N-Acetyl Semax Amidate
$69.00
What is N-Acetyl Semax Amidate?
N-Acetyl Semax Amidate is a stabilized derivative of Semax, a synthetic heptapeptide analog of ACTH(4-10) (the fragment Met-Glu-His-Phe-Pro-Gly-Pro). The N-acetyl and C-terminal amide modifications enhance metabolic stability by protecting against aminopeptidase and carboxypeptidase degradation. Semax was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences and is approved in Russia and several CIS countries as a nootropic and neuroprotective medication, typically administered intranasally. The ACTH(4-10) fragment retains the neurotrophic and cognitive properties of ACTH without its adrenocorticotropic (cortisol-stimulating) activity. N-Acetyl Semax Amidate represents an optimization of this clinically validated peptide for improved pharmacokinetic properties. Semax-class peptides have been studied for their effects on BDNF expression, cerebral blood flow, and cognitive function in both preclinical and clinical settings.
Mechanism of Action
N-Acetyl Semax Amidate has been investigated for its neurotrophic and neuroprotective mechanisms through multiple signaling pathways. Researchers observed that Semax peptides increase BDNF and NGF expression in hippocampal and cortical regions through melanocortin-dependent signaling, activating TrkB and downstream cascades including MAPK/ERK and PI3K/Akt. Studies suggest that the ACTH(4-10) sequence engages melanocortin receptors (MC3R and MC4R) in the brain, though the neurotrophic effects may involve additional receptor-independent mechanisms. Researchers observed that Semax administration was associated with modulation of dopaminergic, serotonergic, and acetylcholinergic neurotransmitter systems. In cerebrovascular research models, Semax has been investigated for its effects on cerebral blood flow regulation through nitric oxide and prostacyclin pathways. The N-acetyl and amide modifications protect the peptide from exopeptidase degradation, extending its functional duration compared to unmodified Semax.
Published Research
BDNF Modulation
Dolotov et al. (2006) investigated Semax’s effects on neurotrophic factor expression in rat brain and observed dose-dependent increases in BDNF and NGF mRNA in hippocampal and basal forebrain regions following intranasal administration [1].
Neuroprotection
Gusev et al. (2005) investigated Semax in clinical stroke models and observed improved neurological outcome scores following early administration, contributing to its clinical adoption in Russia for acute cerebrovascular events [2].
Cognitive Enhancement
Ashmarin et al. (1995) reviewed the regulatory peptide cascade involving ACTH fragments including the Semax sequence, describing how these melanocortin-derived peptides influence synaptic plasticity and memory formation [3].
Product Specifications
| Product | N-Acetyl Semax Amidate Lyophilized Powder |
|---|---|
| Available Sizes | 30mg |
| Purity | ≥99% (HPLC verified) |
| Sequence | Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH₂ |
| Molecular Formula | C₃₉H₅₇N₉O₁₀ |
| Molecular Weight | 815.93 g/mol |
| Appearance | White lyophilized powder in glass vial |
| Storage | Store lyophilized at -20°C protected from light. Reconstituted solution at 2-8°C, use within 14 days. |
| Testing | Third-party tested — Certificate of Analysis available |
Frequently Asked Questions
It is a stabilized version of Semax, a synthetic ACTH(4-10) analog. The modifications improve metabolic stability while preserving the neurotrophic and nootropic properties of the parent peptide.
The N-acetyl and C-terminal amide modifications protect against exopeptidase degradation, extending the functional half-life compared to unmodified Semax.
Semax is approved in Russia and several CIS countries as a nootropic and neuroprotective medication, typically administered intranasally.
Store lyophilized at -20°C protected from light. Once reconstituted, store at 2-8°C and use within 14 days.
No. While Semax is derived from the ACTH sequence, the 4-10 fragment does not activate the MC2R receptor on adrenal cells and does not stimulate cortisol production.
Adamax has an adamantane group for lipophilicity. N-Acetyl Semax Amidate uses N-acetyl/amide caps for stability. Both are Semax/ACTH(4-10) derivatives with different modification strategies.
References
- Dolotov OV, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res. 2006;1117(1):54-60. PMID: 16996040
- Gusev EI, et al. Semax in prevention of disease progress and development of exacerbations in patients with cerebrovascular insufficiency. Zh Nevrol Psikhiatr Im S S Korsakova. 2005;105(2):35-40.
- Ashmarin IP, et al. Regulatory peptides in the brain: new classes and functional interactions. Neurochem Res. 1995;20:1009-1018.
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