Brefeldin A (BFA chemical)

製品コードS7046 バッチS704603

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)は、HCT 116細胞におけるIC50が0.2 μMのタンパク質輸送に対するラクトン系抗生物質およびATPase阻害剤であり、がん細胞の分化とアポトーシスを誘導します。また、HDR（相同組換え修復）効率を向上させ、CRISPRを介したHDRのエンハンサーとなる可能性もあります。Brefeldin Aは、オートファジーおよびマイトファジーの阻害剤でもあります。
in vitro	Brefeldin A (BFA) is a fungal metabolite that blocks the forward transport between the endoplasmic reticulum and Golgi apparatus, causing an impaired distribution of the membrane proteins. When HCT 116 human colon cancer cell is treated with this compound, morphological changes indicating cell differentiation are observed. It exerts its cytotoxic effects mainly by inducing differentiation and apoptosis in tumor cells. The treatment of the strips with 20 μg/mL BFA 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 of this compound substantially abolishes the bradykinin-induced decreases in [Ca²⁺]_i and tension in the range of concentrations between 1 nM and 1 mM. It has no effect on the [Ca²⁺]_i elevation in endothelial cells induced by bradykinin or substance P. Addition of the fungal metabolite 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. It prevents a wide variety of membrane traffic pathways and inhibits an ADP-ribosylation factor-specific guanine nucleotide exchange activity present in Golgi membranes or in brain cytosol. The complete prevention by this compound 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 BFA, even at 300 μM. It induces fusion of the Golgi apparatus with the ER and abolishes the inhibitory effect of the CERT inhibitor HPA-12. Treatment with this compound, which induces fusion of the Golgi apparatus and the ER, rescues the limonoid-induced prevention of sphingomyelin biosynthesis. Its treatment of CHO cells causes a 2 to 3 fold increase in sphingomyelin synthesis. Apart from B-CLL cells, BFA 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 this compound completely blocks growth of HF4.9 and HF28RA cells, whereas higher 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 (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. BFA-induced cell killing is in a dose-dependent manner using YO-PRO 1/PI assay. It could improve the HDR(homology-directed repair) efficiency and is an enhancer of CRISPR-mediated HDR.
in vivo	Brefeldin A (BFA), a lactone antibiotic and specific inhibitor of protein trafficking, blocks the transport of secreted and membrane proteins from endoplasmic reticulum to Golgi apparatus.

製品説明

Brefeldin A (BFA)は、HCT 116細胞におけるIC50が0.2 μMのタンパク質輸送に対するラクトン系抗生物質およびATPase阻害剤であり、がん細胞の分化とアポトーシスを誘導します。また、HDR（相同組換え修復）効率を向上させ、CRISPRを介したHDRのエンハンサーとなる可能性もあります。Brefeldin Aは、オートファジーおよびマイトファジーの阻害剤でもあります。

in vitro

Brefeldin A (BFA) is a fungal metabolite that blocks the forward transport between the endoplasmic reticulum and Golgi apparatus, causing an impaired distribution of the membrane proteins. When HCT 116 human colon cancer cell is treated with this compound, morphological changes indicating cell differentiation are observed. It exerts its cytotoxic effects mainly by inducing differentiation and apoptosis in tumor cells.

The treatment of the strips with 20 μg/mL BFA 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 of this compound substantially abolishes the bradykinin-induced decreases in [Ca²⁺]_i and tension in the range of concentrations between 1 nM and 1 mM. It has no effect on the [Ca²⁺]_i elevation in endothelial cells induced by bradykinin or substance P.

Addition of the fungal metabolite 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. It prevents a wide variety of membrane traffic pathways and inhibits an ADP-ribosylation factor-specific guanine nucleotide exchange activity present in Golgi membranes or in brain cytosol. The complete prevention by this compound 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 BFA, even at 300 μM.

It induces fusion of the Golgi apparatus with the ER and abolishes the inhibitory effect of the CERT inhibitor HPA-12. Treatment with this compound, which induces fusion of the Golgi apparatus and the ER, rescues the limonoid-induced prevention of sphingomyelin biosynthesis. Its treatment of CHO cells causes a 2 to 3 fold increase in sphingomyelin synthesis.

Apart from B-CLL cells, BFA 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 this compound completely blocks growth of HF4.9 and HF28RA cells, whereas higher 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 (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. BFA-induced cell killing is in a dose-dependent manner using YO-PRO 1/PI assay.

It could improve the HDR(homology-directed repair) efficiency and is an enhancer of CRISPR-mediated HDR.

in vivo

Brefeldin A (BFA), a lactone antibiotic and specific inhibitor of protein trafficking, 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 (BFA) 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 this compound, cells are seeded at initial concentration 10⁵ cells/mL and treated with 0-75 ng/mL of it 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

https://pubmed.ncbi.nlm.nih.gov/10722169/
https://pubmed.ncbi.nlm.nih.gov/11522609/
https://pubmed.ncbi.nlm.nih.gov/8576155/

https://pubmed.ncbi.nlm.nih.gov/22566693/
https://pubmed.ncbi.nlm.nih.gov/17428536/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4461869/
https://pubmed.ncbi.nlm.nih.gov/30110907/

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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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