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Merck

SML1974

Sigma-Aldrich

CBLC000 trifluoroacetate

≥95% (HPLC)

Synonym(e):

9H-Carbazole-9-ethanamine, N,N-diethyl-3,6-dinitro- trifluoroacetate, Curaxin CBLC000 trifluoroacetate, N,N-Diethyl-3,6-dinitro-9H-carbazole-9-ethanamine trifluoroacetate

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About This Item

Empirische Formel (Hill-System):
C18H20N4O4 · C2HF3O2
CAS-Nummer:
Molekulargewicht:
470.40
UNSPSC-Code:
12352200
NACRES:
NA.77

Assay

≥95% (HPLC)

Form

powder

Farbe

white to beige

Löslichkeit

DMSO: 2 mg/mL, clear

Lagertemp.

2-8°C

SMILES String

CCN(CC)CCN1C2=C(C=C([N+]([O-])=O)C=C2)C3=C1C=CC([N+]([O-])=O)=C3.FC(F)(C(O)=O)F

InChI

1S/C18H20N4O4.C2HF3O2/c1-3-19(4-2)9-10-20-17-7-5-13(21(23)24)11-15(17)16-12-14(22(25)26)6-8-18(16)20;3-2(4,5)1(6)7/h5-8,11-12H,3-4,9-10H2,1-2H3;(H,6,7)

InChIKey

VFGJIBCWHYFSHE-UHFFFAOYSA-N

Biochem./physiol. Wirkung

CBLC000 is a potent inhibitor of FACT (facilitates chromatin transcription) complex that activates p53 and suppresses NF-kB without genotoxicity. CBLC000 induces chromatin trapping of FACT both in vitro and in vivo. CBLC000 exhibits brad anticancer activity. CBLC000 analog clinical candidate CBL0137 decreases self-renewal of GBM stem cells (GSC).
Potent inhibitor of FACT complex that activates p53 and suppresses NF-kB without genotoxicity

Piktogramme

Exclamation mark

Signalwort

Warning

Gefahreneinstufungen

Acute Tox. 4 Oral - Aquatic Chronic 4 - Skin Irrit. 2

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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Analysenzertifikate (COA)

Lot/Batch Number

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Die Dokumentenbibliothek aufrufen

Alexander V Gasparian et al.
Science translational medicine, 3(95), 95ra74-95ra74 (2011-08-13)
Effective eradication of cancer requires treatment directed against multiple targets. The p53 and nuclear factor κB (NF-κB) pathways are dysregulated in nearly all tumors, making them attractive targets for therapeutic activation and inhibition, respectively. We have isolated and structurally optimized
Josephine Kam Tai Dermawan et al.
Cancer research, 76(8), 2432-2442 (2016-02-28)
The nearly universal recurrence of glioblastoma (GBM) is driven in part by a treatment-resistant subpopulation of GBM stem cells (GSC). To identify improved therapeutic possibilities, we combined the EGFR/HER2 inhibitor lapatinib with a novel small molecule, CBL0137, which inhibits FACT

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