Weight loss · Pill

5-Amino-1MQ

Gray market

Checked 11 Oct 2026 · 24 sources · 11 corrections on this page · No vendors · No affiliates · No one buys a word of it

0 human trials published

Preclinical · Mouse only

Gray market · No FDA ruling — not on any list

Sold as a research chemical. Some clinics and pharmacies still supply it; that’s their risk, not a change in the rule.

Bottom line

A mouse-stage research compound that pharmacies and research-chemical sellers already sell.

Also called: 5-Amino-1-methylquinolinium
5A1MQ
NNMT Inhibitor
Neelakantan / Watowich quinolinium
Category: Small Molecule — NNMT Inhibitor
Class: Small molecule NNMT inhibitor
Molecular Weight: 159.2 Da (cation); 286.1 Da as the iodide salt
Enzyme Target: Nicotinamide N-methyltransferase
IC50 (biochemical): ~1 µM vs NNMT
Route (studied): SubQ, IV, oral (mice) · no human study
Route (sold): Oral capsules (pharmacy Rx); SubQ vials (research chemical)
FDA Status: Not approved
Human Trials: None published
Evidence Strength: Preclinical: Mouse only
Human: None
WADA Status: Not specifically named — prohibited at all times under S0 (no government has approved it for human use)
Cost & Access: Research-only

Also for weight loss

The other four questions

What does it do? It blocks NNMT, an enzyme that uses up nicotinamide and SAM; in cultured fat cells it raised both NAD+ and SAM and suppressed fat-making, and in obese mice it shrank fat cells (Neelakantan et al., 2018).
Who uses it? Research labs plus a small self-experimenter crowd buying it from research-chemical suppliers, and from pharmacies that sell it without any FDA basis for compounding it.
Does the evidence hold up? Obese mice lost body weight and fat mass without eating less (Neelakantan et al., 2018; Babula et al., 2024). The obesity studies all come from the lab that made it; two other groups have used it only in cancer models (Akar et al., 2021; Yang et al., 2024). ClinicalTrials.gov lists no human trial (searched October 4, 2026).
Bottom line? A mouse-stage research compound that pharmacies and research-chemical sellers already sell.

Dosing from the Literature

Published for fat loss: mouse doses from one lab (5–34 mg/kg). Not published: any human dose; no human study exists.

The rows below are mouse doses from the published studies. No human dose has been published, and no FDA-approved dose exists.

Route / Population	Dose	Frequency	Notes
Mouse IV (PK)	5 mg/kg	Single dose	Babula 2024 pharmacokinetic reference dose.
Mouse oral (PK)	30 mg/kg	Single dose	Babula 2024, in lean mice: blood levels stayed low (peak 14.5 ng/mL at 4 h), far below those after IV or subcutaneous dosing.
Mouse subcutaneous (DIO efficacy)	10 or 32 mg/kg	Once daily × ~4 weeks	Babula 2024 efficacy study in diet-induced obese mice; Neelakantan 2018 used about 34 mg/kg a day, as three injections, for 11 days.
Mouse subcutaneous (PK)	25 mg/kg	Daily × 1–5 days	Babula 2024 SubQ characterization.

Dosing Disclaimer

No dose-finding study has been done in humans, and no human dose has been published. Always work with a licensed healthcare provider.

What It Is

5-Amino-1MQ (5-amino-1-methylquinolinium) is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), a cytosolic enzyme that catalyzes the methylation of nicotinamide (vitamin B3 / NAD+ precursor) to 1-methylnicotinamide (1-MNA) using S-adenosylmethionine (SAM) as the methyl donor. It is a quinolinium scaffold — a fused bicyclic aromatic structure carrying a permanent positive charge on the ring nitrogen — that was selected from a structure-activity-relationship (SAR) series developed in the laboratory of Stanley Watowich and Harshini Neelakantan at the University of Texas Medical Branch at Galveston.

