ML327 is a blocker ofMYCwhich can also de-repress E-cadherin transcription and reverse Epithelial-to-Mesenchymal Transition (EMT).

MYC^[1]

Treatment with ML327 induces an elongated morphology in neuroblastoma cells. BE(2)-C cells treated with ML327 demonstrates G1 cell cycle arrest with a concordant decrease in S phase population, and a significant increase in the sub G0 population. ML327 induces the expression ofCDH1in all seven of the neuroblastoma cell lines with a 50 to 1,400-fold induction ofCDH1mRNA expression. ML327 blocks the expression of MYC family of oncogenic transcription factors in all tested neuroblastoma cell lines. Immunoblotting time course demonstrates early repression of N-MYC expression within 2 h of treatment with ML327 (10 μM). p53 levels are also suppressed by treatment with ML327. ML327-pretreated cells demonstrates reduced proliferative potential in both tetrazolium-based (p<0.0001) and adherent 2D colony formation (41 vs. 400; p<0.0001)^[1]. ML327 reduces SW620inv cell invasion through Matrigel by ~60% and reduces H520 cell invasion by ~30% in thesein vitroassays. ML327 partially restores E-cadherin expression at the plasma membrane in NMuMG cells induced to undergo Epithelial-to-Mesenchymal Transition (EMT) by TGF-β1 treatment^[2].

ML327 treatment significantly reduces tumor volume by three-fold over the two-week treatment period (p=0.02). Tumor explant weights are approximately three-fold smaller in the ML327-treated mice (p=0.01). Mice treated with ML327 lost 12% more body weight than vehicle treated mice. ML327 treatment results in a two-fold decrease inMYCNexpression, confirming that ML327 inhibits xenograftMYCNexpression (p=0.0035)^[1].

366.37

Solid

C₁₉H₁₈N₄O₄

1883510-31-3

Room temperature in continental US; may vary elsewhere.

DMSO : 32 mg/mL(87.34 mM;Need ultrasonic and warming)

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