Comparisons

5-Amino-1MQ vs SLU-PP-332: Inhibitor versus Agonist in Metabolic Research

Two compounds shelved side by side in metabolic catalogues turn out to share almost nothing at the molecular level — one switches an enzyme off, the other switches a receptor program on.

In short

5-Amino-1MQ and SLU-PP-332 are unrelated metabolic-research tool compounds. 5-Amino-1MQ is a small-molecule NNMT inhibitor probing NAD+ and methyl-donor biology; SLU-PP-332 is a pan-ERRalpha/beta/gamma nuclear-receptor agonist studied as an exercise mimetic for mitochondrial gene programs. Different targets, opposite logic, distinct chemistry. For research use only.

5-Amino-1MQ vs SLU-PP-332: Inhibitor versus Agonist in Metabolic Research

Catalogue them side by side and they look like rivals; read their mechanisms and they barely belong in the same conversation. 5-Amino-1MQ shuts an enzyme down. SLU-PP-332 switches a receptor program on. One subtracts, the other adds — and that single inversion of logic is the whole story.

Both compounds appear together in metabolic and mitochondrial research catalogues, which invites a direct comparison. In practice they share almost nothing at the molecular level: they engage different targets, act through opposite logic — enzyme inhibition versus nuclear-receptor activation — and have distinct chemistry. This comparison is framed strictly for in vitro and laboratory research use only (RUO). Nothing here describes human use, dosing, or therapeutic outcomes; all mechanisms are characterised as preclinical cell-culture and animal findings.

What is 5-Amino-1MQ in research terms?

5-Amino-1MQ (5-amino-1-methylquinolinium; CAS 685079-15-6) is a small-molecule, membrane-permeable inhibitor of nicotinamide N-methyltransferase (NNMT). The interest is positional: NNMT consumes both nicotinamide, an NAD+ precursor, and S-adenosylmethionine (SAM), the universal methyl donor, placing the enzyme at the intersection of two cellular budgets — the NAD+ pool and the methylation pool. In high-fat-diet mouse models, selective NNMT inhibitors of this chemotype were reported to reduce adiposity,1 and genetic NNMT knockdown produced a comparable protective phenotype,2 establishing the enzyme as a metabolic-research target. That dual budget is what makes NNMT compelling as a probe: inhibit it, and a researcher is nominally tugging on NAD+ availability and methyl-group flux at once. 5-Amino-1MQ has since become a widely cited chemical probe used to interrogate NNMT across adipocyte-energy, fibrosis, and tumour-stroma models,345 with the enzyme increasingly examined as a regulator in hepatocellular-carcinoma metabolism.10 The throughline is consistent: NNMT is treated as a node where energy currency and epigenetic substrate meet, and 5-Amino-1MQ is the reagent used to perturb it.

What is SLU-PP-332 in research terms?

SLU-PP-332 (CAS 303760-60-3) is a synthetic pan-agonist of the estrogen-related receptors ERRalpha, ERRbeta and ERRgamma — orphan nuclear receptors that act as transcriptional master switches for oxidative, mitochondria-rich metabolism. By engaging all three ERR isoforms, SLU-PP-332 is studied as an exercise mimetic: in cell and rodent models it induced an ERRalpha-dependent acute aerobic-exercise transcriptional response and altered exercise-capacity and metabolic endpoints,67 and the receptor-pharmacology rationale has been reviewed more broadly.9 The chemotype continues to be developed, with newer orally characterised ERR agonists such as SLU-PP-915 extending the series.8 Where 5-Amino-1MQ removes an enzymatic constraint, SLU-PP-332 recruits a transcriptional program — it does not block a single reaction but biases the cell toward the broad oxidative, mitochondria-rich gene set the ERR receptors govern. Critically, this is an activator of a receptor program, not an enzyme inhibitor, and that distinction propagates through every downstream readout a researcher might design around it.

The comparison collapses to a single contrast: one compound takes a brake off methylation and NAD+ chemistry, the other puts a foot on the mitochondrial accelerator.

How do the two compounds differ side by side?