NNMT sits at an unusual metabolic intersection. Every molecule of nicotinamide that NNMT methylates is both a NAD+ precursor that has been diverted away from the NAD+ salvage pathway and a methyl group (from SAM) consumed producing 1-MNA (1-methylnicotinamide). Over-expressed NNMT therefore drains both the NAD+ pool and the cellular methyl pool at the same time. NNMT expression is increased in the white adipose tissue (WAT) and liver of obese and diabetic mice, which is what made the enzyme a target of interest for obesity pharmacology in the first place (Kraus et al., Nature 2014; PMID 24717514). The same pattern shows up in people: one group found NNMT mRNA about twice as high in both omental and subcutaneous white adipose tissue of patients with type 2 diabetes as in controls, plasma 1-MNA tracking the degree of insulin resistance, and adipose NNMT expression falling after exercise or bariatric surgery (Kannt et al., Diabetologia 2015; PMID 25596852).

The Neelakantan / Watowich series screened quinolinium analogs for on-target potency, membrane permeability, and selectivity. 5-Amino-1MQ emerged as the lead compound. It demonstrated inhibition of NNMT in biochemical assay with an IC50 of approximately 1 µM, penetrated adipocytes to reduce intracellular 1-MNA concentrations, raised intracellular NAD+ and SAM, and when administered systemically to diet-induced-obese C57Bl/6J mice reversed the obesity phenotype without altering food intake (Neelakantan et al., J Med Chem 2017; Neelakantan et al., Biochem Pharmacol 2018). This result — fat loss without appetite suppression — is what made 5-Amino-1MQ of interest to the optimization / longevity community.

Mechanism of Action

5-Amino-1MQ blocks NNMT, the enzyme that methylates nicotinamide using SAM as the methyl donor (Kraus et al., 2014). In docking models, its quinolinium family binds the enzyme's nicotinamide-binding site (Neelakantan et al., J Med Chem 2017; PMID 28548833).

Direct NNMT enzyme inhibition — Biochemical IC50 around 1 µM (Neelakantan et al., J Med Chem 2017; PMID 28548833). In cultured fat cells, it lowered 1-MNA, the product of NNMT's reaction, at concentrations that did not harm the cells (Neelakantan et al., 2018).
NAD+ — NNMT diverts nicotinamide, an NAD+ precursor, out of the salvage pathway (Dong et al., 2025). In cultured fat cells, NNMT inhibitors raised NAD+, and the authors propose that more NAD+ and SAM may explain how they act (Neelakantan et al., 2018).
SAM — Each NNMT reaction uses SAM, the cell's methyl donor. NNMT inhibitors raised SAM in cultured fat cells (Neelakantan et al., 2018); knocking NNMT down in mouse fat raised SAM there and changed histone methylation and polyamine flux (Kraus et al., 2014).
Fat-cell lipogenesis — In cultured fat cells, NNMT inhibitors suppressed lipogenesis, the making of new fat (Neelakantan et al., 2018).
Energy use — In mice, knocking NNMT down in fat and liver protected against diet-induced obesity by raising energy expenditure, and in fat cells it raised oxygen consumption (Kraus et al., 2014). That was a gene knockdown, not this compound.
Muscle stem cell (satellite cell) niche effects — The same laboratory's muscle work used this inhibitor, not knockdown: in 24-month-old mice given 5 or 10 mg/kg after a barium-chloride muscle injury, muscle stem cell proliferation and fusion rose, regenerating fibers ended nearly twice the cross-sectional area of the controls, and peak torque of the treated muscle was about 70% higher (Neelakantan et al., Biochem Pharmacol 2019; PMID 30753815).
Where it goes — In mice, it was measured in plasma after IV, oral and subcutaneous doses, and after subcutaneous doses it reached fat, muscle and liver (Babula et al., 2024; PMID 39161060).
Not appetite — Obese mice given it lost weight without eating less (Neelakantan et al., 2018; Babula et al., 2024).

What the Research Shows

The entire peer-reviewed 5-Amino-1MQ literature is essentially one laboratory's research program plus a small number of citing reviews. The core papers — and the effect sizes they report — are:

