BAM15

Dosing from the Literature

Published for fat loss: mouse doses only — 0.05 to 0.2% of the diet by weight, about 85 mg/kg a day at 0.1%, for 8 days to 10 weeks (Alexopoulos et al., 2020; Axelrod et al., 2020; Chen et al., 2023; Dantas et al., 2022; Shah et al., 2025). Not published: any dose given to a person, and any measurement of what a dose does in one.

Every row below is an animal dose, with its species. BAM15 barely dissolves in water and the mouse studies could not inject it repeatedly, so the long studies mixed it into food and the dose each animal received was whatever it ate (Axelrod et al., 2020). A percentage of mouse chow is not convertible into a human dose, and no study has tried.

What It Is

BAM15 is not a peptide. It is a small synthetic molecule, 5-N,6-N-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine (C16H10F2N6O, 340.3 Da, CAS 210302-17-3), supplied as a crystalline solid that dissolves in DMSO and barely in water (PubChem; laboratory reagent supplier’s product sheet, read October 5, 2026). The discovery paper wrote the same structure a different way, as (2-fluorophenyl){6-[(2-fluorophenyl)amino](1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl)}amine, and both spellings appear in the literature and the catalogues (Kenwood et al., 2014; PubChem).

It is a mitochondrial uncoupler: a lipophilic weak acid that ferries protons into the mitochondrial matrix past ATP synthase, so nutrient oxidation runs faster while making less ATP per unit of fuel (Kenwood et al., 2014). That class is old and compromised. The classic laboratory uncoupler FCCP and the weight-loss drug 2,4-dinitrophenol also act on the plasma membrane, which brings cytotoxicity and a narrow margin between an effective and a toxic dose (Kenwood et al., 2014). A group at the University of Virginia led by Kyle Hoehn screened a 5,040-compound library in rat L6 myoblasts for compounds that raised oxygen use without raising reactive oxygen species, and in 2014 reported BAM15 as the hit that depolarised mitochondria without changing plasma-membrane current in whole-cell recordings (Kenwood et al., 2014). Two of its authors declared a patent application on the molecule (Kenwood et al., 2014).

The chemistry then moved to Virginia Tech, where Webster Santos’s laboratory mapped which parts of the molecule carry the proton (Kenwood et al., 2015; Childress et al., 2020), and the mouse work to the University of New South Wales, where Hoehn holds a second post and ran the animal studies (Virginia Tech, June 5, 2020; Alexopoulos et al., 2020). Santos and Hoehn founded Continuum Biosciences in 2017; the compounds are patented by Virginia Tech and licensed to that company (Virginia Tech, June 5, 2020). Several papers carry the disclosure: the senior author holds equity in Continuum Biosciences, “a company that develops mitochondrial uncouplers as therapeutics” (Alexopoulos et al., 2020; Axelrod et al., 2020). When this page was written the company had no website at its .com address, which was listed for sale (read October 5, 2026).

BAM15 itself was never put forward as the drug. Its half-life in mice is 1.7 hours (Alexopoulos et al., 2020). The Virginia Tech release that followed the mouse paper gave no figure, but called the half-life short for oral dosing in people and stated in its own words that “the drug won’t necessarily be successful in humans - at least not this same exact molecule.” Santos, quoted in the same release, said his laboratory was looking for “roughly the same type of molecule, but it needs to stay in the body for longer to have an effect” and had “made several hundred molecules related to this” (Virginia Tech, June 5, 2020). Three of those analogs have been published — SHC517, SHD865 and SHS206 — and all of them stop at mice (Chen et al., 2021; Beretta et al., 2024; Salamoun et al., 2024). No uncoupler from this program has entered a registered trial (ClinicalTrials.gov, searched October 5, 2026).

PubMed returns 72 records for “BAM15” (October 5, 2026). Twenty-six name it in the title; most of the rest use it as the reference uncoupler in experiments about something else, which is what it was built to be. WADA added it to the Prohibited List for 2026, among activators of AMP-activated protein kinase, and it is the first mitochondrial uncoupler to get a page on this site (World Anti-Doping Agency, 2026).

Mechanism of Action

All of it comes from artificial membranes, isolated mitochondria, cell lines and rodents. Nothing below has been measured in a person (PubMed and Europe PMC, searched October 5, 2026).

