What it is
Noopept — also written omberacetam or GVS-111 — is the smallest compound in this library, and the one whose presence here needs a sentence of justification.
It is N-phenylacetyl-L-prolylglycine ethyl ester: a dipeptide of proline and glycine, capped with a phenylacetyl group at one end and an ethyl ester at the other. PubChem lists it as CID 180496, formula C₁₇H₂₂N₂O₄, molecular weight 318.4.
Two residues, both termini modified, swallowed as a capsule. That is a peptide-derived small molecule, not a peptide drug — and the modifications are the reason it is orally active at all. This library covers it because the market calls it a peptide nootropic, and a reader looking it up deserves to be told what it chemically is, the way SLU-PP-332 and 5-amino-1MQ are handled here.
Where it came from, and the claim that travelled with it
Noopept was not discovered by screening. It was designed, at the Zakusov Research Institute of Pharmacology in Moscow, by an explicit strategy published in 2003: identify the dipeptide fragments implicit in the structure of a known non-peptide drug, build the peptide analogue that is topologically close to it, test it, then look for the matching endogenous neuropeptide.
The non-peptide drug they worked backwards from was piracetam. The paper reports that the resulting pyroglutamyl- and prolyl-containing dipeptides showed nootropic activity at doses 100 to 10,000 times lower than piracetam's.
That single line is the origin of every "a thousand times stronger than piracetam" claim in the product copy. What it describes is dose potency in animal pharmacology. A compound active at a much lower dose is not thereby producing a larger effect in a person — and no human comparison of the two exists.
The registry finding
ClinicalTrials.gov holds zero records for noopept, omberacetam or GVS-111. Queried 2026-09-15.
Not a terminated trial. Not an unpublished one. None.
For context, this library's entries routinely report thin registries — a handful of observational studies, a phase 1 that never reported. Zero is different, and for a compound with a quarter-century of published pharmacology and a worldwide grey market it is the most informative fact available about it.
The published record matches:
| Query | Records |
|---|---|
noopept[tiab] OR omberacetam[tiab] OR "GVS-111"[tiab] |
107 |
| …in Russian | 51 |
| …mentioning rats or mice | 63 |
| …with PubMed's human tag | 25 |
| …with the "clinical trial" publication type | 3 |
| …with the randomized controlled trial publication type | 0 |
Nearly half the literature is in one language, most of it is animal work, and the strongest study-design tag in the whole file is the broad "clinical trial" type on three records.
The metabolite argument, and the part that is usually left out
The standard mechanistic story is that noopept is a prodrug: it is converted to cyclo-prolyl-L-glycine (CPG), an endogenous dipeptide, and CPG does the work.
The rat evidence for that is real. A 2018 study from the originating institute found CPG in rat plasma and brain after noopept, with pharmacokinetics clearly different from the parent compound but a similar spectrum of effects on memory.
Then read the interspecies study from the same laboratory, published in 2004:
- Elimination slows from rats to rabbits to humans.
- In rats, intensive presystemic metabolism produces a metabolite hydroxylated at the phenyl ring.
- In rabbits, unchanged noopept circulates longer and no analogous metabolite is detected.
- In humans, elimination is slower still, individual variability is considerable, and no drug metabolites were found in human blood plasma — which the authors attribute to the relatively small dose and low concentrations.
So the metabolite that carries the mechanistic explanation has been demonstrated in the species whose metabolism the same authors show is least like ours, and the human dataset shows no metabolites at all. That does not disprove the prodrug story; small concentrations can be real and unmeasured. It does mean the story is an inference from rodents, and it is almost never presented that way.
The one other mechanism proposal is a 2016 cell experiment: in HEK293 cells carrying reporters for nine transcription factors, noopept at 10 μM raised HIF-1 DNA-binding activity and moved none of the other eight, while piracetam at a hundred times the concentration moved nothing. A clean, narrow result, in cells.
Where it stands
A designed compound with a coherent scientific story, a single institutional home, a substantial animal literature, a human pharmacokinetic profile that is variable between people, no randomized trial, and no registered trial anywhere in the world.
It is also the clearest example in this library of a pattern worth naming: being derived from a peptide is not the same as being a peptide, and being sold as one is a third thing again. The endogenous dipeptide behind it, cycloprolylglycine, has 22 papers of its own — a smaller file than the compound built to deliver it.
Related: what a peptide is for why two residues and thirty are not the same kind of molecule, and Semax and the intranasal anxiolytic from the same research tradition for the other Moscow-developed neuroactive peptides, both of which do have registry records.
Sources
- Gudasheva TA, Skoldinov AP. [Design of the novel dipeptide neuropsychotropic drug preparations]. Eksp Klin Farmakol 2003;66(2):15–19. PMID 12962042 — the design strategy and the 100–10,000-fold dose comparison with piracetam.
- Boĭko SS, Korotkov SA, Zherdev VP, et al. [Interspecies differences of noopept pharmacokinetics]. Eksp Klin Farmakol 2004;67(1):40–43. PMID 15079908 — rat, rabbit and human pharmacokinetics; no metabolites detected in human plasma.
- Boyko SS, Zherdev VP, Shevchenko RV. [Pharmacokinetics of noopept and its active metabolite cycloprolyl glycine in rats]. Biomed Khim 2018;64(5):455–58. PMID 30378564 — cyclo-prolyl-L-glycine in rat plasma and brain.
- Vakhitova YV, Sadovnikov SV, Borisevich SS, et al. Molecular mechanism underlying the action of substituted Pro-Gly dipeptide Noopept. Acta Naturae 2016;8(1):82–89. PMID 27099787 — the HIF-1 reporter experiment.
- PubChem CID 180496 (Noopept / omberacetam / GVS-111), retrieved 2026-09-15: formula, molecular weight, IUPAC name and synonyms.
- ClinicalTrials.gov, queried 2026-09-15 for noopept, omberacetam and GVS-111 — zero records.
- PubMed counts, run 2026-09-15 via the NCBI E-utilities
esearchendpoint: the three-name set — 107 records; withrussian[la]— 51; with rat or mouse terms — 63; withhumans[mh]— 25; with"clinical trial"[pt]— 3; with"randomized controlled trial"[pt]— 0;cycloprolylglycine[tiab]— 22.