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Amq2.0
5-Amino-1MQ Research
Mostly mechanism / observationalLimited safety
7 peer-reviewed studies
What the evidence says
Mostly mechanism / observational
Most 5-Amino-1MQ studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2014–2025.
Based on 7 studies
Confidence
Low
By outcome
Weight management
Mostly mechanism / observational6 studies
Glucose & metabolic
Too few graded studies2 studies
Active research area
6 studies in the last 5 years
201420192025
1Animal2014
Nnmt knockdown in WAT and liver protects against diet-induced obesity by augmenting cellular energy expenditure.
Kraus D, Yang Q, Kong D, Banks AS, Zhang L, Rodgers JT, et al. · Nature (2014)
Foundational genetic rationale for targeting NNMT: knockdown of Nnmt in white adipose tissue and liver protected mice from diet-induced obesity
Protection was driven by increased cellular energy expenditure, with elevated adipose SAM and NAD+ levels
NNMT inhibition upregulated polyamine flux (ODC/SSAT) via effects on histone H3K4 methylation in adipose tissue
5A1MQ treatment dose-dependently limited body weight and fat mass gains, improved oral glucose tolerance and insulin sensitivity, and suppressed hyperinsulinaemia in DIO mice.
Treatment with a nicotinamide N-methyltransferase inhibitor (NNMTi; 5-amino-1-methylquinolinium) combined with low-fat diet promoted dramatic whole-body adiposity and weight loss in diet-induced obese (DIO) mice.
Dimet-Wiley A, Wu Q, Wiley JT, Eswar A, Neelakantan H, Savidge T, et al. · Sci Rep (2022)
Used 5-amino-1-methylquinolinium (the compound itself) plus a low-fat-diet switch in diet-induced-obese mice
The combination produced dramatic whole-body adiposity and weight loss, rapidly normalizing these measures toward age-matched lean animals
Low-fat-diet switch alone did not fully restore these measures in the same time frame
A lead molecule, JBSNF-000028... drives insulin sensitization, glucose modulation and body weight reduction in a diet-induced obese mouse model of diabetes.
Discovery and characterization of a different NNMT-inhibitor chemotype (tricyclic series; lead JBSNF-000028), corroborating the target class
JBSNF-000028 reduced 1-methylnicotinamide in plasma, liver and adipose tissue and drove insulin sensitization, glucose modulation and weight reduction in DIO mice
A co-crystal structure showed binding at the nicotinamide pocket; the compound was inactive against a broad metabolism/safety panel
NNMT inhibition led to notable improvements in cardiac function... alongside significant reductions in LV hypertrophy and fibrosis.
Li S, Rodrigues PG, Chakraborty AD, Correia C, Schouten EM, Strömstedt M, et al. · Pharmacol Res (2025)
Tested a separate NNMT inhibitor (AMO-NAM) in an aged-mouse cardiometabolic heart-failure-with-preserved-ejection-fraction (HFpEF) model
Treatment sharply reduced the NNMT product 1-MNA and downstream metabolites in the left ventricle
Improved global longitudinal strain and reduced LV hypertrophy and fibrosis, with less inflammation and reduced macrophage infiltration in heart and visceral fat
Knockdown of NNMT elicits heightened energy expenditure in adipose and hepatic tissues, mitigates lipid accumulation, and enhances insulin sensitivity.
Sun WD, Zhu XJ, Li JJ, Mei YZ, Li WS, Li JH. · Front Pharmacol (2024)
Review framing NNMT as a candidate therapeutic target for metabolic syndrome (obesity, T2D, hyperlipidaemia, hypertension)
Summarizes that elevated NNMT in liver and white adipose tissue characterizes obese/diabetic rodents, and that knockdown improves energy expenditure and insulin sensitivity
Explains the mechanism: NNMT depletes nicotinamide (a NAD+ precursor) and consumes SAM, linking NAD+ and methylation metabolism
5MQ significantly inhibited HeLa cell proliferation in a concentration and time-dependent manner ... 5MQ can effectively inhibit HeLa cell proliferation without apparently affecting HEK-293 cell proliferation.
Akar S, Duran T, Azzawri AA, Koçak N, Çelik Ç, Yıldırım Hİ. · J Obstet Gynaecol (2021)
In-vitro cell study: 0.1-500 microM 5-amino-1-methylquinolinium (5MQ), the actual compound, applied to the HeLa cervical-cancer cell line
5MQ concentration- and time-dependently inhibited HeLa proliferation with morphological signs of apoptosis, while sparing non-cancer HEK-293 cells
Treatment lowered phospho-Akt and SIRT1 protein expression and shifted ZEB1/SIRT1/TWIST mRNA levels