BAM-15 25 mg 60 capsules/units

BAM-15 25 mg – 60 capsules of a mitochondrial uncoupler for laboratory research

Research reagent for laboratory use only. Not for human or veterinary use, diagnostic, or therapeutic purposes.

BAM-15 is an experimental chemical substance from the class of protonophoric mitochondrial uncouplers. It is not registered as a medicine by the EMA, FDA or any other major regulatory authority. It is not a food product – EFSA has not authorized it in this category. This product is sold exclusively as a chemical reagent for in vitro laboratory research and in vivo animal-model research. It is not intended for human consumption, administration to companion animals or any clinical use. Purchase only for qualified research personnel.

Mitochondrial proton uncouplers are a class of molecules that has attracted attention in metabolic pharmacology since the 1930s. The mechanism is elegant in its simplicity: an uncoupler makes the mitochondrial membrane permeable to protons, and the energy from substrate oxidation that would normally drive ATP synthesis is dissipated as heat. To maintain ATP levels, the cell burns more substrate. The same thermodynamic simplicity made 2,4-dinitrophenol (DNP) a lethally dangerous weight-loss drug, banned by the FDA as early as 1938 due to hyperthermia, cataracts and deaths.

BAM-15 is a molecule designed in 2014 as a mild uncoupler with mitochondrial selectivity and a wider safety window in preclinical models. Preclinical animal studies have used BAM-15 to examine body-mass, glucose-handling and hepatic-lipid endpoints in obesity and NAFLD/MASH models – alongside thermal-safety observations relevant to the classical uncoupler class. However, it remains an experimental substance with limited clinical data in humans, offered only as a research reagent.

What is BAM-15 – pharmacological class

Full chemical name: (2-fluorophenyl)-{6-[(2-fluorophenyl)amino]-1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl}-amine.

Pharmacological class: protonophoric mitochondrial uncoupler (proton uncoupler of mitochondrial respiration).

Molecular mechanism: BAM-15 transports protons across the inner mitochondrial membrane, bypassing ATP synthase (complex V). The respiratory chain continues to pump protons into the intermembrane space, but with BAM-15 they return to the matrix without generating ATP. The cell compensates for this deficit by increasing oxygen consumption and the oxidation of fatty acids and glucose.

Mitochondrial selectivity – the difference versus DNP: the key feature of BAM-15 reported in preclinical studies is its preferential action at the mitochondrial membrane. DNP also uncouples other biological membranes (plasma and lysosomal membranes), which translates into systemic consequences once the narrow therapeutic window is exceeded. In animal models, BAM-15 did not cause a marked increase in core temperature even at metabolically active doses.

Reagent characteristics

Mechanism of action in preclinical research

In animal models, BAM-15 affects several axes of energy metabolism that are treated as separate therapeutic targets in obesity pharmacology.

Increased oxygen consumption and substrate oxidation. Uncoupling oxidative phosphorylation forces cells – especially cells with high mitochondrial density (hepatocytes, myocytes and brown adipose tissue) – to intensify respiration. In rodent models fed a high-fat diet (HFD), increased resting energy expenditure has been reported.

AMPK activation. The drop in the ATP/AMP ratio caused by uncoupling ATP synthesis activates AMP-activated protein kinase (AMPK) – the central energy sensor of the cell. AMPK shifts metabolism toward catabolism: it increases fatty-acid oxidation, inhibits de novo lipogenesis and modifies insulin signaling. The same biochemical concept – AMPK as a central node of energy metabolism – explains research interest in the mitochondrial peptide MOTS-c as an alternative research reagent for the AMPK axis.

Models of obesity and hepatic steatosis. Mouse studies have reported changes in body-mass, glucose-handling and hepatic triglyceride endpoints in NAFLD/MASH models (non-alcoholic fatty liver disease / metabolic dysfunction-associated steatohepatitis). These observations are the basis for interest in BAM-15 as a laboratory research candidate in metabolic-disease models.

