| Size | Price | Stock |
|---|---|---|
| 5mg | $75 | In-stock |
| 10mg | $135 | In-stock |
| 25mg | $250 | In-stock |
| 50mg | $400 | In-stock |
| 100mg | $600 | In-stock |
| 250mg | $1000 | In-stock |
| 500mg | $1350 | In-stock |
| 1 g | Get quote | |
| 5 g | Get quote | |
| We match the lowest price on market. | ||
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| Cat. No. : | HY-110284 |
| M.Wt: | 340.29 |
| Formula: | C16H10F2N6O |
| Purity: | >98 % |
| Solubility: | DMSO : 50 mg/mL (ultrasonic) |
BAM 15 is a mitochondrial protonophore uncoupler. BAM 15 is an oxidative phosphorylation (OXPHOS) uncoupler[1]. In Vitro: BAM 15 is able to increase O2 consumption across a broad dosing range without increasing ROS. BAM 15 and FCCP are structurally unrelated and it is observed that low doses of BAM 15 from 100 nM to 1 μM increase cellular O2 consumption rate (OCR) to a similar degree as FCCP, but higher concentrations from 1 μM to 50 μM reveal that BAM 15 is able to maintain uncoupled respiration at a high rate in a range of cell lines. BAM 15 is fully capable of increasing mitochondrial respiration in the presence of oligomycin and does so across a broader concentration range than FCCP in both myoblasts and hepatocytes. BAM 15 induces mitochondrial swelling, demonstrating that BAM 15 is a protonophore. BAM15-treated cells are more viable than FCCP-treated cells when administered across a broad dosing range up to 50 μM[1]. In Vivo: Compare to vehicle-treated mice, animals that receive BAM 15 are protected from kidney injury as indicated by lower plasma creatinine levels at 24 and 48 h post-ischemia, reduced tubular necrosis, less depletion of brush border villi, less obstruction of proximal tubules, and less immune cell infiltration[1].
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