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Brevilin A

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Chemical Structure| 16503-32-5 同义名 : 6-O-Angeloylprenolin;6-O-Angeloylplenolina;6-O-Angeloylplenolin;6-OAP;Brevelin A
CAS号 : 16503-32-5
货号 : A426347
分子式 : C20H26O5
纯度 : 98%
分子量 : 346.418
MDL号 : MFCD04034623
存储条件:

粉末 Sealed in dry,2-8°C

液体 -20°C:3-6个月-80°C:12个月

溶解度 :

DMSO: 105 mg/mL(303.1 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO

动物实验配方:
生物活性
描述 STAT3 is an oncoprotein which participates in essential processes of cell survival, growth and proliferation in many types of tumors, as well as immune diseases[3]. Brevilin A is a sesquiterpene lactone isolated from Centipeda minima with anti-tumor activity. Brevilin A is a selective inhibitor of JAK-STAT signal pathway by attenuating the JAKs activity and blocking STAT3 signaling (IC50 = 10.6 µM) in cancer cells[3]. In vivo investigation suggested that brevilin A significantly inhibited the growth of CT26 tumor compared to adriamycin and concurrently promoted the expressions of LC3-II and cleaved-caspase-3 in tumor tissues[4]. Brevilin A increased ROS levels, decreased MMP and induced apoptosis of CT26 cell in a dose-dependent manner. Higher apoptotic rates were achieved in CT26 cells treated with 2 μg/ml brevilin A compared to 2 μg/ml adriamycin, with a statistical significance of both compounds compared to control, indicating that brevilin A exerts a greater capacity in cell apoptosis induction than adriamycin[4]. Brevilin A significantly down-regulated the phosphorylation of PI3K, AKT and mTOR, and promoted the expression of LC3-II, which was a key protein in cell autophagy, in addition to the expression of autophagy-related proteins Beclin1 and Atg5, which indicated that PI3K/AKT/mTOR signaling was involved in CT26 autophagy induced by brevilin A[4]. Tumor weights of mice treated with brevilin A and adriamycin for 14 days were significantly lower compared to the control group (p < .01, p < .05) while the weight of those treated with brevilin A were significantly lower than that of the adriamycin group (p < .01). Body weights in adriamycin group were clearly lower than brevilin A group (p < .01), indicating that brevilin A exhibites lower toxicity compared to adriamycin[4]. The growth inhibition of the tumors by brevilin A reached 74.89% on day 14 after the inoculation, but the inhibition of tumor growth by adriamycin was 53.18%. In contrast with the control, brevilin A significantly promoted the expressions of LC3-II and cleaved-caspase-3 in tumor tissues[4].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.89mL

0.58mL

0.29mL

14.43mL

2.89mL

1.44mL

28.87mL

5.77mL

2.89mL

参考文献

[1]Chen X, Du Y, et al. Brevilin A, a novel natural product, inhibits janus kinase activity and blocks STAT3 signaling in cancer cells. PLoS One. 2013 May 21;8(5):e63697.

[2]Pu S, Guo Y, Gao W. [Chemical constituents from Centipeda minima] . Zhongguo Zhong Yao Za Zhi. 2009 Jun;34(12):1520-2. Chinese.

[3]Chen X, Du Y, Nan J, Zhang X, Qin X, Wang Y, Hou J, Wang Q, Yang J. Brevilin A, a novel natural product, inhibits janus kinase activity and blocks STAT3 signaling in cancer cells. PLoS One. 2013 May 21;8(5):e63697. doi: 10.1371/journal.pone.0063697. PMID: 23704931; PMCID: PMC3660600.

[4]You P, Wu H, Deng M, Peng J, Li F, Yang Y. Brevilin A induces apoptosis and autophagy of colon adenocarcinoma cell CT26 via mitochondrial pathway and PI3K/AKT/mTOR inactivation. Biomed Pharmacother. 2018 Feb;98:619-625. doi: 10.1016/j.biopha.2017.12.057. Epub 2017 Dec 29. PMID: 29289836.