Important limitations
- Safety, Pharmacokinetics & Comparison to Other Uncouplers: Why BAM-15 is considered distinct from older uncoupling agents
- Future Research: What still needs to be answered before clinical translation
BAM-15
BAM-15 is a synthetic mitochondrial uncoupling compound studied for its ability to increase mitochondrial respiration, energy expenditure, and metabolic flexibility.
Dosing & scaling, explained
No mass-based amount example with adequate calculation context is available for this compound. This is educational source context, not a protocol or recommendation.
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Evidence context
No clinical amount or schedule is inferred from this material. Source verification is pending, and every displayed amount remains educational context rather than guidance.
Storage, handling and interpretation
Product identity
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Storage & handling
Follow the product label, certificate and validated laboratory SOP; no universal storage assumption is applied here.
Prepared solutions
Label concentration and preparation date, use sterile technique where applicable, and follow a validated stability protocol.
Reported protocols for BAM-15
What published studies and recent community write-ups report about amounts, timing and course length. 6 preclinical and 3 community-reported rows, each linked to its source. These are descriptions of what others report, not instructions, and nothing here is medical advice.
| Context | Dose | Frequency | Route | Course | Source |
|---|---|---|---|---|---|
| Preclinical6 rows | |||||
| Discovery paper and kidney injury modelCultured cells and 8-week-old male C57BL/6 mice subjected to 26 minutes of bilateral renal ischemia | 1 or 5 mg/kg | Single injection, 1 hour before the ischemia | Intraperitoneal, in 3% DMSO in 50% PEG400 | Single dose, assessed at 24 and 48 hours after reperfusionNot applicable | Molecular Metabolism (PubMed)2014 |
| The 2014 screen was designed to find an uncoupler that would not collapse the plasma membrane potential, and BAM-15 drove a higher maximum respiration rate than FCCP while being less toxic to cells. A single pretreatment injection lowered plasma creatinine and reduced tubular necrosis, brush border loss and immune cell infiltration against vehicle, which is what made the authors argue for revisiting uncoupling as a therapy. | |||||
| Mouse oral pharmacokinetics and acute dose rangeMale C57BL/6J mice | 50 mg/kg for the tissue distribution work; 10, 50 or 100 mg/kg for the acute energy expenditure test | Single dose | Oral gavage, compared against tail vein injection | Single dose, measured over 4 hoursNot applicable | Nature Communications2020 |
| Oral bioavailability was 67% with a peak plasma level of 8.2 micromolar and a half-life of 1.7 hours, and the drug went mostly to the liver, clearing over about 4 hours. The 10 mg/kg dose did not change oxygen use, 50 mg/kg raised it by 30% in the first hour and 100 mg/kg by 48%, back to baseline by roughly 3 hours. | |||||
| Mouse obesity reversal studySingle-housed male C57BL/6J mice already made obese by 4 weeks of a western diet, with a chow-fed benchmark group | 0.1% by weight mixed into the diet, giving an overnight exposure of 5-10 micromolar | Continuous, by eating | In food, not by injection or gavage | 5 weeks of treatment within a 9-week studyNot applicable | Nature Communications2020 |
| Treated mice ate the same calories as controls but ended 15% lighter, almost entirely from fat, with no difference in lean mass and no sign of fat malabsorption in the stool. An earlier arm had compared 0.05%, 0.10% and 0.15% in the diet, and 0.10% was picked as the lowest concentration that fully prevented diet-induced fat gain. | |||||
| Mouse glycemic control study10-week-old male diet-induced obese C57BL/6J mice on a 60% fat diet | 0.1% by weight in the diet, which worked out to about 85 mg/kg per day eaten freely | Continuous, by eating | Oral, in food | 3 weeksNot applicable | EMBO Molecular Medicine (PubMed Central)2020 |
| Peak serum levels were about 5 micromolar with a half-life near 3 hours, and the drug concentrated in fat depots rather than the liver in this study. Body weight separated from control by day 9 without any change in food intake until day 20, fat mass fell while lean mass held, and fasting glucose, insulin and glucose tolerance all improved. | |||||
| Mouse body temperature safety check16 ten-week-old mice randomized by baseline weight | 0.1, 0.5 or 1 mg/kg | Single injection | Intraperitoneal, in 5% DMSO in corn oil | Temperature measured before, immediately after and 1 and 24 hours laterNot applicable | EMBO Molecular Medicine (PubMed Central)2020 |
