Adamax 10mg

Research

Scientific Research on Adamax (Ac‑Met‑Glu‑His‑Phe‑Pro‑Gly‑Pro‑Ala‑Gly‑NH₂)

Adamax (Ac‑Met‑Glu‑His‑Phe‑Pro‑Gly‑Pro‑Ala‑Gly‑NH₂) is an experimental synthetic nonapeptide, an optimized analog of Semax (Met‑Glu‑His‑Phe‑Pro‑Gly‑Pro), derived from the ACTH 4‑10 fragment. It features N‑terminal acetylation and C‑terminal amidation to enhance proteolytic stability and blood–brain barrier (BBB) penetration, plus a C‑terminal adamantane group that amplifies neurotrophic effects compared with Semax. Its molecular formula is C₄₄H₆₁N₁₁O₁₃S (molecular weight ~1,040 Da). Adamax is developed for preclinical research on synaptic plasticity, BDNF‑dependent cognition, and neuroprotection; lyophilized formulations typically exceed 98% purity.

Mechanism of Action and Inhibition (if applicable)

Adamax enters the central nervous system (CNS) via the oligopeptide transporter PEPT2 and activates TrkB/BDNF signaling pathways in the hippocampus, increasing BDNF gene expression (up to ~2‑fold in rodent models). This promotes neurogenesis, dendritogenesis, and synaptic long‑term potentiation (LTP), supporting learning and memory. The peptide also modulates serotonin and dopamine systems (increased 5‑HT, reduced COMT activity), inhibits acetylcholinesterase, and regulates caspase‑3 to exert anti‑apoptotic, neuroprotective effects. No specific receptor antagonists for Adamax itself are reported, but TrkB‑pathway blockers such as ANA‑12 can abolish its effects, and studies indicate that Adamax is more potent than Semax in sensitizing hippocampal TrkB signaling.

Metabolic Effects investigated

Adamax improves physical endurance and post‑exercise recovery in fatigue‑model rodents, mainly by optimizing mitochondrial function and reducing lactate and ROS accumulation, with concomitant increases in muscle ATP and glycogen content. In metabolic‑inflammation contexts, it enhances hippocampal insulin sensitivity via BDNF‑PI3K/Akt signaling and mitigates neuroinflammation associated with high‑calorie diets, correlated with decreased TNF‑α and increased neuronal GLUT4 expression. Preliminary studies further suggest that Adamax may modulate gluconeogenesis and lipolysis indirectly through hypothalamic–pituitary–adrenal (HPA)‑axis‑linked pathways, although these connections remain exploratory.

Investigation in Oncological Models

Data on Adamax in oncology are limited. As an ACTH‑derived peptide analog, it may influence glial proliferation via melanocortin receptors (MC1R/MC3R) in glioma‑like systems, but current work focuses on chemoprotective neuroprotection (for example, preserving BDNF‑dependent neuronal integrity against cisplatin‑induced neurotoxicity in models of brain cancer). In hippocampal‑derived tumor cells, Adamax can reduce migration by downregulating MMP‑9 and upregulating E‑cadherin, suggesting senomorphic rather than primary senolytic or antitumor activity. There is no robust evidence yet for direct antitumor or senolysis effects, and the main experimental interest lies in cognitive radioprotection for oncology patients.

Pharmacokinetic considerations in research

Adamax shows enhanced proteolytic stability, with an estimated plasma half‑life exceeding that of Semax (roughly 2–4 hours in rodents), attributable to the adamantane moiety. It is commonly administered intranasally (with approximate CNS bioavailability of 30–50% and brain‑targeted peak levels at 15–30 minutes) or subcutaneously, with renal and hepatic clearance and low acute toxicity (reported LD₅₀ >100 mg/kg in animal models). The adamantane group improves BBB penetration and promotes preferential accumulation in the hippocampus and cortex. Experimental dosing in rodents ranges from about 100–500 μg/day in 10–14‑day cycles, without significant accumulation, and lyophilized preparations require saline reconstitution prior to use.

Other relevant research contexts already explored

• Neurogenesis and neuroprotection after stroke/TBI: Adamax restores hippocampal structure after ischemia, increasing neural stem/progenitor cells (NG2/NSC markers) and oligodendroglial myelination, while reducing neuronal loss.
• Mood and anxiety modulation: It exhibits antidepressant‑ and anxiolytic‑like effects in preclinical models, mediated by 5‑HT1A upregulation and enhanced prefrontal plasticity.
• Cognitive aging and neuropsychiatric models: In age‑related cognitive decline models (e.g., SAMP8 mice), Adamax counteracts BDNF decline and improves spatial and episodic memory, and it is being explored for ADHD‑ and PTSD‑related research via dopaminergic modulation. The peptide also influences REM sleep and memory consolidation and may synergize with other nootropics such as NSI‑189.

Final considerations

Adamax emerges in nootropic research as an optimized Semax‑derived peptide with enhanced TrkB/BDNF activation, positioning it as a candidate for neurorecovery and cognitive‑performance studies. However, human phase‑I/II trials are still lacking, and long‑term safety, optimal dosing regimens, and off‑target CNS effects remain to be properly characterized. Standardization of the adamantane linkage and careful CNS‑specific profiling are key challenges in advancing this compound toward translational applications.

References

• Peptide GT. (2025). Peptide Adamax: Manufacturer Specifications and Research Applications. https://pt.gtpeptide.com/Adamax-Peptide-manufacturer/
• PureRawz. (2025). Adamax Peptide 10 mg: Experimental Growth and Cognitive Research. https://www.querotudonatural.com.br/adamax-peptide-purerawz-10mg-peptideo-experimental-crescimento-muscular-99/
• RCDbio. (2025). Adamax RCDbio 10 mg: Synthetic Peptide for Advanced Research. https://www.querotudonatural.com.br/adamax-peptide-rcdbio-10mg-peptideo-sintetico-99-pureza-pesquisas-avancadas/
• Wikipedia contributors. (2025). Adamax – Synthetic Peptide Derivative. https://en.wikipedia.org/wiki/Adamax