SML1257
KU-0060648
≥98% (HPLC), DNA-PK and PI3K inhibitor, powder
别名:
4-Ethyl-N-[4-[2-(4-morpholinyl)-4-oxo-4H-1-benzopyran-8-yl]-1-dibenzothienyl]-1-piperazineacetamide, KU 0060648
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关于此项目
经验公式（希尔记法）:
C33H34N4O4S
化学文摘社编号:
分子量:
582.71
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
产品名称
KU-0060648, ≥98% (HPLC)
Quality Level
assay
≥98% (HPLC)
form
powder
color
white to light brown
solubility
DMSO: 1 mg/mL, clear (warmed)
storage temp.
−20°C
SMILES string
O=C(CN1CCN(CC)CC1)NC2=CC=C(C3=CC=CC4=C3OC(N5CCOCC5)=CC4=O)C6=C2C(C=CC=C7)=C7S6
InChI
1S/C33H34N4O4S/c1-2-35-12-14-36(15-13-35)21-29(39)34-26-11-10-23(33-31(26)25-6-3-4-9-28(25)42-33)22-7-5-8-24-27(38)20-30(41-32(22)24)37-16-18-40-19-17-37/h3-11,20H,2,12-19,21H2,1H3,(H,34,39)
InChI key
AATCBLYHOUOCTO-UHFFFAOYSA-N
Biochem/physiol Actions
KU-0060648 is observed to inhibit proliferation and initiate apoptosis in hepatocellular carcinoma. KU-0060648 is useful in chemotherapy as it increases the efficiency of double stranded breaks initiated by anticancer drugs.
KU-0060648 is a very potent dual inhibitor of DNA-PK and PI3K.
KU-0060648 is a very potent dual inhibitor of DNA-PK and PI3K. The IC50 values for inhibition of DNA-PK in MCF7 and SW620 cells are 19 and 170 nM, respectively. The compound KU-0060648 inhibits MCF7 PI3K activity with an IC50 of 39 nM, but is inactive against PI3K in SW620, suggesting a cell-dependent mechanism of inhibition. KU-0060648 increases sensitivity to DNA damaging cytotoxic drugs such as etoposide and doxorubicin in tumor cell lines expressing DNA-PK. KU-0060648 stimulates Cas9 (CRISPR associated protein 9) mediated genome editing by enhancing the rate of homology directed-repair (HDR) and decreasing the rate of NHEJ (non-homologous end-joining).
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 3 Oral
存储类别
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
KU-0060648 inhibits hepatocellular carcinoma cells through DNA-PKcs-dependent and DNA-PKcs-independent mechanisms.
Chen M B, et al.
Oncotarget, 7(13), 17047-17047 (2016)
Developments of DNA-dependent protein kinase inhibitors as anticancer agents.
Ma C C, et al.
Mini-Reviews in Medicinal Chemistry, 14(11), 884-895 (2014)
Joanne M Munck et al.
Molecular cancer therapeutics, 11(8), 1789-1798 (2012-05-12)
DNA double-strand breaks (DSB) are the most cytotoxic lesions induced by topoisomerase II poisons. Nonhomologous end joining (NHEJ) is a major pathway for DSB repair and requires DNA-dependent protein kinase (DNA-PK) activity. DNA-PK catalytic subunit (DNA-PKcs) is structurally similar to
全球贸易项目编号
| 货号 | GTIN |
|---|---|
| SML1257-5MG | 04061832434742 |
| SML1257-25MG | 04061832434735 |