Skip to main content

Semax · Selank · DSIP

Where do nasalpeptides lead?

The nose sounds like a shortcut. I followed Semax, Selank and DSIP into the papers and arrived at some unexpectedly different places.

A cutaway plaster head showing the nasal cavity beside cobalt paper

The Semax experiment

The first surprise was a decrease. In a Semax experiment in male rats, NGF gene activity fell in the frontal cortex after intranasal administration. Elsewhere, NGF and BDNF gene activity rose in the hippocampus, and BDNF rose in the brainstem and cerebellum. The same nasal entrance led to an uneven pattern across the brain.

NGF and BDNF are neurotrophins, proteins involved in the growth and survival of nerve cells. This experiment measured their messenger RNA, the working copies of genetic instructions used to make proteins. I expected NGF and BDNF to rise together. The regional differences give me something much more interesting to puzzle over: which signal changed, and where?

That is where nasalpeptides begins. The word nasal names an entrance. The experiments take us further inside, where a broad phrase such as brain enhancement starts to lose its usefulness. The Semax page follows those regional results through to protein measurements and injury models.

Selank in the hippocampus

Selank arrives with an anxiety reputation and an immune-system ancestry. It is derived from tuftsin, a peptide fragment of an antibody, and a review discusses GABA-receptor binding modulation in rat-brain membrane assays. That combination makes the neat separation between an immune peptide and a brain peptide feel rather artificial to me.

The nasal experiment here has a precise address: increased BDNF expression in the rat hippocampus. Other Selank studies examine anxiety-like behaviour in rats or immune markers in patients with anxiety-asthenic disorders. I want those different destinations visible at once, because the word calming covers very little of this biology. Follow Selank from tuftsin through the anxiety and immune findings.

DSIP after stroke

DSIP takes the most unexpected turn. A rat experiment using intranasal DSIP after focal stroke reported improved motor recovery by day seven. The difference in infarct volume, the amount of damaged brain tissue, was statistically insignificant. Movement and tissue damage gave different answers in the same experiment.

For a peptide whose name spells out Delta Sleep-Inducing Peptide, that is quite a detour. I trust this particular motor result further than the broad sleep reputation; its relevance remains confined to the rats and conditions studied. The DSIP page starts with movement, then returns to the older sleep work.

Intranasal administration

Semax, Selank and DSIP each have a nasal study here, alongside experiments using other routes. I follow each paper to the last thing it actually measured: a gene signal, a protein, a behaviour or a person. The delivery page follows those distinctions; the comparison puts the experiments beside one another.

None of these compounds is FDA-approved. Semax and Selank have pharmaceutical registrations in Russia; DSIP has no drug approval anywhere. A promising result in these papers leaves substantial questions about human benefit and long-term safety. The nasal route makes the subject fascinating. It also makes nasal irritation an especially relevant concern, as the anecdotal reports on the compound pages describe.