Brefeldin A (BFA)

製品コードS7046 バッチS704604

化学情報

	Synonyms	Cyanein, Decumbin	Storage (From the date of receipt)	3 years -20°C powder 1 years -80°C in solvent
	化学式	C₁₆H₂₄O₄
	分子量	280.36	CAS No.	20350-15-6
Solubility (25°C)*	体外	DMSO	56 mg/mL (199.74 mM)
		Water	Insoluble
		Ethanol	Insoluble
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

溶剤液（一定の濃度）を調合する

生物活性

製品説明	Brefeldin A (BFA) is a lactone antibiotic and ATPase inhibitor for protein transport with IC50 of 0.2 μM in HCT 116 cells, induces cancer cell differentiation and apoptosis. It could also improve the HDR(homology-directed repair) efficiency and be an enhancer of CRISPR-mediated HDR. Brefeldin A is also an inhibitor of autophagy and mitophagy.
in vitro	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. ^[1] 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. ^[2] 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. ^[3] 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. ^[4] 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. ^[5] Brefeldin A could improve the HDR(homology-directed repair) efficiency. It is an enhancer of CRISPR-mediated HDR^[6].
in vivo	Brefeldin A (BFA) is a lactone antibiotic and a specific inhibitor of protein trafficking. Brefeldin A blocks the transport of secreted and membrane proteins from endoplasmic reticulum to Golgi apparatus.

製品説明

Brefeldin A (BFA) is a lactone antibiotic and ATPase inhibitor for protein transport with IC50 of 0.2 μM in HCT 116 cells, induces cancer cell differentiation and apoptosis. It could also improve the HDR(homology-directed repair) efficiency and be an enhancer of CRISPR-mediated HDR. Brefeldin A is also an inhibitor of autophagy and mitophagy.

in vitro

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. ^[1]

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. ^[2]

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. ^[3]

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. ^[4]

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. ^[5]

Brefeldin A could improve the HDR(homology-directed repair) efficiency. It is an enhancer of CRISPR-mediated HDR^[6].

in vivo

Brefeldin A (BFA) is a lactone antibiotic and a specific inhibitor of protein trafficking. Brefeldin A blocks the transport of secreted and membrane proteins from endoplasmic reticulum to Golgi apparatus.

プロトコル(参考用のみ)

細胞アッセイ	細胞株	Human follicular lymphoma cell lines HF1A3, HF4.9 and HF28RA
	濃度	0 ng/mL -75 ng/mL
	反応時間	5 days
	実験の流れ	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.
動物実験	動物モデル	C57BL/6 mice
	投薬量	250 µg
	投与方法	i.p.

参考

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カスタマーフィードバック

: , , J Biol Chem, 2014, 289(32):22284-305.

: Data from [Data independently produced by , , Nanoscale, 2018, 10(18):8796-8805]

: Data from [Data independently produced by , , J Biosci, 2018, 42(1):43-56]

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