BAM-15

A mitochondrial protonophore uncoupler with EC₅₀ 1.4 μM (~7× more potent than DNP at 10.1 μM). Developed through a multi-institutional collaboration: Webster Santos at Virginia Tech and Kyle Hoehn at the University of Virginia (later UNSW Sydney). Selectively accumulates in lipid-rich tissues (liver, adipose). In mice, reversed diet-induced obesity without hyperthermia or reduced food intake. Continuum Biosciences (co-founded by Santos and Hoehn, 2017) is developing it.

Animal studies only Unregulated Exercise Mimetic

Written by WhatPeptide Editorial Team · Last updated 2026-03-18

Half-life

~1.7 hours in mice (oral gavage at 10 mg/kg; Alexopoulos et al.); ~3 hours under food admixture dosing (Axelrod et al.)

Dosage range

Mouse studies: 10 mg/kg oral gavage (PK profiling); efficacy studies used various routes. No established human dosing.

Administration

Oral

Research level

Animal only

How BAM-15 works

Selectively uncouples mitochondrial oxidative phosphorylation by transporting protons across the inner mitochondrial membrane, bypassing ATP synthase. Preferentially active in lipid-rich tissues (liver, adipose). Increases metabolic rate and fat oxidation without the narrow therapeutic window of classical uncouplers like DNP — no hyperthermia or food intake changes observed in animal studies.

Also known as: BAM15, N5,N6-bis(2-Fluorophenyl)[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine

Research relevance

Fat Loss
Moderate relevance 70

Side effects & safety

No obvious toxicity at tested doses in animals No hyperthermia (unlike DNP) No reduction in food intake No human safety data available

Contraindications

No human data — all contraindications theoretical
Pre-existing mitochondrial disorders
Pregnancy

Consult a healthcare provider before use if any of these apply to you.

FAQ

What is BAM-15? +
A mitochondrial protonophore uncoupler with EC₅₀ 1.4 μM (~7× more potent than DNP at 10.1 μM). Developed through a multi-institutional collaboration: Webster Santos at Virginia Tech and Kyle Hoehn at the University of Virginia (later UNSW Sydney). Selectively accumulates in lipid-rich tissues (liver, adipose). In mice, reversed diet-induced obesity without hyperthermia or reduced food intake. Continuum Biosciences (co-founded by Santos and Hoehn, 2017) is developing it. Its mechanism of action is based primarily on animal and in-vitro studies.
What is BAM-15 researched for? +
BAM-15 has the strongest research relevance for Fat Loss. Evidence is based primarily on animal and in-vitro studies.
What are the side effects of BAM-15? +
Reported side effects include No obvious toxicity at tested doses in animals, No hyperthermia (unlike DNP), No reduction in food intake, No human safety data available. Key contraindications: No human data — all contraindications theoretical; Pre-existing mitochondrial disorders; Pregnancy.
Is BAM-15 FDA approved? +
BAM-15 is not FDA-approved. It is available as a research compound or through compounding pharmacies in some jurisdictions.
How is BAM-15 administered? +
BAM-15 is typically administered via oral route. Researched dosage range: Mouse studies: 10 mg/kg oral gavage (PK profiling); efficacy studies used various routes. No established human dosing.. Half-life: ~1.7 hours in mice (oral gavage at 10 mg/kg; Alexopoulos et al.); ~3 hours under food admixture dosing (Axelrod et al.).

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