Compound reference
Semax
Cognitive & Neuro Research · vial. For laboratory research use only. Not for human or veterinary consumption, diagnostic use, therapeutic use, or clinical use.
Chemistry identity
Reference identifiers
COA documentation
Lot record status
COA per lot - on requestView Lab ReportsPublished literature
Research context
Peer-reviewed literature referencing this compound, provided for research context.
Semax peptide targets the μ opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice2025
Liu R, Chen Y, Huang H, Li X, Lv J, Jiang L, et al.
British journal of pharmacology
In a mouse spinal cord injury model (T9-T10 contusion) and a PC12 cell neuroinflammation model, Semax reduced oxidative stress and pyroptosis-related lysosomal membrane permeabilization; RNA-sequencing, network pharmacology, and molecular docking identified the mu-opioid receptor as a target linked to USP18-mediated deubiquitination and functional motor recovery in this preclinical model.
The Potential of the Peptide Drug Semax and Its Derivative for Correcting Pathological Impairments in the Animal Model of Alzheimer's Disease2025
Radchenko AI, Kuzubova EV, Apostol AA, Mitkevich VA, Andreeva LA, Limborska SA, et al.
Acta naturae
In a transgenic APPswe/PS1dE9 mouse model of Alzheimer's disease, Semax and a peptide derivative improved performance on cognitive behavioral tasks (open field, novel object recognition, Barnes maze) and reduced amyloid-beta plaque burden in cortex and hippocampus on histological analysis.
Semax, a Synthetic Regulatory Peptide, Affects Copper-Induced Abeta Aggregation and Amyloid Formation in Artificial Membrane Models2022
Sciacca MFM, Naletova I, Giuffrida ML, Attanasio F
ACS chemical neuroscience
Using spectrofluorometric, calorimetric, and MTT assays in artificial membrane models, Semax inhibited copper-induced amyloid-beta aggregation and fibrillogenesis, preventing formation of amyloid-beta:copper complexes implicated in amyloid plaque formation.
Antistress Action of Melanocortin Derivatives Associated with Correction of Gene Expression Patterns in the Hippocampus of Male Rats Following Acute Stress2021
Filippenkov IB, Stavchansky VV, Glazova NY, Sebentsova EA, Remizova JA, Valieva LV, et al.
International journal of molecular sciences
In a rat model of acute restraint stress, Semax administration prior to stress exposure attenuated stress-induced behavioral changes and modulated hippocampal gene expression pathways related to RNA biogenesis, DNA replication, and immune and nervous system function, as measured by RNA sequencing.
Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain2006
Dolotov OV, Karpenko EA, Seredenina TS, Inozemtseva LS, Levitskaya NG, Zolotarev YA, et al.
Journal of neurochemistry
In rats, intranasally administered Semax bound specifically and reversibly to binding sites in basal forebrain cell membranes and increased brain-derived neurotrophic factor (BDNF) protein levels in this region within hours, suggesting a receptor-mediated mechanism linking Semax to BDNF-dependent synaptic plasticity pathways studied in neuroscience research models.
Catalog access requires an account and acceptance of a research-use disclaimer.
This product is intended strictly for research and laboratory use only. It is designated for in vitro testing and experimental purposes. Any use involving human or animal consumption is prohibited by law. All information provided on this website is for educational purposes only. This product must only be handled by licensed, qualified professionals. It is not intended for use as a drug, food, or cosmetic, and must not be misused, mislabeled, or misrepresented as such.