As of current scientific literature, zero published 5-amino-1-methylquinolinium clinical trials in humans exist in peer-reviewed medical databases. The compound remains exclusively an experimental small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) restricted to in vitro and preclinical animal research models.
As of current scientific literature, zero published 5-amino-1-methylquinolinium clinical trials in humans exist in peer-reviewed medical databases. The compound remains exclusively an experimental small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT) restricted to in vitro and preclinical animal research models.
A rigorous audit of clinical trials registries, including ClinicalTrials.gov and the WHO International Clinical Trials Registry Platform (ICTRP), confirms that there are no published or ongoing 5-amino-1-methylquinolinium clinical trials in humans. 5-Amino-1-methylquinolinium (commonly referred to in biochemical literature as 5-Amino-1MQ) has not received investigational new drug (IND) authorization from the United States Food and Drug Administration (FDA) or international regulatory equivalents. Consequently, no clinical safety profile, pharmacokinetic data in human subjects, or therapeutic dosage ranges exist.
All available empirical data regarding the physiological impacts of this membrane-permeable quinolinium derivative originate from preclinical rodent models, ex vivo tissue assays, and primary cell culture systems. Laboratory investigators evaluating 5-amino-1-methylquinolinium research compounds must contextualize all reported metabolic outcomes—such as accelerated lipolysis and enhanced basal metabolic rate—strictly within controlled experimental designs rather than human clinical applications.
Nicotinamide N-methyltransferase (NNMT) is a cytosolic enzyme responsible for catalyzing the methylation of nicotinamide (NAM) and other pyridines using S-adenosylmethionine (SAM) as the universal methyl donor. This reaction yields 1-methylnicotinamide (1-MNA) and S-adenosylhomocysteine (SAH). In metabolic research, elevated NNMT activity is associated with depleted intracellular nicotinamide adenine dinucleotide (NAD+) pools and compromised mitochondrial oxidative phosphorylation, particularly within white adipose tissue (WAT) and liver parenchymal cells.
5-Amino-1MQ functions as a selective, membrane-permeable small-molecule inhibitor of NNMT. By competitive binding at the catalytic substrate pocket, 5-Amino-1MQ suppresses the conversion of NAM to 1-MNA. Preclinical assays demonstrate that blocking this enzymatic pathway prevents the irreversible clearance of nicotinamide, thereby directing NAM back into the NAD+ salvage pathway via nicotinamide phosphoribosyltransferase (NAMPT). This flux increase raises intracellular NAD+ availability, enhancing Sirtuin-1 (SIRT1) signaling and boosting downstream mitochondrial biogenesis.
In vivo rodent models evaluating diet-induced obesity (DIO C57BL/6J mice) demonstrate that systemic administration of 5-Amino-1MQ yields measurable shifts in systemic energy expenditure without requiring dietary restriction. Preclinical studies indicate a reduction in adipocyte volume and overall fat mass in treated animal cohorts compared to vehicle controls. These phenotypical changes correlate directly with increased expression of genes involved in fatty acid oxidation, including carnitine palmitoyltransferase-1 (CPT-1) and uncoupling protein-1 (UCP-1).
In vitro oxygen consumption rate (OCR) assays using extracellular flux analyzers reveal that 5-Amino-1MQ treatment restores basal mitochondrial respiration in high-fat cultured 3T3-L1 adipocytes. Researchers exploring cellular energy fluxes cross-reference these findings with broader NAD+ pathway research compounds to determine how direct NNMT blockade compares against generalized NAD+ supplementation strategies.
When designing protocols targeting mitochondrial efficiency and lipid utilization, researchers routinely contrast 5-Amino-1MQ against established mitochondrial peptides and secretagogues. While 5-Amino-1MQ operates via small-molecule enzymatic inhibition of NNMT, alternative peptide candidates target distinct receptor networks or mitochondrial open reading frames.
For example, the mitochondrial-derived peptide MOTS-c modulates the folate cycle and activates AMPK, influencing metabolic homeostasis through gene transcription in response to metabolic stress. Conversely, lipid-cleaving compounds like AOD9604 act as modified C-terminal fragments of human growth hormone, stimulating lipolysis via adrenergic mechanisms without perturbing the NAD+ salvage network. Growth hormone secretagogues such as Tesamorelin or CJC-1295 DAC act upstream on the pituitary axis. Selecting the appropriate model depends on whether the laboratory objective requires direct NNMT pathway modulation, peptide-receptor signaling, or mitochondrial genome regulation.
To ensure precise molar calculations in cell culture media and biochemical assays, laboratory personnel must reference verified chemical parameters. 5-Amino-1-methylquinolinium is typically supplied as a iodide or chloride salt to preserve stability and water solubility in aqueous buffers.
• Chemical IUPAC Name: 5-amino-1-methylquinolin-1-ium • Molecular Formula: C10H11N2+ • Molecular Weight: 159.21 g/mol (cationic form) • CAS Registry Number: 42464-96-0 • Physical Form: Crystalline solid / Lyophilized salt • Recommended Solvent: Dimethyl sulfoxide (DMSO) or sterile phosphate-buffered saline (PBS) • Storage Temperature: -20°C (desiccated, protected from light)
Because small-molecule inhibitors are frequently utilized in high-throughput enzymatic screens and quantitative cell assays, analytical purity is critical to eliminate batch-to-batch variation and false-positive data. High-performance liquid chromatography (HPLC) coupled with mass spectrometry (MS) serves as the benchmark quality verification protocol.