| Neither this single injection nor chronic dosing in food raised body temperature, and tail heat dissipation did not change either. This is the specific result that separates BAM-15 from dinitrophenol in the animal record, and it has never been checked in a person. | |||||
| Review of the whole preclinical recordAnimal and cell studies across obesity, diabetes, fatty liver, sepsis and cardiovascular models | The review summarizes rodent studies using 0.1% dietary dosing and injections of 1 to 5 mg/kg | Varies by study | Oral and injected in animals | Days to weeks depending on the modelNot applicable | Frontiers in Endocrinology (PubMed)2023 |
| The 2023 review calls the tolerability in animals encouraging and lists obesity, diabetes, fatty liver disease, sepsis and cardioprotection as areas with positive rodent data. It flags high lipophilicity and the need for better delivery as unresolved problems and states that more research is needed before clinical use. | |||||
| Community-reported3 rows | |||||
| Community range reported by a scoring site | Roughly 50-400 mg per day, with the units and basis described as unverified | Daily, cycled | Oral powder or capsules from research-chemical vendors | Not specifiedCycled, with no pattern given | Community resource2026 |
| A September 2026 review reports what it sees on bodybuilding and biohacking forums while stating that no verified human dose exists and that every figure is a body-weight extrapolation from mouse data with no pharmacokinetic justification. It notes that users treat the compound as a milder dinitrophenol and that no pharmaceutical-grade product exists. | |||||
| Lower community band and contraindication list | 5-60 mg orally, as the range self-report communities describe | Once daily | Oral | Not establishedNot established | Community resource2026 |
| This 2026 page reports a much lower band than the forum figures elsewhere and says there is no scientific basis for any specific number, that any dose on a vendor label is a vendor's guess, and that the delivered amount may differ from the label by an unknown margin. It lists heart disease, thyroid disorders, eating disorders and concurrent metabolic drugs among the situations it says rule out use. | |||||
| Research profile with purity testing data | No safe dose established; the page cites rodent pharmacokinetics of 67% oral bioavailability and a 1.7 hour half-life | Not applicable | Not applicable to humans | Not applicableNot applicable | Community resource2026 |
| This vendor-comparison site declines to publish a protocol, listing any human use as a contraindication because the compound has never been tested in people. It records the class risk of uncouplers, dangerous overheating and metabolic disruption at excess doses, and notes that anti-doping bodies have found BAM-15 as an undeclared ingredient in some online supplements. | |||||
How a course is commonly described
- Hours 0-3 after a dosePreclinical
The only measured human-relevant timing is from mice: a single oral dose peaked at 8.2 micromolar, raised oxygen use within the first hour at 50 mg/kg or more, and returned to baseline about 3 hours later with a 1.7 hour half-life. Nothing like this has been measured in a person.
- Days 1-9Preclinical
In the mouse study with continuous dietary dosing, body weight separated from controls by day 9 with no change in how much the animals ate. Food intake stayed level until day 20, by which point the weight gap was 7.5 grams.
- Weeks 3-5Preclinical
Three weeks of dietary dosing improved fasting glucose, insulin and glucose tolerance in one study, and five weeks reversed established diet-induced obesity in the other, with 15% lower body weight made up almost entirely of fat. Both relied on the drug being present continuously in food.
- Cycling and stoppingCommunity-reported
Community sources describe cycling without specifying a pattern, and one points out that there is no dependency or withdrawal mechanism here, just a metabolic rate that returns toward baseline when dosing stops. No study has looked at what happens after stopping.
- BAM-15 has never been given to a human in a published or registered study. There is no human pharmacokinetic, safety or dose data, so the milligram figures circulating online are body-weight extrapolations from mouse experiments.
- The animal dosing was not a daily pill. Both metabolic studies mixed the compound into food at 0.1% by weight for continuous exposure, which in freely feeding mice amounted to roughly 85 mg/kg per day, and single gavage doses of 50 to 100 mg/kg raised oxygen use for only about 3 hours.
