# Questions From the Research Record > Semax, Selank & DSIP FAQ — nasalpeptides — Frequently asked questions about three Cognitive & Nootropic research peptides — Semax, Selank, and DSIP — answered from the peer-reviewed literature, with citations. **COGNITIVE & NOOTROPIC RESEARCH / FAQ** Direct, citation-anchored answers to the questions readers most often bring to Semax, Selank, and DSIP. ## What is Semax? Semax is a synthetic heptapeptide (H-Met-Glu-His-Phe-Pro-Gly-Pro-OH) built from a fragment of adrenocorticotropic hormone (ACTH) with a stabilizing Pro-Gly-Pro tail added to slow its breakdown. It lacks the cortisol-releasing activity of full ACTH and is studied instead for effects on neurotrophin signaling and neuroprotection. It is registered as a prescription drug in Russia and Ukraine and sold as a research chemical elsewhere, including the United States. ## What is Semax peptide used for? In the research literature, Semax has been studied for neuroprotection after stroke and spinal-cord injury, for upregulating the neurotrophins BDNF and NGF, and for cognitive and antiamnesic (memory-preserving) effects in rodent ischemia models [1][2][3][4][5]. It is used clinically in Russia for ischemic stroke, transient ischemic attack, cognitive impairment, and optic-nerve disease. It has no approved use in the United States and this site names no human protocol for it. ## Is Semax a peptide? Yes. Semax is a synthetic heptapeptide — a chain of seven amino acids — built from a fragment of ACTH combined with a Pro-Gly-Pro stabilizing tripeptide. It is not a hormone, a stimulant, or a small-molecule drug; it is classified in the literature as a neuropeptide and as a synthetic ACTH(4-10) analog. ## How does Semax work? Semax rapidly and region-specifically upregulates the neurotrophins BDNF and NGF in the brain and increases BDNF protein in the basal forebrain, acting through a specific, reversible, calcium-dependent binding site with a dissociation constant of 2.4 nanomolar [4]. It also inhibits enzymes that degrade the body's own opioid-like peptides. In cerebral-ischemia models, its protective effect is described as driven largely by shifts in immune- and vascular-system gene expression rather than a single receptor pathway [2]. ## What is Selank? Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) built from tuftsin, a naturally occurring immune-system tetrapeptide, extended with the same Pro-Gly-Pro stabilizing tail used in Semax. It is studied primarily as a non-benzodiazepine anxiolytic and is registered as such in Russia; it has no FDA or EMA approval and is sold in the US as a research chemical. ## What does Selank do? In animal and limited human research, Selank reduces anxiety-like behavior through positive allosteric modulation of GABA receptors and inhibition of enkephalin-degrading enzymes, distinct from benzodiazepine sedation [6]. It also alters serotonin and dopamine turnover, modulates hippocampal BDNF expression, and — inherited from its tuftsin origin — shifts the immune system's Th1/Th2 cytokine balance in patients with anxiety-asthenic disorders [10]. ## What is Selank peptide used for? Selank has been studied for reducing anxiety-like behavior in stress models, including in combination with diazepam, where the pairing was the most effective intervention tested in one rat study [7]. It has also been studied for effects on hippocampal BDNF expression via intranasal dosing [9] and, in a small human study, for modulating immune markers in patients with anxiety-asthenic disorders [10]. It is not approved for any use in the United States. ## How does Selank work? Selank acts primarily through positive allosteric modulation of GABA receptors, enhancing GABA's own binding rather than acting at a benzodiazepine site, and it shifts GABA-pathway gene expression in a direction that correlates with GABA's own effects [6][8]. A second mechanism — inhibition of enzymes that break down endogenous opioid-like peptides — is thought to contribute to its anxiolytic profile alongside effects on serotonin, dopamine, and BDNF signaling. ## What is DSIP peptide? DSIP, Delta Sleep-Inducing Peptide, is an endogenous nonapeptide (Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu) first isolated from the cerebral venous blood of sleeping rabbits in 1977 [16]. Despite the name, no specific DSIP receptor, gene, or precursor protein has ever been identified, and a 2006 review described the evidence for its signature sleep-promoting effect as "extremely poorly documented and still weak" [12]. It is not approved as a drug anywhere and is sold in the US as a research chemical. ## What is DSIP peptide used for? In the research literature, DSIP has been studied for promoting slow-wave (delta) sleep, for reducing plasma ACTH-like activity in men [14], for improving sleep quality in a small trial of chronic insomniacs [15], for motor-function recovery after stroke in rats when given intranasally [17], and — in a single lineage of Russian studies using the DSIP-containing preparation Deltaran — for lifespan and tumor-incidence effects in mice [13]. None of these are human-use recommendations. ## What are the benefits of DSIP peptide? In cited studies, DSIP-related findings include modestly improved sleep quality and reduced disruption in a small human insomnia trial [15], improved post-stroke motor-function recovery in rats given the peptide intranasally [17], and — from a single Russian research lineage — increased maximum lifespan and reduced tumor incidence in mice given a DSIP-containing preparation [13]. Community reports (anecdotal, not clinical evidence) most often describe an easier transition into sleep and, for people who dream vividly on it, more memorable dreams. A large share of people report no effect at all. ## Does DSIP really work? The honest answer from the literature is: inconsistently. A 2006 review calling DSIP's sleep-promoting evidence "extremely poorly documented and still weak" remains the most comprehensive assessment of the compound [12], and even the positive human insomnia trial was small (six participants) and decades old [15]. A large share of community reports describe no noticeable effect, with one commonly repeated estimate putting the response rate at roughly half of people who try it. A 2024 study using an engineered blood-brain-barrier-crossing fusion of DSIP showed clearer effects than native DSIP in mice [11], which is itself evidence that unmodified DSIP's own effect is limited. --- A review desk for nose-to-brain neuropeptide research — no dosing schedules, no prescriptions, no peptides for sale here.