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COGNITIVEPreclinicalBDNF MIMETICDIPEPTIDEANTIDEPRESSANT

GSB-106

Also known as: Bis-(N-monosuccinyl-L-seryl-L-lysine) hexamethylenediamide

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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.

STRUCTURE

Molecular Composition

FORMULA
C₃₂H₅₈N₈O₁₂ (vendor-sourced)
MOL. WEIGHT
746.85 Da (vendor-sourced)
SEQUENCE LENGTH
2 (dimeric dipeptide)
TARGET
TrkB
ROUTE
Preclinical only
ORIGIN
Zakusov Institute (Russia)
AMINO ACID CHAIN VISUALIZATION
S
Serine
BDNF loop-4 pharmacophore
NH-CO
K
Lysine
BDNF loop-4 pharmacophore
NH-CO
Su
Succinyl caps (×2)
stability, dimerization anchor
NH-CO
C6
Hexamethylenediamine linker
dimerization bridge
SEQUENCES-K-Su-C6
MECHANISMS

How It Works

🎯
TrkB Receptor Activation
Activates TrkB and downstream MAPK/ERK, PI3K/AKT, and PLCγ signaling. Its antidepressant-like activity is completely blocked by a Trk antagonist (K252a) and a PLC inhibitor (U73122), directly confirming Trk/PLC-dependence.
🧠
Antidepressant-Like Effects Across Models
Shown effective in the Porsolt forced swim test, tail suspension test, Nomura water-wheel test, and a chronic social defeat stress model — reversing anhedonia and locomotor deficits at an oral dose of 0.1 mg/kg in rodents.
🔬
Neurotrophic Cell Survival Effect
Beyond behavioral endpoints, GSB-106 promotes survival of serum-deprived cells via TrkB-dependent suppression of apoptosis, indicating a genuine neurotrophic action rather than a purely symptomatic behavioral effect.
OVERVIEW

Research Overview

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.

Mechanism of Action

// TrkB RECEPTOR ACTIVATION

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.

// ANTIDEPRESSANT-LIKE EFFECTS ACROSS MODELS

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.

// NEUROTROPHIC, NOT ONLY BEHAVIORAL, EFFECTS

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.

DOSAGE

Dosage & Administration

RESEARCH (PRECLINICAL) — RODENT MODEL, ORAL
DOSE
0.1 mg/kg
FREQUENCY
Reported effective in a chronic social defeat stress rodent model
NOTES
This is a preclinical (rodent) research dose, not an established or approved human dosing regimen — there is no published human trial data for GSB-106. Do not treat this figure as a human dosing recommendation.

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.

CYCLING

Cycle Duration Guide

ON CYCLE
Not applicable — no human use protocol exists
OFF CYCLE
Not applicable

GSB-106 remains a preclinical research compound with no established human dosing or cycling protocol.

NOTES

Research Notes

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.

Quick Reference
FORMULAC₃₂H₅₈N₈O₁₂ (vendor-sourced, not independently confirmed against primary literature)
MOL. WEIGHT746.85 Da
LENGTH2 amino acids
ORIGINV.V. Zakusov Research Institute of Pharmacology, Russian Academy of Medical Sciences (Gudasheva/Seredenin group)
STATUSPreclinical
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TAGS
BDNF mimeticdipeptideantidepressantpreclinicalTrkB agonist