• Proton transport across the inner mitochondrial membrane (protonophore) — In isolated mitochondria BAM15 caused proton-dependent swelling and collapsed the membrane potential, and in planar lipid bilayers and liposomes it behaved as an anionic protonophore with potency close to the classical uncoupler CCCP (Kenwood et al., 2014; Firsov et al., 2021). In mouse liver cells it raised oxygen consumption with a half-maximal concentration of 1.4 µM against 10.1 µM for 2,4-dinitrophenol, and held maximal respiration from 3 to 100 µM, while dinitrophenol’s window was much narrower and above 30 µM it shut respiration down (Alexopoulos et al., 2020).
• The plasma membrane: the selling point, with one contrary report — In whole-cell voltage and current clamp recordings of rat L6 cells, FCCP produced an inward current and reversible depolarisation while BAM15 produced no appreciable change, and BAM15-treated cells stayed more viable up to 50 µM (Kenwood et al., 2014). A separate group that reproduced the protonophore activity found the opposite in molluscan neurons, where BAM15 did depolarise the plasma membrane and suppress electrical activity, more slowly than CCCP; the same work found that an inhibitor of the adenine nucleotide translocase partly reversed BAM15’s uncoupling of isolated rat liver mitochondria, implicating that carrier protein (Firsov et al., 2021); the discovery paper had run the same test in permeabilised muscle cells and found the carrier was not needed, so the two reports disagree (Kenwood et al., 2014).
• AMPK (AMP-activated protein kinase) — In vascular smooth-muscle cells BAM15 activated AMPK more strongly than CCCP, niclosamide, metformin or AICAR (Tai et al., 2018). In muscle cells, knocking AMPK down with shRNA removed the sustained metabolic response to BAM15, and in diet-induced obese mice AMPK and acetyl-CoA carboxylase were activated in white fat, where lipogenesis genes fell (Axelrod et al., 2020). The other 2020 mouse study found no change in AMPK phosphorylation or activity, and no change in ATP, in the livers of treated mice; the two reports differ by tissue, and whether AMPK is needed for the fat loss is unsettled (Alexopoulos et al., 2020; Axelrod et al., 2020). WADA classifies it as an AMPK activator (World Anti-Doping Agency, 2026).
• Where it goes in the body — Given by mouth to mice it was 67% bioavailable, peaked at 8.2 µM in plasma, cleared with a 1.7-hour half-life and distributed mainly to the liver, where palmitate oxidation rose 51% an hour after a 100 mg/kg dose and tissue oxygen use rose 54% an hour after 50 mg/kg (Alexopoulos et al., 2020). The second group measured a peak of about 5 µM, a half-life of about 3 hours and highest enrichment in fat depots, then liver, heart and kidney (Axelrod et al., 2020). Both report little of it in skeletal muscle, which the second group gives, together with unchanged food intake, as the reason lean mass was spared (Axelrod et al., 2020; Zunica et al., 2021).
• Fat oxidation, not appetite — Mice fed BAM15 ate the same amount as controls and kept normal locomotor activity; their respiratory exchange ratio fell (0.86 to 0.82 across the dark period), plasma free fatty acids rose 40% in the fed state, and faecal fat was unchanged, so the fat was being oxidised rather than not absorbed (Alexopoulos et al., 2020; Axelrod et al., 2020).
• Proposed anti-inflammatory and antioxidant effects — Liver metabolomics in treated mice showed a higher glutathione ratio and fewer oxidised lipids (Alexopoulos et al., 2020); in cells and mice, uncoupling by BAM15 lowered mitochondrial reactive oxygen species and the release of mitochondrial DNA, which the authors propose as the reason it limited kidney injury in sepsis (Tsuji et al., 2023). A review by an unrelated group collects these proposals and states plainly that the delivery problem and the lipophilicity are unresolved (Xiong et al., 2023).

What the Research Shows

Mice, worms, cells and tissue (PubMed, searched October 5, 2026). The Human Data section below is short because it is empty.

