Mechanism: NNMT Inhibition → NAM Salvage → NAD⁺-Linked Signaling

At the core, 5-Amino-1MQ competitively inhibits NNMT. When NNMT activity drops, NAM is less frequently methylated into 1-MNA and can instead be routed into the NAMPT-dependent salvage pathway that regenerates NAD⁺. Increased NAD⁺ availability can, in turn, support sirtuin deacetylases (e.g., SIRT1/SIRT3) and influence PARP-mediated repair, tying NNMT inhibition to chromatin, mitochondrial enzyme acetylation state, and DNA-damage responses.

In adipocyte and hepatocyte models, this mechanism is frequently read out via NAD⁺/NADH ratios, acetyl-lysine footprints on metabolic enzymes, mitochondrial respiration (OCR), and transcriptional signatures (AMPK–PGC-1α, fatty-acid oxidation, UCPs). Because methyl-donor flux is involved, researchers may also quantify SAM/SAH, 1-MNA, and related methylome endpoints.

What preclinical data generally report

While specific results vary by model, dosing, and readouts, multiple preclinical studies report that NNMT inhibition can shift adipocyte energetics toward a more oxidative phenotype. Typical observations include reduced adipocyte size in diet-induced models, higher NAD⁺ pools, increased mitochondrial markers, and favorable changes in lipid handling. These outcomes are hypothesis-generating and model-dependent; they motivate continued investigation of methyl-donor economy, NAD⁺ salvage, and mitochondrial control in metabolic research.

Importantly, any translation beyond benchtop contexts remains an open research question. Dose, delivery matrix, and tissue specificity can substantially shift findings. We recommend pairing 5-Amino-1MQ with multi-omic panels—metabolites, epigenetic marks, and respiration—to produce a richer causal picture.

Related research tools: mitochondria & energy balance

Ipamorelin 10 mg Popular Slug validated: /product/ipamorelin-10-mg/ A selective GH secretagogue often profiled alongside metabolic markers. In projects investigating 5-Amino-1MQ, Ipamorelin may be used to probe GH/IGF axis interactions with mitochondrial readouts (OCR, citrate-synthase activity) and NAD+-linked enzymes. View Ipamorelin product page

MOTS-c 10 mg Slug validated: /product/mots-c-10mg/ A mitochondrial-encoded peptide investigated for AMPK-linked metabolic reprogramming and exercise-responsive signals. Because 5-Amino-1MQ influences NAD+ salvage, pairing MOTS-c can help clarify cross-talk among AMPK, sirtuins, and downstream transcriptional programs (e.g., PGC-1α, NRF1). View MOTS-c product page

SLU-PP-332 Slug validated: /product/slu-pp-332/ A tool compound characterized as an ERR agonist with “exercise-mimetic” transcriptional effects in preclinical experiments. When studied with 5-Amino-1MQ, researchers often profile fatty-acid oxidation, mitochondrial gene sets, and acetylproteomics to differentiate NAD+ salvage effects from nuclear receptor program activation. View SLU-PP-332 product page

Popular product highlight: GLP3 online

In incretin-focused experiments, triple-agonist GLP-3 research compounds engage GLP-1R, GIPR, and GCGR—networks tightly coupled to hepatic lipid flux, adipocyte signaling, and skeletal-muscle substrate use. Because 5-Amino-1MQ touches NAD⁺ salvage, running the two in parallel (separate arms) can reveal whether metabolic outcomes stem primarily from endocrine signaling or redox/epigenetic modulation.

How this fits into your catalog workflow

Researchers often position 5-Amino-1MQ within a broader metabolic methods panel: an NNMT inhibitor for methyl-donor/NAD⁺ salvage, a mitochondrial peptide like MOTS-c for AMPK-linked stress signals, an exercise-mimetic such as SLU-PP-332 for nuclear receptor activation, and a GH-axis control arm using Ipamorelin. That factorial approach can separate endocrine from redox/epigenetic causes of any observed shift in lipid handling or mitochondrial capacity.

To browse additional research compounds and reference testing information, visit:
All Peptides for Sale or the
Pure Tested Peptides homepage.