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:
产品名称
PHA 767491 hydrochloride, ≥98% (HPLC)
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
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Medicinal Chemistry: Fusion of Traditional and Western Medicine, 382-382 (2014)
Transcription-replication conflict orientation modulates R-loop levels and activates distinct DNA damage responses
Hamper S, et al.
Cell, 170(4), 774-786 (2017)
The Initiation of DNA Replication in Eukaryotes, 289-289 (2016)
Co-transcriptional R-loops are the main cause of estrogen-induced DNA damage
Stork CT, et al.
eLife, 5, e17548-e17548 (2016)
Irene Gallina et al.
Molecular cell, 81(3), 442-458 (2020-12-16)
Lesions on DNA uncouple DNA synthesis from the replisome, generating stretches of unreplicated single-stranded DNA (ssDNA) behind the replication fork. These ssDNA gaps need to be filled in to complete DNA duplication. Gap-filling synthesis involves either translesion DNA synthesis (TLS)
商品
Review properties, activators and inhibitors, and available products for researching cyclin-dependent kinases (CDKs).
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