Research Use Only: This product is supplied for laboratory research and in-vitro studies. Not for human or veterinary administration.
BAM15 (15mg) 60 capsules
- Mitochondrial Uncoupler: Selective protonophore (C₁₆H₁₀F₂N₆O), ≥98% purity
- AMPK Activation: 1,000-fold greater potency than metformin per unit concentration
- Metabolic Research: 50+ publications since 2014, validated in Nature Communications
- Mechanistic pathway studies
- In vitro receptor profiling
- HPLC verified identity and purity
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Research Overview
BAM15 (N5,N6-bis(2-fluorophenyl)[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine) is a synthetic small-molecule mitochondrial protonophore uncoupler that has emerged as a paradigm-shifting research tool for metabolic disease investigation since its initial characterization in 2014 by researchers at the University of New South Wales and Virginia Tech. Unlike classical uncouplers such as DNP (2,4-dinitrophenol) and FCCP, BAM15 selectively uncouples oxidative phosphorylation in mitochondria without affecting plasma membrane potential, a critical distinction that confers a substantially wider therapeutic window and reduced cytotoxicity. As of early 2026, BAM15 has been the subject of over 50 peer-reviewed publications spanning metabolic disease, oncology, sepsis, cardiovascular biology, neurodegeneration, and aging research.
The compound demonstrates an EC50 of approximately 270 nM for mitochondrial uncoupling in L6 myoblasts while maintaining cellular viability at concentrations where FCCP becomes cytotoxic. Landmark studies published in Nature Communications and EMBO Molecular Medicine demonstrated that oral BAM15 administration reverses diet-induced obesity, normalizes glycemic control, reduces hepatic steatosis, and preserves lean body mass in murine models without affecting food intake, core body temperature, or producing observable organ toxicity. A 2025 comprehensive comparison evaluating 15 structurally unrelated mitochondrial uncouplers confirmed BAM15 as the top-performing compound across both in vitro and in vivo metabolic parameters, outperforming all other uncouplers and calorie restriction in diabetic db/db mice.
Beyond metabolic applications, BAM15 has demonstrated significant anti-inflammatory activity through metabolic reprogramming of immune cells, cardiovascular protection via NLRP3 inflammasome inhibition and endothelial pyroptosis suppression, sepsis survival improvement from 25% to 75% with kidney injury protection, and lifespan extension in invertebrate aging models. BAM15's selective action on mitochondrial membranes, preservation of plasma membrane potential, and exceptional dose tolerance range (effective from 0.5-50 µM without mitochondrial inhibition) collectively position it as the leading next-generation mitochondrial uncoupler for investigating energy homeostasis, metabolic flexibility, and mitochondrial biology across diverse disease contexts.
Primary Research Applications
Mechanism of Action
Mitochondrial Protonophoric Activity
Selective Proton Shuttling — BAM15 functions as a lipophilic weak acid that facilitates proton transport across the inner mitochondrial membrane independent of ATP synthase, thereby uncoupling oxidative phosphorylation from ATP production. The protonophoric cycle involves protonation in the acidic intermembrane space, membrane translocation in the neutral form, deprotonation in the alkaline mitochondrial matrix, and return transport of the anionic form. Critically, BAM15's activity is strongly modulated by membrane dipole potential, which differs between mitochondrial inner membranes (high dipole) and plasma membranes (low dipole), conferring selectivity that preserves cellular electrophysiology at effective uncoupling concentrations.
AMPK Activation and Metabolic Signaling
Master Metabolic Regulator — The reduction in ATP/ADP ratio caused by mitochondrial uncoupling triggers robust activation of AMP-activated protein kinase (AMPK), with BAM15 demonstrating approximately 1,000-fold greater potency per unit concentration than metformin and AICAR in vascular smooth muscle cells. AMPK activation triggers enhanced glucose uptake via GLUT4 translocation, increased glycolysis, phosphorylation and inhibition of acetyl-CoA carboxylase (reducing de novo lipogenesis), activation of fatty acid oxidation, promotion of PGC-1alpha upregulation for mitochondrial biogenesis, activation of autophagy and mitophagy pathways, and insulin sensitization through enhanced glucose disposal.
Anti-Inflammatory and Anti-Pyroptotic Pathways
Metabolic Immune Reprogramming — BAM15 attenuates LPS-induced inflammatory cytokine production (IL-6, TNF-alpha, IL-10), downregulates proinflammatory M1 macrophage polarization genes, and promotes metabolic reprogramming from glycolytic M1 toward oxidative M2 macrophage phenotypes. In cardiovascular tissues, BAM15 inhibits endothelial pyroptosis by reducing mitochondrial ROS production and oxidized mitochondrial DNA release, thereby suppressing the NLRP3/ASC/caspase-1 inflammasome signaling pathway. In ApoE-knockout mice, BAM15 treatment reduced atherosclerotic plaque formation, lipid deposition, and vascular inflammation.
