BAM-15
BAM15 is a small-molecule mitochondrial protonophore uncoupler studied for its effects on cellular energy expenditure and metabolic regulation. Unlike most compounds in this catalog, it is not a peptide; it is a fluorophenyl-substituted oxadiazolopyrazine with the IUPAC name N5,N6-bis(2-fluorophenyl)[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine. The compound is catalogued under CAS number 210302-17-3, with a molecular formula of C₁₆H₁₀F₂N₆O and a molecular weight of approximately 340.29 g/mol (PubChem CID 565708). A defining feature reported in the literature is its mitochondrial selectivity: it acts as a lipophilic weak-acid protonophore at the inner mitochondrial membrane with a reported EC₅₀ of approximately 270 nM in L6 myoblast mitochondria.
BAM15 has been studied predominantly in vitro and in rodent models, where investigators have examined mitochondrial respiration, nutrient oxidation, and metabolic endpoints. It is supplied here strictly as a research-use chemical for laboratory investigation of these pathways. BAM15 is not approved by the FDA, EMA, or any other regulatory authority for any indication, and no completed human clinical trials have established efficacy or a safety profile.
Important note on the evidence base: The peer-reviewed BAM15 literature consists of in vitro mitochondrial characterization and in vivo rodent work, primarily in diet-induced obesity and ischemia-reperfusion models, produced by a small number of research groups. No completed Phase 2 or Phase 3 clinical trials of BAM15 in human participants exist, and no mitochondrial-uncoupler small molecule has reached broad regulatory approval for metabolic indications. Researchers consulting this page should weight the evidence accordingly and refer to the primary literature in the References section for full methodological detail.
Available Products
Mechanism of Action
The mechanistic literature on BAM15 centers on mitochondrial uncoupling — the dissipation of the inner-membrane proton gradient independently of ATP synthase — and the downstream metabolic consequences of forcing mitochondria to oxidize more substrate per unit of ATP produced. The pathways described below are drawn from preclinical work and have not been independently confirmed in human clinical studies.
Mitochondrial protonophore activity
Mitochondrial uncouplers are lipophilic weak acids that shuttle protons into the mitochondrial matrix through a pathway independent of ATP synthase, uncoupling nutrient oxidation from ATP production. In the foundational characterization study, BAM15 was identified as a protonophore that stimulates maximal mitochondrial respiration over a broad concentration range without causing respiratory collapse, establishing the basic mechanism on which subsequent metabolic work was built [1]. The net effect of this controlled proton leak is that mitochondria oxidize more glucose and fatty-acid substrate to maintain the same ATP output, increasing overall energy expenditure at the cellular level.
Selectivity relative to earlier uncouplers
A central theme in the BAM15 literature is its profile relative to classical uncouplers such as FCCP and 2,4-dinitrophenol (DNP). In comparative experiments, BAM15 matched the potency of FCCP in increasing oxygen flux while supporting a higher maximum rate of mitochondrial respiration, and — unlike FCCP — it did not depolarize the plasma membrane, a property associated with reduced cytotoxicity across the tested concentration range [1]. This mitochondrial selectivity is the reason BAM15 became a widely used research tool for isolating the effects of mitochondrial uncoupling.
AMPK-dependent nutrient handling
Downstream of uncoupling, mechanistic work reported that BAM15 enhanced mitochondrial respiratory kinetics, improved insulin action, and stimulated nutrient uptake through sustained activation of AMP-activated protein kinase (AMPK), with activation of AMPK and acetyl-CoA carboxylase observed in white adipose tissue and effects on genes regulating de novo lipogenesis [2]. This positions BAM15 within the broader cellular-energetics and AMPK-signaling research framework.
None of the mechanisms summarized here have been independently verified in adequately powered human clinical trials of BAM15 specifically.
Forms and Use in the Research Literature
The amount ranges and routes described below reflect the protocols used in the published preclinical BAM15 literature. They are reported strictly for research-reference purposes and do not constitute administration recommendations of any kind.
Diet-induced obesity protocol. In the pivotal rodent study, mice fed an obesigenic western diet received BAM15 by oral administration, and the investigators reported that the compound was orally bioavailable, dose-dependently increased nutrient oxidation, and decreased body fat mass without altering food intake, lean body mass, or body temperature, alongside reduced hepatic fat and improved insulin sensitivity across multiple tissue types in hyperinsulinemic-euglycemic clamp studies [3]. Tissue oxygen-consumption measurements were taken following oral gavage in the milligram-per-kilogram range.
In vitro characterization. Cell and isolated-mitochondria work has characterized BAM15 as a mitochondrial-selective protonophore in the low-micromolar range, with respiration and membrane-potential endpoints assessed by respirometry and compared directly against FCCP [1].
Other research models. Beyond metabolic work, BAM15 has been investigated in models of acute renal ischemia-reperfusion injury, where intraperitoneal administration was reported to be protective — one of the earliest in vivo demonstrations of the compound’s activity [1]. It has also appeared in exploratory work in additional tissue and disease models.
Pharmacokinetic profile. The lipophilic small-molecule structure produces oral bioavailability in rodent models, with reported selectivity for lipophilic tissues. Published human pharmacokinetic data are not available.
Stability and storage. BAM15 is typically supplied as a solid and stored frozen, protected from light, with stock solutions prepared in an organic solvent such as DMSO, aliquoted, and frozen. Each lot supplied by Captide Labs is accompanied by a batch-specific Certificate of Analysis documenting identity and purity by HPLC.
Adverse-event profile. No human clinical-trial adverse-event database exists for BAM15. The available preclinical literature reported a wider apparent therapeutic window and less cytotoxicity than earlier uncouplers such as DNP and FCCP, and the rodent obesity study reported no changes in haematological or biochemical markers of toxicity at the studied amounts; however, this is not equivalent to a regulated human safety dataset, and the well-documented historical toxicity of the uncoupler drug class (notably DNP) warrants particular caution in interpreting these preclinical findings. Safety in humans has not been established.
References
- Kenwood BM, Weaver JL, Bajwa A, et al. Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane. Mol Metab. 2013;3(2):114–123. doi:10.1016/j.molmet.2013.11.005 · PubMed: 24634817
- Axelrod CL, King WT, Davuluri G, et al. BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control. EMBO Mol Med. 2020;12(7):e12088. doi:10.15252/emmm.202012088 · PMC: PMC7338798
- Alexopoulos SJ, Chen SY, Brandon AE, et al. Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice. Nat Commun. 2020;11(1):2397. doi:10.1038/s41467-020-16298-2 · PMC: PMC7224297