Kraus 2014 (Nature; PMID 24717514) — Demonstrated that NNMT knockdown (antisense oligonucleotide) in white adipose tissue of DIO mice protects against diet-induced obesity. This is the foundational "NNMT as obesity target" paper and the rationale for pharmacologic NNMT inhibition. Does not use 5-Amino-1MQ but frames the target.
Neelakantan 2017 (J Med Chem; PMID 28548833) — Structure-activity relationship paper for small-molecule NNMT inhibitors. Describes the quinolinium scaffold SAR (enzyme IC50 around 1 µM) and how the inhibitors dock in the enzyme's nicotinamide-binding site. The membrane-permeability and cellular 1-MNA results came in the 2018 paper.
Neelakantan 2018 (Biochem Pharmacol; PMID 29155147) — The pivotal in vivo paper. C57Bl/6J male mice on a high-fat diet received 5-Amino-1MQ systemically for 11 days. Treated mice lost about 5% of their starting body weight over the 11 days while controls gained about 1%, epididymal white fat mass and size fell about 35%, adipocyte size fell more than 30%, and plasma total cholesterol was about 30% lower. Food intake was unchanged. Intracellular adipocyte NAD+ and SAM rose; 1-MNA fell. This is the single most-cited 5-Amino-1MQ study and the basis for essentially all downstream interest in the compound.
Babula 2024 (PMID 39161060) — Characterized plasma pharmacokinetics and tissue distribution of 5A1MQ after single IV (5 mg/kg) and oral (30 mg/kg) dosing and single/multiple subcutaneous dosing (25 mg/kg, once daily for 1 or 5 days) in C57Bl/6J mice. Extended the DIO mouse phenotype to include liver pathology improvements and characterized drug exposure in peripheral tissues. Validated NNMT inhibition as a pharmacologic approach to obesity-related metabolic dysfunction in the mouse.
Sampson 2021 (Sci Rep; PMID 33707534) and Dimet-Wiley 2022 (Sci Rep; PMID 35013352) — Same laboratory, same setup: 5-Amino-1MQ plus a switch from the high-fat diet to a lean one, in diet-induced obese mice. Sampson reports the pair beat the diet switch alone on body weight and fat loss, lean-mass-to-body-weight ratio, liver and epididymal white fat weight and hepatic steatosis, and brought body composition and liver fat to the levels of age-matched lean-diet controls, with a shifted adipose metabolome. Dimet-Wiley looked at the gut in that setting: the cecal microbiome of treated mice clustered apart from vehicle mice, with less Erysipelatoclostridium and more Lactobacillus. Mice, one laboratory, and a diet change doing part of the work.
Dimet-Wiley 2024 (Sci Rep; PMID 38969654) — Same laboratory, with a muscle group at the University of Kentucky. Mice aged 22 months got 5-Amino-1MQ once daily for eight weeks, with or without an intensive exercise program. Sedentary treated mice ended with about 40% more grip strength than sedentary controls; exercise alone gave about 20%; the two together about 60%. Grip strength in old mice, not a human outcome.
Two groups outside the originating laboratory — on the enzyme, not the compound — Liang 2024 (Aging Cell; PMID 38838088) picked NNMT out of skeletal-muscle transcriptomics as raised in sarcopenia, and reports that inhibiting it raised grip strength in aging mice and slowed the age-related fall in quadriceps mass index and whole-body lean mass, with muscle NAD+, PGC1α and p-AMPK up. Dong 2025 (Physiol Rep; PMID 41108586) found NNMT mRNA and protein raised in the gastrocnemius of patients with peripheral artery disease and persistently raised in the muscle stem cells of mice after hindlimb ischemia, and reports that an NNMT inhibitor improved ischemic muscle strength, power and total work without changing limb perfusion or capillary density. Neither paper prints the chemical name of the inhibitor it used, so both read as evidence about the enzyme rather than about this molecule, and neither touches the diet-induced-obesity phenotype.
Ulanovskaya / Cravatt / Campagna reviews — Multiple review articles frame NNMT as a target in obesity, cancer, fatty-liver disease, aging, and Alzheimer's, often citing the 5-Amino-1MQ SAR series as the pharmacological probe of choice. These are review articles, not independent efficacy replications.
Muscle / stem-cell line of work — The muscle line of work is three papers: the originating laboratory's own injury study in aged mice (Neelakantan 2019; PMID 30753815), its exercise study in 22-month-old mice (Dimet-Wiley 2024; PMID 38969654), and one paper on NNMT in the skeletal muscle of patients with COPD (Kim 2010; PMID 20110558). Two further groups report that inhibiting the enzyme improves muscle function in aging mice and in a mouse model of peripheral artery disease, without printing the chemical name of the inhibitor they used (Liang 2024; PMID 38838088, Dong 2025; PMID 41108586).

