5-hydroxy-7,4'-diacetoxyflavanone-N-phenyl hydrazone | 1334290-09-3

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 2-芳基苯并呋喃类黄酮
• 英文名称: 5-hydroxy-7,4'-diacetoxyflavanone-N-phenyl hydrazone
• 英文别名: 5-hydroxy-7,4'-diacetyloxyflavanone-N-phenyl hydrazone；[4-[7-acetyloxy-5-hydroxy-4-(phenylhydrazinylidene)-2,3-dihydrochromen-2-yl]phenyl] acetate
• CAS: 1334290-09-3
• 化学式: C₂₅H₂₂N₂O₆
• 分子量: 446.459
• InChiKey: COLHXDDUGXENKH-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.2
• 重原子数：
  33
• 可旋转键数：
  7
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.16
• 拓扑面积：
  106
• 氢给体数：
  2
• 氢受体数：
  8

反应信息

• 作为产物：
  描述：

  5,7,4'-trihydroxyflavanone N-phenyl hydrazone 、 乙酰氯 在 三乙胺 作用下， 以 四氢呋喃 为溶剂， 反应 0.34h， 以91.3%的产率得到5-hydroxy-7,4'-diacetoxyflavanone-N-phenyl hydrazone
  参考文献：
  名称：

  A Synthetic Naringenin Derivative, 5-Hydroxy-7,4′-diacetyloxyflavanone-N-phenyl Hydrazone (N101-43), Induces Apoptosis through Up-regulation of Fas/FasL Expression and Inhibition of PI3K/Akt Signaling Pathways in Non-Small-Cell Lung Cancer Cells

  摘要：

  Naringenin, a well-known naturally occurring flavonone, demonstrates cytotoidcity in a variety of human cancer cell lines; its inhibitory effects on tumor growth have spurred interest in its therapeutic application. In this study, naringenin was derivatized to produce more effective small-molecule inhibitors of cancer cell proliferation, and the anticancer effects of its derivative, 5-hydroxy-7,4'-diacetyloxyflavanone-N-phenyl hydrazone (N101-43), in non-small-cell lung cancer (NSCLC) cell lines NCI-H460, A549, and NCI-H1299 were investigated. Naringenin itself possesses no cytotoxicity against lung cancer cells. In contrast, N101-43 inhibits proliferation of both NCI-H460 and A549 cell lines; this capacity is lost in p53-lacking NCI-H1299 cells. N101-43 induces apoptosis via sub-G(1) cell-cycle arrest in NCI-H460 and via G(0)/G(1) arrest in A549 cells. Expression of apoptosis and cell-cycle regulatory factors is altered: Cyclins A and D1 and phospho-pRb are down-regulated, but expression of CDK inhibitors such as p21, p27, and p53 is enhanced by N101-43 treatment; N101-43 also increases expression levels of the extrinsic death receptor Fas and its binding partner FasL. Furthermore, N101-43 treatment diminishes levels of cell survival factors such as PI3K and p-Akt dose-dependently, and N101-43 additionally induces cleavage of the pro-apoptotic factors caspase-3, caspase-8, and poly ADP-ribose polymerase (PARP). Cumulatively, these investigations show that the naringenin derivative N101-43 induces apoptosis via up-regulation of Fas/FasL expression, activation of caspase cascades, and inhibition of PI3K/Akt survival signaling pathways in NCI-H460 and A549 cells. In conclusion, these data indicate that N101-43 may have potential as an anticancer agent in NSCLC.

  DOI：

  10.1021/jf2017594