BAM 15 |
| Catalog No.GC19056 |
BAM15 is a novel mitochondrial protonophore uncoupler (2-fluorophenyl){6-[(2-fluorophenyl)amino](1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl)}amine, that does not depolarize the plasma membrane.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 210302-17-3
Sample solution is provided at 25 µL, 10mM.
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BAM15 is a novel mitochondrial protonophore uncoupler (2-fluorophenyl){6-[(2-fluorophenyl)amino](1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl)}amine, that does not depolarize the plasma membrane[1].
BAM15 has an average EC50 value of 1.4 µM and is capable of maintaining high levels of mitochondrial respiration over a wide concentration range of 3 to 100 µM in OCR[2]. In fully differentiated C2C12 mouse myotubes, BAM15 (100 µM;16h) did not alter cell viability or number,but BAM15 improves cellular respiratory kinetics by sustained mitochondrial uncoupling[3]. Wild-type animals treated with both 50 µM BAM15 showed reduced mechanosensory neuronal defects during aging, which correlates with the maintenance of touch responses and short-term memory during aging in Caenorhabditis elegans[4]. BAM15(1mM) depolarized mitochondrial membrane potential, induced mitochondrial fission, increased mitochondrial ROS production, and increased mitochondrial oxygen consumption rate in A10 cells[5].
BAM15(1 mg/kg; i.p.; 3 hours before injection of LPS) attenuated serum cytokines, organ damage (liver enzymes and serum creatinine) and tissue cytokines (liver and kidney), and reduced inflammatory mononuclear/macrophages in the liver, in part by enhancing phosphorylated αAMPK in LPS-administered mice[6]. BAM15 was seen to reduce mortality after injection at 0, 6 and 12 hours after cecal ligation and puncture (CLP), and reduced kidney damage and spleen apoptosis even after 12 hours when the mice were sick[7].
References:
[1]. Kenwood BM, Weaver JL, et,al. Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane. Mol Metab. 2013 Nov 28;3(2):114-23. doi: 10.1016/j.molmet.2013.11.005. PMID: 24634817; PMCID: PMC3953706.
[2]. Alexopoulos SJ, Chen SY, et,al. Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice. Nat Commun. 2020 May 14;11(1):2397. doi: 10.1038/s41467-020-16298-2. PMID: 32409697; PMCID: PMC7224297.
[3]. Axelrod CL, King WT, et,al. BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control. EMBO Mol Med. 2020 Jul 7;12(7):e12088. doi: 10.15252/emmm.202012088. Epub 2020 Jun 10. PMID: 32519812; PMCID: PMC7338798.
[4]. Cho I, Song HO, et,al. BAM15 Relieves Neurodegeneration in Aged Caenorhabditis elegans and Extends Lifespan. Metabolites. 2022 Nov 17;12(11):1129. doi: 10.3390/metabo12111129. PMID: 36422268; PMCID: PMC9698188.
[5]. Tai Y, Li L, et,al. Mitochondrial uncoupler BAM15 inhibits artery constriction and potently activates AMPK in vascular smooth muscle cells. Acta Pharm Sin B. 2018 Oct;8(6):909-918. doi: 10.1016/j.apsb.2018.07.010. Epub 2018 Jul 26. PMID: 30505660; PMCID: PMC6251816.
[6]. Dang CP, Issara-Amphorn J, et,al. BAM15, a Mitochondrial Uncoupling Agent, Attenuates Inflammation in the LPS Injection Mouse Model: An Adjunctive Anti-Inflammation on Macrophages and Hepatocytes. J Innate Immun. 2021;13(6):359-375. doi: 10.1159/000516348. Epub 2021 Jun 1. PMID: 34062536; PMCID: PMC8613553.
[7]. Tsuji N, Tsuji T, et,al. BAM15 treats mouse sepsis and kidney injury, linking mortality, mitochondrial DNA, tubule damage, and neutrophils. J Clin Invest. 2023 Feb 9:e152401. doi: 10.1172/JCI152401. Epub ahead of print. PMID: 36757801.
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