KU-55933 (ATM Kinase Inhibitor)

Apparatus

Kits and Reagent

Consumables

KU-55933 (ATM Kinase Inhibitor)

Solutions：Cell Biology,Life Science

Origin：USA

Product description

KU-55933 (ATM Kinase Inhibitor) is an effective, specific inhibitor of ATM, which has a high selectivity to ATM in IC50/Ki, PI3K/PI4K, ATR and mTOR compared with DNA-PK, nM/2.2, nM in a cell-free trial.

Target

ATM [1]
(Cell-free assay)

DNA-PK [1]
(Cell-free assay)

mTOR [1]
(Cell-free assay)

PI3K [1]
(Cell-free assay)

ATR [1]
(Cell-free assay)

PI4K [1]
(Cell-free assay)

IC50

12.9 nM

2.5 μM

9.3 μM

16.6 μM

>100 μM

In vitro study

KU-55933 is effective for specific ATM inhibitors, IC50 13 nM, Ki value of 2.2 nM. KU-55933 also inhibited DNA-PK and PI3K, and the IC50 was 2.5 and 16.6 M, respectively. KU-55933 also inhibited mTOR activity, IC50 was 9.3 M. KU-55933 acts on ATM dependent phosphorylation. KU-55933 inhibited the ATM dependent phosphorylation, which was dose dependent and IC50 was 300 nM. When was less than 30 M, KU-58050 could not inhibit the ATM- dependent phosphorylation of p53 (site of serine). In the UV- induced H2AX (position 139th serine), NBS1 (343rd to serine sites), CHK1 (position 345th serine), and SMC1 (position 966th, adding KU-55933 serine) had no obvious effect. KU-55933 removal of ATM phosphorylated substrates induced by ionizing radiation during UV treatment. KU-55933 makes HeLa cells sensitive to ionizing radiation. In cancer cells, KU-55933 inhibits growth factor induced phosphorylation of Akt. KU-55933 inhibits proliferation of cancer cells. KU-55933 inhibits ATM, by blocking the activation of downstream TAp63 alpha, improve survival.

Cell Data

Cell Lines	Assay Type	Activity Description	PMID
DU-145	Growth Inhibition Assay	IC50=3.27352 μM	SANGER
HuO-3N1	Growth Inhibition Assay	IC50=4.17142 μM	SANGER
LAMA-84	Growth Inhibition Assay	IC50=4.58465 μM	SANGER

... Click to View More Cell Line Experimental Data

In vivo study

KU-55933 inhibited the activation of ATM dependent STAT3, and increased the apoptosis of TRAIL regulated by up regulation of DR5 expression, and the inhibition of STAT3 and NF- kappa B was associated with down-regulation of cFLIP, accompanied by an increase in apoptosis. The effect of ATM inhibitor KU-55933 on apoptosis regulated by TRAIL was higher than that of JAK2 inhibitor AG490 or STAT3.