• Diet-induced obesity in mice — Mixed into a western diet at 0.10 and 0.15% by weight, BAM15 prevented fat-mass gain entirely over 8 days, while 0.05% prevented more than half of it; food intake, lean mass and body temperature were unchanged. In the reversal arm, mice fed a western diet for four weeks and then 0.1% BAM15 for five more ended 15% lighter than controls on the same calories, with liver triglycerides back to the level of chow-fed mice and glucose clearance on a hyperinsulinemic-euglycemic clamp back to the level of chow-fed mice (Alexopoulos et al., 2020). In 10-week-old diet-induced obese mice eating about 85 mg/kg a day, a second group saw weight diverge from day 9 and reach a 7.5 g mean difference at day 20, the point from which cumulative food intake also differed; fat fell without a change in lean mass, and energy expenditure rose without a change in body temperature (Axelrod et al., 2020).
• Against calorie restriction, and with semaglutide — In db/db mice, 0.2% BAM15 in the diet lowered body weight as much as about 50% calorie restriction and controlled glucose better, normalising fasting glucose and glucose tolerance to the level of lean controls; 0.1% improved glucose tolerance without changing weight (Chen et al., 2023). In a head-to-head in female db/db mice, BAM15 and calorie restriction improved body weight and liver steatosis more than semaglutide, niclosamide ethanolamine or rosiglitazone, while BAM15, semaglutide and rosiglitazone improved glucose tolerance more than calorie restriction or niclosamide ethanolamine (Chen, Beretta et al., 2024). Of 15 uncouplers compared in cells, five went on to db/db mice; there 0.2% BAM15 significantly improved body weight, fat-pad weight, glucose tolerance, blood glucose, HbA1c, liver weight and liver triglycerides, and was “the only intervention which statistically decreased fat pad weight and maintained or statistically increased the raw weight of gastrocnemius muscle in this study” (Shah et al., 2025).
• Old mice: muscle as well as fat — In 80-week-old obese male mice given 0.1% in a high-fat diet for 10 weeks, body weight fell from 54.0 ± 2.0 to 42.3 ± 1.3 g, muscle mass rose as a share of body weight, strength rose from 91.1 ± 1.3 to 124.9 ± 1.2 g and locomotor activity from 347.0 ± 14.4 to 432.7 ± 32.0 m, with lower muscle interleukin-6 and markers of mitochondrial quality control up (Dantas et al., 2022).
• Liver — In mice with diet-induced steatohepatitis, 0.1% BAM15 for eight weeks drove the fat loss and the thyroid-receptor agonist resmetirom drove the ALT and cholesterol improvements, with the combination better than either alone on energy expenditure, liver fat, glucose and disease activity score; no treatment changed fibrosis (Zhou et al., 2024; a correction to that paper was published in 2025). A separate group reported that BAM15 lowered liver lipid in high-fat-diet mice and tied the effect to AMPK-driven mitophagy (Liu et al., 2026).
• Sepsis and kidney injury in mice — A single 5 mg/kg injection into the belly at the time of cecal ligation and puncture raised 7-day survival to 75% from 25%, cut kidney tubule injury scores and splenic apoptosis, and lowered circulating mitochondrial DNA; given 6 or 12 hours later, when the mice were already ill, it still lowered mortality (Tsuji et al., 2023). The original 2014 paper had found the same protection in a kidney ischemia model at 1 and 5 mg/kg (Kenwood et al., 2014).
• Blood vessels, worms and tumour cells — BAM15 relaxed constricted rat mesenteric arteries with and without endothelium (Tai et al., 2018), and at 5 mg/kg a day under the skin it reduced plaque and inflammatory markers in ApoE-knockout mice on a high-fat diet (Zhong et al., 2025). At 50 µM it extended mean lifespan in Caenorhabditis elegans and preserved touch responses with age (Cho et al., 2022). In breast-cancer cells it lowered proliferation, ATP and membrane potential, and in mice bearing mammary tumours it slowed growth; distribution was again to fat, liver and tumour, with little in skeletal muscle (Zunica et al., 2021).
• Where the field is now — Work since 2023 mostly uses BAM15 as a tool or as a cargo: a dual-layer microneedle patch carrying capsaicin and BAM15 nanoparticles into mouse fat (Zeng et al., 2026), CAR-T cell work (Ma et al., 2025), and a published molluscicide screen (Wang et al., 2026). The therapeutic program has moved to the analogs SHC517, SHD865 and SHS206, each tested in mice only (Chen et al., 2021; Beretta et al., 2024; Salamoun et al., 2024).

Human Data

There is none. No published study has given BAM15 to a person, and no trial of it has ever been registered: a ClinicalTrials.gov search for “BAM15” returns one record, a monoclonal-antibody study in which “BAM” abbreviates bamlanivimab (NCT04634409), and searches of PubMed and Europe PMC return no human study (searched October 5, 2026).

• Human cells in a dish, never a person — Human material has only ever met BAM15 in a dish. Testing uncouplers as possible contraceptives, one group applied it to donated human sperm: it uncoupled sperm mitochondria specifically and significantly lowered progressive motility, but did not lower sperm ATP, which the authors read as sperm falling back on glycolysis (Skinner et al., 2023). A 2026 group added BAM15 to a sperm freezing medium and reported higher total and progressive motility, less DNA fragmentation and better-preserved structure after thawing than untreated controls (Chen, Liu et al., 2026). Earlier, a group shipping human iPS-derived retinal tissue for five days reported that adding BAM15 lowered the apoptosis markers cleaved caspase-3, p53, NF-κB and TNF-α and protected neuronal structure (Tang et al., 2019), and the CAR-T work in the research section added BAM15 to T cells taken from human blood (Ma et al., 2025). Cells and tissue in a dish are laboratory data, not human data, and these experiments asked different questions.
• What the lab and its university said about people — The half-life measured in mice was 1.7 hours (Alexopoulos et al., 2020). The Virginia Tech release that followed that paper called it short for oral dosing in people and said, in its own words, that “the drug won’t necessarily be successful in humans - at least not this same exact molecule”; Santos, quoted there, said his laboratory was looking for “roughly the same type of molecule, but it needs to stay in the body for longer to have an effect” (Virginia Tech, June 5, 2020). The laboratory’s published successors, SHC517, SHD865 and SHS206, are also untested in people (Chen et al., 2021; Beretta et al., 2024; Salamoun et al., 2024).
• The only human experience of this class is DNP’s — 2,4-dinitrophenol was sold as a slimming agent in the 1930s and banned by FDA after reports of severe toxicity; a 2011 review counted 62 deaths attributed to it in the medical literature, and two more poisonings, one fatal, were described in 2026 (Grundlingh et al., 2011; Lindeman et al., 2026). The 2020 mouse paper cites that experience as its proof of principle that uncoupling causes weight loss in people — patients taking DNP lost weight without eating less — and as the reason for the whole search for a safer molecule, noting the narrow window between DNP’s effective and its toxic dose and the 1938 FDA ban (Alexopoulos et al., 2020). DNP is a different compound; nothing in its record tells a reader what BAM15 does in a person.
• The evidence meter — The meter on the BAM15 card reads “Animal only”: it counts published human data on BAM15 itself, for fat loss, and there is none (PubMed, Europe PMC and ClinicalTrials.gov, searched October 5, 2026). The mouse results, however strong, leave it there.

