PZ0178
PHA 767491 hydrochloride
≥98% (HPLC)
别名:
1,5,6,7-Tetrahydro-2-(4-pyridinyl)-4H-pyrrolo[3,2-c]pyridin-4-one hydrochloride, 2-Pyridin-4-yl-1,5,6,7-tetrahydro-pyrrolo[3,2-c]pyridin-4-one hydrochloride, PHA-00767491 hydrochloride
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关于此项目
经验公式（希尔记法）:
C12H11N3O · xHCl
化学文摘社编号:
分子量:
213.24 (free base basis)
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
51111800
MDL number:
InChI key
IMVNFURYBZMFDZ-UHFFFAOYSA-N
SMILES string
Cl.O=C1NCCc2[nH]c(cc12)-c3ccncc3
InChI
1S/C12H11N3O.ClH/c16-12-9-7-11(8-1-4-13-5-2-8)15-10(9)3-6-14-12;/h1-2,4-5,7,15H,3,6H2,(H,14,16);1H
assay
≥98% (HPLC)
form
powder
storage condition
desiccated
color
off-white to yellow
solubility
H2O: >25 mg/mL
Quality Level
Application
PHA 767491 hydrochloride has been used to study its effect on estrogen-induced DNA damage. It has also been used in western blot analysis and to study the S9.6 nuclear signal in HeLa cells.
Biochem/physiol Actions
PHA 767491 serves as a potential anticancer drug. It shows an ameliorating effect against acute myeloid leukemia, colon and breast cancer models. PHA 767491 possesses anti proliferating and apoptotic effect.
PHA-767491 is a potent and selective ATP-competitive dual inhibitor cdc7/cdk9.
PHA-767491 is a potent and selective ATP-competitive dual inhibitor cdc7/cdk9. PHA-767491 blocks DNA synthesis and affects the phosphorylation of the replicative DNA helicase at Cdc7-dependent phosphorylation sites.
存储类别
11 - Combustible Solids
flash_point_f
Not applicable
flash_point_c
Not applicable
Transcription-replication conflict orientation modulates R-loop levels and activates distinct DNA damage responses
Hamper S, et al.
Cell, 170(4), 774-786 (2017)
Medicinal Chemistry: Fusion of Traditional and Western Medicine, 382-382 (2014)
Co-transcriptional R-loops are the main cause of estrogen-induced DNA damage
Stork CT, et al.
eLife, 5, e17548-e17548 (2016)
The Initiation of DNA Replication in Eukaryotes, 289-289 (2016)
Lin Deng et al.
Molecular cell, 73(5), 915-929 (2019-03-09)
DNA replication errors generate complex chromosomal rearrangements and thereby contribute to tumorigenesis and other human diseases. One mechanism that triggers these errors is mitotic entry before the completion of DNA replication. To address how mitosis might affect DNA replication, we
商品
Review properties, activators and inhibitors, and available products for researching cyclin-dependent kinases (CDKs).
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