BAM15 Capsules 50mg 60ct by Omnix Peptides — research-grade capsules

BAM15 Capsules 50mg

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BAM15 (N5,N6-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine) is a small-molecule mitochondrial protonophore that uncouples oxidative phosphorylation from ATP synthesis without depolarizing the plasma membrane.

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Research goals: Metabolic & Weight

Description

BAM15 (N5,N6-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine) is a small-molecule mitochondrial protonophore that uncouples oxidative phosphorylation from ATP synthesis without depolarizing the plasma membrane. Originally identified by Kenwood and colleagues at the University of Virginia in 2014, BAM15 was developed as a safer alternative to the historical uncoupler 2,4-dinitrophenol (DNP), which was discontinued in humans in the 1930s due to a narrow therapeutic window and lethal hyperthermia. BAM15 has been characterized in multiple peer-reviewed mouse studies as orally bioavailable and effective against diet-induced obesity, hepatic steatosis, and insulin resistance.

The strongest preclinical finding comes from the Alexopoulos et al. Nature Communications study: in C57BL/6J mice on a Western diet, oral BAM15 reversed diet-induced obesity, decreased hepatic fat and inflammatory lipids, and improved insulin sensitivity in multiple tissues — without altering food intake, lean body mass, or body temperature.2

Important Note on the Evidence Base

The published evidence base for BAM15 is preclinical. All controlled studies referenced below were conducted in cell culture (L6 myoblasts, hepatocytes, primary cardiomyocytes) or rodent models (diet-induced obese C57BL/6J mice, db/db mice, NASH models). No human clinical trials of BAM15 have been published in peer-reviewed journals as of 2026, and the compound’s pharmacokinetics, safety, and efficacy in humans remain uncharacterized in the published literature. Mitochondrial uncouplers as a drug class carry historical safety concerns (DNP) related to hyperthermia and cardiovascular adverse effects, although BAM15 specifically has shown a wider therapeutic window in preclinical models. This product is for laboratory research only.

Published Research on BAM15

Original Identification and Characterization — Kenwood et al., Molecular Metabolism (2014)

The foundational paper that introduced BAM15 as a mitochondrial protonophore that uncouples oxidative phosphorylation without depolarizing the plasma membrane — the key pharmacological distinction from FCCP and CCCP that gives BAM15 a wider effective concentration range in living cells. In L6 myoblast mitochondria, BAM15 had an EC50 of 270 nM. Compared with FCCP, BAM15 stimulated a higher maximum rate of mitochondrial respiration before inducing respiratory inhibition. The authors framed the membrane-selectivity profile as the basis for therapeutic development of mitochondrial uncouplers in obesity, NAFLD, and metabolic disease.1

Reversal of Diet-Induced Obesity in Mice — Alexopoulos et al., Nature Communications (2020)

This study tested oral BAM15 in C57BL/6J mice on a Western diet and demonstrated that the compound increased nutrient oxidation and decreased body fat mass without altering food intake, lean body mass, or body temperature. BAM15 also decreased hepatic fat, decreased inflammatory lipids, and exerted antioxidant effects. Hyperinsulinemic-euglycemic clamp studies showed BAM15 improved insulin sensitivity in multiple tissue types. The findings established pharmacologic mitochondrial uncoupling as a tractable approach to reverse obesity in mice without compromising lean mass.2

Body Composition and Glycemic Control — Axelrod et al., EMBO Molecular Medicine (2020)

This independent confirmation study, published in parallel with the Alexopoulos work, showed BAM15 was orally bioavailable, selectively distributed to lipid-rich tissues, and protected mice against diet-induced obesity. Notably, the improvements in body composition and glycemic control were observed independently of weight loss, suggesting tissue-selective effects on lipid storage and insulin sensitivity beyond simple caloric inefficiency. BAM15 enhanced mitochondrial respiratory kinetics, improved insulin action, and stimulated nutrient uptake by sustained activation of AMPK in vitro.3

Therapeutic Potential for NAFLD and NASH — Goedeke & Shulman, Molecular Metabolism (2021)

This Yale-led review synthesizes the preclinical case for mitochondrial uncouplers as a class of treatment for metabolic-associated fatty liver disease and NASH, with detailed coverage of BAM15 and its second-generation derivatives (compound 10b, SHS4121705). In a STAM murine model of NASH, BAM15 derivatives at 25 mg/kg/day for 21 days decreased hepatic triglyceride content and improved markers of liver toxicity including plasma ALT, hepatic inflammation, fibrosis, and NAFLD activity score — independently of changes in food intake, body weight, or body temperature. The review situates BAM15 within the broader pipeline of selective mitochondrial uncouplers in development for human metabolic disease.4

About the Compound

BAM15 is a small-molecule (non-peptide) mitochondrial uncoupler from the oxadiazolopyrazine class. Its mechanism is direct protonophore activity: BAM15 transports protons across the inner mitochondrial membrane via a pathway independent of ATP synthase, dissipating the proton gradient that normally drives ATP production. Because the inner mitochondrial membrane is uncoupled, electron transport runs at high rate while producing less ATP per unit of substrate oxidized; the cell compensates by burning more nutrients (fat, glucose) to maintain energy homeostasis. The compound’s defining property versus older protonophores (DNP, FCCP, CCCP) is its lack of plasma membrane depolarization, which substantially widens the effective concentration range and reduces non-mitochondrial off-target effects.

  • Compound class: small-molecule mitochondrial protonophore uncoupler; oxadiazolopyrazine
  • IUPAC name: N5,N6-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine
  • CAS Number: 210302-17-3
  • Molecular Formula: C16H10F2N6O
  • Molecular Weight: 340.30 g/mol
  • Solubility: soluble in DMSO; low aqueous solubility (lipophilic, membrane-permeable)
  • Mechanism: mitochondrial proton transport without plasma membrane depolarization; uncouples oxidative phosphorylation from ATP synthesis
  • Regulatory status: not approved by the FDA or EMA. No human clinical trials published as of 2026

Product Specifications

  • Format: capsules
  • Strength: 50 mg per capsule
  • Count: 60 capsules per bottle
  • Purity: ≥98% (HPLC verified)
  • Container: sealed amber bottle
  • Certificate of Analysis: lot-specific COA available

See the FDA Disclosure, Storage Instructions, and RUO tabs for handling, storage, and regulatory information.

References

  1. Kenwood BM, Weaver JL, Bajwa A, et al. Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane. Mol Metab. 2014;3(2):114-123. doi:10.1016/j.molmet.2013.11.005
  2. Alexopoulos SJ, Chen SY, Brandon AE, et al. Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice. Nat Commun. 2020;11(1):2397. doi:10.1038/s41467-020-16298-2
  3. Axelrod CL, King WT, Davuluri G, et al. BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control. EMBO Mol Med. 2020;12(7):e12088. doi:10.15252/emmm.202012088
  4. Goedeke L, Shulman GI. Therapeutic potential of mitochondrial uncouplers for the treatment of metabolic associated fatty liver disease and NASH. Mol Metab. 2021;46:101178. doi:10.1016/j.molmet.2021.101178

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For research use only. Not for human consumption.