Reconstitution & Storage

There is nothing to reconstitute for human use: no label and no trial document exists, and the published route is a powder mixed into animal food or given by gavage (Alexopoulos et al., 2020; Axelrod et al., 2020). What is on record is how laboratories handle it.

• It does not dissolve in water — A laboratory reagent supplier’s product sheet gives solubility as about 1 mg/mL in ethanol and about 20 mg/mL in DMSO or dimethyl formamide, and about 0.16 mg/mL in a 1:5 mixture of DMSO and phosphate-buffered saline; the compound is supplied as a crystalline solid of at least 98% purity (read October 5, 2026). The mouse studies made the same point in their own words: BAM15 is “highly lipophilic, and as a result, it is not suitable for chronic injection in vivo,” which is why the long studies put it in food (Axelrod et al., 2020), and at 150 and 200 mg/kg by gavage the suspension became a paste that could not be dosed further (Alexopoulos et al., 2020).
• Storage, as the catalogue states it — The same product sheet gives storage at −20 °C with stability of at least four years for the solid, and one supplier’s datasheet gives −20 °C for three years as powder and −80 °C for a year in solvent (read October 5, 2026). These are reagent-handling specifications, not instructions for a person.
• What the injection studies used — For single injections into the belly, the vehicle was 3% DMSO in 50% PEG400 (Kenwood et al., 2014) or 5% DMSO in corn oil (Axelrod et al., 2020); for pharmacokinetics, the intravenous vehicle was N-methylpyrrolidone and Kolliphor EL in water and the oral one methylcellulose with Tween-80 and DMSO (Alexopoulos et al., 2020).
• What is sold — Bulk powder: packages of 1 mg to 1 g from chemical catalogues, and 1 g and 10 g from a peptide shop at a fraction of the reagent price per gram (see Legal Status). No study has tested a product bought from either, and no independent analysis of one has been published.

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Side Effects & Risks

• Body temperature in mice — Unchanged over four hours after single oral doses up to 200 mg/kg, after injections of 0.1, 0.5 and 1 mg/kg into the belly, and across chronic feeding; tail heat dissipation also did not change (Alexopoulos et al., 2020; Axelrod et al., 2020). At the two highest gavage doses the mice showed transient lethargy that the authors could not separate from being given a paste (Alexopoulos et al., 2020).
• Blood chemistry in mice — After five weeks at 0.1% in the diet, ALT, AST, glutamate dehydrogenase and creatine kinase were unchanged, triglycerides fell 29%, blood urea nitrogen rose 22% within the strain’s normal range, and no ketosis appeared; free fatty acids in the fed state rose 40% (Alexopoulos et al., 2020). In db/db mice at 0.15 and 0.2% for four weeks, no marker of liver or kidney damage rose above control values, and glutamate dehydrogenase returned to the level of lean controls (Shah et al., 2025).
• Cytotoxicity in cells — BAM15 was less cytotoxic than FCCP across a range up to 50 µM and did not trigger caspase 3/7 up to 40 µM, where dinitrophenol did at 5 µM and FCCP at 10 µM (Kenwood et al., 2014; Axelrod et al., 2020). In cancer cells the same uncoupling is used deliberately to kill: it inhibited proliferation and promoted apoptosis in acute myeloid leukemia cells, which the authors link to reactive oxygen species, and did the same in breast-cancer cells (Gao et al., 2022; Zunica et al., 2021).
• The “mitochondria only” claim is not unanimous — In molluscan neurons BAM15 depolarised the plasma membrane and suppressed electrical activity (Firsov et al., 2021). That is one preparation in one species, against whole-cell recordings in mammalian cell lines showing no effect (Kenwood et al., 2014), and no one has recorded electrically from a human neuron treated with it: the one experiment on human neural tissue, iPS-derived retina during transport, stained it rather than recording from it (Tang et al., 2019).
• Sperm — In donated human sperm, BAM15 lowered progressive motility without lowering ATP; the authors were testing uncouplers as candidate contraceptives (Skinner et al., 2023). A different group found improved motility when it was added to a freezing medium before thawing (Chen, Liu et al., 2026).
• What has not been tested — No published study covers pregnancy, and none covers any amount given to a person. The only reproductive work is a 2026 report that BAM15 improved oocyte quality in an obesity model; PubMed carries no abstract for it and the article itself could not be read for this page, so its species, dose and design are not known here (Ma et al., 2026). No toxicology study in a live mammal other than mice has been published, and no study of how BAM15 changes another drug’s handling in the body: the published combinations are the two mouse ones in the stacking section and a cell experiment with the chemotherapy drug cytarabine (Gao et al., 2022). The longest exposure in a mammal is 10 weeks, in 80-week-old mice (Dantas et al., 2022). Products sold as research chemicals carry no regulatory review of their contents, and no analysis of a BAM15 product has been published (PubMed and Europe PMC, searched October 5, 2026).
• WADA — BAM15 is named on the 2026 Prohibited List, in section S4.4.1 among activators of AMP-activated protein kinase, beside AICAR and MOTS-c. Section S4 is prohibited at all times, in and out of competition, and substances in S4.4 are non-specified substances (World Anti-Doping Agency, 2026). The US Anti-Doping Agency’s advisory on the 2026 list describes it as one of two additions “found in supplements and products marketed as ‘research chemicals’” (US Anti-Doping Agency, 2026).

