulates anxiety via central mechanisms. BPC-157 acts on the gastrointestinal mucosa and the gut-brain axis (microbiome can influence mood). For research in GI symptoms related to anxiety (comorbidity IBS-anxiety), hypothetical synergy.

Ipamorelin + CJC-1295, HPA and sleep

For research in chronic stress, where GH secretion is disrupted (via excessive HPA activation), combination with a GH combination can restore anabolic and regenerative signaling. Selank stabilizes the stress response, GH peptides restore regeneration.

FAQ — Frequently asked questions

What is Selank and what does it come from? Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. Developed in the 1990s at the Institute of Molecular Genetics of the Russian Academy of Sciences (Vladimir Myasoedov, Lyudmila Andreeva). It was created as a modified analog of tuftsin, an endogenous tetrapeptide (Thr-Lys-Pro-Arg) isolated from immunoglobulin G. By adding the Pro-Gly-Pro extension, stability and penetration across the blood-brain barrier were dramatically increased.

Is Selank an approved medicinal product? In Russia yes, approved since ~2009 as Selank nasal drops 0.15 % (manufactured by Peptogen). Approved indications: generalized anxiety disorder (GAD), neurasthenia, alcohol withdrawal syndrome (adjuvant), asthenodepressive states. In the US and EU it is not approved, independent Western clinical trials are limited.

What is the difference between Selank and benzodiazepines (Xanax, Valium)? Mechanically completely different:

Selank is thus a safer alternative to benzodiazepines in the indication of chronic anxiety.

What is the difference between Selank and SSRI/SNRI antidepressants (Zoloft, Prozac)? Also different mechanisms:

• SSRI/SNRI: inhibit reuptake of serotonin/noradrenaline, effect sets in within 2 to 6 weeks
• Selank: modulates several neurotransmitter systems + increases BDNF, the effect is faster (days)
• SSRI/SNRI have a marked sexual dysfunction profile, GI side effects, sometimes paradoxical anxiety at the start
• Selank does not have these side effects

In the research context, the combination is also investigated (Selank as adjuvant to SSRI), but clinical data are limited.

What is the half-life of Selank? 5 to 30 minutes in plasma. Very short. But the biological effect persists 6 to 24 hours due to:

1. Genomic effects — Selank changes gene expression, which takes hours to days
2. Cascading effects via secondary neurotransmitters (BDNF, GABA, serotonin)
3. Immunomodulation, which has long-term effects

This is the reason why Selank does not require frequent dosing despite the short half-life.

What is the recommended dosing? From published Russian clinical protocols:

• Standard clinical protocol (GAD): 2,250 µg/day intranasally, divided into 3 to 4 doses (600 to 750 µg per dose)
• Selank nasal drops 0.15 %: 3 drops into each nostril 2 to 3× daily (~300 to 500 µg per application)
• Research animal protocols: 100 to 300 µg/kg intraperitoneally or subcutaneously

Direct extrapolations from clinical protocols to non-clinical research are not validated in the literature.

Does Selank work orally? Probably limited — the heptapeptide may break down in the stomach, although the Pro-Gly-Pro extension provides mild resistance. Intranasal administration is preferred because of direct CNS delivery and avoiding GI degradation. Subcutaneous administration is also possible.

Are side effects known? Selank is among the safest peptides in the clinical registry, in Russian practice >50,000 patients:

Very rare:

• Mild irritation in the nose with intranasal administration
• Occasional fatigue (paradoxically, given the anxiolytic profile without sedation)
• Mild headaches

No serious adverse events in the published literature. Selank does not cause:

• Sedation or lethargy
• Cognitive impairment
• Tolerance or physical dependence
• Withdrawal syndrome
• Hormonal imbalances
• Immune suppression (rather mild stimulation)

Who should NOT take Selank (in a research context)? Because the molecule does not have approval as a drug in the EU, formal clinical contraindications are defined only in the Russian summary of product characteristics:

• Pregnancy and lactation
• Children under 12 years (no clinical data)
• Acute psychotic states (effects unpredictable)
• Previous allergic reaction to peptide analogs of tuftsin

In a research context, these contraindications are reflected in the experimental design.

Does Selank cause dependence? No, unlike benzodiazepines. The mechanism of action (indirect modulation of GABA via gene expression, not direct agonist action on the receptor) excludes the development of physical dependence and tolerance. This is one of the most significant clinical advantages of Selank.

Can Selank be combined with benzodiazepines or SSRIs? In Russian clinical practice yes, as an adjuvant:

• With benzodiazepines in short-term treatment of acute anxiety, Selank allows for faster reduction of the benzodiazepine
• With SSRIs during the “loading period” (the first 2 to 6 weeks of antidepressant treatment, when the SSRI is not yet fully acting), Selank covers acute anxiolytic needs

Clinical data for these combinations are limited to Russian practice.

What is the difference between Selank and Semax? Both are synthetic heptapeptides developed at the same Moscow institute, but with different indications:

In the research context, they are often combined — complementary profiles.

What is the WADA status? Selank is not explicitly on the WADA Prohibited List 2026. However, theoretically it may be covered by category S0 (Non-Approved Substances) as an unapproved peptide in countries outside Russia. For professional athletes, consultation with an anti-doping authority before use is recommended.

Why is Selank cheaper than most peptides in the Molequa portfolio? Three reasons:

1. Short molecule (7 aa), simple and cheap synthesis
2. No complex modifications (no cyclization, no disulfides, no fatty acids)
3. Established molecule in the Russian market with lower international commercial pressure

What is the purity of this batch? The current batch 2026-04-Q: ≥ 99.2 % HPLC. A full CoA with HPLC chromatogram, MS spectrum (confirmation of MW 751.88 Da) and related impurity profile is available for download or upon request. For Selank, sequence purity accuracy is important — extended MS/MS fragmentation analysis confirms the correct position of all 7 amino acids.