N-Acetyl Semax Amidate — Research, Dosing & Price Guide

N-Acetyl Semax Amidate (NASA) is a modified form of Semax, a synthetic heptapeptide analog of ACTH(4-10), with enhanced stability and blood-brain barrier penetration. The N-acetyl and C-terminal amide modifications protect the peptide from enzymatic degradation, extending its half-life and nootropic potency. It is widely regarded as one of the most effective peptide nootropics for focus, memory, and neuroprotection.

N-Acetyl Semax Amidate works through multiple synergistic neurotrophin and neurotransmitter pathways. Its core mechanism involves potent upregulation of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the hippocampus and prefrontal cortex — regions critical for memory formation and executive function. BDNF upregulation enhances long-term potentiation (LTP), the molecular basis of learning and memory, and promotes neuronal survival, dendritic branching, and synaptic plasticity. Additionally, NASA modulates dopaminergic, serotonergic, and cholinergic neurotransmission, increasing dopamine and serotonin turnover in the prefrontal cortex. The N-acetyl group improves lipophilicity for enhanced blood-brain barrier penetration, while the amide modification prevents carboxypeptidase degradation, resulting in 5–10x longer activity compared to native Semax. It also demonstrates neuroprotective effects against oxidative stress and excitotoxicity through upregulation of antioxidant enzyme expression.

• Levitskaya et al. (2008) in Neuroscience and Behavioral Physiology demonstrated Semax analogs increased BDNF mRNA expression by 2–3 fold in the rat hippocampus
• Russian clinical trials on Semax (the parent compound) showed improved cognitive recovery in ischemic stroke patients, leading to its approval in Russia for this indication
• Research in the Journal of Neurochemistry showed ACTH(4-10) analogs enhance dopaminergic neurotransmission in the mesolimbic pathway
• Preclinical studies demonstrate neuroprotection against MPTP-induced neurotoxicity (a Parkinson's model) through BDNF and antioxidant mechanisms
• Glazova et al. (2005) showed Semax peptides promote neurite outgrowth and neuronal differentiation in cell culture models
• Studies in Doklady Biological Sciences demonstrated Semax modulates expression of over 1,000 genes in the rat brain, with effects on immune, inflammatory, and neurotrophic pathways

• Intranasal: 200–600 mcg per nostril, 1–2 times daily
• Subcutaneous injection: 100–500 mcg once daily
• Start with 200 mcg intranasally to assess response before increasing
• Best used in the morning or early afternoon; may cause insomnia if dosed late
• Cycle: 2–4 weeks on, 1–2 weeks off to prevent tolerance
• Some users prefer 5 days on, 2 days off for sustained cognitive support
• Effects are noticeable within 15–30 minutes intranasally, making acute dosing effective for cognitive demands

Known Side Effects

• Nasal irritation — dryness or mild burning sensation when administered intranasally, typically temporary
• Headache — occasionally reported, usually during the first few doses and resolves with continued use
• Insomnia — if dosed too late in the day due to increased alertness and dopaminergic stimulation
• Mild anxiety or overstimulation — some users sensitive to dopaminergic compounds may experience restlessness at higher doses
• Hair shedding — a rare but reported side effect attributed to melanocortin receptor activity of ACTH-derived peptides; typically reversible
• Appetite changes — mild appetite suppression reported by some users

Safety Profile

N-Acetyl Semax Amidate has an excellent safety profile based on extensive use of its parent compound Semax in Russian clinical medicine since the 1990s. Semax has been prescribed to hundreds of thousands of patients for stroke recovery, cognitive impairment, and optic nerve disorders with minimal adverse events. The modified form (NASA) has no formal clinical trial data of its own but is pharmacologically similar with enhanced stability. It does not appear to cause dependence or withdrawal effects. The primary caution is for individuals with anxiety disorders, as the dopaminergic stimulation may exacerbate symptoms at high doses. There are no known dangerous drug interactions, though concurrent use with stimulants should be approached carefully.

Within minutes (intranasal): Increased mental clarity and alertness within 15–30 minutes. Users describe a 'fog-lifting' effect with improved verbal fluency and focus. Days 1–3: Acute cognitive enhancement is immediately noticeable. Improved ability to sustain attention on complex tasks. Some users report enhanced color perception and sensory acuity. Weeks 1–2: Cumulative neurotrophin effects begin. Memory recall improves, learning capacity increases, and multitasking becomes easier. Mood is generally elevated with a calm, focused quality. Weeks 3–4: Peak effects. Users report the clearest cognitive improvements — faster processing speed, better working memory, enhanced creativity. After cessation, benefits taper over 1–2 weeks as BDNF levels gradually normalize.

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