BAM15 is a synthetic small molecule, not a peptide, that works as a mitochondrial protonophore uncoupler, meaning it lets protons leak across the inner mitochondrial membrane, causing cells to burn more fuel to maintain their normal function. It has reversed diet-induced obesity and insulin resistance in mice without observed toxicity in that research, but it has never been tested in a human being. It shares its basic mechanism with 2,4-dinitrophenol (DNP), a chemical with a documented history of fatal overheating deaths in people who used it for weight loss, and no human safety margin for BAM15 has ever been established.
Ask about BAM15
Research snapshot
| Category | Current information |
|---|---|
| Peptide category | Small-molecule mitochondrial uncoupler (not a peptide) |
| Primary research interest | Diet-induced obesity and insulin resistance reversal |
| Highest available evidence | Published animal research (mouse); no human data of any kind |
| Human research available | No — never administered to a human being in any published or registered trial |
| Development status | Preclinical only |
| Regulatory status | Not approved anywhere; no regulatory pathway underway |
| Last reviewed | September 27, 2026 |
Technical identity
| Technical property | Information |
|---|---|
| Primary name | BAM15 |
| Alternative names | BAM 15, N5,N6-bis(2-fluorophenyl)[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine, mitochondrial uncoupler, protonophore |
| Peptide sequence | Not applicable — BAM15 is a small-molecule compound, not a peptide or amino-acid sequence |
| Amino-acid length | Not applicable |
| Molecular formula | C16H10F2N6O |
| Molecular weight | 340.29 g/mol |
| CAS Registry Number | 210302-17-3 |
| PubChem CID | Not established |
| Chemical modifications | Not applicable |
| Peptide class | Not a peptide — mitochondrial uncoupler / protonophore |
| Primary biological target | Inner mitochondrial membrane (proton gradient uncoupling) |
| Developer or originator | Characterized in academic mouse research (Alexopoulos et al. 2020, Nature Communications) |
| Development status | Preclinical (mouse studies only); no human trials registered |
What it is
BAM15 is a non-peptide small molecule in the oxadiazolopyrazine chemical class, developed as a research tool to study mitochondrial uncoupling with more selectivity and less toxicity than older uncouplers like DNP. Research groups, including work highlighted by Virginia Tech, developed and characterized it specifically to avoid DNP’s narrow safety margin and excess reactive oxygen species production. As of September 2026, every published finding on BAM15 comes from cell and mouse studies; it has never been administered to a human in a registered clinical trial, and it has no regulatory status anywhere.
How does it work?
Plain-English explanation
Cells normally use a precise, controlled process to turn food into usable energy, storing some of that energy as fat when there is a surplus. A mitochondrial uncoupler like BAM15 makes that process deliberately less efficient: cells have to burn more fuel just to keep functioning normally, which in mice translated into losing fat without eating less or moving more.
Technical explanation
BAM15 acts as a chemical protonophore, shuttling protons across the inner mitochondrial membrane independent of ATP synthase, which dissipates the proton gradient that mitochondria normally use to generate ATP. This forces increased substrate oxidation to maintain the gradient, increasing whole-body energy expenditure. Unlike DNP, BAM15 was designed and has been reported in mouse studies to uncouple mitochondria without the same degree of excess reactive oxygen species generation, and without raising core body temperature to a dangerous degree in the mouse studies conducted.
Potential benefits and research applications
Reversal of diet-induced obesity (mouse studies only)
What is being investigated: whether mitochondrial uncoupling can reverse established, diet-induced obesity without reducing food intake or increasing activity. How the effect might occur: increased whole-body energy expenditure from mitochondrial proton leak. Evidence: a mouse study (Alexopoulos et al., published in Nature Communications) using a high-fat, high-sucrose Western diet found chronic BAM15 treatment produced about 15 percent lower body weight than untreated obese mice, almost entirely from reduced fat mass with no reduction in lean mass, and completely prevented diet-induced fat gain at higher doses. Strength: has been shown in a well-controlled, peer-reviewed mouse study, including dose-response and pharmacokinetic characterization. Limitation: entirely a mouse result; whether the same effect, at any dose, would occur safely in a human has never been tested.
Improved insulin sensitivity and glucose tolerance (mouse studies only)
What is being investigated: whether mitochondrial uncoupling improves insulin sensitivity independent of weight loss. How the effect might occur: increased fatty acid oxidation reducing lipid accumulation in liver and muscle, tissues where excess fat interferes with insulin signaling. Evidence: the same mouse study found BAM15 reversed diet-induced glucose intolerance within 3 weeks, improved insulin sensitivity across multiple tissues by clamp study, and normalized elevated liver triglycerides, with a reported 51 percent increase in fatty acid (palmitate) oxidation. Strength: has been shown in a peer-reviewed mouse study using gold-standard insulin clamp methodology. Limitation: no human metabolic study of any kind exists for BAM15.
Comparative safety profile versus older uncouplers like DNP (mouse studies only)
What is being investigated: whether a more selective mitochondrial uncoupler can avoid the fatal hyperthermia risk associated with DNP. How the effect might occur: proposed reduced reactive oxygen species generation and a different pharmacokinetic profile compared with DNP. Evidence: the mouse study reported no observed toxicity, normal body temperature, unchanged lean mass, and normal blood chemistry and blood cell counts at the doses tested. Strength: has been reported in a controlled mouse toxicity assessment alongside the efficacy study. Limitation: DNP itself looked comparably promising in early, non-human research decades ago before its narrow human safety margin became apparent through real-world deaths; a favorable mouse toxicity profile is not evidence of human safety, and no such evidence exists for BAM15.
