Adamax — Research, Dosing & Price Guide

Adamax is a modified derivative of Semax incorporating an adamantane moiety, designed for enhanced nootropic effects with improved blood-brain barrier penetration and extended half-life. It combines the neurotrophin-boosting properties of the ACTH(4-10) fragment with superior pharmacokinetic properties. Users in the nootropic community report improved focus, verbal fluency, mental clarity, and motivation, with effects often described as cleaner and more sustained than the parent compound Semax.

Adamax works through multiple converging neurotrophin and neurotransmitter pathways. As a derivative of the ACTH(4-10) melanocortin fragment, it retains the core sequence's ability to upregulate brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) expression, particularly in the hippocampus and prefrontal cortex — regions critical for memory consolidation and executive function. The adamantane modification serves dual purposes: it dramatically improves lipophilicity, enhancing penetration across the blood-brain barrier, and it extends the peptide's half-life by conferring resistance to enzymatic degradation by aminopeptidases. This means more of the compound reaches the brain and remains active longer compared to unmodified Semax. At the receptor level, Adamax modulates melanocortin receptors (MC3R and MC4R) in the CNS, influencing dopaminergic and serotonergic neurotransmission. It enhances cholinergic signaling in the basal forebrain, supporting attention and working memory. Downstream, it activates the CREB (cAMP response element-binding protein) transcription factor, promoting the expression of genes involved in synaptic plasticity and long-term potentiation — the molecular basis of learning and memory. It also upregulates antioxidant enzymes (SOD, catalase) in neuronal tissue, providing neuroprotective effects against oxidative stress.

• Semax and its analogs have been shown to increase BDNF mRNA expression by 2–3 fold in rodent hippocampal neurons within 24 hours of administration, with effects persisting up to 48 hours.
• Russian clinical studies on the parent compound Semax demonstrated improved cognitive function, attention, and memory in stroke patients during rehabilitation — supporting the nootropic potential of the ACTH(4-10) fragment class.
• ACTH(4-10) derivatives demonstrate significant neuroprotective effects against ischemia-reperfusion injury in rodent models, reducing infarct volume and preserving neuronal viability.
• Preclinical data shows enhanced long-term potentiation (LTP) in hippocampal CA1 circuits following melanocortin peptide administration, providing a mechanistic basis for memory enhancement.
• Adamantane-modified peptides show 3–5x improved blood-brain barrier penetration compared to unmodified analogs in pharmacokinetic studies.
• Semax analogs have demonstrated antidepressant-like effects in forced swim test models, likely mediated through BDNF upregulation and serotonergic modulation.

• Intranasal administration: 100–300 mcg per nostril, 1–2 times daily. This is the most common route for nootropic use, providing rapid onset (5–15 minutes) via the olfactory mucosa.
• Subcutaneous injection: 100–500 mcg once daily, typically in the morning. Provides more consistent bioavailability than intranasal.
• Start with the lowest effective dose (100 mcg) for the first 3–5 days to assess individual response and tolerance.
• Standard cycle: 2–4 weeks on, 2 weeks off. Extended cycles of up to 6 weeks are reported but lack safety data.
• Best used in the morning or early afternoon. Avoid evening dosing as enhanced dopaminergic and noradrenergic activity may interfere with sleep onset.
• Can be combined with NA-Selank-Amidate (intranasal) for a balanced cognitive-anxiolytic stack, using Adamax for focus and Selank for calm.
• Onset of effects: intranasal 5–15 minutes, subcutaneous 15–30 minutes. Duration: 4–8 hours depending on dose and route.

Known Side Effects

• Nasal irritation or mild burning sensation with intranasal use — most common side effect, typically mild and transient.
• Headache — reported occasionally, particularly during the first few days of use or at higher doses.
• Insomnia or sleep disruption if taken too late in the day, related to enhanced catecholaminergic activity.
• Mild anxiety or overstimulation in sensitive individuals, particularly at doses above 300 mcg. Dose reduction usually resolves this.
• Transient hair shedding — reported anecdotally by a subset of users, possibly related to melanocortin receptor modulation affecting the hair growth cycle. Reversible upon discontinuation.
• Appetite changes — some users report reduced appetite, consistent with melanocortin system activation.

Safety Profile

Adamax inherits much of its safety profile from the parent compound Semax, which has over 20 years of clinical use in Russia with a well-established safety record. The adamantane modification improves pharmacokinetics without introducing fundamentally new toxicity concerns based on available data. Adamantane derivatives (such as memantine, amantadine) have well-characterized safety profiles in other pharmaceutical applications. Contraindications include a history of seizure disorders (melanocortin peptides may lower seizure threshold at high doses), active psychotic conditions, and pregnancy/breastfeeding. Individuals with anxiety disorders should start at the lowest dose, as enhanced catecholaminergic activity may initially exacerbate anxiety. Long-term safety data specific to Adamax (as opposed to Semax) is limited. It should not be combined with MAO inhibitors or high-dose stimulants due to potential for excessive catecholamine accumulation.

Days 1–3: Initial effects are noticeable within 15–30 minutes of first dose — improved verbal fluency, mental clarity, and a sense of cognitive 'sharpness.' Effects are subtle but distinctly present. Some users notice enhanced color perception or auditory clarity. Days 4–7: The nootropic effects deepen as BDNF upregulation takes hold. Working memory, task switching, and sustained attention improve. Verbal articulation becomes notably smoother. The cognitive enhancement feels more consistent day-to-day. Weeks 2–3: Peak effects are typically reached during this period. Users report the strongest improvements in focus, creativity, and mental stamina. Mood elevation and motivation are commonly noted. Some users report vivid dreams. Week 4+: Effects maintain at a steady state with continued use. Upon cycling off, residual benefits in cognitive function may persist for 1–2 weeks, likely reflecting sustained BDNF elevation. Tolerance does not appear to develop significantly within a 4-week cycle.

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