99% PURITY
Nootropics
Semax 11mg
MW: 813.93 g/molCAS: 80714-61-0
£29.99
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High-purity compounds for investigating BDNF expression, NNMT inhibition, and cognitive pathway biology.
Cognitive neuroscience research increasingly focuses on the molecular substrates of neuroplasticity, neuroprotection, and cellular metabolic health in neurons and glial cells. The compounds in this category represent two mechanistically distinct research tools. Semax is a synthetic heptapeptide derived from the adrenocorticotropic hormone (ACTH) 4–10 fragment, with an added Pro-Gly-Pro sequence that confers enhanced stability. It has been extensively studied in animal models for its ability to upregulate brain-derived neurotrophic factor (BDNF) and its receptor TrkB, placing it within research programmes examining neurotrophin signalling and its role in synaptic plasticity, learning, and neuroprotection against ischaemic or excitotoxic insults.
5-Amino-1MQ (5-amino-1-methylquinolinium) is a selective, cell-permeable small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) — an enzyme that transfers a methyl group from S-adenosylmethionine (SAM) to nicotinamide, producing 1-methylnicotinamide. NNMT activity consumes the methyl donor pool and reduces NAD+ precursor availability, and its expression is elevated in senescent and metabolically dysfunctional cells. By inhibiting NNMT, 5-Amino-1MQ provides a tool for studying how methyl group flux and NAD+ biosynthesis influence cellular energy status, adipocyte function, and potentially neuronal metabolic health. Together, these compounds offer complementary entry points into the molecular underpinnings of brain and metabolic function relevant to cognitive research.
In rodent models, intranasal and systemic Semax administration has been shown to increase hippocampal and cortical BDNF mRNA and protein levels, and to enhance TrkB receptor phosphorylation — a marker of active neurotrophin signalling. Downstream of TrkB, this translates to activation of the MAPK/ERK, PI3K/Akt, and PLCγ pathways, which regulate synaptic protein synthesis, dendritic spine remodelling, and neuronal survival. Researchers use Semax as a comparator or positive control in studies investigating pro-BDNF and mature BDNF processing, and in models of neuroplasticity where neurotrophin support is experimentally manipulated.
Nicotinamide N-methyltransferase (NNMT) diverts nicotinamide — a precursor for NAD+ biosynthesis via the salvage pathway — into 1-methylnicotinamide, simultaneously consuming S-adenosylmethionine (the universal methyl donor). Elevated NNMT activity therefore represents a dual metabolic drain: reducing NAD+ availability (with downstream effects on sirtuin and PARP activity) and depleting the SAM pool needed for epigenetic methylation reactions. NNMT is overexpressed in adipose tissue in obesity models and in senescent cells, making its inhibition via compounds like 5-Amino-1MQ a tractable experimental approach to studying the intersection of one-carbon metabolism, NAD+ biology, and cellular ageing.
Semax has been studied primarily in rodent models of focal cerebral ischaemia, traumatic brain injury, and excitotoxicity (NMDA or kainic acid administration), where its effects on infarct volume, BDNF expression, and behavioural outcomes have been characterised. In vitro, it has been applied to primary neuronal cultures and neuronal cell lines subjected to oxidative stress or growth factor withdrawal to assess pro-survival signalling. These models allow researchers to examine whether Semax-induced BDNF upregulation is sufficient to activate downstream neuroprotective cascades, or whether direct receptor interactions play an additional role independent of BDNF induction.
Published selectivity profiling data indicate that 5-Amino-1MQ shows substantial selectivity for NNMT over a panel of other SAM-dependent methyltransferases, including DNMT1, COMT, and PRMT1, at the concentrations typically used in cell culture research. Its cell permeability — measured by its ability to reduce intracellular 1-methylnicotinamide levels — makes it preferable to earlier NNMT inhibitor scaffolds that showed limited cellular uptake. Researchers should, however, include appropriate methyltransferase selectivity controls in experimental designs, particularly when studying SAM-dependent epigenetic processes in the same system, to confirm that observed phenotypes are attributable to NNMT inhibition specifically.
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