The record
| Class | nootropic |
|---|---|
| Also known as | N-Acetyl Semax, Acetyl Semax, Ac-Semax |
| Chain length | - |
| Molecular weight | 854.98 Da |
| Half-life | 2-10 hours (tissue dependent) |
| Route | IN (intranasal) / SC / IM |
| Studied for | Stroke recovery (Russia/Ukraine); Cognitive enhancement; ADHD (investigational); Traumatic brain injury |
| Research use | Neuroprotection studies; BDNF pathway research; Cognitive enhancement models |
| What has been shown | Increases BDNF 500% (animal models); Improves memory and learning; Neuroprotective in stroke; Enhances focus and attention |
| How it works | N-acetylated heptapeptide analog of ACTH(4-10) with Pro-Gly-Pro added for stability. Enhances BDNF/TrkB signaling up to 500%, increases hippocampal neurogenesis, modulates serotonergic and dopaminergic systems. N-acetylation improves BBB penetration and metabolic stability. Shows neuroprotective effects against stroke and hypoxia. Enhances attention, memory consolidation, and learning without horm |
| Patent status | various formulation patents |
| Regulatory status | approved in Russia; research elsewhere |
Blank = not established in the record. Nothing is estimated to fill a gap.
Where it is matched
- Nerve Support / Neuro-repair Environment (affection, 65%)
- Cognitive Enhancement / Focus (affection, 66%)
- Neuroprotection Signaling (affection, 51%)
- ADHD (illness, 100%)
- Alzheimer's disease (illness, 45%)
- Chronic inflammatory conditions (illness, 30%)
- Cognitive enhancement (illness, 100%)
- Diabetic neuropathy (illness, 30%)
- Neuropathic pain (illness, 30%)
- Sarcoidosis-associated small fiber neuropathy (illness, 30%)
- Stroke recovery (illness, 100%)
- Traumatic brain injury (illness, 100%)
- Vascular dementia (illness, 45%)
- Low mood (symptom, 67%)
- Brain fog or poor focus (symptom, 50%)
- Memory lapses (symptom, 75%)