SML2399
ML327
≥98% (HPLC)
Sinônimo(s):
1,2-Dihydro-2-oxo-N-[3-[[(5-phenyl-3-isoxazolyl)carbonyl]amino]propyl]-3-pyridinecarboxamide, CID 60167648
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About This Item
Produtos recomendados
Ensaio
≥98% (HPLC)
forma
powder
cor
white to beige
solubilidade
DMSO: 2 mg/mL, clear
temperatura de armazenamento
2-8°C
Ações bioquímicas/fisiológicas
ML327 is a regulator of E-cadherin transcription that restores E-cadherin expression in cancer cell lines and partially reverses Epithelial-to-Mesenchymal Transition (EMT). It is a potent inducer of mesenchymal-to-epithelial transition (MET) in epithelial cancers. Apparently ML327 blocks MYC expression in neuroblastomas. It induces apoptosis in cancer cells and sensitizes Ewing sarcoma cells to TRAIL.
Código de classe de armazenamento
11 - Combustible Solids
Classe de risco de água (WGK)
WGK 3
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
Certificados de análise (COA)
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ML327 induces apoptosis and sensitizes Ewing sarcoma cells to TNF-related apoptosis-inducing ligand.
Biochemical and biophysical research communications, 491(2), 463-468 (2017-07-19)
Ewing sarcomas are rare mesenchymal-derived bone and soft tissue tumors in children. Afflicted children with distant metastases have poor survival despite aggressive therapeutics. Epithelial-to-mesenchymal transition in epithelial carcinomas is associated with loss of E-cadherin and resistance to apoptosis. ML327 is
Oncotarget, 6(26), 22934-22948 (2015-06-18)
Transcriptional repression of E-cadherin is a hallmark of Epithelial-to-Mesenchymal Transition (EMT) and is associated with cancer cell invasion and metastasis. Understanding the mechanisms underlying E-cadherin repression during EMT may provide insights into the development of novel targeted therapeutics for cancer.
Oncotarget, 8(60), 101072-101086 (2017-12-20)
Epithelial cancers (carcinomas) comprise the top four causes of cancer-related deaths in the United States. While overall survival has been steadily improving, therapy-resistant disease continues to present a major therapeutic challenge. Carcinomas often exploit the normal developmental program, epithelial-to-mesenchymal transition
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