What dosage information circulates?
No established or reliably sourced human dosing information was identified for BAM15, because it has never been administered to a human being in any published or registered trial. This site does not reproduce a circulating dosage table for BAM15. That omission is deliberate: BAM15 is a mitochondrial uncoupler, the same mechanism as DNP, a compound with a well-documented history of fatal hyperthermia in people who dosed themselves for weight loss without any human safety data to guide them. Publishing a table of mouse-study amounts, even clearly labeled, risks being read as a translatable human protocol for a mechanism where that translation has already killed people using a closely related chemical.
| Reported use or research objective | Route reported | Amount reported | Frequency reported | Reported duration | Evidence or source category |
|---|---|---|---|---|---|
| Short pharmacological studies (mouse) | Oral gavage | 10-200 mg/kg (mouse body weight) | Single or short-course dosing | Up to 4 hours | Published animal research |
| Diet-induced obesity model (mouse) | Dietary admixture | 0.05-0.15% of diet by weight | Continuous dietary exposure | Up to 9 weeks | Published animal research |
| Pharmacokinetic characterization (mouse) | Intravenous | Approximately 1 mg/kg | Single dose | Not applicable | Published animal research |
This table intentionally omits a circulating or community-reported dosing row. This site does not document a community or practitioner dosing pattern for BAM15, because it shares its basic mechanism with DNP (2,4-dinitrophenol), a chemical with a well-documented history of fatal human hyperthermia deaths from self-dosing, and because literally no human dose of BAM15 itself has ever been tested at any level. The mouse figures above are a controlled research protocol and cannot responsibly be converted into a human amount.
Amounts studied in animal research
Mouse studies used oral gavage doses in the range of 10 to 200 mg per kilogram of mouse body weight for short (up to 4 hour) pharmacological studies, and chronic dietary admixture at 0.05 to 0.15 percent of the diet by weight over as long as 9 weeks, in a diet-induced obesity model, with intravenous dosing of about 1 mg per kilogram used separately for pharmacokinetic characterization. These are mouse-to-mouse comparisons within a controlled research protocol and are not, and cannot responsibly be converted into, a human amount.
Practitioner and community-reported protocols
This site does not document a community or practitioner dosing pattern for BAM15, in line with its policy of excluding circulating-figures tables for compounds whose only mechanism-comparable human history (DNP) is one of documented overdose deaths, and for which literally no human dose of BAM15 itself has ever been tested at any level.
Side effects, risks, and limitations
No human safety data exist for BAM15. Its mechanism, mitochondrial uncoupling, is the same one used by 2,4-dinitrophenol (DNP), a chemical still sold illegally as a weight-loss aid that has caused confirmed deaths from severe hyperthermia, particularly when combined with heat, exercise, or dehydration, and for which there is no antidote. While BAM15’s mouse studies reported a favorable safety profile relative to DNP at the doses tested, that finding describes mice, not people, and does not establish any margin of safety for a human dose, which has never been determined because no human trial has been conducted.
Regulatory and developmental status
BAM15 is not approved for any use anywhere and has not entered human clinical trials as of September 2026. It remains a preclinical research tool compound used to study mitochondrial bioenergetics, with academic and pharmaceutical-industry interest in developing safer, more selective uncoupler chemistry, including newer oxadiazolopyridine derivatives reported in the medicinal chemistry literature as potential successors.
Frequently asked questions
What is BAM15?
A non-peptide, small-molecule mitochondrial uncoupler studied in mice for obesity and insulin resistance. It has never been tested in humans and is not approved for any use.
Is BAM15 a peptide?
No. It is a small molecule in the oxadiazolopyrazine chemical class, unrelated in structure to peptides.
How does it work?
It uncouples mitochondria, forcing cells to burn more fuel to maintain their normal energy state, the same general mechanism as DNP, though BAM15 was designed to be more selective.
What dosage has been studied?
No established or reliably sourced human dosing information was identified, because BAM15 has never been given to a human in any published or registered trial. This site does not publish its mouse-study dosing as a circulating figure for that reason.
Is it safe?
Unknown in humans. Its mechanism is shared with DNP, a chemical that has caused confirmed deaths from overheating in people using it without medical supervision. A favorable mouse safety result does not establish human safety, and no human study of BAM15 has ever been conducted.
Has it been studied in humans?
No. Every published finding on BAM15 comes from cell and mouse studies. There is no human trial and no human dosing, safety, or efficacy data of any kind.
Is it approved?
No. It has no regulatory status anywhere and is not an approved drug in any country.
How is it different from DNP?
Both are mitochondrial uncouplers, but BAM15 was designed to reduce the excess reactive oxygen species and toxicity associated with DNP, and mouse studies reported no observed toxicity at the doses tested. Neither compound has an established safe human dose; DNP’s human use has caused confirmed deaths, and BAM15 has simply never been tried in a person at all.
What remains unknown?
Essentially everything about its effects, dosing, and safety in humans, since no human study of any kind has been conducted, and whether the favorable mouse safety profile would hold at any dose in a person.
Bottom line
BAM15 is a genuine, peer-reviewed mitochondrial uncoupler that reversed diet-induced obesity and insulin resistance in mice without observed toxicity in that research, a real and interesting finding. But it shares its basic mechanism with DNP, a chemical with a documented history of fatal human overheating deaths, and BAM15 itself has never been given to a human being in any study. There is no established human dose, no human safety data, and no regulatory pathway underway. This site does not publish a circulating dosage table for BAM15 because doing so, for a mitochondrial uncoupler with zero human testing and a mechanism-mate with a body count, would risk presenting an untested mouse amount as something closer to guidance than it is.