Critical Context — Single Lab, Mouse Only

Every peer-reviewed in vivo study of the obesity phenotype is from the Neelakantan / Watowich laboratory at University of Texas Medical Branch at Galveston; the one in vivo study of this compound from an independent group is a bladder-cancer mouse study (Yang 2024; PMID 39067875). There is no independent replication of the DIO-mouse body-composition phenotype from a different laboratory. No human trial has been registered, conducted, or published.

Human Data

There is no published human clinical trial of 5-Amino-1MQ. A ClinicalTrials.gov search for "5-amino-1-methylquinolinium," "5-Amino-1MQ," and "5A1MQ" returns no registered human studies (searched October 11, 2026).

No published human pharmacokinetics — All plasma-concentration data is from C57Bl/6J mice (Babula 2024). Whether the mouse subcutaneous or oral exposure translates proportionally to humans has not been established.
No published human safety database — There is no Phase I healthy-volunteer safety, tolerability, or maximum-tolerated-dose study. The absence of data is not evidence of absence of risk.
No published human efficacy data for any indication — Not for obesity, not for fatty liver, not for muscle preservation, not for NAD+ biology, not for any clinical endpoint.
Compounding pharmacy activity is not evidence — A compounding pharmacy dispensing 5-Amino-1MQ under a prescriber's signature does not constitute human clinical data. Pharmacy dispensing and FDA-recognized evidence are different phenomena.

Reconstitution & Storage

5-Amino-1MQ is sold as oral capsules by pharmacies and as powder in vials by research-chemical sellers. No label or guideline gives a strength, storage condition or shelf life for either.

Quaternary ammonium chemistry — The permanent positive charge on the ring nitrogen means 5-Amino-1MQ is very water-soluble as a salt. The counter-ion (typically chloride or iodide) depends on the synthesis route.

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Side Effects & Risks

Important

No person has taken 5-Amino-1MQ in a published study, so its effects in people are unknown (ClinicalTrials.gov and PubMed, searched October 4, 2026). Consult a licensed healthcare provider.

In the 11-day obesity study, the mice showed no observable adverse effects (Neelakantan et al., 2018); PubMed lists no toxicology study of the compound (searched October 4, 2026).

Methylation — NNMT's reaction uses up SAM, and in cancer cells high NNMT lowered histone methylation (Ulanovskaya et al., 2013). Whether blocking it shifts methylation elsewhere in the body is a theoretical question that no study cited here has measured.
NNMT outside fat — The liver makes the most NNMT; in mice, suppressing it there changed glucose and cholesterol metabolism (Hong et al., 2015). What blocking it does in the human liver has not been studied.
Cancer — NNMT is overexpressed in many human cancers, where it helps tumours form (Ulanovskaya et al., 2013). The cancer work with the compound itself points the other way. In cells, a group outside the originating laboratory tested 0.1–500 µM on HeLa cervical-cancer cells and reports that proliferation fell with concentration and time, while HEK-293 cells were apparently unaffected (Akar et al., J Obstet Gynaecol 2021; PMID 33645410). In mice, another group reports that NNMT in cancer-associated fibroblasts tracked non-response to PD-L1 blockade and worse prognosis in urothelial bladder cancer, and that 5-amino-1-methylquinolinium iodide cut tumor growth and added to the effect of an anti-PD-L1 antibody in their mouse models (Yang et al., J Immunother Cancer 2024; PMID 39067875). Cancer models, not people.
Pregnancy and breastfeeding — No reproductive toxicology study has been published (PubMed, searched October 4, 2026).
Drug interactions — Unstudied. NNMT methylates drugs and other foreign compounds; its activity in human liver varies two ways across people, which the paper that cloned it flagged as a possible source of differences in drug and xenobiotic toxicity (Aksoy et al., J Biol Chem 1994; PMID 8182091).
What is in a vial — 5-Amino-1MQ is sold as a research chemical and by pharmacies; no analysis of such products appears in the documents read for this page.
WADA status — Not named on the Prohibited List, but prohibited at all times under S0, non-approved substances, because no government has approved it for human therapeutic use (WADA Prohibited List 2026).

