Explore BAM-15 dosage trends, reconstitution volumes, and vial size patterns from anonymized WPA peptide calculator data.
BAM-15 is a small-molecule mitochondrial uncoupler studied in animal models for energy-expenditure and fat-loss research. It is a chemical compound, not a peptide or SARM, so the certificate of analysis (COA) is about chemical purity and accurate dose per unit.
BAM-15 partitions into the inner mitochondrial membrane and acts as a protonophore — transporting protons back across the inner membrane and dissipating the electrochemical gradient that ATP synthase normally uses to make ATP. The mitochondria respond by accelerating substrate oxidation (especially fatty-acid β-oxidation) to maintain the gradient, increasing whole-body energy expenditure. **Unlike DNP, BAM-15 is reportedly specific to mitochondrial inner-membrane and does not significantly uncouple the plasma membrane, which is the published mechanistic basis for the wider therapeutic window: in mouse studies, BAM-15 produces fat-loss and metabolic-improvement effects without the dangerous hyperthermia DNP causes at near-effective doses.[1][2][4]**
Kenwood et al. (Mol Metab 2014) characterised BAM-15 as a protonophore uncoupler with mitochondrial specificity.[1] Alexopoulos et al. (Nat Commun 2020) demonstrated that BAM-15 produced substantial fat-loss, reversal of diet-induced obesity, improved insulin sensitivity, and reduced hepatic steatosis in mice without hyperthermia or tachycardia at effective doses — the breakthrough in-vivo result that brought BAM-15 to broader attention.[2] Follow-on work has extended BAM-15 into models of metabolic-dysfunction-associated steatohepatitis (MASH), aging, and acute kidney injury.[4][5] No human trial has been registered in ClinicalTrials.gov for BAM-15.[3]
Not FDA-approved. No registered human clinical trial. Pre-clinical mouse data only. Published as a safer alternative to DNP, but human pharmacokinetic and safety profiles are entirely uncharacterised. Research-grade material only.
BAM-15 has a reported half-life of ~4 hours (estimated). The pharmacokinetic reference models an interval of once daily (oral); this is not a measured community cadence or a dosing recommendation. Short-acting, so a once-daily dose clears before the next with little buildup. The effect tracks each dose rather than a steady level. Pharmacokinetic source: No human PK data; pre-clinical mitochondrial uncoupler (Alexopoulos et al. Nat Commun 2020). It is catalogued under Other Peptides on WPA.
4 BAM-15 reconstitution calculations have been logged by the WPA community.
This is the lifetime header population. Each chart and its associated analysis below use their own selected period and denominator; frequency responses are a separate cohort.
These figures come from anonymized WPA peptide calculator sessions, not verified administrations or unique people. Separate modal inputs do not establish a joint protocol. They are community input statistics — not dosing recommendations, and not medical advice.
These figures come from anonymized WPA peptide calculator sessions.
All figures shown are aggregated from anonymized calculator inputs and are provided strictly for independent laboratory research and educational purposes. They are community usage statistics — not dosing recommendations, and not medical advice.