Peptide enthusiasts often ask “What is Selank and why do researchers use it for anxiety and cognition?” In short: Selank is a tuftsin‑derived heptapeptide explored for anxiolytic and nootropic effects without sedation. Below you’ll find an answer‑first overview of how it works, research-use handling, comparisons (Semax/benzodiazepines), and FAQs—written for education, not medical advice.
Fast Answer / Executive Summary (40–60 words)
Selank is a synthetic tuftsin‑analog heptapeptide (sequence TKPRPGP) studied for reducing anxiety and sharpening cognition while sparing alertness. Mechanistically, studies show modulation of GABA‑related gene expression, monoamines/serotonin, BDNF, enkephalin preservation, and immune cytokines (e.g., IL‑6)—a multi‑system profile that explains its calm‑yet‑clear outcomes in clinical and preclinical models. (PMC)
Entity Properties (for researchers)
Normalization note: You may see “Selanc” or “TP‑7” used; the standardized name here is Selank.
| Property | Details |
|---|---|
| Aliases / Synonyms | Selanc; TP‑7; UNII: TS9JR8EP1G. (GSRS) |
| Family / Pathway | Tuftsin analog (immunomodulatory peptide family) with glyproline (PGP) motif aiding stability. (Most Wiedzy) |
| Sequence (AA) | Thr–Lys–Pro–Arg–Pro–Gly–Pro (TKPRPGP). (PubChem) |
| Molecular Weight (Da) | ~751.9 g/mol. (PubChem) |
| CAS | 129954‑34‑3. (PubChem) |
| Typical Diluent(s) | Sterile water for injection (often bacteriostatic water 0.9% benzyl alcohol) or 0.9% saline (research use). Use promptly unless manufacturer of the solute specifies otherwise. (DailyMed) |
| Example Concentrations (educational) | 5 mg vial + 2 mL diluent → 2.5 mg/mL (2,500 µg/mL). 0.10 mL ≈ 250 µg. (Calculation example only.) |
| Storage | Lyophilized peptides are typically kept refrigerated or frozen; reconstituted solutions should be kept 2–8 °C, minimize freeze–thaw, and used relatively soon, per stability best practices for peptides. (PMC) |
Core Concepts & Key Entities
What is Selank and why is it studied?
Selank is a seven–amino‑acid analog of the immune peptide tuftsin engineered to provide anxiolysis without sedative trade‑offs. In a head‑to‑head clinical study in patients with generalized anxiety disorder (GAD) and neurasthenia, Selank’s anxiolytic effect matched medazepam (a benzodiazepine) while adding antiasthenic/psychostimulant benefits. (PubMed)
How does Selank modulate neurotransmission?
Selank influences GABA‑related and monoaminergic signaling in ways that reduce anxiety while preserving cognition. Transcriptomic work shows broad regulation of GABAergic genes after Selank administration; researchers interpret this as indirect GABAergic modulation (not classic benzodiazepine receptor agonism). (PMC)
In parallel, BDNF—a key neuroplasticity factor—rises in hippocampus after intranasal Selank in vivo, supporting pro‑cognitive effects. (PubMed)
Enkephalin preservation: a unique lever
Selank inhibits human serum enkephalin‑degrading enzymes (enkephalinases), prolonging endogenous enkephalin tone linked to stress relief and analgesia. Reported IC₅₀ values are ~20 µM (Selank), stronger than bacitracin/puromycin comparators in the same assay. This mechanism complements its anxiolytic phenotype. (PubMed)
Immune–brain crosstalk (IL‑6 and cytokine balance)
As a tuftsin analog, Selank shows immunomodulatory effects—notably altered expression of cytokine/chemokine genes (≈34 targets in mouse spleen) and normalization of inflammatory signals under stress. This may explain reports of improved stress resilience. (PubMed)
Antiviral signal: an information‑gain angle
Beyond anxiety, Selank demonstrated antiviral activity against influenza A/H3N2 in vitro and in vivo with strongest effect via preventive pre‑exposure administration, hinting at innate‑immunity priming. While not an antiviral drug, this result strengthens the “stress‑immune” narrative. (PubMed)
Why “calm without sedation” matters
Across clinical and translational work, Selank reduces anxiety without typical benzodiazepine downsides (amnesia, withdrawal). This has been explicitly noted in mechanistic and gene‑expression studies tied to GABA modulation, and in patient‑level data showing preserved—or improved—mental energy. (PMC)
Step‑by‑Step / How‑To (Research Use Only)
Educational only—no medical advice. The steps below outline laboratory‑style handling common in peptide research.
