SEMAX

Chemical Makeup:

• Molecular Formula: C37, H51, N9, O10, S
• Molecular Weight: 813.92 g/mol
• Synonyms: ACTH(4-10) analogue; ACTH(4-7)Pro-Gly-Pro; MEHFPGP

Sequence:

• Met-Glu-His-Phe-Pro-Gly-Pro

Semax and Cognitive Function (BDNF Expression)

Research conducted on murine models suggests that Semax may influence the expression of neurotrophins in the forebrain and hippocampus. In a study involving rat subjects, a rapid elevation in BDNF and trkB mRNA levels was observed following administration. It is hypothesized that this upregulation of neurotrophic factors contributes to synaptic plasticity and cellular survival. Experimental data indicates that subjects treated with the peptide displayed altered behavioral responses in passive avoidance tasks, suggesting a potential role in memory formation and retention mechanisms.

Semax and Ischemic Stroke (Neuroprotection)

The peptide has been extensively studied for its potential neuroprotective properties in models of cerebral ischemia. In studies utilizing middle cerebral artery occlusion (MCAO) models, Semax administration was correlated with a reduction in infarct volume and improved neurological scores. Researchers postulate that the peptide may mitigate oxidative stress and inflammation during reperfusion injury. Furthermore, gene expression analysis in these models revealed that Semax might influence the regulation of immune response genes (e.g., Il1a, Il1b, Il6) and vascular system genes, potentially stabilizing the blood-brain barrier post-trauma.

Semax and Attention Deficit (ADHD)

Theoretical models have explored Semax as a modulator of the dopaminergic system, which is often dysregulated in attention-deficit/hyperactivity disorder (ADHD). Comparative studies in rodent models have observed that Semax may increase the extracellular concentration of dopamine in the striatum. Researchers have noted that, unlike traditional psychostimulants, this modulation appears to occur without significant depletion of neurotransmitter reserves. Consequently, the peptide is a subject of investigation for its potential to improve selective attention and task completion in models of neurodevelopmental disorders.

Semax and Stress Response (Enkephalins)

Investigations into the peptide's analgesic and anxiolytic potential suggest an interaction with the endogenous opioid system. It has been proposed that Semax inhibits enkephalinases, the enzymes responsible for breaking down enkephalins. By delaying this degradation, the peptide may prolong the activity of endogenous opioids. In "open field" and "elevated plus maze" tests, animal subjects administered the peptide demonstrated alterations in stress-induced behaviors and locomotion, providing data on its potential role in modulating the hypothalamic-pituitary-adrenal (HPA) axis response to acute stress.

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Side Effects & Withdrawal: 

In animal toxicology studies, Semax has shown a high safety profile with low toxicity. However, observed effects in high-dose rodent studies have included mild sedation or transient hyperactivity depending on the dosage relative to body weight. Withdrawal phenomena have not been extensively characterized in the literature, though rapid cessation after chronic high-exposure protocols in test subjects is theoretically associated with transient downregulation of receptor sensitivity.

Disclaimer: 

ALL PRODUCTS ARE FOR RESEARCH USE ONLY. This product is not intended for human consumption, diagnostic use, or therapeutic application. It is strictly for laboratory research and development purposes. The statements made regarding this material have not been evaluated by the FDA or any other regulatory body. The purchaser assumes all responsibility for compliance with local, state, and federal regulations regarding the use and handling of this chemical.