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Brefeldin A(BFA)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Brefeldin A(BFA)图片
CAS NO:20350-15-6
规格:≥98%
包装与价格:
包装价格(元)
250mg电议
500mg电议
1g电议
2g电议

产品介绍
Brefeldin A (also known as BFA), a fungal metabolite, is a potent macrocyclic lactone antibiotic and ATPase inhibitor for intracellular vesicle formation and protein transport (protein trafficking between the endoplasmic reticulum (ER) and the Golgi apparatus) with IC50 of 0.2 μM in HCT 116 cells. It has antitumor, antifungal, and antiviral effects. It induces cancer cell differentiation and apoptosis. Treatment with BFA could attenuate stimulus-dependent hyperalgesia phenomenon via inhibiting vesicular exocytosis which process is important for ATP release. BFA induced cells apoprosis (colorectal cancer cell line HCT116 ) by inhibiting ATP which functioned in the process of cellular vesicle trafficking.
理化性质和储存条件
Molecular Weight (MW)280.36
FormulaC16H24O4
CAS No.20350-15-6
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: 4 mg/mL (14.3 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Other infoChemical Name: (1S,2E,7S,10E,12R,13R,15S)-12,15-Dihydroxy-7-methyl-8-oxabicyclo[11.3.0]hexadeca-2,10-dien-9-one
InChi Key: KQNZDYYTLMIZCT-KQPMLPITSA-N
InChi Code: InChI=1S/C16H24O4/c1-11-5-3-2-4-6-12-9-13(17)10-14(12)15(18)7-8-16(19)20-11/h4,6-8,11-15,17-18H,2-3,5,9-10H2,1H3/b6-4+,8-7+/t11-,12+,13-,14+,15+/m0/s1
SMILES Code: O=C1O[C@@H](C)CCC/C=C/[C@]2([H])C[C@H](O)C[C@@]2([H])[C@H](O)/C=C/1
SynonymsBrefeldin A; BFA; Cyanein; Decumbin; Brefeldin-A; Ascotoxin; Cyanein; Decumbin; Bredfeldin A; Synergisidin
实验参考方法
In Vitro

In vitro activity: Brefeldin A is a fungal metabolite and blocks the forward transport between the endoplasmic reticulum and Golgi apparatus, Brefeldin A causes an impaired distribution of the membrane proteins. When HCT 116 human colon cancer cell is treated with Brefeldin A, morphological changes indicating cell differentiation are observed. Brefeldin A exerts its cytotoxic effects mainly by inducing differentiation and apoptosis in tumor cells. The treatment of the strips with 20 μg/mL Brefeldin A for 6 hours completely abolishes the relaxation induced by bradykinin in the presence of 10mM indomethacin and 30 μM L-NOARG. The treatment with 20 μg/mL Brefeldin A substantially abolishes the bradykinin-induced decreases in [Ca2+]i and tension in the range of concentrations between 1 nM and 1 mM. Brefeldin A has no effect on the [Ca2+]i elevation in endothelial cells induced by bradykinin or substance P. Addition of the fungal metabolite Brefeldin A does not affect the spontaneous phospholipid-dependent GTPS binding to myr-rARF1 but totally abolishs the retinal isotonic extract (RIE)-catalyzed exchange, with half-maximal inhibition at 2 μM Brefeldin A. Brefeldin A prevents a wide variety of membrane traffic pathways. Brefeldin A inhibits an ADP-ribosylation factor-specific guanine nucleotide exchange activity present in Golgi membranes or in brain cytosol. The complete prevention by Brefeldin A strongly suggests that the retinal extract contains an ARF-specific guanine nucleotide exchange factor. Retinal isotonic extract (RIE)-catalyzed GTPS release from both ADP-ribosylation factors (ARFs) is only partly inhibited by Brefeldin A, even at 300 μM. Brefeldin A induces fusion of the Golgi apparatus with the ER. Brefeldin A abolishes the inhibitory effect of the CERT inhibitor HPA-12. Brefeldin A treatment, which induces fusion of the Golgi apparatus and the ER, rescues the limonoid-induced prevention of sphingomyelin biosynthesis. BFA treatment of CHO cells causes a 2 to 3 fold increase in sphingomyelin synthesis. Apart from B-CLL cells, Brefeldin A reportedly causes apoptosis in multiple myeloma (U266, NCI-H929), Jurkat, HeLa, leukaemia (HL60, K562, BJAB), colon (HT-29) and prostate, as well as adenoid cystic sarcoma cells. The administration of 25 ng/mL of Brefeldin A completely blocks growth of HF4.9 and HF28RA cells, whereas higher Brefeldin A doses (75 ng/mL) are required to achieve the same effect in HF1A3 cells. Cell proliferation is inhibited within 24 hours in a dose-dependent manner and, depending on the cell line, almost complete cessation of 3H-thymdine incorporation is observed at 50-75 ng/mL of Brefeldin A (26%, 76%, 87% inhibition at 50 ng/ml and 75%, 87%, 92% inhibition at 75 ng/mL for HF1A3, HF4.9 and HF28RA cells respectively. Brefeldin A-induced cell killing is in a dose-dependent manner using YO-PRO 1/PI assay.


Cell Assay: HF1A3, HF4.9 cell viability upon the treatments is tested using double staining of cells with YO-PRO 1/PI and SYTO16/PI probes. To access cell proliferation, cells are treated with 0–100 ng/mL Brefeldin A in complete medium for 20 hours before adding 1 μCi/mL [methyl-3H]-thymidine for additional 4 hours at 37 °C. The incorporated radioactive thymidine is quantified by scintillation counting with Microbeta counter. To examine long-term effects of Brefeldin A treatment, cells are seeded at initial concentration 105 cells/mL and treated with 0-75 ng/mL Brefeldin A for up to 5 days. At the time indicated, a sample of cells is removed and viable cell number is assessed by standard Trypan Blue exclusion assay.

In Vivo
Animal model
Formulation & Dosage
ReferencesBioorg Med Chem. 2000 Feb;8(2):455-63; Leuk Res. 2007 Dec;31(12):1687-700.