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SML1260

Sigma-Aldrich

HLM006474

≥98% (HPLC)

Synonyma:

7-[(4-Ethoxy-3-methylphenyl)(2-pyridinylamino)methyl]-2-methyl-8-quinolinol

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About This Item

Empirický vzorec (Hillův zápis):
C25H25N3O2
Číslo CAS:
353519-63-8
Molekulová hmotnost:
399.48
MDL number:
MFCD02168344
UNSPSC Code:
12352200
PubChem Substance ID:
329825752
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 5 mg/mL, clear (warmed)

storage temp.

2-8°C

SMILES string

CC1=CC(C(NC2=NC=CC=C2)C3=C(O)C(N=C(C)C=C4)=C4C=C3)=CC=C1OCC

InChI

1S/C25H25N3O2/c1-4-30-21-13-11-19(15-16(21)2)23(28-22-7-5-6-14-26-22)20-12-10-18-9-8-17(3)27-24(18)25(20)29/h5-15,23,29H,4H2,1-3H3,(H,26,28)

Inchi Key

CYNZBLNMIJNBSF-UHFFFAOYSA-N

Application

HLM006474 has been used as an E2 factor (E2F) inhibitor in human nasopharyngeal carcinoma hone-1 cells and T. annulata-infected TBL20 cells.

Biochem/physiol Actions

HLM006474 activates p53 and induces DNA damage and apoptosis in mouse tumor models.
HLM006474 is a pan-E2F transcription factor inhibitor. E2F s part of the CDK/Rb/E2F pathway. When phosphorylated by CDKs, the tumor suppressor retinoblastoma protein (Rb) is inactivated, releasing E2Fs and allowing cell cycle progression. HLM006474 inhibited DNA-binding of all E2F complexes and down-regulated expression of E2F4 protein. HLM006474 induced apoptosis of A375 melanoma cells and synergized with paclitaxel in lung cancer cell lines.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Osvědčení o analýze (COA)

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Osteosarcoma (OS) is characterized by TP53 mutations in humans. In mice, loss of p53 triggers OS development, and osteoprogenitor-specific p53-deleted mice are widely used to study the process of osteosarcomagenesis. However, the molecular mechanisms underlying the initiation or progression of
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Clinical studies suggest a positive association between malignant progression of nasopharyngeal carcinoma (NPC) and Rta, a transcription factor of Epstein-Barr virus (EBV). However, Rta induces cellular senescence in vitro. To provide an underlying mechanism integrating these clues, we adapted a concept
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Retinoblastoma, a childhood cancer, is most frequently caused by bi-allelic inactivation of RB1 gene. However, other oncogenic mutations such as MYCN amplification can induce retinoblastoma with proficient RB1. Previously, we established RB1-proficient MYCN-overexpressing retinoblastoma models both in human organoids and

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