Bloodwork & Monitoring

No monitoring guidance for BAM15 has been published, because no one has been monitored on it. The animal studies measured these:

• Liver and kidney markers — ALT, AST, glutamate dehydrogenase, creatine kinase, creatinine and blood urea nitrogen, in mice after five weeks and after four weeks in db/db mice (Alexopoulos et al., 2020; Shah et al., 2025).
• Glucose and insulin — Fasting glucose, glucose tolerance tests, fed and fasted insulin, HOMA-IR, HbA1c in diabetic mice, and hyperinsulinemic-euglycemic clamps (Alexopoulos et al., 2020; Axelrod et al., 2020; Chen et al., 2023; Shah et al., 2025).
• Lipids — Plasma triglycerides, free fatty acids, cholesterol, β-hydroxybutyrate, liver triglyceride content and faecal fat (Alexopoulos et al., 2020; Axelrod et al., 2020).
• Body temperature and energy expenditure — Rectal and infrared temperature, thermal imaging of the tail, indirect calorimetry for oxygen consumption and respiratory exchange ratio, and locomotor activity (Alexopoulos et al., 2020; Axelrod et al., 2020).
• Haematology — Full blood counts and clinical biochemistry panels at euthanasia (Alexopoulos et al., 2020).
• Which tests fit a given person — A question for a licensed healthcare provider. This page can’t answer it.

Commonly Stacked With

Two published drug combinations exist, both in mice, and both were run by the laboratories that develop the compound; a third published pairing is with a feeding schedule rather than a compound. A seller listing read for this page pitched BAM15 alongside three other research chemicals; no study has tested any of those pairs, and a seller’s menu is not a pairing. Searches of PubMed and Europe PMC on October 5, 2026 found no study of BAM15 with any other compound on this site except semaglutide.

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Legal Status

Related Compounds

People researching BAM15 often also look at these:

