Brefeldin A 20350-15-6

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Molecular Weight:

280.36 Brefeldin A 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.

Biological 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.

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Product Categories : Transmembrane Transporters > ATPase Inhibitor