Peptides›Metabolic, Longevity›BAM-15

BAM-15

/ Selective mitochondrial protonophore uncoupler (small molecule)

TIER 3 · PreclinicalN = 0 · TESTING PENDINGMW 400.34 g·mol⁻¹

ALIAS · BAM15 · BAM-15

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Research use onlyAny dose figures below describe what specific cited studies used, reported factually. Nothing on this page is guidance for human use.READ FIRST →

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§ A · Identity

Primary sequence— sequence not captured —

MW · 400.34CLASS · Selective mitochondrial protonophore uncoupler (small molecule)CATEGORY · Metabolic, Longevity

Tier 3. Rodent and in vitro literature on BAM15 as a selective mitochondrial protonophore uncoupler with a wider therapeutic index than DNP. No human Phase 1 trial published as of early 2026.

§ B · Mechanism of action

BAM15 is a small-molecule protonophore that shuttles protons across the inner mitochondrial membrane, dissipating the proton-motive force and uncoupling oxidative phosphorylation from ATP synthesis. The result is increased oxygen consumption, increased substrate oxidation, and dissipation of energy as heat - the same broad pharmacology as 2,4-dinitrophenol (DNP) but with reportedly greater selectivity for the mitochondrial inner membrane and a wider window between active and toxic exposures in rodent models. The structural class (aromatic N-aryl-substituted fluoroamine) was specifically optimised in academic medicinal-chemistry programs to avoid the plasma-membrane uncoupling and acute hyperthermia toxicity that ended DNP development for human use.

§ C · Human clinical evidence

Tier 3. Kenwood 2014 (Mol Metab) characterised BAM15 in vitro and in mouse models, demonstrating uncoupler pharmacology with substantially less plasma-membrane depolarisation than DNP. Alexopoulos 2020 (Nat Commun) extended the rodent data to a diet-induced obesity model, reporting reduced fat mass, improved glucose tolerance, and improved hepatic steatosis without observed hyperthermia. No published human trial.

§ D · Primary literature

PubMed24634817Kenwood BM et al. — Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane · Molecular Metabolism · in-vitroBAM15 was identified from a high-throughput screen as a selective mitochondrial uncoupler producing oxygen-consumption-rate increases without plasma-membrane depolarisation; rodent tolerability studies suggested a wider therapeutic index than DNP.Limitations: Discovery and in-vitro characterisation; rodent dosing studies short duration; no human data.2014

PubMed32409697Alexopoulos SJ et al. — Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice · Nature Communications · rodentOral BAM15 in diet-induced-obese mice reduced fat mass, improved glucose tolerance and insulin sensitivity, and reduced hepatic steatosis without measurable hyperthermia at the doses studied.Limitations: Rodent only; single-laboratory replication; chronic human exposure profile not established.2020

§ F · Safety signal

No human safety database. The class concern with all mitochondrial uncouplers - the historical DNP toxicity profile of hyperthermia, cataract formation, and fatal overdose - frames the regulatory caution around any uncoupler reaching human exposure. The published BAM15 rodent therapeutic index is wider than DNP, but a wider rodent window does not constitute a human safety signal.

§ H · Regulatory status

Regulatory status

FDA status:: Not FDA-approved

§ I · Notable gaps and controversies

Vendor sale of BAM15 as a research chemical for human-exposure use sits outside any approved or characterised clinical pathway. The 'safer DNP' framing is supported in rodents but has not been validated in humans, and the historical DNP fatalities in non-medical weight-loss use motivate regulatory caution about any uncoupler being marketed to non-clinical buyers. Identity and purity of vendor material vary substantially.