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经验公式(希尔记法):
C27H21ClN2O2
化学文摘社编号:
分子量:
440.92
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
solubility
DMSO: 2 mg/mL, clear
InChI
1S/C27H21ClN2O2/c1-30-25-13-10-21(28)16-23(25)26(19-8-11-22(31)12-9-19)29-24(27(30)32)15-17-6-7-18-4-2-3-5-20(18)14-17/h2-14,16,24,29H,15H2,1H3
SMILES string
ClC1=CC=C2C(C(C3=CC=C(O)C=C3)=NC(CC4=CC=C(C=CC=C5)C5=C4)C(N2C)=O)=C1
InChI key
IJEUIRDNQUQMFU-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
storage temp.
2-8°C
Quality Level
Application
Bz-423 has been used as a mitochondrial inner membrane pore (MIMP) reagent to study its effect on oxygen consumption rate (OCR) and ATP synthesis in HepG2 cells.
Biochem/physiol Actions
Bz-423 is an inhibitor of mitochondrial F1F0 ATP synthase. It binds the oligomycin sensitivity conferring protein (OSCP) component of mitochondrial F1F0-ATPase, resulting in superoxide generation and apoptosis. BZ-423 was shown to block multidrug-resistant melanoma cells. In another study, Bz-423 selectively increased superoxide and induced the apoptosis of alloreactive T cells, which arrested established Graft versus Host Disease.
Bz-423 stimulates mitochondrial inner membrane pore (MIMP) opening in isolated mitochondria.
Inhibitor of mitochondrial F1F0-ATP synthase
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Propionate Enhances Cell Speed and Persistence to Promote Intestinal Epithelial Turnover and Repair.
Anthony J Bilotta et al.
Cellular and molecular gastroenterology and hepatology, 11(4), 1023-1044 (2020-11-26)
Gut bacteria-derived short-chain fatty acids (SCFAs) play crucial roles in the maintenance of intestinal homeostasis. However, how SCFAs regulate epithelial turnover and tissue repair remain incompletely understood. In this study, we investigated how the SCFA propionate regulates cell migration to
Abby Hearne et al.
Toxicology in vitro : an international journal published in association with BIBRA, 67, 104907-104907 (2020-06-06)
Oligomycin is a classical mitochondrial reagent that binds to the proton channel on the Fo component of ATP synthase. As a result, oligomycin blocks mitochondrial ATP synthesis, proton translocation, and O2 uptake. Here we show that oligomycin induces proton uncoupling
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