PX1 Research enforces stringent quality control measures for all incoming batches. Every lot undergoes independent analytical testing at an ISO 17025-accredited laboratory, confirming high chemical purity (typically ≥98.0% by RP-HPLC peak area integration) and structural identity via electrospray ionization mass spectrometry (ESI-MS). Furthermore, reagents undergo chromogenic LAL assays to verify endotoxin levels remain below strict thresholds (<0.01 EU/mg), preventing confounding inflammatory responses in sensitive cell lines or rodent models. All orders ship directly from US-based facilities in California and Arizona with lot-specific Certificate of Analysis (COA) access.
For in vitro cellular assays, 5-Amino-1MQ solid should be reconstituted under sterile laminar flow conditions. Dimethyl sulfoxide (DMSO) is the preferred primary solvent for preparing high-concentration stock solutions (e.g., 10 mM to 50 mM). After complete dissolution in DMSO, working stocks can be diluted into culture media (such as DMEM or RPMI-1640), maintaining final DMSO vehicle concentrations below 0.1% v/v to eliminate organic solvent toxicity.
Stock solutions prepared in DMSO should be aliquoted into sterile microcentrifuge tubes to avoid repeated freeze-thaw cycles and stored at -80°C. Working concentrations reported in peer-reviewed in vitro literature range from 1 µM to 50 µM, depending on the exposure duration and the NNMT expression density of the specific cell line under evaluation.
Procurement officers and principal investigators seeking reliable supply chains for analytical grade compounds can review documentation standardizations via our centralized PX1 Research database. Institutional laboratories requiring high-volume reagents for longitudinal animal studies or high-throughput assay screening can establish bulk research accounts to access standardized batch testing, dedicated account management, and bulk lot reservation.
Are there any published 5-amino-1-methylquinolinium clinical trials in humans?
No. As of current peer-reviewed literature and clinical registry databases, zero human clinical trials have been conducted or published for 5-amino-1-methylquinolinium. The compound is strictly an experimental small molecule limited to preclinical animal and in vitro laboratory research.
What is the primary mechanism of action of 5-amino-1-methylquinolinium?
5-Amino-1-methylquinolinium acts as a selective inhibitor of nicotinamide N-methyltransferase (NNMT). By blocking NNMT activity, it prevents the methylation of nicotinamide to 1-methylnicotinamide, thereby preserving intracellular nicotinamide pools and promoting NAD+ synthesis via the salvage pathway.
How does 5-amino-1MQ raise NAD+ levels in cellular assays?
NNMT normally consumes nicotinamide (NAM) and S-adenosylmethionine (SAM). By inhibiting NNMT, 5-amino-1MQ prevents the clearance of NAM, allowing nicotinamide phosphoribosyltransferase (NAMPT) to convert NAM back into NMN and subsequently NAD+.
Is 5-amino-1-methylquinolinium approved by the FDA?
No. 5-Amino-1-methylquinolinium is not approved by the FDA or any global regulatory agency for human or veterinary use. It is designated solely as a laboratory research chemical.
What analytical testing is performed on PX1 Research 5-amino-1MQ?
Every lot undergoes Reverse-Phase High-Performance Liquid Chromatography (RP-HPLC) for purity determination (≥98.0%) and Electrospray Ionization Mass Spectrometry (ESI-MS) for identity verification. Products are also tested for endotoxin levels via chromogenic LAL testing in an ISO 17025 accredited laboratory.
What solvents are recommended for reconstituting 5-amino-1MQ powder?
For in vitro protocols, stock solutions are best prepared using research-grade Dimethyl Sulfoxide (DMSO). Once dissolved, aliquots can be diluted into aqueous buffers or cell culture media immediately prior to application, keeping solvent concentrations non-toxic to cells.
How should 5-amino-1MQ be stored upon receipt?
Lyophilized or crystalline 5-amino-1MQ solid should be stored at -20°C in a desiccated environment protected from direct light. Liquid DMSO stock solutions should be stored in single-use aliquots at -80°C.
How does 5-amino-1MQ compare to MOTS-c in fat metabolism models?
5-Amino-1MQ is a synthetic small-molecule NNMT inhibitor that functions by elevating intracellular NAD+ pools. MOTS-c is a mitochondria-derived peptide that activates the AMPK pathway. Both are studied in metabolic research, but operate via entirely distinct biochemical signaling cascades.
What are the endotoxin limits for PX1 Research compounds?
PX1 Research compounds undergo strict endotoxin testing to ensure levels remain below <0.01 EU/mg, minimizing inflammatory interference in cell culture assays and preclinical models.
Where are PX1 Research compounds manufactured and shipped from?
All PX1 Research compounds are manufactured in US-based GMP-compliant facilities and shipped directly from fulfillment centers in California and Arizona with same-day shipping available Monday through Friday.
All products are sold strictly for laboratory and research use only. Not for human or veterinary use, diagnosis, treatment or consumption. Statements have not been evaluated by the FDA.