Semax (11mg)
$60.00
Description
Description
A single-component research material supplied for controlled research environments. Suitable for studies involving peptide characterization and method development in model systems.
Composition
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Semax: 11 mg
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Appearance: lyophilized powder in a sealed research vial
Research Focus (non-clinical)
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Peptide identity and purity assessment via HPLC/LC-MS
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Assay development and calibration for quantitative analysis
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Chromatographic method optimization for impurity profiling and peak resolution
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Stability characterization of a lyophilized peptide under laboratory storage conditions
Documentation
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COA pending — third-party verification in progress
Important Notice
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For research use only
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Not for human consumption
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Not intended to diagnose, treat, cure, or prevent any disease
Quality & Manufacturing
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COA pending — third-party verification in progress
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Lyophilized for transit stability; batch traceable
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Tamper-evident seal; lot & test date on each vial
Additional information
| Weight | 0.5 lbs |
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Research Use Only
These studies reference research-grade peptides for laboratory and scientific investigation only. Not for human consumption. Not intended to diagnose, treat, cure, or prevent any disease.
Published Scientific Research
Peer-reviewed laboratory research investigating research peptides from leading scientific databases
Semax peptide targets the μ opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice.
Given the key roles of LMP and ubiquitination in SCI pathophysiology, this study investigated how Semax could modulate these pathways to affect functional recovery following SCI. Network pharmacology and docking revealed the μ-opioid receptor as a Semax target.
View Full StudySemax, a Copper Chelator Peptide, Decreases the Cu(II)-Catalyzed ROS Production and Cytotoxicity of aβ by Metal Ion Stripping and Redox Silencing.
Alzheimer's disease (AD) is the most common neurodegenerative disorder associated with cognitive decline and loss of memory. It is postulated that the generation of reactive oxygen species (ROS) in Fenton-like reaction connected with Cu(II)/Cu(I) redox cycling of the Cu(II)-aβ complex can play a key role in the molecular mechanism of neurotoxicity in AD.
View Full StudyBrain Protein Expression Profile Confirms the Protective Effect of the ACTHPGP Peptide (Semax) in a Rat Model of Cerebral Ischemia-Reperfusion.
Previously, studies of the molecular mechanisms underlying the actions of Semax using models of cerebral ischemia in rats showed that the peptide enhanced the transcription of neurotrophins and their receptors and modulated the expression of genes involved in the immune response. At 24 h after tMCAO, we observed the upregulation of active CREB in subcortical structures, including the focus of the ischemic damage; downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex; and downregulation of active JNK in both tissues under the action of Semax.
View Full StudyAntistress Action of Melanocortin Derivatives Associated with Correction of Gene Expression Patterns in the Hippocampus of Male Rats Following Acute Stress.
Here, we studied the behavioral effects and molecular genetic mechanisms of two synthetic MC derivatives-ACTH(4-7)PGP (Semax) and ACTH(6-9)PGP under normal and acute restraint stress (ARS) conditions. Administration of Semax or ACTH(6-9)PGP (100 μg/kg) to rats 30 min before ARS attenuated ARS-induced behavioral alterations.
View Full StudyNovel Insights into the Protective Properties of ACTHPGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats.
However, its molecular mechanisms of action within the brain are not yet fully understood. Therefore, the neuroprotective action of Semax may be associated with a compensation of mRNA expression patterns that are disrupted during ischaemia-reperfusion conditions.
View Full Study[POSSIBLE ROLE OF TRANSTHYRETIN IN THE BIOLOGICAL MECHANISM OF THE REGULATORY PEPTIDE NEUROPROTECTION.].
However, the mechanisms of its action are insufficiently understood and actively studied. High similarity between the effects of Ttr and coupled molecular systems with the Semax effects in ischemic stroke allowed us to suggest that the neuroprotection mechanisms of Semax (and, possibly, of other neuroprotection mechanisms of Semax) could be mediated by Ttr.
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