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Merck

SML0140

Sigma-Aldrich

BV02

≥98% (HPLC)

Synonym(e):

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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About This Item

Empirische Formel (Hill-System):
C20H15N3O5
CAS-Nummer:
Molekulargewicht:
377.35
MDL-Nummer:
UNSPSC-Code:
12352200
PubChem Substanz-ID:
NACRES:
NA.77

Beschreibung

The structure of BV02 differs slightly from the published form, but has been internally verified by Sigma-Aldrich quality control.

Qualitätsniveau

Assay

≥98% (HPLC)

Form

powder

Farbe

white to off-white

Löslichkeit

DMSO: >5 mg/mL

Lagertemp.

room temp

SMILES String

CN1N(c2ccccc2)C(=O)C(N3C(=O)c4ccc(cc4C3=O)C(O)=O)=C1C

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)

InChIKey

ZFYSDSINNOLWGO-UHFFFAOYSA-N

Anwendung

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. Wirkung

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.

Piktogramme

Environment

Signalwort

Warning

H-Sätze

Gefahreneinstufungen

Aquatic Acute 1

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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Die Dokumentenbibliothek aufrufen

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
BAP1 induces cell death via interaction with 14-3-3 in neuroblastoma
Sime W, et al.
Cell Death & Disease, 9(5), 458-458 (2018)
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)
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
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

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