Peptide encyclopedia
3 of 20 peptides match the filters. Each entry carries mechanism, route of administration, half-life, legal status in your jurisdiction, and the primary sources backing every claim.
- Compounds
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- Source links
- 39
- Therapeutic classes
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Dihexa
Also: PNB-0408, N-hexanoyl-Tyr-Ile-(6)aminohexanoic amide
Dihexa is a chemically modified hexapeptide derivative engineered from the cognition-relevant fragment of angiotensin IV by Joseph Harding's laboratory at Washington State University ([McCoy et al., *J Pharmacol Exp Ther* 2013, 344:141–154](https://doi.org/10.1124/jpet.112.199497)). The modifications — an N-terminal hexanoyl group and a C-terminal 6-aminohexanoic acid extension — were designed to increase lipophilicity and protect against enzymatic degradation, producing a metabolically stable, orally active, blood-brain-barrier-permeant analog. Mechanistically, the cognitive activity of angiotensin IV had originally been attributed to the AT4 receptor; the Harding group's later work demonstrated that the relevant target is actually the hepatocyte growth factor (HGF) receptor c-Met. Dihexa binds HGF with high affinity and potentiates HGF activity at c-Met, driving downstream PI3K/Akt signaling and synaptogenesis. In cell-culture assays the group reported synapse-formation activity orders of magnitude greater than equivalent concentrations of brain-derived neurotrophic factor — the much-quoted "10 million times more potent than BDNF" framing originates here, and applies specifically to a synaptogenesis-in-culture endpoint, not to broad cognitive efficacy in vivo.
Research use only
02·Cognitive
Selank
Also: TKPRPGP, Selanc
Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) built by extending the immunoglobulin-derived tetrapeptide tuftsin with a Pro-Gly-Pro tail that resists enzymatic degradation. The proposed mechanism is multimodal rather than single-receptor. Published work has documented allosteric modulation of GABA-A receptor sensitivity, reshaping of GABA-induced gene-expression patterns in human IMR-32 neuroblastoma cells (Selank alone produced no baseline mRNA changes — its effect appeared only in combination with GABA or olanzapine; [Filatova et al., *Front Pharmacol* 2017, 8:89](https://doi.org/10.3389/fphar.2017.00089)), elevated brain-derived neurotrophic factor (BDNF) in rat hippocampus, and modulation of leu-enkephalin turnover in human plasma. Unlike benzodiazepines, Selank does not appear to bind the benzodiazepine site of the GABA-A receptor directly, which is the hypothesis underlying its reported non-sedating, non-dependency-forming profile. In Russian clinical use it is administered intranasally; subcutaneous and intravenous routes appear in the experimental rodent literature.
Research use only
03·Cognitive
Semax
Also: MEHFPGP, ACTH(4-7) Pro-Gly-Pro, et al.
Semax is a synthetic heptapeptide built by attaching a Pro-Gly-Pro tail to the C-terminus of ACTH(4-7) — the four-residue fragment Met-Glu-His-Phe — yielding the sequence MEHFPGP. The Pro-Gly-Pro extension protects against enzymatic degradation, and follow-up work has shown that the tail itself carries independent neurotrophic activity in rodent stroke models. Mechanistically Semax appears to act through several coupled pathways: in rodents it rapidly elevates brain-derived neurotrophic factor (BDNF) and TrkB receptor expression in the hippocampus, modulates dopaminergic and serotoninergic systems, and influences melanocortin-receptor signaling consistent with its ACTH origin. A representative Western-journal mechanism study reported a 25% rise in striatal 5-HIAA at two hours after Semax administration in rats, with serotonin-metabolite levels reaching 180% of baseline within 1–4 hours; dopamine concentrations were unaltered by Semax alone, but Semax pretreatment substantially enhanced the dopamine response to D-amphetamine ([Eremin et al., *Neurochem Res* 2005, 30:1493–1500](https://doi.org/10.1007/s11064-005-8826-8)). The reading is consistent with Semax acting as a neuromodulatory amplifier rather than a primary releaser.
Research use only