规格: | 98% |
分子量: | 398.41 |
包装 | 价格(元) |
1mg | 电议 |
5mg | 电议 |
10mg | 电议 |
Background:
Deoxypodophyllotoxin (DPT), a derivative of podophyllotoxin, is a lignan with potent antimitotic, anti-inflammatory and antiviral properties isolated from rhizomes of Sinopodophullumhexandrum (Berberidaceae). Deoxypodophyllotoxin, targets the microtubule, has a major impact in oncology not only as anti-mitotics but also as potent inhibitors of angiogenesis[1]. Deoxypodophyllotoxin induces cell autophagy and apoptosis[2]. Deoxypodophyllotoxin evokes increase of intracellular Ca2+ concentrations in DRG neurons[3].
Deoxypodophyllotoxin (25-75 nM; 6-48 hours) increases the percentage of early apoptotic cell population from 2.05 to 5.62 and 18.49% for 24 h and 48 h, respectively[1].Deoxypodophyllotoxin (25-75 nM; 6-48 hours) treats SGC-7901 cells arrested in G2/M phase in time- and dose- dependent manners[1]. Deoxypodophyllotoxin (25-75 nM; 6-48 hours) results in a remarkably time- and dose-dependent decrease in Cdc2 and Cdc25C expression levels and increases cyclin B1 within 6h, decreases PARP, Bcl-2 and caspase-3 activity[1]. Apoptosis Analysis[1] Cell Line: SGC-7901 cells
Deoxypodophyllotoxin (intravenously injected; 5, 10, and 20 mg/kg; 3 times a week; 28 days) suppresses the tumors in a dose-dependent manner, the growth of tumors is inhibited by 22.19%, 47.91% and 50.93% with DPT at 5, 10 and 20 mg/kg, respectively[1]. Animal Model: Xenograft model of gastric cancer in nude mice with SGC-7901 cells[1]
[1]. Wang YR, et al. Deoxypodophyllotoxin induces G2/M cell cycle arrest and apoptosis in SGC-7901 cells and inhibits tumor growth in vivo. Molecules. 2015 Jan 20;20(1):1661-75. [2]. Kim SH, et al. Deoxypodophyllotoxin induces cytoprotective autophagy against apoptosis via inhibition of PI3K/AKT/mTOR pathway in osteosarcoma U2OS cells. Pharmacol Rep. 2017 Oct;69(5):878-884. [3]. Xu P, et al. Pharmacological effect of deoxypodophyllotoxin: a medicinal agent of plant origin, on mammalian neurons. Neurotoxicology. 2010 Dec;31(6):680-6.