Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of 5-Amino-1MQ and MOTS-c — mechanism, side effects, legal status, and pricing.
5-Amino-1MQ is a small heterocyclic molecule (not a peptide) that acts as a selective, membrane-permeable inhibitor of nicotinamide N-methyltransferase (NNMT). It is under preclinical investigation for obesity and non-alcoholic fatty liver disease. It is not FDA-approved and has not completed human clinical trials; it is commonly tracked alongside peptides because grey-market vendors sell it for metabolic protocols.
MOTS-c is a 16-amino-acid mitochondrial-derived peptide (MDP) encoded within the mitochondrial 12S rRNA, discovered by Lee and Cohen at USC in 2015 (sequence: MRWQEMGYIFYPRKLR). It is an investigational, research-only peptide studied as a metabolic regulator; it has not been approved by the FDA for any indication.
5-Amino-1MQ
MOTS-c
Category
Legal Status
Mechanism
Half-life
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
5-Amino-1MQ
MOTS-c
COA corpus from Disclosed Labs — independently tested batches only.
5-Amino-1MQ
80
COAs
99.5%
Avg purity
12
Labs
MOTS-c
193
COAs
99.5%
Avg purity
16
Labs
Neelakantan et al. (2018, Biochem Pharmacol, PMID 29155147) reported that 5-Amino-1MQ and related selective, membrane-permeable methylquinolinium NNMT inhibitors reversed high-fat-diet-induced obesity in mice, reducing body weight, white adipose mass, adipocyte size, and plasma cholesterol without changing food intake. A separate NNMT inhibitor program (Kannt et al., 2018, Sci Rep, PMID 29483571, JBSNF-000088) produced similar metabolic effects in rodents. Dimet-Wiley et al. (2022, Sci Rep, PMID 35013352) reported microbiome changes with NNMT inhibition plus low-fat diet in DIO mice, and Babula et al. (2024, Diabetes Obes Metab, PMID 39161060) showed 5A1MQ dose-dependently limited weight and fat gain and reduced NAFLD-like liver pathology in DIO mice. No human clinical trials of 5-Amino-1MQ have been completed or published as of 2026; grey-market oral protocols are not clinically validated.
Key references
Lee et al. (Cell Metabolism, 2015; PMID 25738459) identified MOTS-c and showed that exogenous administration in mice prevented diet-induced obesity and insulin resistance via AMPK activation in skeletal muscle. Kim et al. (Cell Metabolism, 2018; PMID 29983246) demonstrated that MOTS-c translocates to the nucleus under metabolic stress and regulates antioxidant response element (ARE) genes. Reynolds et al. (Nature Communications, 2021; PMID 33473109) reported that exercise induces MOTS-c in human skeletal muscle and that MOTS-c treatment improved physical capacity in young, middle-aged, and aged mice. Human clinical data are limited to CohBar's Phase 1a/1b study of the analog CB4211 in healthy volunteers and obese NAFLD subjects, which reported acceptable tolerability and exploratory signals on ALT/AST and glucose; CohBar wound down the program in 2023. No completed Phase 2 or Phase 3 trials exist for MOTS-c or its analogs, and grey-market dosing (typically ~10 mg SubQ 2-3x/week) is not clinically validated.
5-Amino-1MQ and MOTS-c are both in the Metabolic category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Contraindications
Lab Testing
Key references