K4 Elite
K4 Elite
Cognitive & Nootropic
This vial contains two synthetic heptapeptides developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, co-lyophilised at a 1:1 ratio (10 mg Semax plus 10 mg Selank, 20 mg total). Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is an analogue of the adrenocorticotropin fragment ACTH(4-7) extended with a C-terminal Pro-Gly-Pro tail that slows enzymatic degradation. Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) is the same Pro-Gly-Pro tail attached to tuftsin, a natural immunomodulatory tetrapeptide derived from immunoglobulin G. Both compounds share the “glyproline” design principle, but they act on different systems and were developed for different indications: Semax as a neuroprotective and cognitive agent, Selank as a peptide anxiolytic. Both are registered as medicines in Russia and neither is approved by the FDA or EMA.
The pairing is a practical one rather than a mechanistic discovery. Semax is the more studied of the two for neurotrophin signalling and attention-related endpoints, while Selank is the more studied for anxiety-related behaviour and GABAergic gene expression. Laboratories interested in the melanocortin-neurotrophin axis on one hand and the tuftsin-GABA axis on the other frequently use both reference compounds, and a fixed-ratio co-lyophilised vial removes the need to weigh two separate powders. It is important to state at the outset that no published study has examined the two peptides in combination; every finding summarised below concerns one peptide alone.
The best-characterised effect of Semax in the rodent brain is on brain-derived neurotrophic factor (BDNF). In rats, a single intranasal application of Semax produced a maximal 1.4-fold increase in hippocampal BDNF protein, a 1.6-fold increase in phosphorylation of its receptor TrkB, and 3-fold and 2-fold increases in exon III BDNF and TrkB mRNA respectively [1]. The same group reported that Semax binds specifically to rat basal forebrain membranes and raises BDNF protein there. Transcriptome work in a rat transient middle cerebral artery occlusion model identified 394 differentially expressed genes 24 hours after Semax relative to saline, with suppression of inflammation-related genes and activation of neurotransmission-related genes [2]. The Russian clinical literature includes a 1997 open series of 30 patients in the acute phase of hemispheric ischaemic stroke and a 2018 study relating Semax to plasma BDNF and Barthel index after stroke [3]; both are Russian-language reports without placebo-controlled, blinded design.
Selank was designed as a stabilised tuftsin analogue. Early work from the Zozulya group linked its anxiolytic-like behavioural effects in mice to inhibition of enkephalin-degrading enzymes in plasma [4]. Later gene-expression work in rat frontal cortex compared Selank with GABA itself: of 84 neurotransmission genes profiled, 45 changed expression one hour after either compound and 22 after three hours, with a positive correlation between the Selank and GABA response patterns, which the authors interpreted as allosteric modulation of the GABAergic system [5]. Separate mouse spleen work from the same institute showed altered expression of inflammation-related genes, consistent with its tuftsin ancestry. The principal human report is a 2008 Russian-language comparison of Selank against medazepam in 62 patients with generalised anxiety disorder or neurasthenia (30 Selank, 32 medazepam), which was not placebo-controlled [6].
The 1:1 mass ratio is a convenience for laboratories comparing the two compounds on equal-mass terms. Because Semax (813.9 g/mol) and Selank (751.9 g/mol) have different molecular weights [7][8], 10 mg of each corresponds to roughly 12.3 µmol of Semax and 13.3 µmol of Selank; researchers requiring equimolar conditions should account for this when reconstituting.
No peer-reviewed study has tested Semax and Selank together, so no synergy, additivity or interaction has been demonstrated or ruled out. The literature on both peptides is predominantly Russian-language, produced largely by the originating institute and its collaborators, and consists of small rodent studies and small, mostly unblinded clinical series; there are no large randomised placebo-controlled trials in indexed Western journals. The mechanistic findings summarised above are transcript- and protein-level observations in rats and mice and do not establish clinical efficacy for any cognitive or anxiety-related endpoint in humans. Neither compound has FDA or EMA approval. This material is supplied for in-vitro laboratory research only.
| Amino-acid sequence | Semax: Met-Glu-His-Phe-Pro-Gly-Pro; Selank: Thr-Lys-Pro-Arg-Pro-Gly-Pro |
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Format. Co-lyophilised white powder, 20 mg per vial (10 mg Semax + 10 mg Selank), supplied in a sealed glass vial with a rubber stopper and aluminium crimp cap.
Reconstitution. Add bacteriostatic water slowly down the side of the vial and allow the cake to dissolve without shaking; swirl gently. Use the reconstitution calculator to convert the 20 mg combined content to a working concentration. Note that concentration figures refer to total peptide, with each component at half that value.
Storage. Lyophilised vials: 2–8 °C, protected from light; suitable for longer-term storage at −20 °C. Reconstituted solution: 2–8 °C and use within 14 days; avoid repeated freeze–thaw cycles.
Handling. Both peptides carry a proteolysis-resistant Pro-Gly-Pro tail but remain sensitive to methionine oxidation (Semax) and to prolonged room-temperature exposure. Wear gloves and eye protection; avoid generating dust from the lyophilised cake. For in-vitro laboratory research only — not for human or veterinary use.