Next Steps

References

1. Kenwood BM, Weaver JL, Bajwa A, Poon IK, et al. Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane. Mol Metab. 2014;3(2):114-123. PMID: 24634817. DOI: 10.1016/j.molmet.2013.11.005. (Full text at PMC3953706, read October 5, 2026: the 5,040-compound screen, the whole-cell recordings, the 1 and 5 mg/kg intraperitoneal doses, and “BMK and KLH are co-inventors on a patent application involving BAM15.”)
2. National Library of Medicine. PubChem: BAM15, CID 565708 (C16H10F2N6O, 340.29 g/mol; CAS 210302-17-3; IUPAC name 5-N,6-N-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine; synonyms include BAM 15 and the (1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl) spelling). pubchem.ncbi.nlm.nih.gov. Read October 5, 2026.
3. Alexopoulos SJ, Chen SY, Brandon AE, Salamoun JM, et al. Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice. Nat Commun. 2020;11(1):2397. PMID: 32409697. DOI: 10.1038/s41467-020-16298-2.
4. Axelrod CL, King WT, Davuluri G, Noland RC, et al. BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control. EMBO Mol Med. 2020;12(7):e12088. PMID: 32519812. DOI: 10.15252/emmm.202012088.
5. Kenwood BM, Calderone JA, Taddeo EP, Hoehn KL, Santos WL. Structure-activity relationships of furazano[3,4-b]pyrazines as mitochondrial uncouplers. Bioorg Med Chem Lett. 2015;25(21):4858-4861. PMID: 26119501. DOI: 10.1016/j.bmcl.2015.06.040.
6. Childress ES, Salamoun JM, Hargett SR, Alexopoulos SJ, et al. [1,2,5]Oxadiazolo[3,4-b]pyrazine-5,6-diamine Derivatives as Mitochondrial Uncouplers for the Potential Treatment of Nonalcoholic Steatohepatitis. J Med Chem. 2020;63(5):2511-2526. PMID: 32017849. DOI: 10.1021/acs.jmedchem.9b01440.
7. Chen SY, Beretta M, Alexopoulos SJ, Shah DP, et al. Mitochondrial uncoupler SHC517 reverses obesity in mice without affecting food intake. Metabolism. 2021;117:154724. PMID: 33548253. DOI: 10.1016/j.metabol.2021.154724.
8. Beretta M, Dai Y, Olzomer EM, Vancuylenburg CS, et al. Liver-Selective Imidazolopyrazine Mitochondrial Uncoupler SHD865 Reverses Adiposity and Glucose Intolerance in Mice. Diabetes. 2024;73(3):374-384. PMID: 37870907. DOI: 10.2337/db23-0233.
9. Salamoun JM, Krinos EL, Foutz MA, Hargett SR, et al. Design, synthesis, and biological evaluation of imidazo[4,5-b]pyridine mitochondrial uncouplers for the treatment of metabolic dysfunction-associated steatohepatitis (MASH). Eur J Med Chem. 2024;280:116916. PMID: 39406121. DOI: 10.1016/j.ejmech.2024.116916.
10. Firsov AM, Popova LB, Khailova LS, Nazarov PA, Kotova EA, Antonenko YN. Protonophoric action of BAM15 on planar bilayers, liposomes, mitochondria, bacteria and neurons. Bioelectrochemistry. 2021;137:107673. PMID: 32971482. DOI: 10.1016/j.bioelechem.2020.107673.
11. Tai Y, Li L, Peng X, Zhu J, et al. Mitochondrial uncoupler BAM15 inhibits artery constriction and potently activates AMPK in vascular smooth muscle cells. Acta Pharm Sin B. 2018;8(6):909-918. PMID: 30505660. DOI: 10.1016/j.apsb.2018.07.010.
12. Dantas WS, Zunica ERM, Heintz EC, Vandanmagsar B, et al. Mitochondrial uncoupling attenuates sarcopenic obesity by enhancing skeletal muscle mitophagy and quality control. J Cachexia Sarcopenia Muscle. 2022;13(3):1821-1836. PMID: 35304976. DOI: 10.1002/jcsm.12982.
13. Chen SY, Beretta M, Olzomer EM, Shah DP, et al. Targeting negative energy balance with calorie restriction and mitochondrial uncoupling in db/db mice. Mol Metab. 2023;69:101684. PMID: 36731653. DOI: 10.1016/j.molmet.2023.101684.
14. Chen SY, Telfser AJ, Olzomer EM, Vancuylenberg CS, et al. Beneficial effects of simultaneously targeting calorie intake and calorie efficiency in diet-induced obese mice. Clin Sci (Lond). 2024;138(4):173-187. PMID: 38315575. DOI: 10.1042/CS20231016.
15. Chen SY, Beretta M, Olzomer EM, Alexopoulos SJ, et al. Head-to-head comparison of BAM15, semaglutide, rosiglitazone, NEN, and calorie restriction on metabolic physiology in female db/db mice. Biochim Biophys Acta Mol Basis Dis. 2024;1870(1):166908. PMID: 37793464. DOI: 10.1016/j.bbadis.2023.166908.
16. Zhou M, Li C, Byrne FL, Vancuylenburg CS, et al. Beneficial effects of MGL-3196 and BAM15 combination in a mouse model of fatty liver disease. Acta Physiol (Oxf). 2024;240(10):e14217. PMID: 39152636. DOI: 10.1111/apha.14217. Correction: Acta Physiol (Oxf). 2025;241(1):e14250. PMID: 39533750. DOI: 10.1111/apha.14250.