The cited papers include Kenwood et al. (2014), describing the discovery of BAM-15, Alexopoulos et al. (2020), covering obesity models, and Goedeke et al. (2019), covering NAFLD/MASH models – full bibliographic details are provided in the References section. All data come from animal models and cell cultures – translating these observations to human physiology remains a working hypothesis, not an established fact.

BAM-15 vs DNP – a safer uncoupler from a preclinical perspective

Comparison with DNP is unavoidable and scientifically relevant because both compounds act within the same mechanistic class.

DNP (2,4-dinitrophenol). A classical uncoupler briefly used as a weight-loss drug in the 1930s, banned by the FDA in 1938 after a series of deaths caused by malignant hyperthermia. Its uncoupling activity involves plasma membranes in many cell types, leading to a rapid systemic increase in heat production. A narrow therapeutic window, accumulation with repeated administration and cataract risk made DNP unsuitable as a medicine.

BAM-15. Designed de novo as a mild uncoupler with preference for the mitochondrial membrane. In rodent models, substantial separation has been reported between metabolically effective doses and toxic doses – LD50 is markedly higher than the effective dose.

The limit of this narrative. The safety profile of BAM-15 is described almost exclusively in preclinical studies. Publicly available phase II/III human data did not exist at the time this description was prepared. Any claim that “BAM-15 is safe in humans” goes beyond the current evidence base – the substance remains a research tool.

Research context and laboratory endpoints

• HFD obesity models in rodents – measurements of body weight, body composition, energy expenditure and plasma lipid profile.
• NAFLD/MASH models – assessment of hepatic triglyceride content, steatosis markers and inflammatory profile.
• Insulin-sensitivity research – glucose tolerance tests (GTT), insulin tolerance tests (ITT) and euglycemic-hyperinsulinemic clamps. Complementary to the incretin axis – GLP-1 analogues such as Sema G PEN and tri-agonists such as Triple G PEN act on different axes of glycemic regulation.
• In vitro bioenergetics experiments – OCR (oxygen consumption rate) and ECAR (extracellular acidification rate) measurements on platforms such as Seahorse, and thermogenesis studies in brown-adipose-tissue cultures.
• Comparative pharmacology of uncouplers – BAM-15 as a reference mild uncoupler in comparative studies with DNP, FCCP or CCCP.

One Peptides quality specification

• HPLC purity ≥98% – high-performance liquid chromatography.
• MS structural confirmation – mass spectrometry for each batch.
• Certificate of Analysis (COA) per batch – available to the purchaser.
• Batch traceability – full batch identification.
• Cold chain 2-8°C – refrigerated transport and storage. After receipt, capsules should be stored in a refrigerator in the original packaging, protected from light and moisture.
• Stability – BAM-15 powder in capsules is stable when the cold chain is maintained. Working solutions in DMSO prepared by the researcher should be stored according to standard practice for small lipophilic molecules.

Details of the QA process and each control stage are described in HPLC/COA methodology & batch lookup.

Working with capsules in a laboratory protocol

The capsule form was selected to make it easier to handle microdoses of powder under laboratory conditions – each capsule contains a weighed portion of approximately 417 µg BAM-15, eliminating the need to use an analytical balance for every prepared sample.

Typical laboratory workflow:

• Removing capsule contents – open the capsule and transfer the powder into an Eppendorf tube or a weighed vial.
• Primary solvent – BAM-15 is lipophilic; the standard stock solvent in cell-culture work is DMSO (commonly a 10 mM stock).
• Working concentrations – in cell cultures, submicromolar to low micromolar ranges are used; details depend on the cell line and readout (Seahorse, viability, signaling).
• In vivo models – rodent studies have reported administration in diets supplemented with BAM-15 or in gavage solutions; details should always follow the protocol approved by the ethics committee.
• Oral bioavailability – reported as limited in animal models, which remains one of the main pharmacokinetic challenges for this class.

