NA-831; cyclic glycine-proline (cGP); cycloprolylglycine (CPG); (S)-Hexahydropyrrolo[1,2-a]pyrazine-1,4-dione · Evidence-based safety and harm-reduction overview.
| Also known as | NA-831; cyclic glycine-proline (cGP); cycloprolylglycine (CPG); (S)-Hexahydropyrrolo[1,2-a]pyrazine-1,4-dione |
| Category | Peptide (research chemical) |
| Chemical class | Diketopiperazine (2,5-diketopiperazine); endogenous cyclic dipeptide |
| Developer | NeuroActiva Inc. (subsidiary of Biomed Industries Inc.) |
| Highest clinical stage (as of July 2026) | Phase 3 - Alzheimer's disease (combination with donanemab and lecanemab) |
| Endogenous status | Found naturally in human plasma, cerebrospinal fluid, and breast milk |
| Approximate serum half-life | ~7 hours (reported); crosses blood-brain barrier; oral bioavailability |
| Phase 2 primary outcome (AD/MCI trial) | ADAS-Cog-13: 4.1-point improvement vs. placebo (p=0.001); n=112; 24 weeks |
| US legal status | Not approved for any indication in the United States. Traneurocin (NA-831) holds Investigational New Drug (IND) status with the FDA and is available only within the context of registered clinical trials. It is not a scheduled controlled substance. It cannot be legally marketed, sold, or distributed for human use outside of approved clinical study protocols. |
Traneurocin (development code NA-831) is a small endogenous diketopiperazine peptide - specifically cyclic glycine-proline (cGP), the chemical designation (S)-Hexahydropyrrolo[1,2-a]pyrazine-1,4-dione - found naturally in human plasma, cerebrospinal fluid, and breast milk. It is being investigated as a neuroprotective and pro-cognitive agent with a primary mechanism centered on modulating insulin-like growth factor-1 (IGF-1) bioavailability and activity. It was first synthesized in Russia in 1991 under the name cycloprolylglycine and is currently in active clinical development by NeuroActiva Inc. (a subsidiary of Biomed Industries Inc.) for Alzheimer's disease and several other neurological indications.
Traneurocin has two described primary mechanisms. First, it acts as a positive allosteric modulator of AMPA and GABA-A receptors, a pharmacological profile with some resemblance to racetam-class compounds. Second, and more distinctively, it functions as an IGF-1 metabolite that competes with IGF-1-binding protein 3 (IGFBP-3) for IGF-1 binding, thereby normalizing IGF-1 bioavailability in a homeostatic fashion - promoting IGF-1 activity when levels are deficient and attenuating it when excessive. Downstream effects observed in preclinical models include increased brain-derived neurotrophic factor (BDNF) levels, promotion of neurogenesis, and neuroprotection. The compound is orally bioavailable, reported to cross the blood-brain barrier, and has an approximate serum half-life of seven hours. This mechanism is mechanistically distinct from amyloid-targeting monoclonal antibodies and is being studied in combination with such agents (donanemab, lecanemab) in Phase 3.
Cycloprolylglycine was first described in Russia in 1991. Subsequent research characterized it as a naturally occurring endogenous diketopiperazine present in human biological fluids. NeuroActiva Inc. advanced it into formal IND development under the name NA-831, later branded as Traneurocin. Phase 1 work established initial safety signals; Phase 2 randomized controlled trials in mild cognitive impairment and mild-to-moderate Alzheimer's disease were completed, with results published in 2024 in Alzheimer's and Dementia (PMCID: PMC11712904). As of December 2025, Phase 3 trials were reported at the Clinical Trials on Alzheimer's Disease (CTAD) conference, including combination protocols with the anti-amyloid antibodies lecanemab and donanemab. Parallel Phase 2 trials in Fragile X syndrome, Rett syndrome, and COVID-19-related cognitive impairment, as well as Phase 1 in major depressive disorder, were ongoing as of that reporting.
The most substantial published human clinical evidence is the Phase 2 randomized, placebo-controlled trial (n=112; 32 MCI participants and 24 mild-to-moderate AD participants) spanning 24 weeks. The ADAS-Cog-13 primary outcome showed a 4.1-point improvement versus placebo (p=0.001); the CIBIC-Plus global impression scale showed 78% patient improvement versus placebo (p=0.01). No serious adverse events were reported at doses of 10 mg/day (MCI) or 30 mg/day (AD). These results should be interpreted with appropriate caution given the relatively small sample size and single-trial basis; independent replication and Phase 3 outcomes are pending. Preclinical evidence in APP/PS1 transgenic mouse models showed reduced amyloid-beta plaque burden and improved memory function. Phase 3 combination trials with lecanemab and donanemab are the definitive efficacy tests currently underway. Evidence in Fragile X syndrome, Rett syndrome, MDD, and post-COVID cognitive impairment remains at Phase 1-2 and no efficacy conclusions can be drawn from those programs yet.
