Also known as: Bis-(N-monosuccinyl-L-seryl-L-lysine) hexamethylenediamide
GSB-106 is a dimeric dipeptide mimetic of brain-derived neurotrophic factor (BDNF), developed alongside GK-2 by the Gudasheva/Seredenin group at Russia's Zakusov Institute. It activates TrkB and has shown antidepressant-like effects across multiple rodent behavioral models, but like GK-2 has no human trial data — a preclinical, animal-model-only compound.
GSB-106 (bis-(N-monosuccinyl-L-seryl-L-lysine) hexamethylenediamide) is a dimeric dipeptide engineered to mimic brain-derived neurotrophic factor (BDNF), built from a Ser-Lys dipeptide core derived from BDNF's fourth loop, dimerized via a hexamethylenediamine linker — the same general design strategy used for the NGF-mimetic GK-2, developed by the same Gudasheva/Seredenin group at the V.V. Zakusov Research Institute of Pharmacology.
GSB-106 has been studied for antidepressant-like and neurotrophic effects across a range of rodent behavioral paradigms, including the forced swim test, tail suspension test, a water-wheel test, and a chronic social defeat stress model, where it was reportedly effective at an oral dose of 0.1 mg/kg. As with GK-2, there is no published human trial data — this is a preclinical, animal-model-only research compound.
GSB-106 activates TrkB and its downstream MAPK/ERK, PI3K/AKT, and PLCγ signaling pathways. Its antidepressant-like activity in the forced swim test is completely blocked by the Trk antagonist K252a and the PLC inhibitor U73122, directly confirming Trk/PLC-dependence of its behavioral effects rather than an off-target mechanism.
GSB-106 has shown antidepressant-like activity in the Porsolt forced swim test, tail suspension test, and Nomura water-wheel test, as well as in a chronic social defeat stress model — effective orally at 0.1 mg/kg, reversing anhedonia and locomotor deficits — an inflammation-induced depression model, and a model of post-stroke depressive-like behavior and memory impairment.
Beyond behavioral endpoints, GSB-106 has also been shown to promote survival of serum-deprived cells via TrkB-dependent suppression of apoptosis, indicating a genuine neurotrophic action rather than a purely symptomatic behavioral effect.
GSB-106 is a dimeric dipeptide BDNF mimetic developed alongside GK-2 by the Gudasheva/Seredenin group at Russia's Zakusov Institute. It activates TrkB and has shown antidepressant-like effects across multiple rodent behavioral models (forced swim test, tail suspension test, chronic social defeat stress). This is strictly a preclinical research compound — no human trials exist.
GSB-106 remains a preclinical research compound with no established human dosing or cycling protocol.
No human trial data exists for GSB-106 — all identified studies are in mice and rats, spanning roughly 2013–2023. This should not be presented as a clinically studied or dosed compound.
Molecular formula (C₃₂H₅₈N₈O₁₂) and molecular weight (746.85) are sourced from a commercial peptide vendor listing rather than the primary pharmacology literature — reasonably likely accurate but not independently cross-verified, and flagged here accordingly.
One secondary aggregator source described the sequence as "seryl-methionine" rather than "seryl-lysine" — this conflicts with both the primary literature and the vendor listing, which consistently describe a seryl-lysine core; the "seryl-methionine" variant is treated as a likely error and not used here.
Ask anything about GSB-106 — mechanisms, dosing protocols, interactions, or research comparisons.
Selank is a synthetic heptapeptide developed at the Russian Institute of Molecular Genetics, derived from the endogenous…
Semax is a synthetic heptapeptide analog of the adrenocorticotropic hormone (ACTH) 4–10 fragment, developed at the Insti…
Delta Sleep-Inducing Peptide (DSIP) is an endogenous nonapeptide first isolated from rabbit thalamus in 1977 by Schoenen…
Dihexa is a potent peptidomimetic derived from angiotensin IV that acts as a superagonist of the HGF/MET signaling syste…