| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 25mg | 电议 |
| 100mg | 电议 |
Cell lines | Mouse primary bone marrow-derived macrophages (BMDMs) from the femurs of C57BL/6 or Nlrp-/- mice |
Preparation Method | Quantification of IL-6 and IL-1β in the culture supernatants of mouse BMDMs untreated (Unt) or treated with LPS in the presence of Golgi-Plug, Brefeldin A (2 or 5 ug/ ml), or MCC950 for 3 h followed by ATP treatment |
Reaction Conditions | 2 or 5 ug/ ml Brefeldin A for 3 h |
Applications | Inhibition of vesicle trafficking by Brefeldin A between ER and golgi attenuates IL-1β production from BMDMs upon stimulation with NLRP3 agonists |
Animal models | Female BALB/ C mice (20 ± 2 g, 5-6 weeks) |
Preparation Method | HepG2 tumor-bearing nude mice were injected with M- Brefeldin A daily for 14 days( intravenous injection) |
Dosage form | 5 mg/kg and 10 mg/kg Brefeldin A for 14 days |
Applications | M- Brefeldin A 10 mg/kg group showed effective antitumor effect and significantly delayed tumor progression, while M- Brefeldin A 5 mg/kg mice did not show significant inhibitory effect. |
| 产品描述 | Brefeldin A (BFA) is a fungal macrocyclic lactone and a potent, reversible inhibitor of intracellular vesicle formation and protein trafficking between the endoplasmic reticulum (ER) and the Golgi apparatus[1][2].Brefeldin A is an ATPase inhibitor with IC50 value of 0.2 μM[9].Brefeldin A and its analogs are promising inhibitors in drug development due to a number of key features such as apoptosis?inducing properties as well as antitumor, antifungal, and antiviral effects [3,6].Brefeldin A is a CRISPR/Cas9 activator. Brefeldin A inhibits HSV-1 and has anti-cancer activity[4]. Perturbation of ER-Golgi trafficking by brefeldin A (BFA) treatment attenuated nucleotide-binding oligomerization domain-like receptor family, pyrin-domain-containing 3 (NLRP3) inflammasome activation in mouse bone marrow-derived macrophages (BMDMs)[5].ADP-ribosylation of BARS is mediated by formation of a conjugate between Brefeldin A and ADPR. BARS shows BAC binding when incubated with the medium from the brefeldin A-treated CD38+ HeLa cells[3].Brefeldin A induces anchorage-independent cell death in MDA-MB-231 breast cancer cells with an EC50 of 0.016 μg/mL, inhibits the formation of MDA-MB-231 colonies in 3D and 2D cultures and inhibits the migration and MMP 9 activity of MDA-MB-231[2]. In tumor-bearing mice, M-brefeldin A can prolong blood circulation, improve tumor accumulation ability, and show effective inhibition of tumor growth, M-brefeldin A 10 mg/kg group showed effective antitumor effect and significantly delayed tumor progression, while M-brefeldin A 5 mg/kg mice did not show significant inhibitory effect[7]. Mice were treated with the Golgi blocker Brefeldin A. Since most cytokines are processed and secreted via the classical secretion pathway through the Golgi, brefeldin A blocks cytokine secretion, leading to their accumulation within immune cells, which are eventually detected by flow cytometry. Thus, treatment of mice with brefeldin A allows in situ assessment of cytokine production without the use of reporter mice[8]. References: |
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