4-Hydroperoxy cyclophosphamide
国际站：4-Hydroperoxy cyclophosphamide
CAS：39800-16-3
品牌：MedChemExpress (MCE)
存储条件：-20°C, stored under nitrogen
生物活性：4-Hydroperoxy cyclophosphamide 是前体药物 Cyclophosphamide 的活性代谢物形式。 4-Hydroperoxy cyclophosphamide 交联 DNA 并诱导 T 细胞细胞凋亡，与死亡受体激活无关，但通过产生活性氧 (ROS). 4-Hydroperoxy cyclophosphamide 具有治疗淋巴瘤和自身免疫性疾病的潜力。
体外：4-Hydroperoxy cyclophosphamide (1 或 3 μg/mL, 24, 48, 72 h) 通过氧化应激诱导的线粒体凋亡因子 AIF 和 EndoG 的核重新定位介导 caspase 非依赖性 T 细胞凋亡[1]。 4-Hydroperoxy cyclophosphamide (1 μg/mL, 72, 96 h) 和甲氨蝶呤 (HY-14519) 联用通过抑制 JAK2/STAT3 和 p38MAPK 信号通路抑制 IL-6/sil-6r 诱导的成纤维细胞样滑膜细胞中 RANKL 的表达[2]。 MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内：4-Hydroperoxy cyclophosphamide (200 mg/kg, 腹腔注射) 在小鼠中不依赖 caspase 的 T 细胞和 B细胞死亡[1]。 MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: BALB/c mice[1] Dosage: 200 mg/kg Administration: i.p. Result: Exhibited a marked depletion of immature double-positive CD4 þ CD8 þ thymocytes and mature single-positive CD4+ and CD8+ T cells.
参考文献：[1]. Niu HQ, et al. Combination of 4-hydroperoxy cyclophosphamide and methotrexate inhibits IL-6/sIL-6R-induced RANKL expression in fibroblast-like synoviocytes via suppression of the JAK2/STAT3 and p38MAPK signaling pathway. Int Immunopharmacol. 2018 Aug;61:45-53.[2]. Strauss G, et al. 4-hydroperoxy-cyclophosphamide mediates caspase-independent T-cell apoptosis involving oxidative stress-induced nuclear relocation of mitochondrial apoptogenic factors AIF and EndoG. Cell Death Differ. 2008 Feb;15(2):332-43.
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