This is not an instruction for human use. The above information applies only to laboratory handling of the reagent in authorized research units.

Regulatory status – research reagent

BAM-15 as a medicine. BAM-15 is not registered by the European Medicines Agency (EMA), U.S. Food and Drug Administration (FDA), Pharmaceuticals and Medical Devices Agency (PMDA, Japan), Therapeutic Goods Administration (TGA, Australia) or any other major jurisdiction. The substance remains at the preclinical / early-clinical development stage.

BAM-15 as a food product. EFSA (European Food Safety Authority) has not authorized BAM-15 under any framework for food products or novel food ingredients. The substance does not fall under the dietary-supplement regulatory framework in the European Union.

Market status: chemical reagent for laboratory research (Research Use Only – RUO). Sales are intended for scientific units, pharmacology laboratories and qualified researchers.

WADA. BAM-15 (BAM15) is named on the World Anti-Doping Agency Prohibited List for 2026 — section S4.4.1 (metabolic modulators, AMPK activators). It is prohibited at all times, in and out of competition. Athletes and individuals subject to anti-doping programs should check the current version of the List, which is updated every year.

Frequently asked questions (FAQ)

How does BAM-15 differ from DNP?

Both compounds belong to the mitochondrial uncoupler class. DNP also uncouples other cellular membranes and has a narrow therapeutic window – it has been banned as a medicine since 1938 because of hyperthermia and deaths. BAM-15 was designed as a mild uncoupler with mitochondrial preference and a wider safety window in animal models. The advantage of BAM-15 remains preclinical, however – human data are limited.

Is BAM-15 registered as a medicine?

No. BAM-15 is not registered by the EMA, FDA or any other major regulatory agency. It remains a substance at the preclinical and early-clinical research stage.

Is BAM-15 a food product?

No. EFSA has not authorized BAM-15 as a food ingredient or food product. In the European market, BAM-15 does not meet the definition of a food product and does not fall under that regulatory framework.

What are the limitations of current preclinical research?

Most data come from animal models (mainly mice on an HFD diet) and cell cultures. Translating metabolic observations from rodent models to human physiology is a hypothesis that requires clinical validation. Human pharmacokinetics, optimal therapeutic exposure, long-term safety and interactions remain insufficiently studied areas.

Are there phase I/II clinical data in humans?

Early clinical phases are reported as ongoing or planned by entities developing BAM-15 as a drug candidate. Publicly available, peer-reviewed phase II/III human data were not available at the time this description was prepared. Full assessment of safety and efficacy in humans requires completion of the clinical pathway.

Is BAM-15 on the WADA list?

Yes. BAM-15 (BAM15) is named on the WADA Prohibited List for 2026 — section S4.4.1 (metabolic modulators, AMPK activators). It is prohibited at all times, in and out of competition. The List is updated every year — any athlete or researcher subject to an anti-doping program should check its current version.

References

1. Kenwood BM et al. (2014). Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane
2. Alexopoulos SJ et al. (2020). Mitochondrial uncoupler BAM-15 reverses diet-induced obesity and insulin resistance in mice
3. Goedeke L et al. (2019). Controlled-release mitochondrial protonophore (CRMP) reverses dyslipidemia and hepatic steatosis in dysmetabolic nonhuman primates
4. Kalinovich AV, Shabalina IG (2015). Novel mitochondrial cationic uncoupler C4R1 is an effective treatment for combating obesity in mice

The product One-Peptides BAM-15 25 mg – 60 capsules is sold exclusively as a chemical reagent for in vitro laboratory research and animal-model studies. It is not a medicine, not a food product and not a product intended for human consumption. It is not intended to diagnose, treat, mitigate or prevent any disease. Sales are intended for qualified research personnel, scientific units and pharmacology laboratories. The purchaser assumes full responsibility for lawful and safe use of the reagent under laboratory conditions compliant with applicable regulations and institutional guidelines.