Mitochondrial ROS Modulation
Source-Level ROS Reduction — By decreasing the proton gradient, BAM15 reduces electron dwell time in the electron transport chain, minimizing electron leak to molecular oxygen that generates superoxide. This represents a mechanistically distinct anti-oxidant pathway that prevents ROS generation at the source rather than scavenging existing species. In sepsis models, BAM15 decreases damaging mitochondrial ROS production and reduces circulating cell-free mitochondrial DNA (cfmtDNA), a damage-associated molecular pattern that drives systemic inflammation.
“Mechanistic summaries on this page are provided for laboratory reference and should be interpreted within controlled experimental settings only.”
Preclinical Research Summary
In preclinical obesity and metabolic disease models, BAM15 has demonstrated remarkable efficacy. A landmark study by Alexopoulos et al. (2020) published in Nature Communications showed that oral BAM15 (10-50 mg/kg daily) completely reversed high-fat diet-induced weight gain in C57BL/6J mice, normalizing body weight to lean controls without affecting food intake. Fat mass was selectively reduced with preservation of lean body mass, fasting glucose normalized, glucose tolerance was restored, and liver triglycerides significantly decreased. Critically, no effects on body temperature were observed and no detectable tissue toxicity was found across comprehensive histopathological, hematological, and biochemical assessments.
A comprehensive 2025 comparative study by Shah et al. published in Molecular Metabolism evaluated 15 structurally unrelated mitochondrial uncouplers and confirmed BAM15 as the top-performing compound. BAM15 demonstrated the broadest effective dosing range in vitro (maximum oxygen consumption rate approximately 286% of basal at 5 µM, sustained from 0.5-50 µM without mitochondrial inhibition) and delivered the best overall metabolic improvements in diabetic db/db mice. Treatment with 0.2% BAM15 completely normalized glucose tolerance, restored HbA1c to approximately 4%, and significantly reduced body weight, fat pads, liver steatosis, and triglycerides.
Beyond metabolic applications, BAM15 demonstrated significant protective effects in critical care models. Tsuji et al. (2023) published in the Journal of Clinical Investigation showed that BAM15 (5 mg/kg IP) increased sepsis survival from 25% to 75% at 7 days, with efficacy even when treatment was delayed 6-12 hours post-induction. Serum creatinine decreased from 0.43 to 0.12 mg/dL and BUN decreased from 103.8 to 53.4 mg/dL, indicating robust kidney protection. In aging research, BAM15 extended lifespan by approximately 9% on normal diet and 24% on high-fat diet in male Drosophila, with 125% improvement in locomotor activity. Body weight reduction was driven by decreased triglyceride accumulation while thorax muscle mass was preserved.
Academic References
- Kenwood BM et al. (2014). Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane. Molecular Metabolism.
- Alexopoulos SJ et al. (2020). Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice. Nature Communications.
- Kirkland RA et al. (2020). BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control. EMBO Molecular Medicine.
- Tsuji N et al. (2023). BAM15 treats mouse sepsis and kidney injury, linking mortality, mitochondrial DNA, tubule damage, and neutrophils. Journal of Clinical Investigation.
- Shah DP et al. (2025). Diverse actions of 15 structurally unrelated mitochondrial uncouplers in cells and mice. Molecular Metabolism.
- Tomar N et al. (2021). Protonophoric action of BAM15 on planar bilayers, liposomes, mitochondria, bacteria and neurons. Biochimica et Biophysica Acta (BBA) - Biomembranes.
- Tai Y et al. (2018). Mitochondrial uncoupler BAM15 inhibits artery constriction and potently activates AMPK in vascular smooth muscle cells. Acta Pharmaceutica Sinica B.
- Cheng CW et al. (2021). BAM15 attenuates inflammation in the LPS injection mouse model. International Journal of Molecular Sciences.
- Zhong S et al. (2025). BAM15 inhibits endothelial pyroptosis via the NLRP3/ASC/caspase-1 pathway to alleviate atherosclerosis. Atherosclerosis.
- Taylor AL et al. (2024). Restricting bioenergetic efficiency enhances longevity and mitochondrial redox capacity in Drosophila melanogaster. Aging Cell.
This product is intended exclusively for in vitro laboratory research by qualified professionals. Not for human consumption. Not approved by the FDA.