Cognition & Mood

A nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) isolated in 1977 by Marcel Monnier and Guido Schoenenberger at the University of Basel from the cerebral venous blood of rabbits subjected to electrical thalamic stimulation that induced slow-wave (delta) sleep. The peptide was named for the electroencephalographic signature it was thought to induce. Fifty years of subsequent research has broadened the picture without fully resolving it: DSIP has been shown to modulate GABAergic, serotonergic and monoaminergic tone, to influence adrenocorticotropic hormone secretion patterns, and to interact with opioid systems. It crosses the blood-brain barrier. It is not a classical receptor agonist — no single receptor accounts for its whole pharmacology. Small human clinical studies conducted mostly in the 1980s and 1990s in narcolepsy, chronic pain and opioid withdrawal produced mixed signals. It has never been approved by any regulator.

A synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) developed at the Institute of Molecular Genetics of the Russian Academy of Sciences (Myasoedov group) and the Zakusov Institute of Pharmacology. Its parent sequence tuftsin (Thr-Lys-Pro-Arg) is a naturally occurring tetrapeptide released from the IgG heavy chain that modulates macrophage and neutrophil activity; the added -Pro-Gly-Pro C-terminal tripeptide dramatically increases the peptide's plasma stability and centrally-active anxiolytic profile. Selank has been registered in Russia and some CIS countries as a prescription anxiolytic under the brand name Selank® (Селанк) as a 0.15% intranasal solution. Mechanism studies indicate BDNF and NGF upregulation, modulation of monoamine and GABAergic systems, and inhibition of enkephalin-degrading enzymes (protecting endogenous opioid tone). It has no MHRA / EMA / FDA authorisation.

A two-component neuro / nootropic research blend combining Selank 5 mg + Semax 5 mg (10 mg total) in a single lyophilized vial. Both compounds come from the same Russian regulator-peptide tradition at the Institute of Molecular Genetics — see the individual Selank and Semax pages. The blend pairs their complementary neurological effects: Selank as a positive allosteric modulator at a benzodiazepine-independent GABA-A site (anxiolysis without sedation or dependence) and Semax as an ACTH(4-10)-derived BDNF and NGF upregulator (cognitive activation and neuroplasticity). The two act on non-overlapping receptor systems and produce no pharmacological conflict. Both routes documented in the source PDF are available: subcutaneous injection and intranasal (bacteriostatic water for subQ, sterile saline for intranasal).

A synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) that reproduces the ACTH(4-10) neuropeptide fragment — the portion of adrenocorticotropic hormone stripped of its corticotropic activity — extended at the C-terminus with a Pro-Gly-Pro tail that dramatically increases plasma stability and central nervous system penetration. Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences (Ivanov, Myasoedov and colleagues), Semax has been registered in Russia since 1994. Its approved indications include acute ischaemic stroke (Semax 1% intranasal), transient ischaemic attack, discirculatory encephalopathy, chronic fatigue, optic nerve atrophy and cognitive impairment. Mechanism studies indicate BDNF and NGF upregulation, monoamine and cholinergic modulation, and neuroprotection through reduced excitotoxicity. It has no MHRA / EMA / FDA authorisation.