RPEP-00939 · 2004Daily intranasal administration of Semax (an ACTH(4-10) analog peptide, sequence MEHFPGP) at 0.2 mg/kg reduced the severity of behavioral disturbances caused by the neurotoxin MPTP in rats. MPTP selectively destroys dopamine neurons — the same neurons lost in Parkinson's disease — causing decreased movement and increased anxiety. Semax treatment lessened both of these deficits.
The researchers proposed two mechanisms for Semax's protective effects: direct modulation of the dopaminergic system and broader neurotrophic (nerve-supporting) activity of the peptide.
Levitskaya, N G; Sebentsova, E A; Andreeva, L A; Alfeeva, L Yu; Kamenskii, A A; Myasoedov, N F · Animal
RPEP-01129 · 2006Semax upregulated BDNF mRNA and TrkB receptor expression in the rat hippocampus, providing the neurotrophic molecular mechanism for its documented cognitive enhancement and neuroprotective effects — BDNF is the brain's primary growth and survival factor.
Dolotov, Oleg V; Karpenko, Ekaterina A; Inozemtseva, Lyudmila S; Seredenina, Tamara S; Levitskaya, Natalia G; Rozyczka, Joanna; Dubynina, Elena V; Novosadova, Ekaterina V; Andreeva, Lyudmila A; Alfeeva, Lyudmila Yu; Kamensky, Andrey A; Grivennikov, Igor A; Myasoedov, Nikolay F; Engele, Jürgen · Animal Study
RPEP-01130 · 2006Semax (ACTH 4-10 analog) showed specific binding to rat brain tissue and increased brain-derived neurotrophic factor (BDNF) protein levels, confirming receptor-mediated neurotrophin enhancement as the mechanism for its nootropic and neuroprotective activities.
Dolotov, Oleg V; Karpenko, Ekaterina A; Seredenina, Tamara S; Inozemtseva, Lyudmila S; Levitskaya, Natalia G; Zolotarev, Yuriy A; Kamensky, Andrey A; Grivennikov, Igor A; Engele, Juergen; Myasoedov, Nikolay F · Animal Study
RPEP-05052 · 2020Both Selank and Semax modulated functional connectivity between right amygdala and right temporal cortex regions (fusiform, inferior/middle temporal, parahippocampal gyri) with both shared and peptide-specific effects.
Panikratova, Ya R; Lebedeva, I S; Sokolov, O Yu; Rumshiskaya, A D; Kupriyanov, D A; Kost, N V; Myasoedov, N F · Rct
RPEP-05410 · 2021Neonatal fluvoxamine (postnatal days 1-14) caused long-term anxiety, impaired learning, and altered brain monoamines. Subsequent Semax treatment (postnatal days 15-28) reduced anxiety, improved learning, and normalized brain biogenic amine levels.
Glazova, Nataliya Yu; Manchenko, Daria M; Volodina, Maria A; Merchieva, Svetlana A; Andreeva, Ludmila A; Kudrin, Vladimir S; Myasoedov, Nikolai F; Levitskaya, Natalia G · Preclinical Animal Study