17. Shah DP, Vancuylenburg CS, Olzomer EM, Chen SY, et al. Diverse actions of 15 structurally unrelated mitochondrial uncouplers in cells and mice. Mol Metab. 2025;99:102204. PMID: 40639664. DOI: 10.1016/j.molmet.2025.102204.
18. Zunica ERM, Axelrod CL, Cho E, Spielmann G, et al. Breast cancer growth and proliferation is suppressed by the mitochondrial targeted furazano[3,4-b]pyrazine BAM15. Cancer Metab. 2021;9(1):36. PMID: 34627389. DOI: 10.1186/s40170-021-00274-5.
19. Tsuji N, Tsuji T, Yamashita T, Hayase N, Hu X, Yuen PS, Star RA. BAM15 treats mouse sepsis and kidney injury, linking mortality, mitochondrial DNA, tubule damage, and neutrophils. J Clin Invest. 2023;133(7):e152401. PMID: 36757801. DOI: 10.1172/JCI152401.
20. Zhong S, Shen H, Dai X, Liao L, Huang C. BAM15 inhibits endothelial pyroptosis via the NLRP3/ASC/caspase-1 pathway to alleviate atherosclerosis. Atherosclerosis. 2025;406:119226. PMID: 40393254. DOI: 10.1016/j.atherosclerosis.2025.119226.
21. Cho I, Song HO, Ji HE, Yang S, Cho JH. BAM15 Relieves Neurodegeneration in Aged Caenorhabditis elegans and Extends Lifespan. Metabolites. 2022;12(11):1129. PMID: 36422268. DOI: 10.3390/metabo12111129.
22. Gao ZX, Cui ZL, Zhou MR, Fu Y, et al. The new mitochondrial uncoupler BAM15 induces ROS production for treatment of acute myeloid leukemia. Biochem Pharmacol. 2022;198:114948. PMID: 35192847. DOI: 10.1016/j.bcp.2022.114948.
23. Skinner WM, Petersen NT, Unger B, Tang S, et al. Mitochondrial uncouplers impair human sperm motility without altering ATP content. Biol Reprod. 2023;109(2):192-203. PMID: 37294625. DOI: 10.1093/biolre/ioad064.
24. Chen B, Liu C, Xiong M, Xu L, et al. Mitochondrial uncoupler BAM15 attenuates cryopreservation-induced damage in human sperm by stabilizing mitochondrial homeostasis. Biol Reprod. 2026;115(3):777-788. PMID: 42295994. DOI: 10.1093/biolre/ioag123.
25. Tang M, Luo Z, Wu Y, Zhuang J, et al. BAM15 attenuates transportation-induced apoptosis in iPS-differentiated retinal tissue. Stem Cell Res Ther. 2019;10(1):64. PMID: 30795805. DOI: 10.1186/s13287-019-1151-y.
26. Ma RJ, Zhang HL, Wu X, Lu PS, et al. BAM15 improves oocyte quality against obesity via PPARγ-dependent mitochondrial function. Protein Cell. 2026 (advance online publication). PMID: 42178393. DOI: 10.1093/procel/pwag035. (PubMed carries no abstract for this record and the article was not reachable for this page, so its species, dose and design are not described here. Read October 5, 2026.)
27. Liu Z, Wang W, Wang S, Lv R, Li C, Sun C. Mitochondrial uncoupler BAM15 ameliorates liver lipid metabolism disorders by activating the AMPK pathway. FEBS J. 2026;293(10):2999-3014. PMID: 41527408. DOI: 10.1111/febs.70400.
28. Ma Y, Zhang H, Dou L, Sun H, et al. Mitochondrial uncoupler BAM15 enhances the function of CD7CAR-T CD7- cells and reduces the release of cytokines for the therapy of T-cell malignancies. Int Immunopharmacol. 2025;155:114577. PMID: 40215779. DOI: 10.1016/j.intimp.2025.114577.
29. Zeng F, Liu Q, Xiang Y, Hu H, Zheng J, Yang Z, Tao R. A Programmed Drug-Loaded and Penetration-Delivery Functionalized Microneedle Patch for Synergistic Obesity Treatment. Adv Healthc Mater. 2026;15(30):e71409. PMID: 42403298. DOI: 10.1002/adhm.71409.
30. Wang L, Yu H, Qu G, Jin J, Wang J, Xing Y. BAM 15 Exerts Molluscicidal Effects on Pomacea canaliculata Through the Induction of Oxidative Stress, Impaired Energy Metabolism, and Tissue Damage. Molecules. 2026;31(2):361. PMID: 41599409. DOI: 10.3390/molecules31020361.
31. Xiong G, Zhang K, Ma Y, Song Y, et al. BAM15 as a mitochondrial uncoupler: a promising therapeutic agent for diverse diseases. Front Endocrinol (Lausanne). 2023;14:1252141. PMID: 37900126. DOI: 10.3389/fendo.2023.1252141.
32. Grundlingh J, Dargan PI, El-Zanfaly M, Wood DM. 2,4-dinitrophenol (DNP): a weight loss agent with significant acute toxicity and risk of death. J Med Toxicol. 2011;7(3):205-212. PMID: 21739343. DOI: 10.1007/s13181-011-0162-6.
33. Lindeman E, Sommer T, Leffler M, Sekine S, Elmér E, Sjövall F, Wallquist W. Runaway uncoupling in 2,4-dinitrophenol poisoning: Clinical and mitochondrial observations from two cases. Toxicol Rep. 2026;16:102183. PMID: 41487961. DOI: 10.1016/j.toxrep.2025.102183.
