Bufalin

  Cat. No.:  DC6501   Featured
Chemical Structure
465-21-4
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More than 5000 active chemicals with high quality for research!
Field of application
Bufalin inhibits steroid receptor coactivator 1 (SRC-1) and SRC-3 at doses as low as 5 nM, promotes the degradation of SRC-3 protein, and inhibits cancer cell growth both in vitro and in vivo.
Cas No.: 465-21-4
Chemical Name: NSC 89595,NSC-89595,NSC89595
Synonyms: NSC 89595,NSC-89595,NSC89595
SMILES: O=C1C=CC([C@H]2CC[C@]3(O)[C@]4([H])CC[C@]5([H])C[C@@H](O)CC[C@]5(C)[C@@]4([H])CC[C@]23C)=CO1
Formula: C24H34O4
M.Wt: 386.52
Purity: >98%
Sotrage: 4°C for 1 year, -20°C for more than 2 years
Description: Bufalin a major digoxin-like immunoreactive component of the Chinese medicine Chan Su; has been shown to exert a potential for anticancer activity against various human cancer cell lines in vitro.
In Vivo: bufalin (0.3 and 0.6 mg/kg, i.p.) potently decreased carrageenan-induced paw edema. Bufalin down regulated the expression levels of nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) during these treatments [5].
In Vitro: bufalin remarkably inhibited growth in human gallbladder cancer cells by decreasing cell proliferation, inducing cell cycle arrest and apoptosis in a dose-dependent manner. Bufalin also disrupted the mitochondrial membrane potential (ΔΨm) and regulated the expression of cell cycle and apoptosis regulatory molecules. Activation of caspase-9 and the subsequent activation of caspase-3 indicated that bufalin may be inducing mitochondria apoptosis pathways [1]. bufalin suppressed the protein levels associated with DNA damage and repair, such as a DNA dependent serine/threonine protein kinase (DNA-PK), DNA repair proteins breast cancer 1, early onset (BRCA1), 14-3-3 σ (an important checkpoint keeper of DDR), mediator of DNA damage checkpoint 1 (MDC1), O6-ethylguanine-DNA methyltransferase (MGMT) and p53 (tumor suppressor protein) [2]. TNF-α significantly increased p65 translocation into nucleus (P < 0.01) and enhanced NF-κB DNA-binding activity, which were dose-dependently inhibited by bufalin. Furthermore, bufalin attenuated the TNF-α-induced interleukin-1beta (IL-1β), IL-6, and IL-8 production in RAFLSs in a concentration-dependent manner [3]. bufalin enhanced TRAIL-induced apoptosis in MCF-7 and MDA-MB-231 breast cancer cells by activating the extrinsic apoptotic pathway. Bufalin also promoted the clustering of death receptor 4 (DR4) and DR5 in aggregated lipid rafts [4].
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
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