KC7F2

CAS号

927822-86-4

分子式

C16H16Cl4N2O4S4

主要靶点

HIF|HIF/HIF Prolyl-Hydroxylase

仅限科研使用

Cat No : CM04468

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Synonyms

Inhibitor|KC7F2|KC-7F2|inhibit|HIF/HIFProlylHydroxylase|HIF/HIF Prolyl-Hydroxylase|HIF ProlylHydroxylase|HIF/HIF ProlylHydroxylase|HIF Prolyl-Hydroxylase|HIF|HIFProlylHydroxylase|HIF-PH|HIF-1α|HIFs|Hypoxia-inducible factors



产品信息

CAS号 927822-86-4
分子式 C16H16Cl4N2O4S4
主要靶点 HIF|HIF/HIF Prolyl-Hydroxylase
主要通路 血管生成|表观遗传|代谢|表观遗传
分子量 570.38
纯度 99.11%, 此纯度可做参考,具体纯度与批次有关系,可咨询客服
储存条件 Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice.
别名 Inhibitor|KC7F2|KC-7F2|inhibit|HIF/HIFProlylHydroxylase|HIF/HIF Prolyl-Hydroxylase|HIF ProlylHydroxylase|HIF/HIF ProlylHydroxylase|HIF Prolyl-Hydroxylase|HIF|HIFProlylHydroxylase|HIF-PH|HIF-1α|HIFs|Hypoxia-inducible factors

靶点活性

HIF1α:20 μM

体内活性

KC7F2在戊四氮癫痫模型大鼠中显著缩短潜伏期,并在慢性阶段增加了锂-毛果芸香碱大鼠模型中自发性复发性癫痫的发作率。[3]

体外活性

KC7F2在LN229-HRE-AP细胞中抑制HRE驱动的转录并降低HIF-1α蛋白水平。对于MCF7、LNZ308、A549、U251 mg和LN229癌细胞,KC7F2表现出剂量响应性细胞毒性,IC50约为15至25μM。在D54 mg胶质瘤细胞中,尤其在缺氧条件下,KC7F2抑制了集落形成。[1] 在缺氧的小胶质细胞培养中,KC7F2下调TfR和DMT的表达,并减少了HIF-1α介导的铁积累。[2]

溶解度

DMSO:57 mg/mL (99.93 mM)

细胞实验

Cells are seeded onto 96-well plates (4 × 103/well) and cultured under normoxic (21% O2) and hypoxic (1% O2) conditions with different concentrations of KC7F2 for 72 h or treated for various times with 20 μM KC7F2. For proliferation analysis, cells are fixed with 50% trichloroacetic acid for 1 h at 4°C, followed by staining with 0.4% sulforhodamine B dissolved in 1% acetic acid for 30 min at room temperature. Plates are washed five times with 1% acetic acid to remove unbound dye. Bound dye is dissolved by adding 10 mM unbuffered Tris base. Cell proliferation is calculated by measuring OD values at 564 nm using a spectrophotometer.(Only for Reference)

参考文献

1.Narita T, et al. Clin Cancer Res. 2009, 15(19), 6128-6136.
2.Rathnasamy G, et al. Neuropharmacology. 2014, 77, 428-440.
3.Li J, et al. Synapse. 2014, 68(9), 402-409.
4.Yang X L, Zeng M L, Shao L, et al. NFAT5 and HIF-1α Coordinate to Regulate NKCC1 Expression in Hippocampal Neurons after Hypoxia-Ischemia[J]. Frontiers in Cell and Developmental Biology. 2019, 7: 339.

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