Attribute 5-Amino-1MQ SLU-PP-332
Chemical class Small-molecule quinolinium (NNMT inhibitor) Small-molecule pan-nuclear-receptor agonist
Molecular target Nicotinamide N-methyltransferase (NNMT enzyme) Estrogen-related receptors ERRα/β/γ
Mechanism investigated (preclinical) Enzyme inhibition — modulates NAD+/SAM (methyl-donor) pools Receptor activation — drives oxidative/mitochondrial gene programs
Formula / CAS C10H11N2+ (iodide salt) · CAS 685079-15-6 C18H14N2O2 · CAS 303760-60-3
Molecular weight 159.21 g/mol 290.32 g/mol
Solubility Soluble in water and DMSO Soluble in DMSO
Research themes Adipocyte energy, fibrosis/ageing, tumour-stroma metabolism Endurance/oxidative metabolism, fatty-acid handling, doping-control analysis
Condor formats 10 mg vial (≥99% HPLC) · 60 caps, 50 mg (≥98% HPLC) 5 mg vial (≥99% HPLC) · 60 caps, 500 mcg/1 mg (≥98% HPLC)
Characterisation Third-party tested, COA available, EU warehoused Third-party tested, COA available, EU warehoused

Side-by-side identity, mechanism and format specifications for the two compounds as supplied for research use.

131 g/mol separate the two molecules — 159.21 for 5-Amino-1MQ against 290.32 for SLU-PP-332 — a reminder that nothing about their chemistry is shared.

Which format suits which research question?

Both compounds are offered in two formats. The lyophilised or powder vial — 5-Amino-1MQ at 10 mg; SLU-PP-332 at 5 mg, DMSO-soluble — suits in vitro work where a defined stock concentration is reconstituted by the investigator. The HPMC capsule format provides a fixed, pre-portioned quantity of reference material per unit, with 5-Amino-1MQ at 50 mg and SLU-PP-332 in 500 mcg and 1 mg research tiers, and no reconstitution. Capsule purity is specified at ≥98% (HPLC) and vial purity at ≥99% (HPLC). Format selection is a handling and study-design choice for the researcher; it does not imply any route of administration, and neither product is intended for human or animal consumption.

Is the evidence clinical or preclinical?

Honest appraisal: the evidence for both compounds is preclinical. The findings cited here come from cell-culture and rodent studies. For 5-Amino-1MQ, the NNMT-inhibition and anti-obesity signals derive from mouse high-fat-diet models1 and supporting genetic-knockdown work in mice,2 with newer reports extending NNMT inhibition into fibrosis and oncology models.345 For SLU-PP-332, the exercise-mimetic and metabolic-syndrome data are from in vitro reporter assays and rodent studies,67 with the receptor-pharmacology rationale reviewed more broadly.9 Neither compound has established efficacy or safety in humans, and no controlled human clinical trials define a therapeutic role for either. Researchers should treat both strictly as experimental tool compounds.

Because both sit firmly in the preclinical column, reproducibility rests on knowing exactly what is in the vial or capsule. Both are supplied strictly for research use only — not a drug, supplement, food, or cosmetic — and each batch ships with a third-party Certificate of Analysis. Where a study turns on a clean mechanistic readout, that COA and the underlying HPLC and mass-spectrometric identity and purity data are the difference between a result and an artefact.

The takeaways
  • Opposite logic: 5-Amino-1MQ inhibits the enzyme NNMT, whereas SLU-PP-332 activates the ERRalpha/beta/gamma nuclear receptors.
  • Distinct targets and chemistry — an NNMT inhibitor sitting at the NAD+/SAM crossroads versus a transcriptional master switch for oxidative metabolism.
  • They are not interchangeable: choose 5-Amino-1MQ for methylation- and NAD+-pool questions, SLU-PP-332 for mitochondrial and oxidative gene programs.
  • Both are strictly preclinical — the supporting data come from cell-culture and rodent studies, with no controlled human trials for either.
  • Both are supplied as vials and HPMC capsules, third-party tested with a batch-specific Certificate of Analysis and EU warehoused.
  • Neither is a drug, supplement, food, or cosmetic; both are experimental tool compounds for research use only.
Reference data
CAS number
685079-15-6
Molecular formula
C₁₀H₁₁N₂⁺
Molecular weight
159.21
Purity
≥99% (HPLC)
Presentation
10mg/vial
Storage
Store at -20°C, protect from light
Frequently asked
Are 5-Amino-1MQ and SLU-PP-332 the same kind of compound?

