SML0140
BV02
≥98% (HPLC)
동의어(들):
2-(2,3-Dihydro-1,5-dimethyl-3-oxo-2-phenyl-1H-pyrazol-4-yl)-2,3-dihydro-1,3-dioxo-1H-isoindole-5-carboxylic acid
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크기 선택
제품정보 (DICE 배송 시 비용 별도)
실험식(Hill 표기법):
C20H15N3O5
CAS 번호:
Molecular Weight:
377.35
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
제품 이름
BV02, ≥98% (HPLC)
InChI
1S/C20H15N3O5/c1-11-16(19(26)23(21(11)2)13-6-4-3-5-7-13)22-17(24)14-9-8-12(20(27)28)10-15(14)18(22)25/h3-10H,1-2H3,(H,27,28)
SMILES string
CN1N(c2ccccc2)C(=O)C(N3C(=O)c4ccc(cc4C3=O)C(O)=O)=C1C
InChI key
ZFYSDSINNOLWGO-UHFFFAOYSA-N
description
The structure of BV02 differs slightly from the published form, but has been internally verified by Sigma-Aldrich quality control.
assay
≥98% (HPLC)
form
powder
color
white to off-white
solubility
DMSO: >5 mg/mL
storage temp.
room temp
Quality Level
Application
BV02 has been used to study the effects of 14-3-3σ on P-glycoprotein and pregnane X receptor protein xpression. It has also been used as a control in studying BAP1 (BRCA1 (breast cancer gene)-associated protein 1) inducing cell death via interaction with 14-3-3 in neuroblastoma.
BV02, an inhibitor of the 14-3-3 scaffolding protein docking sites, may be used to study the roles and functions of 14-3-3 scaffolding proteins in signaling pathways involved in the cell cycle, and processes such as apoptosis, stress response, and malignant cell transformation.
Biochem/physiol Actions
BV02 is an inhibitor of the 14-3-3 scaffolding proteins docking site.
BV02 is an inhibitor of the 14-3-3 scaffolding proteins docking site. BV02 promotes the apoptotic death of cells expressing either wt Bcr-Abl construct or T315I mutation. It induces apoptosis by c-Abl release from 14-3-3? and re-location to nuclear compartment and at mitochondrial membranes.
signalword
Warning
hcodes
pcodes
Hazard Classifications
Aquatic Acute 1
저장 등급
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Dara K Mohammad et al.
The international journal of biochemistry & cell biology, 78, 63-74 (2016-07-07)
The Protein kinase B (AKT) regulates a plethora of intracellular signaling proteins to fine-tune signaling of multiple pathways. Here, we found that following B-cell receptor (BCR)-induced tyrosine phosphorylation of the cytoplasmic tyrosine kinase SYK and the adaptor BLNK, the AKT/PKB
Role of 14-3-3 sigma in over-expression of P-gp by rifampin and paclitaxel stimulation through interaction with PXR
Kim SW, et al.
Cellular Signalling, 31, 124-134 (2017)
BAP1 induces cell death via interaction with 14-3-3 in neuroblastoma
Sime W, et al.
Cell Death & Disease, 9(5), 458-458 (2018)
Boaz Musafia et al.
PloS one, 9(5), e97696-e97696 (2014-05-23)
This study describes the development of aptamers as a therapy against influenza virus infection. Aptamers are oligonucleotides (like ssDNA or RNA) that are capable of binding to a variety of molecular targets with high affinity and specificity. We have studied
Chevaun D Morrison et al.
Cell death & disease, 8(6), e2899-e2899 (2017-07-01)
We recently established c-Abl as a potent suppressor of triple-negative breast cancer (TNBC) progression through its reactivation of a p53:p21 signaling axis coupled to senescence. Moreover, we observed co-expression of p53 and c-Abl to be essential for normal mammary epithelial
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