BAM15

a preclinical mitochondrial protonophore that reduced fat gain and improved metabolic measures in mice, with no human exposure, dose-finding, or safety study.

tier C · weight loss · 0 human exposure studies

verdict

BAM15 has a coherent mechanism and credible mouse metabolic data, but no human bridge and no basis for calling a research-chemical exposure safe.

if you're asking whether BAM15 is a peptide — no. it is a 340.29 Da small-molecule mitochondrial protonophore.

if you're asking whether BAM15 caused weight loss — in diet-induced-obese mice, dietary BAM15 reduced fat-mass accumulation and improved metabolic measures. those findings are preclinical and do not establish human efficacy.

if you're asking whether it is safer than DNP — the mouse work reported a wider preclinical window and no measurable hyperthermia at one acute oral exposure. no human study has tested the comparison, so the site does not turn a mouse difference into a human safety claim.

if you're asking what its half-life is — the primary paper reports a 1.7-hour plasma half-life in male C57BL/6J mice after a single 10 mg/kg oral gavage. that number is displayed unchanged as animal-only and is not converted into a human value.

All exposures below describe animal experiments. No human-equivalent dose or use schedule is calculated.

why C-tier

C-tier reflects a coherent mechanism and a strong integrated mouse paper with oral PK, dose-ranging, metabolic efficacy, and acute tolerability work. It cannot rise to B because no human has been studied, no human PK exists, and the class mechanism carries safety questions that animal temperature measurements cannot settle.

the core tension

The preclinical program was designed to produce controlled uncoupling without DNP-like thermal toxicity. The only evidence that it succeeded comes from animal models, while the human concentration-response and failure modes are completely unmeasured.

what it is

BAM15 is a synthetic fluorinated small molecule, C16H10F2N6O, 340.29 g/mol, CAS 210302-17-3. It functions as a protonophore at the inner mitochondrial membrane. It is not a peptide, not an approved medicine, and not a characterized consumer product.

what it does

BAM15 carries protons across the inner mitochondrial membrane, partially dissipating the electrochemical gradient. Cells then oxidize more fuel to maintain energy demand while less of that oxidation is captured as ATP. In mice, the resulting increase in energy expenditure reduced fat accumulation and improved several metabolic measures without reducing food intake.

origin

BAM15 was developed as a mitochondrial uncoupler designed to separate beneficial metabolic uncoupling from the extreme thermal toxicity associated with older protonophores. The strongest obesity paper is a 2020 mouse study with oral PK, dietary dose-ranging, efficacy, and acute tolerability experiments.

why researchers are interested

It offers a non-appetite weight-loss story and a preclinical claim of a broader therapeutic window than DNP. Those are both attractive. Neither answers how a human formulation distributes, how narrow the exposure-response curve becomes in people, or what chronic organ risks appear.

does it work

It works as a mitochondrial uncoupler and produced meaningful metabolic effects in mice. C-tier is the correct translation status: real and reproducible preclinical biology, zero human exposure evidence.

claims vs the data

• BAM15 reduces fat without suppressing appetite — preclinical — supported in the Western-diet mouse experiment, with no human outcome study.
• BAM15 does not cause hyperthermia — overreach — no measurable hyperthermia appeared in one acute mouse experiment. species, exposure, duration, and formulation limit that finding.
• BAM15 is a safe version of DNP — unsupported — no controlled human exposure or direct human comparison exists.
• BAM15 has a 1.7-hour human half-life — contradicted — 1.7 hours is a mouse plasma value after a single oral gavage and is labeled animal-only.

key facts

• molecular formula: C16H10F2N6O
• molecular weight: 340.29 g/mol
• amino acids: n/a (small molecule, not a peptide)
• half-life: 1.7 hours in mouse plasma after 10 mg/kg oral gavage; no human half-life
• type: preclinical mitochondrial protonophore and oxidative-phosphorylation uncoupler
• CAS: 210302-17-3
• 0 human exposure studies
• 1.7 h reported mouse plasma half-life, not human PK
• 67% reported oral bioavailability in mice
• 5 wk duration of the main Western-diet mouse experiment

frequently asked questions

What is BAM15?

BAM15 is an investigational small-molecule mitochondrial protonophore. It uncouples fuel oxidation from ATP production and has been studied in cells and animals, not people.

Does BAM15 burn fat?

It reduced fat-mass accumulation in obese mice by increasing energy expenditure. No human weight-loss study exists.

Does BAM15 cause hyperthermia?

One mouse study did not measure hyperthermia after a high acute oral exposure. That does not establish human thermal safety, chronic safety, or overdose behavior.

What is the half-life of BAM15?

The reported value is 1.7 hours in mouse plasma after a single 10 mg/kg oral gavage. No human half-life has been measured.

Is BAM15 safe for humans?

Unknown. There is no published human exposure or safety dataset, and mitochondrial uncoupling can affect heat generation, ATP availability, and organ function.

related peptides

• 2,4-dinitrophenol (DNP) — the historical uncoupler whose human efficacy and lethal toxicity are both documented
• slu-pp-332 — an animal-only metabolic compound working through ERR signaling rather than proton transport
• ATX-304 (formerly O304) — an AMPK program with early controlled human data

reptides grades the research record and cites the literature behind every call. research reference only; not medical advice.