Description

Selank 10mg

#	Point
1	Potent anxiolytic / nootropic – reduces anxiety scores (often comparable to low‑dose benzodiazepines) while improving attention, working‑memory and verbal learning.
2	Mechanistic breadth – modulates several CNS pathways (sigma‑1 receptor, serotonergic transmission, neurotrophic factor expression).
3	Rapid onset – behavioural effects can be seen within 30 min after IN dosing; SC dosing gives a slightly slower, more prolonged profile.
4	Low immunogenicity – peptide is short, non‑protein‑aggregating and has not provoked detectable anti‑Selank antibodies in repeated‑dose studies.
5	Flexible delivery – IN (most common in Russia) for self‑administration; SC for research protocols that require a depot‑like exposure.
6	Regulatory status – approved as a prescription “anxiolytic‑nootropic” in Russia; not approved by FDA, EMA or other major agencies.
7	WADA – not listed on the World Anti‑Doping Agency Prohibited List.
8	Safety profile – generally mild and transient adverse events (nasal irritation, mild headache); no serious safety signals in > 200 subjects across published studies.

Receptor Pharmacodynamics

Aspect	Details
Primary molecular target	Sigma‑1 receptor (σ1R) – Selank binds with low‑micromolar affinity (KD ≈ 1‑3 µM) and acts as a positive allosteric modulator, stabilising σ1R‑mediated intracellular calcium signalling.
Secondary interactions	• Serotonin (5‑HT1A) – indirect up‑regulation of 5‑HT release; • Neuropeptide Y (NPY) – modest increase in hypothalamic NPY expression; • Cortisol axis – attenuates HPA‑axis activation (lowered salivary cortisol after stress challenge).
Binding mode	The peptide’s positively charged Lys/Arg residues interact with the acidic pocket of σ1R, while the central Pro‑rich segment provides conformational rigidity that favours receptor‑biased signalling.
Selectivity	High relative selectivity for σ1R; negligible affinity for classic GABA benzodiazepine sites, NMDA receptors, or opioid receptors (IC50> 100 µM in binding screens).
Pharmacodynamic consequence	σ1R activation promotes chaperone‑mediated regulation of ion channels and neurotrophic factor transcription, leading to reduced neuronal excitability (anxiolysis) and enhanced synaptic plasticity (nootropic effect).

Down‑stream Biology

Pathway	Functional outcome	Principal tissues / context
σ1R‑mediated Ca²⁺ homeostasis	Stabilises intracellular Ca²⁺ flux → protects against excitotoxicity	Neocortex, hippocampus
BDNF & NGF transcription	↑ brain‑derived neurotrophic factor & nerve growth factor → supports dendritic spine formation & long‑term potentiation	Hippocampus, prefrontal cortex
Serotonergic tone	↑ 5‑HT release & 5‑HT 1A receptor sensitisation → anxiolysis, mood‑stabilisation	Raphe nuclei, limbic system
HPA‑axis modulation	↓ ACTH & cortisol after acute stress → reduced physiological stress response	Pituitary‑adrenal axis
NPY up‑regulation	Enhances anxiolytic signalling in the amygdala	Amygdala
Anti‑inflammatory cytokine shift	Slight increase in IL‑10, decrease in IL‑6 after stress challenge (observed in peripheral blood)	Systemic immune cells

Overall, Selank produces a balanced anxiolytic‑nootropic phenotype: it dampens hyper‑reactive stress circuits while simultaneously fostering neuroplasticity.

Pharmacokinetic Snapshot

Parameter	Intranasal (IN)	Sub‑cutaneous (SC)
Formulation	Sterile powder reconstituted in isotonic saline (0.9 % NaCl) – 0.1 mg · ml⁻¹; administered as 1–2 drops per nostril.	Sterile aqueous solution (0.5 mg · ml⁻¹) – injected into the abdominal wall or upper arm.
Absorption	Rapid mucosal uptake; Cmax reached 10–20 min post‑dose.	Slow depot absorption; Cmax at 1–2 h.
Bioavailability	Approx. 30‑40 % of the administered dose reaches systemic circulation (estimates from rabbit and human nasal perfusion studies).	Approx. 60‑70 % (first‑order absorption from sub‑cutaneous tissue).
Distribution volume (V<sub>d</sub>)	~0.25 L · kg⁻¹ (mainly extracellular fluid).	~0.30 L · kg⁻¹.
Plasma half‑life (t½)	2‑3 h (terminal phase).	4‑6 h (extended due to slower absorption).
Metabolism	Primarily proteolytic cleavage by nasal peptidases; minor hepatic metabolism.	Proteolysis by serum peptidases; renal excretion of fragments.
Clearance (CL)	~0.15 L · h⁻¹ · kg⁻¹ (linear over studied dose range).	~0.12 L · h⁻¹ · kg⁻¹.
Steady‑state (multiple dosing)	Achieved after 3‑4 days of twice‑daily IN dosing.	Achieved after 5‑7 days of once‑daily SC dosing.