No. They are mechanistically unrelated. 5-Amino-1MQ is an enzyme inhibitor that blocks NNMT, affecting NAD+ and SAM pools, while SLU-PP-332 is a nuclear-receptor agonist that activates the ERRalpha, ERRbeta and ERRgamma transcription factors. They differ in target, mechanism (inhibition versus activation), and chemistry. Both are studied only in vitro and in animal models.

5-Amino-1MQ vs SLU-PP-332: which is better for research?

Neither is universally better. The choice depends entirely on the research question, framed strictly for research use only. 5-Amino-1MQ is the appropriate probe for NNMT, NAD+ and methylation-pool biology; SLU-PP-332 is appropriate for ERR-driven mitochondrial and oxidative-metabolism gene programs. They are not interchangeable, and we make no human-use or efficacy claims for either.

What targets do these compounds act on?

5-Amino-1MQ inhibits nicotinamide N-methyltransferase (NNMT), an enzyme that consumes nicotinamide and the methyl donor SAM. SLU-PP-332 is a pan-agonist of the estrogen-related receptors ERRalpha, ERRbeta and ERRgamma, orphan nuclear receptors governing mitochondrial and oxidative metabolism. These are entirely distinct molecular targets.

Is the evidence for either compound clinical or preclinical?

Strictly preclinical. The published data for both come from cell-culture and rodent studies, for example mouse high-fat-diet models for 5-Amino-1MQ and rodent exercise-capacity models for SLU-PP-332. No controlled human clinical trials establish efficacy or safety for either compound. They are experimental tool compounds only.

What formats and purity does Condor Research supply?

5-Amino-1MQ is available as a 10 mg vial (≥99% HPLC) and as 60 HPMC capsules at 50 mg (≥98% HPLC). SLU-PP-332 is available as a 5 mg vial (≥99% HPLC, DMSO-soluble) and as 60 HPMC capsules in 500 mcg and 1 mg research tiers (≥98% HPLC). All are third-party tested with a Certificate of Analysis and EU warehoused.

Can these compounds be combined in research?

Some metabolic-research designs use NNMT inhibitors and ERR agonists as orthogonal probes of overlapping mitochondrial and NAD+ biology, but any combination is an experimental design decision for the investigator and must remain in vitro or in validated animal models. We provide no dosing, administration, or combination protocols, and make no human-use claims.

References
1Neelakantan H, Vance V, Wetzel MD, et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018 Jan;147:141-152. link
2Kraus D, Yang Q, Kong D, et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014 Apr 10;508(7495):258-262. link
3Akar S, Duran T, Azzawri AA, et al. Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells. J Obstet Gynaecol. 2021 Nov;41(8):1240-1245. link
4Yang M, Wang B, Hou W, et al. 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 Jul 27;12(7):e009281. link
5Ren N, Li R, Tao Q, et al. Nicotinamide N-Methyltransferase Inhibition Mitigates Cerulein-Induced Pancreatic Fibrosis via Galectin-3-Mediated Regulation of Stellate Cell Activation and Macrophage M2 Polarization in Mice. Inflammation. 2026;49(1):135. link
6Billon C, Sitaula S, Banerjee S, et al. Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity. ACS Chem Biol. 2023 Apr 21;18(4):756-771. link
7Billon C, Schoepke E, Avdagic A, et al. A Synthetic ERR Agonist Alleviates Metabolic Syndrome. J Pharmacol Exp Ther. 2024 Jan 17;388(2):232-240. link
8Billon C, Appourchaux K, Côté I, et al. An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity. J Pharmacol Exp Ther. 2026 Jan;393(1):103787. link
9de Souza-Lima J, Astrosa-Martin BD, Galaz-Rodríguez CA, et al. [Pharmacological Activation of ERRα/β/γ as an Exercise Mimetic: Potential Therapeutic Applications]. Rev Med Chil. 2026 Feb;154(2):237-245. link
10Prajapati S, Yadav S, Singh AP, et al. Nicotinamide N-Methyltransferase (NNMT): A Central Regulator in Hepatocellular Carcinoma Metabolism and Therapeutic Targeting - A Systematic Review. Curr Drug Metab. 2026 Jun 4. link
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