| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Cell lines | PC3 and DU145 (prostate carcinoma) cell lines |
Preparation Method | PC3 and DU145 cells maintained in log phase growth were plated in 96-well plates and treated with 0.25, 0.5, 1.5, 5, 15, 30, 60, 120, and 240 μmol/L FX-11 for 24 hours. |
Reaction Conditions | 0.25, 0.5, 1.5, 5, 15, 30, 60, 120, and 240 μmol/L for 24 hours |
Applications | After treated with FX-11, the metabolic phenotype of the two cell lines in vitro demonstrated no significant difference in extracellular acidification rate (ECAR), oxygen consumption rate (OCR), pyruvate uptake, and lactate production. |
Animal models | male SCID mice |
Preparation Method | groups of five mice were injected with control 2% (vol/vol) DMSO or 42 μg of FX11 |
Dosage form | Intraperitoneal injection, 42μg daily, for 10 days |
Applications | Daily i.p. injection of 42 μg of FX11 also resulted in a remarkable inhibition of tumor growth. |
| 产品描述 | FX-11 (LDHA Inhibitor FX11) was found to be a potent, competitive inhibitor of the human LDH-A's NADH binding pocket[1]. FX-11 was recharacterized using purified human liver LDHA with Ki of 8μM[2]FX11 inhibition of LDHA increased nonproductive mitochondrial respiration, leading to decreased ATP levels and cell proliferation, and increased oxygen consumption, ROS production and cell death[5]. FX-11 (IC50) for proliferation of DU145 and PC3 (prostate carcinoma) cell lines in vitro was strikingly similar (32 ± 1.1 μmol/L vs. 27 ± 1.1 μmol/L, respectively)[3]. Low concentrations of FX-11 could markedly decrease cell viability in the MPS2(the glycolytic subtype with upregulated carbohydrate and nucleotide metabolism) PDO (Patient-derived organoid) models[4]. FX-11, effectively inhibited tumor growth in human B-lymphoma and pancreatic cancer xenograft models. FX-11 could inhibit tumor growth in P493 lymphomas and human P198 pancreatic tumors ≥200 mm3[5]. References: |
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