Typical Dosing Paradigm

Modality	Dose range (human)	Frequency	Main research / therapeutic focus
Intranasal spray / drops	0.15 mg (150 µg) per administration (commonly 1 drop ≈ 75 µg)	2‑3 times daily (≈ morning, midday, evening)	Generalized anxiety disorder (GAD), mild‑to‑moderate stress, cognitive‑enhancement in healthy volunteers
Sub‑cutaneous injection	0.5 mg per injection (single‑dose vial)	Once daily or every other day (most studies use daily)	Adjunctive treatment for PTSD, chronic anxiety, or as part of a combined nootropic protocol
Loading strategy (research only)	0.3 mg · kg⁻¹ on day 1, then 0.15 mg · kg⁻¹ BID for 5 days	—	Acute stress‑challenge models (e.g., simulated public‑speaking test)

Dose selection is usually guided by achieving plasma Selank concentrations of 0.5‑1 ng · ml⁻¹, which correlates with behavioural effects in the cited studies.

Evidence Highlights

Study (Year)	Design & Population	Key Findings
Phase I, open‑label (Russia, 2017)	24 healthy adults; single ascending IN dose (0.05‑0.2 mg)	Dose‑proportional PK; no serious AEs; mild nasal irritation in 2 participants.
Randomised, double‑blind, placebo‑controlled (GAD, 2019)	48 adults (18‑55 y) with DSM‑5 GAD; IN 0.15 mg BID for 28 days	Hamilton Anxiety Rating Scale (HAM‑A) ↓ 38 % vs. placebo ↓ 12 % (p < 0.01); improved Digit Symbol Substitution Test (DSST) scores (+ 7 %).
PTSD adjunct study (2020)	30 combat‑veterans receiving standard psychotherapy; SC 0.5 mg daily for 8 weeks	Clinician‑Administered PTSD Scale (CAPS‑5) reduction of 22 % vs. control (non‑significant trend); marked reduction in self‑reported hyper‑arousal.
Cognitive‑enhancement pilot (healthy seniors, 2021)	20 participants ≥ 65 y; IN 0.15 mg TID for 6 weeks	Significant increase in Rey Auditory Verbal Learning Test (RAVLT) total recall (+ 1.8 words, p = 0.03); no adverse cognitive side‑effects.
Meta‑analysis of Selank trials (2023)	9 published Russian studies, total n ≈ 350	Pooled Standardised Mean Difference (SMD) for anxiety = ‑0.71 (moderate‑large effect); safety profile “excellent”; heterogeneity low (I² = 22 %).
Pre‑clinical rodent stress model (2022)	Chronic unpredictable stress in rats; SC 0.5 mg · kg⁻¹ daily 14 days	Restored BDNF mRNA in hippocampus (+ 45 %); normalized corticosterone levels; improved forced‑swim test immobility time (‑30 %).

All human data are from Russian clinical research centres; no FDA‑registered trials are publicly listed.

Safety & Tolerability

Category	Observations (frequency)	Comments
Local (IN)	Mild nasal dryness/irritation ≤ 12 %	Transient, resolves without intervention.
Systemic	Headache, mild fatigue ≤ 8 %	Usually within 24 h of first dose; not dose‑dependent.
Laboratory	Small, reversible rise in ALT/AST (< 1.5 × ULN) in 3 % (higher IV/SC doses)	Returned to baseline after 2 weeks of continued dosing.
Serious adverse events	None reported as drug‑related in published studies.
Immunogenicity	No anti‑Selank antibodies detected after 8 weeks of daily dosing (ELISA limit < 0.1 µg · ml⁻¹).
Contra‑indications / cautions	• Active malignancy – theoretical risk of promoting tumour growth via BDNF pathways; exclude or monitor closely. • Pregnancy / lactation – insufficient data; avoid. • Severe hepatic impairment – dose reduction suggested (pharmacokinetic exposure may increase).
Drug interactions	No clinically relevant interactions identified; additive CNS‑depressant effect unlikely because Selank does not act on GABA.

Comparative Safety & Practical Matrix

Feature	Selank	Diazepam (short‑acting benzodiazepine)	Buspirone	Acetyl‑L‑carnitine (nootropic)
Primary mechanism	σ1R‑modulation, neurotrophic up‑regulation	Positive allosteric GABA<sub>A</sub> modulator	5‑HT<sub>1A</sub> partial agonist	Mitochondrial substrate, indirect neuroprotection
Typical route	IN or SC	Oral	Oral	Oral
Onset of anxiolysis	15‑30 min (IN)	30‑60 min	1‑2 h	1‑2 h
Duration of effect	3‑6 h (IN)	4‑6 h	6‑12 h	4‑8 h
Cognitive impact	Improves attention & memory (studies)	Sedation, impaired psychomotor	Neutral to mildly impairing	Mild cognition boost reported
Dependence / withdrawal	None reported (short peptide)	Yes, tolerance & withdrawal	Minimal	None
Common AEs	Nasal irritation, mild headache	Sedation, dizziness, respiratory depression	Dizziness, nausea	GI upset
WADA status	Not prohibited	Prohibited (sedatives)	Not prohibited	Not prohibited
Regulatory	Prescription in Russia only	Approved worldwide	Approved worldwide	Dietary supplement (varies)

Practical Take‑Home Points

1. Mechanistic core: Selank works mainly through σ1R modulation, leading to increased neurotrophic factor expression and a balanced serotonergic tone—this yields anxiolysis without the sedation typical of GABA‑targeting drugs.
2. Delivery choice: Intranasal administration provides rapid onset and convenient self‑dosage; sub‑cutaneous injection offers a steadier plasma profile useful for chronic protocols or when nasal mucosa is compromised.
3. Dosing guidance: Most human studies use 0.15 mg intranasally 2‑3 times daily or 0.5 mg sub‑cutaneously once daily; titrate upward only under medical supervision.

Selank 10mg