What doses and routes the Selank literature has actually studied

What these numbers mean

The doses on this page come directly from published studies — what researchers administered to animals and patients, in specific species, by specific routes, under supervision. They are not a guide for taking Selank, and nothing here is a dosing recommendation. Selank is not approved by the FDA, and there is no labeled human dose to report. In rodent studies, 100 to 300 micrograms per kilogram of body weight was the typical range, given by injection or directly into the nose. In Russian clinical work, a 0.15% nasal solution was administered over multi-week courses as an alternative or adjunct to benzodiazepine therapy. Because the intact peptide clears the body quickly, the route and timing of administration in studies mattered as much as the amount. Every figure here is study description, not a recommendation for any use.

Doses used in preclinical rodent studies

The most commonly used dose across the Selank rodent literature is 0.3 mg/kg (300 microg/kg), administered by either intraperitoneal injection or intranasal application. This dose appears across anxiety, memory, opioid withdrawal, and monoamine studies, making it the best-characterized dose in the preclinical record.

Specific examples from the published literature:

• 0.3 mg/kg, intraperitoneal, single dose: Used in the morphine-withdrawal attenuation study (Konstantinopolsky et al. 2022), where it reduced the total withdrawal syndrome index by 39.6% compared to control ^[8]. The same dose in a single injection eliminated anxiety induced by ethanol withdrawal in alcohol-preferring rats on elevated plus maze and social interaction tests ^[9].
• 0.3 mg/kg/day, intraperitoneal, 7 days: Used in the ethanol-withdrawal memory protection study (Kolik et al. 2019). This regimen prevented ethanol-induced memory impairment (p<0.01), prevented the associated BDNF elevation in hippocampus and frontal cortex (p<0.05), and produced cognitive enhancement in non-alcoholic control animals ^[4].
• 300 microg/kg, intranasal, single dose: Used in the serotonin turnover and memory consolidation study (Semenova et al. 2010), where it elevated 5-HT turnover in hypothalamus and caudal brainstem for 30 to 120 minutes post-administration and enhanced 30-day memory retention ^[14]. Also used by Volkova et al. (2016) to map the biphasic gene expression changes in rat frontal cortex, finding 45-gene changes at 1 hour that partially reversed by 3 hours ^[16].
• 300 microg/kg/day, intranasal, 5 days: Used in the strain-comparison study (Vasil'eva et al. 2016), where intranasal administration produced anxiolytic and nootropic effects exclusively in BALB/c mice and increased hippocampal NMDA receptor binding by 23% ^[12].
• 0.25 mg/kg, intraperitoneal: Used in the naloxone interaction study (Kozlovskii et al. 2012) in BALB/c and C57BL/6 mice, where Selank reduced anxiety and increased locomotor activity before naloxone pretreatment was tested ^[13].
• 100 microg/kg/day, intraperitoneal, 20 days: Used in the cytokine suppression study under chronic social stress (Yasenyavskaya et al. 2021), where it significantly reduced IL-1beta, IL-6, TNF-alpha, and TGF-beta1 toward control levels ^[10].
• 300 microg/kg, intranasal, 14 days (with diazepam comparator): In the chronic mild stress combination study (Kasian et al. 2017), Selank (300 microg/kg/day intranasal) plus diazepam (1 mg/kg/day oral) produced the most complete anxiety reduction, normalizing behavior to pre-stress baseline ^[5].

Doses studied in human clinical research

Human dosing data for Selank is limited to intranasal administration, consistent with the Russian regulatory formulation (a nasal spray). No intravenous human data is available in the public literature.

2700 microg/day intranasal (Syunyakov et al. 2012): The most precisely reported human dose in the literature. This was administered as nine individual doses of 300 microg each throughout the study day in a 20-patient GAD trial ^[7]. In rapid responders (40% of the cohort), this dose produced clinically significant HARS reductions within 1-3 days. In conventional responders (60% of the cohort), HARS reduction reached significance by day 14.

Intranasal dose not specified (Zozulia et al. 2008): The 62-patient RCT comparing Selank against medazepam does not report the exact intranasal dose in its available abstract ^[6]. The dosing was presumably consistent with the Russian prescribing formulation, but the specific daily dose is not established in the publicly available record.

10(-7) M, in vitro (Uchakina et al. 2008): The immunomodulatory human study used this concentration in cell culture experiments with peripheral blood lymphocytes from anxiety-asthenic patients ^[17]. This is not translatable to an in vivo dose without pharmacokinetic data that does not currently exist in the public literature.

An important caveat applies to all of these figures: Selank's human pharmacokinetic parameters — Cmax, Tmax, plasma half-life, and bioavailability by the intranasal route — have not been published in English-language peer-reviewed sources. Extrapolating from rodent doses to human doses requires PK data that is currently absent from the public record.

Route-of-administration considerations from the research

Route of administration is not a trivial variable in the Selank literature — it has been shown to affect which receptor populations are engaged and which behavioral outcomes are observed.

The Vasil'eva et al. (2016) strain-comparison study directly compared intranasal and intraperitoneal routes in the same animal model ^[12]. Intraperitoneal Selank (300 microg/kg/day, 5 days) increased GABA receptor binding by 38% in the frontal cortex. Intranasal Selank at the same dose and duration instead increased NMDA receptor binding by 23% in the hippocampus. The route changed which receptor population was most affected — a finding that cannot be collapsed into a single pharmacological profile.

Behaviorally, both routes produced anxiolytic and nootropic effects in BALB/c mice, but not in C57BL/6 mice — the strain, not just the route, determined efficacy ^[12]. For any cross-study comparison, noting whether the study used intranasal or intraperitoneal administration is essential context.

The human clinical studies universally used the intranasal route, consistent with the Russian regulatory formulation. Intravenous administration has been referenced in the Russian literature but is not well-characterized in publicly available English-language sources.

Metabolic stability and formulation context. Selank's Pro-Gly-Pro C-terminal extension was engineered specifically to resist tissue peptidases that rapidly degrade native tuftsin. Kozlovskaya et al. (2003) identified this structural feature as conferring the improved metabolic stability and predictable anxiolytic direction relative to tuftsin analogs that lack the extension ^[18]. The lyophilized powder form requires refrigeration; reconstituted forms require sterile or bacteriostatic water as diluent in research settings. A formal half-life in human subjects has not been published in the available literature.

Research context and regulatory framing

All dosage information on this page is extracted directly from the published research literature and presented as historical context for how investigators have studied this compound — not as guidance for human use.

Selank is approved in Russia as a prescription nasal spray (trade name Selanc) for generalized anxiety disorder and neurasthenia. In the United States and European Union, it holds no regulatory approval and is classified as a research chemical. No physician in the US can legally prescribe Selank as a licensed medication.

Athletes subject to anti-doping regulations should be aware that Selank may fall under the S0 (non-approved substances) category of the WADA Prohibited List despite not being specifically named. Governing bodies should be consulted before any research involving Selank is considered in an athletic context.

This site is an independent editorial digest of the published research record — not a clinic, not a vendor, and not a source of dosing or medical guidance.