# FAQ — Semax, Selank & DSIP — NewGen Peptides

> Frequently asked questions about Semax, Selank and DSIP: what they are, how they work, regulatory status and what the research shows.

Answers drawn from the published literature and this desk's cited evidence base.

## What is Semax?

Semax is a synthetic heptapeptide (seven amino acids, sequence Met-Glu-His-Phe-Pro-Gly-Pro) derived from a fragment of ACTH — the pituitary hormone that triggers cortisol release — but without cortisol-releasing activity itself. It was developed at the Institute of Molecular Genetics in Moscow and is registered as a prescription drug in Russia and Ukraine for ischemic stroke, transient ischemic attacks, cognitive impairment, and optic-nerve disease. In the United States and most other countries it is an unscheduled research chemical, not an approved medicine.

## What is Semax peptide used for?

In Russian clinical practice, Semax is indicated for ischemic stroke, TIA, cognitive impairment and optic-nerve disease. In preclinical research (rodent models), it has been studied for neuroprotection in cerebral ischemia [2][5], BDNF/NGF upregulation [3][4], spinal cord injury recovery [1], and inhibition of enkephalin-degrading enzymes [7]. In nootropic communities, it is used off-label as a cognitive enhancer for focus, verbal fluency and mood — these are anecdotal reports, not clinical indications.

## Is Semax a peptide?

Yes. Semax is a synthetic peptide — a chain of seven amino acids (a heptapeptide). Peptides are shorter than proteins but built from the same amino-acid building blocks. Semax is derived from part of the ACTH hormone sequence and is not a naturally occurring compound; it is entirely synthetic.

## How does Semax work?

The best-characterized mechanisms are: (1) rapid, region-specific upregulation of the neurotrophins BDNF and NGF in rodent brain [3][4]; (2) inhibition of enkephalin-degrading (neprilysin-type) enzymes in human serum in vitro, which may prolong endogenous opioid-peptide signaling [7]; and (3) broad immune-system and vascular gene-expression modulation in ischemia models, framing neuroprotection as immunomodulatory rather than receptor-specific [2]. It also binds a specific, reversible, calcium-dependent site in rat basal-forebrain membranes with a KD of approximately 2.4 nM [4].

## What is Selank?

Selank (also called TP-7) is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) derived from tuftsin, an endogenous immune tetrapeptide. The C-terminal Pro-Gly-Pro tail improves metabolic stability. It is registered as an anxiolytic drug in Russia; in most other countries it is an unregulated research chemical with no approved medical indication.

## What does Selank do?

In published research, Selank acts as a positive allosteric modulator of GABA receptor binding [8], shifts the expression of GABA-pathway genes in rat frontal cortex [10], increases BDNF expression in the rat hippocampus [11], modulates Th1/Th2 cytokine balance in human anxiety patients [12], and inhibits enkephalin-degrading enzymes in human serum [7]. In rodent chronic-stress models it reduces anxiety, and in combination with diazepam it produced the largest anxiety reduction in one study [9].

## What is Selank peptide used for?

In Russian clinical practice, Selank is registered as an anxiolytic — specifically for anxiety-asthenic disorders. In preclinical research it has been studied for anxiety reduction via GABAergic modulation, BDNF upregulation in the hippocampus, and immunomodulation. In nootropic communities it is used for situational anxiety relief, social anxiety, stress resilience and cognitive clarity. These community uses are anecdotal; there are no Western RCTs for any indication.

## How does Selank work?

The primary studied mechanism is positive allosteric modulation of GABA receptor binding — a distinct site from benzodiazepines, with subtype-selective, concentration-dependent effects [8]. It also shifts GABA-related gene expression in frontal cortex (45 genes affected at one hour [10]), inhibits enkephalin-degrading enzymes [7], upregulates BDNF in hippocampus [11], and modulates cytokine balance in human patients [12]. Its tuftsin lineage gives it an immune-signaling dimension not seen in most anxiolytics.

## What is DSIP peptide?

DSIP stands for Delta Sleep-Inducing Peptide. It is a nine-amino-acid endogenous peptide (sequence WAGGDASGE) first isolated in 1977 from the cerebral venous blood of sleeping rabbits by Schoenenberger and Monnier. It is named for its ability to enhance slow-wave delta EEG activity. It occurs naturally in the brain and periphery, crosses the blood-brain barrier via a saturable transporter, and has been studied for sleep regulation, HPA-axis modulation, and neuroendocrine function. No receptor, gene or precursor has been identified despite over forty years of research [14].

## What is DSIP peptide used for?

In research, DSIP has been studied for sleep promotion (small human insomnia pilot showing improved sleep duration and quality [17]), HPA-axis modulation (ACTH reduction in men [16]), longevity and tumor-incidence reduction in mice [15], and more recently, sleep improvement in a mouse insomnia model using a BBB-crossing fusion peptide [13]. In nootropic communities it is used in attempts to improve sleep quality. There is no approved medical indication in any country; it is a research chemical only.

## What are the benefits of DSIP peptide?

The most consistently reported potential benefit in the literature is improved sleep quality — a 1981 human pilot found longer sleep duration, fewer interruptions, slightly more REM and no daytime sedation in six chronic insomniacs given intravenous DSIP [17]. A 2006 critical review tempers this, describing the sleep-promotion evidence as "extremely poorly documented and still weak" [14]. Anecdotally (not clinical evidence), respondents in the research community describe faster sleep onset, deeper sleep, and clear-headed mornings. These reports are unreliable across individuals, and a large share of users report no effect.

## Does DSIP really work?

The honest answer is: for some people, sometimes, modestly — but the evidence is thin and inconsistent. The best controlled human data are a six-person insomnia study from 1981 [17], and a 2006 review concluded the sleep-promotion hypothesis is "extremely poorly documented and still weak" [14]. A 2024 study using a modified BBB-crossing fusion version showed large effects in mouse insomnia models [13], but that is a preclinical finding with a modified peptide. Community reports show a meaningful non-response rate — estimated at roughly half of users. No identified receptor, no modern RCT, and no approved product make DSIP one of the most uncertain peptides in this category.

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A peer-reviewed literature digest on research peptides — not a clinic, not a vendor, not a dosing guide.