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Brefeldin A ATPase inhibitor

Catalog No.B1400
Size Price Stock Qty
10mM (in 1mL DMSO)
$60.00
In stock
Evaluation Sample
$28.00
In stock
5mg
$50.00
In stock
25mg
$190.00
In stock
100mg
$470.00
In stock

Tel: +1-832-696-8203

Email: [email protected]

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Sample solution is provided at 25 µL, 10mM.

Product Citations

1. Rutter BD, Innes RW. "Extracellular Vesicles Isolated from the Leaf Apoplast Carry Stress-Response Proteins." Plant Physiol. 2017 Jan;173(1):728-741. doi: 10.1104/pp.16.01253. PMID:27837092

Quality Control

Chemical structure

Brefeldin A

Related Biological Data

Brefeldin A

Protocol

Cell experiment [1-4]:

Cell lines

Colorectal cancer cell line HCT116 cells; MCF-7 cells; Hela cells; Normal rat kidney cells (NRK); MDA-MB-231 cells

Preparation method

The solubility of this compound in DMSO is >4.7mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.

Reacting condition

5 μg/ml, 1 μg/ml; 3-40 h; 37℃

Applications

BFA treatment (15 h or 40 h) of normal rat kidney (NRK) cells caused dramatic swelling of the Endoplasmic Reticulum (ER) and shifted its localization to the periphery of the cells. BFA affected Golgi structure and MT and actin organization. BFA preferentially induced cell death in MDA-MB-231 suspension cultures with the EC50 of 0.016 μg/mL. BFA effectively inhibited clonogenic activity and the migration and matrix metalloproteinases-9 (MMP-9) activity of MDA-MB-231 cells by down-regulating the breast CSC marker CD44 and anti-apoptotic proteins Bcl-2 and Mcl-1, as well as the reversal of epithelial-mesenchymal transition. Treatment with BFA (1 μg/ml) induced p53 expression in MCF-7 cells and Hela cells. In colorectal cancer cell line HCT116 cells, BFA induced cells apoptosis.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1]. Alvarez C, et al. Brefeldin A (BFA) disrupts the organization of the microtubule and the actin cytoskeletons. Eur J Cell Biol. 1999 Jan;78(1):1-14.

[2]. Tseng CN, et al. Brefeldin A reduces anchorage-independent survival, cancer stem cell potential and migration of MDA-MB-231 human breast cancer cells. Molecules. 2014 Oct 29;19(11):17464-77.

[3]. W.C. Lin, Y.C. Chuang, Y.S. Chang, M.D. Lai, Y.N. Teng, I.J. Su, C.C. Wang, K.H. Lee, J.H. Hung, Endoplasmic reticulum stress stimulates p53 expression through NF-kappaB activation, PLoS One, 7 (2012) e39120.

[4]. P.M. Wierzbicki, M. Kogut, J. Ruczynski, K. Siedlecka-Kroplewska, L. Kaszubowska, A. Rybarczyk, M. Alenowicz, P. Rekowski, Z. Kmiec, Protein and siRNA delivery by transportan and transportan 10 into colorectal cancer cell lines, Folia Histochem Cytobiol, (2014).

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Chemical Properties

Cas No. 20350-15-6 SDF Download SDF
Chemical Name (1S,2E,7S,10E,12R,13R,15S)-12,15-dihydroxy-7-methyl-8-oxabicyclo[11.3.0]hexadeca-2,10-dien-9-one
Canonical SMILES CC1CCCC=CC2CC(CC2C(C=CC(=O)O1)O)O
Formula C16H24O4 M.Wt 280.36
Solubility >4.7mg/mL in DMSO Storage Store at -20°C
Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.

Background

Brefeldin A (BFA) is an inhibitor of ATPase with IC50 value of 0.2 μM [1]
ATPase is a chemical enzyme which is essential in the ADP/ATP exchange which process provides chemical potential energy. ATP supplies the energy for many physiological activities such as importing metabolites necessary for cell metabolism, exporting toxins, wastes, and solutes that can hinder cellular processes, cell proliferation, ER stress and so forth [2].
Treatment with BFA could attenuate stimulus-dependent hyperalgesia phenomenon via inhibiting vesicular exocytosis which process is important for ATP release [3]. When tested with cell line HEK293 cells (stably express wild-type (wt) CRELD2), BFA treatment nearly abolished the secretion of wtCRELD2 completely via inhibiting the transportation of proteins from the ER to the Golgi apparatus [4]. In MCF-7 cells and Hela cells, treatment with BFA induced p53 expression via inhibiting ATP which enhanced ER stress [5]. When treated with colorectal cancer cell line HCT116 cells, BFA treatment induced cells apoprosis by inhibiting ATP which functioned in the process of cellular vesicle trafficking [1].
BFA also is reported as an inhibitor for GTP/GDP exchange in a dose-dependent way, which is important in vesicular trafficking [6].
References:
[1] P.M. Wierzbicki, M. Kogut, J. Ruczynski, K. Siedlecka-Kroplewska, L. Kaszubowska, A. Rybarczyk, M. Alenowicz, P. Rekowski, Z. Kmiec, Protein and siRNA delivery by transportan and transportan 10 into colorectal cancer cell lines, Folia Histochem Cytobiol, (2014).
[2] M. Westerterp, A.E. Bochem, L. Yvan-Charvet, A.J. Murphy, N. Wang, A.R. Tall, ATP-binding cassette transporters, atherosclerosis, and inflammation, Circulation research, 114 (2014) 157-170.
[3] E.K. Joseph, P.G. Green, J.D. Levine, ATP release mechanisms of endothelial cell-mediated stimulus-dependent hyperalgesia, The journal of pain : official journal of the American Pain Society, 15 (2014) 771-777.
[4] K. Oh-hashi, Y. Kanamori, Y. Hirata, K. Kiuchi, Characterization of V-ATPase inhibitor-induced secretion of cysteine-rich with EGF-like domains 2, Cell biology and toxicology, 30 (2014) 127-136.
[5] W.C. Lin, Y.C. Chuang, Y.S. Chang, M.D. Lai, Y.N. Teng, I.J. Su, C.C. Wang, K.H. Lee, J.H. Hung, Endoplasmic reticulum stress stimulates p53 expression through NF-kappaB activation, PLoS One, 7 (2012) e39120.
[6] D. Prieto, P. Corchete, Transport of flavonolignans to the culture medium of elicited cell suspensions of Silybum marianum, Journal of plant physiology, 171 (2014) 63-68.