34. Virginia Tech. Virginia Tech drug researcher develops ‘fat burning’ molecule that has implications for treatment of obesity. News release, June 5, 2020 (Webster Santos on the half-life, the analogs, and Continuum Biosciences, co-founded with Kyle Hoehn in 2017). news.vt.edu/articles/2020/05/FralinLifeSci-Webster-Santos-Nature-Comms-Obesity.html. Read October 5, 2026.
35. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S4.4.1, metabolic modulators: “Activators of the AMP-activated protein kinase (AMPK), e.g. 5-N,6-N-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine (BAM15), AICAR, mitochondrial open reading frame of the 12S rRNA-c (MOTS-c)”; S4 is prohibited at all times and substances in S4.3 and S4.4 are non-Specified Substances; S0, non-approved substances. wada-ama.org. Read October 5, 2026.
36. US Anti-Doping Agency. Athlete Advisory: What’s New on the 2026 WADA Prohibited List? Published October 16, 2025, updated May 13, 2026: BAM15 and 2-phenylbenzo[h]chromen-4-one added as “substances that have been found in supplements and products marketed as ‘research chemicals’”. usada.org/spirit-of-sport/2026-wada-prohibited-list/. Read October 5, 2026.
37. US Food and Drug Administration. Drugs@FDA and the National Drug Code Directory through openFDA (api.fda.gov/drug/drugsfda.json, api.fda.gov/drug/ndc.json): searches for BAM15 and CAS 210302-17-3, October 5, 2026 (no applications, no listings). Bulk Drug Substances Nominated for Use in Compounding Under Section 503A (categories 1–3), updated May 14, 2026, fda.gov/media/94155/download, and under Section 503B, updated March 21, 2025, fda.gov/media/94164/download: neither names BAM15 or any of its chemical names.
38. US Code of Federal Regulations. 21 CFR 216.23 (bulk drug substances that can be used to compound under section 503A) and 21 CFR 216.24 (drug products withdrawn or removed because unsafe or not effective). ecfr.gov (version of October 1, 2026): neither names BAM15. Read October 5, 2026.
39. ClinicalTrials.gov. Searches for “BAM15”, “BAM 15”, “mitochondrial uncoupler”, “uncoupler obesity”, “oxadiazolopyrazine” and “Continuum Biosciences”, API v2, October 5, 2026: no registration of BAM15 or of any uncoupler from this program. The single record returned for “BAM15”, NCT04634409 (Eli Lilly, BLAZE-4), is a monoclonal-antibody study in which “BAM” abbreviates bamlanivimab.
40. Laboratory reagent supplier product information sheet for BAM15 (CAS 210302-17-3), dated February 5, 2025: crystalline solid, purity ≥98%, storage −20 °C, stability ≥4 years; solubility about 1 mg/mL in ethanol, about 20 mg/mL in DMSO and dimethyl formamide, about 0.16 mg/mL in 1:5 DMSO:PBS; “THIS PRODUCT IS FOR RESEARCH ONLY — NOT FOR HUMAN OR VETERINARY DIAGNOSTIC OR THERAPEUTIC USE”; “This material should be considered hazardous until further information becomes available.” A second supplier’s datasheet gives −20 °C for three years as powder and −80 °C for one year in solvent, and is headed “For Research Use Only”. Suppliers not named. Read October 5, 2026.
41. Chemical catalogue price aggregator, listing page for BAM15 (CAS 210302-17-3): 45 prices from 15 brands, 39 to 2,014 US dollars a package, packages from 1 mg to 1 g, including 100 mg at 570 dollars in a listing updated May 26, 2026. Brands not named. Read October 5, 2026.
42. Seller listing for BAM15 powder, 10 g at 300 US dollars and 1 g at 5,300 roubles, claimed batch purity 99.5%, star ratings for “fat burning” and the statement that “human data are practically absent — all compelling results are from mice”, under the shop’s own disclaimer that “any introduction of these products into the human or animal body is strictly prohibited”; its linked compound guide is behind a paid membership and was not read. Seller not named. Read October 5, 2026.
43. Searches of October 5, 2026: PubMed, “BAM15” (72 records; 26 with BAM15 in the title), “BAM15 toxicity” (7), “BAM15 AND pharmacokinetics” (5), “BAM15 AND doping” (0); Europe PMC, “BAM15 AND (human OR patients OR volunteers OR trial)” (355 hits, none a study in people); ClinicalTrials.gov as above; openFDA Drugs@FDA and NDC Directory as above; grep of the WADA 2026 Prohibited List, FDA’s 503A and 503B category lists and 21 CFR part 216 for BAM15, BAM 15, its CAS number, “oxadiazolo”, “fluorophenyl”, “uncoupler” and “dinitrophenol”; chemical catalogues and one seller shop for what is sold (not named).

Related Research

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