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19-Hydroxybufalin Sale

(Synonyms: 19-羟基蟾毒灵) 目录号 : GC60444

19-Hydroxybufalin是一种蟾二烯羟酸内酯,可抑制上皮间质转化,减弱PC3细胞的迁移和侵袭。

19-Hydroxybufalin Chemical Structure

Cas No.:39844-86-5

规格 价格 库存 购买数量
5mg
¥3,600.00
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产品描述

19-Hydroxybufalin is a bufadienolide, inhibits epithelial-mesenchymal transition and attenuates the migration and invasion of PC3 cells[1].

[1]. Chen L, et al. Arenobufagin inhibits prostate cancer epithelial-mesenchymal transition and metastasis by down-regulating β-catenin. Pharmacol Res. 2017 Sep;123:130-142.

Chemical Properties

Cas No. 39844-86-5 SDF
别名 19-羟基蟾毒灵
Canonical SMILES O=C(C=C1)OC=C1[C@H]2CC[C@]3(O)[C@]4([H])CC[C@]5([H])C[C@@H](O)CC[C@]5(CO)[C@@]4([H])CC[C@]23C
分子式 C24H34O5 分子量 402.52
溶解度 DMSO: 100 mg/mL (248.43 mM) 储存条件 4°C, protect from light
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1 mM 2.4843 mL 12.4217 mL 24.8435 mL
5 mM 0.4969 mL 2.4843 mL 4.9687 mL
10 mM 0.2484 mL 1.2422 mL 2.4843 mL
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Research Update

19-Hydroxybufalin inhibits non-small cell lung cancer cell proliferation and promotes cell apoptosis via the Wnt/β-catenin pathway

Exp Hematol Oncol 2021 Oct 25;10(1):48.PMID:34696818DOI:PMC8543904

Background: Bufadienolides derived from the skin of toads are often regarded as the main active components with antitumor effects. 19-Hydroxybufalin (19-HB) is a monomer of bufadienolides; however, its effects and underlying molecular mechanisms on tumor growth remain to be ascertained. In this report, we focused on the antitumor effects of 19-HB on non-small cell lung cancer to provide a scientific basis for its further development and utilization. Methods: The antitumor effects of 19-HB on the human NSCLC cell lines NCI-H1299 and NCI-H838 were examined in vitro. The cells were treated with different concentrations of 19-HB, and the inhibition of cell growth was measured by CCK-8 and colony formation assays. Furthermore, cell apoptosis was analyzed by flow cytometry, TUNEL staining, JC-1 staining, and western blotting. The effects on migration and invasion were evaluated by wound-healing assay, transwell assay, and western blotting. Finally, the antitumor effects of 19-HB were evaluated in vivo using a xenograft mouse model. Results: 19-HB-treated NSCLC cells showed inhibited cell viability and increased apoptosis. The expression levels of cleaved caspase-3, cleaved-PARP, and Bax/Bcl-2 were upregulated, while the mitochondrial membrane potential decreased. In contrast, migration, invasion, as well as the expression of MMP2, MMP7, MMP9, the epithelial-mesenchymal transition-related proteins N-cadherin and Vimentin, and the transcription factors Snail and Slug were inhibited. Furthermore, the expression levels of the key molecules in the Wnt/β-catenin signaling pathway (CyclinD1, c-Myc, and β-catenin) were decreased. In vivo, the growth of xenograft tumors in nude mice was also significantly inhibited by 19-HB, and there were no significant changes in biochemical indicators of hepatic and renal function. Conclusions: 19-HB inhibited the proliferation, migration, and invasion, and promoted the apoptosis of NSCLC cells via the Wnt/β-catenin pathway. In addition, 19-HB inhibited the growth of xenograft tumors in nude mice with little toxicity to the liver and kidney. Thus, 19-HB may be a potential antitumor agent for treating NSCLC.