SML2399
ML327
≥98% (HPLC)
Sinónimos:
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
Fórmula empírica (notación de Hill):
C19H18N4O4
Número de CAS:
Peso molecular:
366.37
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
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assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Biochem/physiol Actions
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.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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ML327 induces apoptosis and sensitizes Ewing sarcoma cells to TNF-related apoptosis-inducing ligand.
Eric J Rellinger et al.
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
Hanbing An et al.
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.
Chandrasekhar Padmanabhan et al.
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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