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for 5-Amino-1MQ, and no human has been studied. The mouse studies tracked body weight and fat mass, food intake and blood cholesterol (Neelakantan et al., 2018), and glucose tolerance, insulin, liver fat and liver enzymes (Babula et al., 2024). Homocysteine is a product of the reaction NNMT runs: adipocytes and adipose-tissue explants released it, and released less when treated with a different NNMT inhibitor, 1-methylnicotinamide (Riederer et al., Atherosclerosis 2009; PMID 18996527).

Commonly Stacked With

PubMed lists no study giving 5-Amino-1MQ with another peptide or weight-loss drug (searched October 4, 2026). In mice, the lab that made it has combined it with a switch to a lean diet (Sampson et al., 2021) and with exercise (Dimet-Wiley et al., 2024).

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Legal Status

Current Status — April 2026

5-Amino-1MQ is not FDA-approved for any indication. It has not entered human clinical trials, and no IND has been publicly disclosed. It is a research compound.

5-Amino-1MQ is not an ingredient of any FDA-approved drug, is not on FDA’s 503A or 503B bulks lists, is not in any of FDA’s nomination categories, and has no USP or NF drug monograph (FDA’s substance registry has no record of it). Section 503A allows compounding only from a substance with such a monograph, a component of an approved drug, or one on the 503A bulks list, so a pharmacy compounding 5-Amino-1MQ meets none of the conditions. A “USP-grade bulk powder” is not one of them.

5-Amino-1MQ is not named on the WADA Prohibited List 2026, but S0 prohibits it at all times: no government has approved it for human therapeutic use (WADA Prohibited List 2026).

5-Amino-1MQ is a small molecule, not a peptide; it was not among the 12 peptides FDA removed from Category 2 in April 2026, and FDA’s 503A categories list, updated May 14, 2026, does not name it (FDA 503A categories list, April 22 and May 14, 2026).

Cost & Access

5-Amino-1MQ is not approved for human use in the United States. It is available through research suppliers for laboratory research purposes only. Some pharmacies sell it on prescription, but it meets none of the conditions for compounding under section 503A or 503B.

Pricing and availability vary by provider, state, and prescription status. Kalios does not sell compounds.