- The advantage claimed over 2,4-dinitrophenol is that BAM-15 does not depolarize the plasma membrane and did not raise body temperature in mice at working doses. That is a published mechanistic distinction in rodents, not a demonstrated safety margin in people, and overheating remains the class risk.
- BAM-15 was added to the 2026 WADA prohibited list at S4.4.1 among AMPK activators, prohibited at all times in and out of competition, and anti-doping bodies have reported finding it as an undeclared ingredient in supplements.
Sources for this section (7)
- Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane
- Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice
- BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control
- BAM15 as a mitochondrial uncoupler: a promising therapeutic agent for diverse diseases
Plus 3 community resources (dosing guides, forum threads and vendor write-ups), reported above but not linked.
How BAM-15 is being studied to work
This process map organizes available educational context. Individual claims remain subject to source-level verification.
- 1
Mechanism of Action
How BAM-15 uncouples oxidative phosphorylation
- 2
Cellular Energy Signaling
AMPK, PGC-1α, mitochondrial biogenesis, and quality control
- Activates AMPK in response to ATP depletion
- Promotes glucose uptake and fatty acid oxidation
- Enhances PGC-1α-related mitochondrial biogenesis
- Supports mitochondrial quality control pathways
Overview
BAM-15 is a small synthetic molecule that carries protons across the inner mitochondrial membrane, letting them bypass ATP synthase so that nutrient oxidation runs faster while producing heat instead of ATP. It was found in a chemical screen at the University of Virginia and published in 2014, and the point of interest was that unlike 2,4-dinitrophenol and FCCP it does not depolarize the outer cell membrane, which is the off-target effect that gave the older uncouplers a narrow margin between a working dose and a fatal one. In mice it reversed diet-induced obesity and insulin resistance when mixed into food, taking off fat without touching lean mass, food intake or body temperature. It has never been given to a human, has no pharmacokinetic or safety data in people, is not approved or sold as a medicine anywhere, and was added to the WADA prohibited list for 2026 as an AMPK activator under S4.4.1.
What researchers are exploring
These themes organize the educational information currently available. Individual claims remain under source review and are not treatment claims.
- 1
Mechanism of Action
How BAM-15 uncouples oxidative phosphorylation
- 2
Cellular Energy Signaling
AMPK, PGC-1α, mitochondrial biogenesis, and quality control
- 3
BAM-15 and Obesity
Effects on fat accumulation, energy expenditure, and mitochondrial health
- 4
BAM-15 and Diabetes
Insulin sensitivity, glucose control, and hepatic glucose output
- 5
BAM-15 and NAFLD / NASH
Liver fat, oxidative stress, inflammation, and mitochondrial dysfunction
- 6
Inflammation, Sepsis & Kidney Protection
How BAM-15 may reduce tissue damage and inflammatory injury
What is known and what still needs verification
Available context is organized without assigning unsupported study models or evidence grades.
- Not graded
Research Status & Administration Notes
Important context about the current state of evidence
- Not graded
Mechanism of Action
How BAM-15 uncouples oxidative phosphorylation
- Not graded
Cellular Energy Signaling
AMPK, PGC-1α, mitochondrial biogenesis, and quality control
- Not graded
BAM-15 and Obesity
Effects on fat accumulation, energy expenditure, and mitochondrial health
Chemistry identifiers
Sequence, synonyms and registry identifiers as recorded in PubChem, the National Library of Medicine's open chemistry database. Formula, mass and CAS number are summarized at the top of the page.
Also listed as
BAM15, BAM 15, N5,N6-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine, CHEMBL3627755, CHEBI:233585, MFCD00373912, HY-110284
InChIKey
OEGJBRZAJRPPHL-UHFFFAOYSA-N
Primary Functional Role
Selective disruption of mitochondrial coupling between electron transport and ATP synthesis
Pharmacokinetic Notes
Reported oral bioavailability of 67%, half-life of 1.7 hours, primary liver localization, and tissue clearance within approximately four hours in preclinical discussion
IUPAC name
5-N,6-N-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine
Limitations and unknowns
Sources
0 links carried over from the earlier page, awaiting verification.