Brain-protective research peptide (SALLRSIPA)
A tiny lab-made fragment of a natural brain-support protein that helps neurons survive in lab studies; used only as a research tool, not an approved drug.
A researcher, an agent, or an algorithm wrote down the sequence and picked a target to hit.
An AI model like OpenFold3 or AlphaFold built a 3D structure and scored how well it fits the binding site.
A second contributor repeated the computation on their own hardware and the scores matched.
Named peptide fragment — synthesized for research; ClinicalTrials.gov trials registered for parent compound or class
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Endogenous peptide fragment — receptor binding/activity established in published literature; CT.gov evidence
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What this is
SAL (also written SALLRSIPA, and known as ADNF-9) is a 9-amino-acid research peptide derived from activity-dependent neurotrophic factor (ADNF), a protein that brain cells release to help neighbouring neurons survive. It is not a drug — it is a laboratory tool used to study how very small fragments of a much larger protein can reproduce that protein's neuron-protecting effect. SAL has only ever been studied in cell culture and preclinical models; it is not approved for any human use anywhere in the world.
History
The parent protein, activity-dependent neurotrophic factor, was characterised by Douglas Brenneman and colleagues at the US National Institutes of Health. In 1996 they reported that the survival-promoting activity of the full ADNF protein could be recapitulated by a much shorter 14-residue fragment (ADNF-14) that acts at extraordinarily low — femtomolar — concentrations on cultured cortical neurons stressed with tetrodotoxin (Brenneman 1996). The sequence shares homology with heat-shock protein 60. SAL / ADNF-9 emerged from later work on this same family as a still-shorter active fragment, and it became one of the standard short peptides used to probe the so-called "neuroprotective core" of ADNF.
What it does
In cultured brain cells, peptides in the ADNF family keep neurons alive under conditions that would otherwise kill them — for example, when electrical activity is silenced by tetrodotoxin (Brenneman 1996). The effect appears at strikingly low concentrations, which is part of what made ADNF and its short derivatives interesting to neuroscience: a 9- or 14-residue peptide reproducing the survival signal of a full-size protein is unusual. SAL has been used in research as a minimal probe of that effect.
Evidence
- Human: No human trials. SAL / ADNF-9 has not been tested in people.
- Animal: Limited; the ADNF family has been explored in rodent models of neuronal injury, but the dossier here does not contain specific animal studies on the SAL nonapeptide itself.
- In vitro: The foundational cell-culture work on the ADNF active site is Brenneman (1996), which demonstrated femtomolar-range survival-promoting activity for short ADNF-derived peptides in tetrodotoxin-treated cerebral cortical cultures.
Regulatory status
- US / EU: Not approved for any indication. Research-use only.
- WADA: Not listed by name on the WADA Prohibited List.
Related peptides
SAL is part of a small family of short ADNF-derived neuroprotective peptides; the closest sibling is ADNF-14, the 14-residue fragment that was the original "active site" identified by Brenneman and colleagues.
Research directions for this peptide, selected from the current sources — hypotheses you can explore and model. None of it is proven yet; tap any one to see the full thinking.
Does SALLRSIPA work the way a molecular cleaning crew works, rather than like a key fitting a lock?
If true, this would explain a 30-year mystery about why such a small amount of this peptide keeps brain cells alive, and could point researchers toward a whole new family of brain-protective drugs built around protein quality-control pathways.
Could inhaling this peptide get it into the brain better than swallowing it?
If intranasal delivery works, it could make this neuroprotective peptide a more practical candidate for Alzheimer's or other brain diseases, since getting drugs past the gut and into the brain is one of the hardest problems in neurology.
▸full evidence table1 metrics
| metric | value | tool |
|---|---|---|
| ranking score | 0.7970947623252869 | boltz-2 |
▸3-letter notation
▸recipeboltz-2 2.2.1
| parameter | value |
|---|---|
| model | boltz-2 2.2.1 |
| weights | — |
| hardware | vast_v100_32gb |
| mlx version | — |
| python | — |
| random seed | 1 |
| msa strategy | none_monomer |
| runtime | — |
| predicted by | — |
| predicted at | 2026-05-23 |
▸citationbibtex
@peptide{pep10779,
sequence = {SALLRSIPA},
target = {longevity},
author = {peptidemodel},
year = {2026},
status = {bioassayed}
}