1) Plan your target concentration
Decide on a working solution that makes microgram‑level measurements easy. Example: 5 mg vial + 2 mL diluent → 2.5 mg/mL; 0.10 mL = 250 µg. For higher precision at smaller volumes, consider 5 mg + 4 mL → 1.25 mg/mL (0.10 mL = 125 µg).
2) Reconstitute with sterile technique
Use sterile water for injection (often bacteriostatic water) or 0.9% saline. Clean the stopper with alcohol; direct the diluent along the vial wall; swirl gently to dissolve. (DailyMed cautions to mix thoroughly and use promptly unless the solute’s manufacturer specifies otherwise.) (DailyMed)
3) Select an administration route (research contexts)
- Subcutaneous (SC): common in research for reliable bioavailability.
- Intranasal (IN): supported by mechanistic data (hippocampal BDNF upregulation after IN dosing), and widely used in Russian clinical practice. (PubMed)
4) Educational dosing ranges (by literature context)
Human clinical and translational literature frequently explores hundreds of micrograms per day, with some Russian protocols using multiple daily IN administrations; onset can be rapid in some patients (days). Researchers adjust by symptoms and tolerability in protocolized settings. (Cambridge University Press & Assessment)
5) Document outcomes and adjust
Track standardized anxiety/cognition scales (e.g., HAM‑A, Zung) akin to published trials, along with time‑of‑day and route, to understand response patterns and potential day‑to‑day variability. (PubMed)
6) Store to maintain integrity
Keep lyophilized material refrigerated/frozen; keep reconstituted material 2–8 °C, avoid repeated freeze–thaw, and minimize storage time consistent with peptide‑stability best practices; when in doubt, prepare fresh aliquots. (PMC)
Comparison / Alternatives
What makes Selank different? Selank vs. Semax vs. benzodiazepines boils down to calm‑focus vs. active‑focus vs. sedative‑anxiolysis. The table below summarizes.
| Dimension | Selank | Semax | Benzodiazepines (e.g., diazepam/medazepam) |
|---|---|---|---|
| What it is | Tuftsin‑analog heptapeptide (TKPRPGP). (PubChem) | ACTH(4‑10)‑analog heptapeptide (MEHFPGP). (PubMed) | Small‑molecule GABA_A positive allosteric modulators. |
| Primary outcome | Anxiolysis without sedation, with pro‑cognitive signal. (PubMed) | Cognitive enhancement / neuroprotection (BDNF‑centric). (PubMed) | Anxiolysis with sedation; risks of amnesia, tolerance, withdrawal. |
| Key mechanisms | GABA‑related gene modulation; ↑BDNF (hippocampus); enkephalinase inhibition; immune cytokine balancing (e.g., IL‑6). (PMC) | ↑BDNF/TrkB signaling; dopaminergic/serotonergic effects; clinical use post‑stroke in Russia. (PubMed) | Directly boost GABA_A receptor activity (broad CNS depression). |
| Clinical signals | Comparable anxiolysis to medazepam, added anti‑asthenic/psychostimulant effects; rapid responders reported in GAD cohorts. (PubMed) | BDNF increases and functional gains in stroke rehabilitation cohorts. (PubMed) | Effective for acute anxiety; cognitive/psychomotor impairment common. |
| Cognition | Often preserved or improved as anxiety falls. (PMC) | Enhanced attention/memory; potential stimulation. (PubMed) | Impaired memory/attention at therapeutic doses. |
| Tolerance / dependence | Not associated with benzodiazepine‑type dependence in literature to date. (PMC) | Not associated with benzo‑type dependence. | Tolerance/dependence risks with chronic use are well‑described. |
| Notable extra | Antiviral/immune signals in models; cytokine gene normalization. (PubMed) | Neuroprotection under ischemia; rehabilitative settings. (PubMed) | N/A |
Bottom line: Selank is best when anxiety + cognitive clarity are dual aims; Semax when pure cognition/neuroprotection is paramount; benzodiazepines remain potent but sedating and potentially habit‑forming.