Published Phase 2 trial protocols used 10 mg/day orally in MCI participants and 30 mg/day orally in mild-to-moderate Alzheimer's disease participants over 24 weeks. These figures are reported here for informational and reference purposes only, drawn from the published clinical trial literature. They do not constitute a dosing recommendation or protocol. No dosing guidance for any use outside of a registered clinical trial can be provided. Anyone seeking to participate in a Traneurocin trial should consult a qualified clinician and refer to ClinicalTrials.gov for active enrollment information.
This is general research/context information, not medical advice or a recommended protocol.
No evidence-based stacking protocols exist for Traneurocin outside of the structured clinical trial combination programs (NA-831 + lecanemab; NA-831 + donanemab). These combination approaches are being studied precisely because the mechanisms are hypothesized to be complementary - anti-amyloid clearance paired with neurogenesis/IGF-1 normalization - but efficacy and safety of the combination remain under investigation. No conclusions about stacking with nootropics, racetams, or other research chemicals can be drawn from available data.
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Get tested with Ulta Lab Tests →Traneurocin (NA-831) is a small endogenous diketopiperazine peptide that modulates IGF-1 bioavailability and acts as a positive allosteric modulator of AMPA and GABA-A receptors. Unlike the current leading Alzheimer's therapies (lecanemab, donanemab), which target amyloid-beta clearance directly, Traneurocin's proposed mechanism centers on neurogenesis support and IGF-1 homeostasis normalization. Phase 3 trials are explicitly testing it in combination with those anti-amyloid antibodies on the hypothesis that the mechanisms are complementary. Whether this translates to additive clinical benefit in humans is currently under investigation.
Promising Phase 2 data exists: a randomized, placebo-controlled trial in 112 participants (MCI and mild-to-moderate AD) showed statistically significant improvement on the ADAS-Cog-13 cognitive scale (4.1 points, p=0.001) and the CIBIC-Plus global impression measure over 24 weeks. However, this is a single Phase 2 trial with a relatively small sample. Definitive efficacy conclusions require Phase 3 replication in larger populations, which is currently underway. Effectiveness has not been established to the standard required for FDA approval.
Based on the published Phase 2 trial (n=112, 24 weeks, up to 30 mg/day), no serious adverse events were reported. The compound is endogenous to the human body, which is sometimes cited as a favorable safety indicator, though this reasoning does not replace full clinical safety data. Long-term safety beyond 24 weeks is not established in published human trials. The full Phase 3 safety profile is pending. This should not be interpreted as a clean bill of health for use outside of clinical trials.
Traneurocin holds IND status in the US and is available only within registered clinical trials. It cannot be legally purchased or used for human consumption outside of that context. To find active enrollment opportunities, search 'NA-831' on ClinicalTrials.gov. Any product sold as NA-831 or cGP outside a clinical trial framework has no regulatory oversight and cannot be assumed to be authentic or safe.
The published Phase 2 trial used 10 mg/day for mild cognitive impairment participants and 30 mg/day for mild-to-moderate Alzheimer's disease participants, administered orally over 24 weeks. These are reported here as literature reference points only and do not constitute a dosing recommendation. Dosing outside a clinical trial context is not appropriate, and a qualified clinician should be consulted regarding any participation in ongoing studies.
Beyond Alzheimer's disease (Phase 3) and mild cognitive impairment (Phase 2 completed), active or recently completed programs include Phase 2 trials in Fragile X syndrome and Rett syndrome, Phase 2/3 in COVID-19-related cognitive impairment, and Phase 1 in major depressive disorder. Evidence in these indications is preliminary and no efficacy conclusions can be drawn from programs at those early stages.
Medical & legal disclaimer. This site is for informational and harm-reduction purposes only. It is not medical advice and is not a substitute for a licensed healthcare professional. The compounds discussed are largely not approved by the FDA for human use and many are sold strictly as research chemicals 'not for human consumption.' Nothing here is an endorsement to purchase, possess, or use any substance. Laws vary by jurisdiction. Always consult a qualified physician and follow the law where you live.
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