Next Steps

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References

Neelakantan H, Brightwell CR, Graber TG, Maroto R, Wang HL, McHardy SF, Papaconstantinou J, Fry CS, Watowich SJ. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol. 2019;163:481-492. PMID: 30753815.
Neelakantan H, Wang HY, Vance V, Hommel JD, McHardy SF, Watowich SJ. Structure-Activity Relationship for Small Molecule Inhibitors of Nicotinamide N-Methyltransferase. J Med Chem. 2017;60(12):5015-5028. PMID: 28548833.
Neelakantan H, Vance V, Wetzel MD, Wang HL, McHardy SF, Finnerty CC, Hommel JD, Watowich SJ. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018;147:141-152. PMID: 29155147. (The pivotal in vivo DIO-mouse paper.)
Babula JJ, Bui D, Stevenson HL, Watowich SJ, Neelakantan H. Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes Obes Metab. 2024;26(11):5272-5282. PMID: 39161060. (Pharmacokinetic characterization of 5A1MQ after IV, oral, and SubQ dosing in DIO mice, plus extension of the efficacy phenotype.)
Sampson CM, Dimet AL, Neelakantan H, Ogunseye KO, Stevenson HL, Hommel JD, Watowich SJ. Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice. Sci Rep. 2021;11(1):5637. PMID: 33707534.
Dimet-Wiley A, Wu Q, Wiley JT, Eswar A, Neelakantan H, Savidge T, Watowich S. Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice. Sci Rep. 2022;12(1):484. PMID: 35013352.
Dimet-Wiley AL, Latham CM, Brightwell CR, Neelakantan H, Keeble AR, Thomas NT, Noehren H, Fry CS, Watowich SJ. Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. Sci Rep. 2024;14(1):15554. PMID: 38969654.
Akar S, Duran T, Azzawri AA, Koçak N, Çelik Ç, Yıldırım Hİ. Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells. J Obstet Gynaecol. 2021;41(8):1240-1245. PMID: 33645410. (Cell culture; a group outside the originating laboratory.)
Yang M, Wang B, Hou W, Zeng H, He W, Zhang XK, Yan D, Yu H, Huang L, Pei L, Li K, Qin H, Lin T, Huang J. NAD+ metabolism enzyme NNMT in cancer-associated fibroblasts drives tumor progression and resistance to immunotherapy by modulating macrophages in urothelial bladder cancer. J Immunother Cancer. 2024;12(7):e009281. PMID: 39067875. (Used 5-amino-1-methylquinolinium iodide in mouse tumor models.)
Liang R, Xiang Q, Dai M, Lin T, Xie D, Song Q, Liu Y, Yue J. Identification of nicotinamide N-methyltransferase as a promising therapeutic target for sarcopenia. Aging Cell. 2024;23(9):e14236. PMID: 38838088.
Dong G, Choi J, Li Y, Muller DC, Li Z, Luo YE, Ryan TE. Nicotinamide N-methyltransferase inhibition improves limb function in experimental peripheral artery disease. Physiol Rep. 2025;13(20):e70615. PMID: 41108586.
Kraus D, Yang Q, Kong D, Banks AS, Zhang L, Rodgers JT, Pirinen E, Pulinilkunnil TC, Gong F, Wang YC, Cen Y, Sauve AA, Asara JM, Peroni OD, Monia BP, Bhanot S, Alhonen L, Puigserver P, Kahn BB. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014;508(7495):258-262. PMID: 24717514. (Foundational target-validation paper.)
Pissios P. Nicotinamide N-Methyltransferase: More Than a Vitamin B3 Clearance Enzyme. Trends Endocrinol Metab. 2017;28(5):340-353. PMID: 28291578.
Kannt A, Pfenninger A, Teichert L, Tönjes A, Dietrich A, Schön MR, Klöting N, Blüher M. Association of nicotinamide-N-methyltransferase mRNA expression in human adipose tissue and the plasma concentration of its product, 1-methylnicotinamide, with insulin resistance. Diabetologia. 2015;58(4):799-808. PMID: 25596852.
Riederer M, Erwa W, Zimmermann R, Frank S, Zechner R. Adipose tissue as a source of nicotinamide N-methyltransferase and homocysteine. Atherosclerosis. 2009;204(2):412-417. PMID: 18996527.
Aksoy S, Szumlanski CL, Weinshilboum RM. Human liver nicotinamide N-methyltransferase. cDNA cloning, expression, and biochemical characterization. J Biol Chem. 1994;269(20):14835-14840. PMID: 8182091.
Campagna R, Pozzi V, Sartini D, Salvolini E, Brisigotti V, Molinelli E, Campanati A, Offidani A, Emanuelli M. Beyond Nicotinamide Metabolism: Potential Role of Nicotinamide N-Methyltransferase as a Biomarker in Skin Cancers. Cancers (Basel). 2021;13(19):4943. PMID: 34638427.
Roberti A, Fernández AF, Fraga MF. Nicotinamide N-methyltransferase: At the crossroads between cellular metabolism and epigenetic regulation. Mol Metab. 2021;45:101165. PMID: 33453420.
Ulanovskaya OA, Zuhl AM, Cravatt BF. NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink. Nat Chem Biol. 2013;9(5):300-306. PMID: 23455543.
Komatsu M, Kanda T, Urai H, Kurokochi A, Kitahama R, Shigaki S, Ono T, Yukioka H, Hasegawa K, Tokuyama H, Kawabe H, Wakino S, Itoh H. NNMT activation can contribute to the development of fatty liver disease by modulating the NAD+ metabolism. Sci Rep. 2018;8(1):8637. PMID: 29872122.
Hong S, Moreno-Navarrete JM, Wei X, Kikukawa Y, Tzameli I, Prasad D, Lee Y, Asara JM, Fernandez-Real JM, Maratos-Flier E, Pissios P. Nicotinamide N-methyltransferase regulates hepatic nutrient metabolism through Sirt1 protein stabilization. Nat Med. 2015;21(8):887-894. PMID: 26168293.
Brightwell CR, Latham CM, Thomas NT, Keeble AR, Murach KA, Fry CS. A glitch in the matrix: the pivotal role for extracellular matrix remodeling during muscle hypertrophy. Am J Physiol Cell Physiol. 2022;323(3):C763-C771. PMID: 35876284. (Extracellular-matrix remodeling in loaded muscle; shares authors with the NNMT muscle work but reports no NNMT result.)
FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances. wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. Read October 3, 2026.