Templates / Checklist / Example
Copy‑ready Researcher Checklist (Selank)
- Define objective: State the outcome of interest (e.g., acute anxiolysis vs. sustained cognitive clarity).
- Standardize naming: Record “Selank (TKPRPGP; CAS 129954‑34‑3)” to avoid confusion with “Selanc/TP‑7.” (PubChem)
- Select route: SC for bioavailability; IN if modeling translational use supported by hippocampal BDNF data. (PubMed)
- Set concentration: Choose mL to make µg math easy (e.g., 5 mg → 2 mL → 2.5 mg/mL).
- Practice asepsis: Alcohol swab stoppers/skin, sterile needle/syringe, avoid touching sterile parts; mix gently. (DailyMed)
- Start low, titrate: Begin in the lower hundreds of µg per day if modeling human‑adjacent paradigms; adjust per outcome scales. (PubMed)
- Record with scales: Log HAM‑A, Zung, or similar at baseline and intervals. (PubMed)
- Avoid long warm storage: Keep reconstituted aliquots 2–8 °C, minimize freeze–thaw; prepare fresh as needed. (PMC)
- Note immune endpoints: If studying stress‑immune crosstalk, include cytokine panels (e.g., IL‑6) pre/post. (PubMed)
- Plan a washout: Build in off‑periods to observe persistence and reversibility of effects.
FAQs (Answer‑first, PAA‑style)
1) What is Selank?
Selank is a synthetic heptapeptide (TKPRPGP) derived from tuftsin that’s studied for anxiolytic and cognitive effects without sedation. Core mechanisms include GABA‑related gene modulation, BDNF increases, enkephalinase inhibition, and cytokine balancing, explaining calm‑yet‑clear outcomes observed across models and clinical cohorts. (PMC)
2) How fast can Selank work?
Selank can act quickly in some patients: clinical observations in GAD cohorts report rapid responders within days, and mechanistically, intranasal dosing alters hippocampal BDNF expression in vivo, a plausible substrate for earlier cognitive/affective change. (Cambridge University Press & Assessment)
3) Does Selank cause sedation like benzodiazepines?
Selank is non‑sedating in the literature and has even shown antiasthenic/psychostimulant signals, contrasting with benzodiazepines’ cognitive/psychomotor impairment. In a comparative clinical study, Selank matched medazepam’s anxiolysis without sedative downsides. (PubMed)
4) What’s unique about Selank’s mechanism vs. other nootropics?
Selank uniquely combines neurochemical (GABA/monoamines/BDNF) and immunomodulatory actions and inhibits enkephalinases, prolonging endogenous anti‑stress peptides—an uncommon multi‑axis profile among nootropics. (PMC)
5) Is Selank approved anywhere?
Selank is used clinically in Russia (including GAD contexts), with abstracts and conference proceedings noting status and rapid‑ vs slow‑response phenotypes. Outside Russia, it’s primarily a research compound. (Cambridge University Press & Assessment)
6) Where can researchers source Selank and find dosing math?
Researchers typically procure Selank as lyophilized powder (5 mg or 10 mg vials), then reconstitute and calculate microgram‑level aliquots. For purchase as research‑grade material, see Selank 5 mg or Selank 10 mg (COA‑driven supply). For step‑by‑step dilution math, see PeptideDosages guides linked below. (Educational; not medical advice.)
Next Steps
- Go deeper on practical handling: See PeptideDosages protocols for reconstitution math and unit conversions:
• Selank 5 mg Vial Dosage Protocol
• Selank 10 mg Vial Dosage Protocol - Procure research‑grade Selank with COAs:
• PureLabPeptides — Selank 5 mg
• PureLabPeptides — Selank 10 mg
Key takeaway: Selank’s value is its rare combination of anxiolysis without sedation plus cognitive support, underpinned by GABA/BDNF/enkephalin/immune mechanisms—making it a compelling peptide to study when calm clarity is the goal. (PubMed)