Phenoxodiol

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

Phenoxodiol 激活线粒体 caspase 系统，抑制 X 连锁凋亡抑制剂 (XIAP)，破坏 FLICE 抑制蛋白 (FLIP) 表达，并使癌细胞对 Fas 介导的凋亡敏感。

Phenoxodiol activates the mitochondrial caspase system, inhibits X-linked inhibitor of apoptosis(XIAP), disrupts FLICE inhibitory protein(FLIP) expression, and sensitizes the cancer cells to Fas-mediated apoptosis. Phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle and upregulates p21WAF1 via a p53 independent manner. Phenoxodiol also inhibits DNA topoisomerase II.(In Vitro):Phenoxodiol, at concentrations >or=1 microg/ml (4 microM), inhibited proliferation and reduced the viability of healthy donor-derived PBMC. In contrast, lower Phenoxodiol concentrations (0.05-0.5 microg/ml) augmented, upon 3-day incubation, peripheral blood mononuclear cells cytotoxicity. Experiments with purified CD56(+) lymphocytes revealed that Phenoxodiol enhanced the lytic function of natural killer cells by directly stimulating this lymphocytic subpopulation.(In Vivo):Balb/C mice administered low-dose Phenoxodiol exhibited significantly reduced tumour growth rates and prolonged survival (in 40% of the animals) in a colon cancer model.

Phenoxodiol (Idronoxil) (0-10 μg/mL; 24 h) decreases cell viability of primary ovarian cancer cells.Phenoxodiol (0-10 μg/mL; 24 h) induces apoptosis and restores sensitivity to Fas-mediated apoptosis in ovarian cancer cells.Phenoxodiol (0-10 μg/mL; 24 h) induces caspase-8 activation and FLIP downregulation through the Akt-pathway. Phenoxodiol-induced apoptosis involves activation of the mitochondrial pathway and is caspase dependent. Phenoxodiol treatment results in downregulation and cleavage of XIAP.Phenoxodiol (10 and 30 μM; 24 and 48 h) induces cell cycle arrest in the G1/S phase of the cell cycle in prostate cancer cells. Cell Viability Assay Cell Line:R182s, R127, Hey, CP70, A2780, R187, R188, R207 and OSE cells Concentration:0, 0.01, 0.1, 1 and 10 μg/mL Incubation Time:24 h Result:A significant decrease in cell viabilityin all the ovarian cancer cell cultures was observed at a concentration of 10 μg/mL (41.6 μM) and did not affect ovarian surface epithelial (OSE) cells’ viability. In CP70 cells, the IC50 was 1.35 μM.Apoptosis Analysis Cell Line:CP70 and OSE cells Concentration:10 μg/mL Incubation Time:24 h Result:Induced apoptosis and resulted in a twofold increase in caspase-3 activity. No change in caspase-3 activity was found in normal OSE cells. Western Blot Analysis Cell Line:Ovarian cancer cells Concentration: 10 μg/mL Incubation Time:24 h Result:Induced caspase-8 activation, characterized bycleavage of procaspase-8 into its p43/41 and p28 forms and in downregulation of the p43 form of FLIPC in all the primarycultures as well as in the CP70 and Hey cell lines. Decreased the levels of Akt expression. Resulted in XIAP downregulation and cleavage to its 30 kDa inactive form.Cell Cycle Analysis Cell Line:LNCaP, DU145 and PC3 cells Concentration:10 and 30 μM Incubation Time:24 and 48 h Result:Induced significantly decreased G2 phase cell populations versus DMSO vehicle control, over 24 hours for both 10 μM and 30 μM treatments. The S phase cell population was found to increase versus DMSO vehicle control. RT-PCRCell Line:LNCaP, DU145 and PC3 cellsConcentration:10 and 30 μMIncubation Time:24 and 48 hResult:PC3 cells were found to significantly increase the expression of c-Myc at 30 μM after 48 h. Decreased the expression of Cyclin-D1 after 24 hours of treatment with 30 μM in DU145 and PC3 cells. Decreased the expression of Ki-67 after 24 hours of treatment with 10 and 30 μM in LNCaP and PC3 cells. Increased the expression of p21 in LNCaP and PC3 cells.

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Idronoxil | Dehydroequol | Haginin E

Apoptosis

Apoptosis

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81267-65-4

240.258

C15H12O3

>98% (HPLC)

In Vitro:?DMSO : ≥ 100 mg/mL (416.23 mM)

Oc1ccc(cc1)C1=Cc2ccc(O)cc2OC1

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(-20℃)

With Ice Pack

≥ 2 years