Molecular Formula | C21H17NO3S2 |
Molar Mass | 395.49 |
Density | 1.419±0.06 g/cm3(Predicted) |
Boling Point | 628.0±55.0 °C(Predicted) |
Solubility | Soluble in DMSO (up to 40 mg/ml) or in Ethanol (up to 20 mg/ml) |
Appearance | powder |
Color | white to beige |
pKa | 0.33±0.20(Predicted) |
Storage Condition | -20°C |
Stability | Stable for 2 years from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20° for up to 1 month. |
In vitro study | KU-55933 is a potent specific ATM inhibitor with an IC50 of 13 nM and a Ki value of 2.2 nM. KU-55933 also inhibited DNA-PK and PI3K with IC50 of 2.5 and 16.6 μm, respectively. KU-55933 also inhibited mTOR activity with an IC50 of 9.3 μm. KU-55933 effective for ATM dependent phosphorylation. KU-55933 inhibits ATM-dependent phosphorylation in a dose-dependent manner with an IC50 of 300 nM. Below 30 μm, KU-58050 failed to inhibit the ATM-dependent phosphorylation of p53 (site serine 15). In the UV-induced H2AX (site 139 serine), NBS1 (site 343 serine), CHK1 (site 345 serine), and SMC1 (serine at position 966), the addition of KU-55933 had no significant effect. Upon UV treatment, KU-55933 cleaves the substrate of ATM phosphorylation induced by ionizing radiation. KU-55933 HeLa cells were sensitive to ionizing radiation. In cancer cells, KU-55933 inhibited growth factor-induced phosphorylation of Akt. KU-55933 inhibition of cancer cell proliferation. KU-55933 inhibition of ATM, by blocking the activation of downstream TAp63α, improve the viability. KU-55933 is a potent specific ATM inhibitor with an IC50 of 13 nM and a K I value of 2.2 nM. KU-55933 also inhibited DNA-PK and PI3K with IC50 of 2.5 and 16.6 μm, respectively. KU-55933 also inhibited mTOR activity with an IC50 of 9.3 μm. KU-55933 effective for ATM dependent phosphorylation. KU-55933 inhibits ATM-dependent phosphorylation in a dose-dependent manner with an IC50 of 300 nM. Below 30 μm, KU-58050 failed to inhibit the ATM-dependent phosphorylation of p53 (site serine 15). In the UV-induced H2AX (site 139 serine), NBS1 (site 343 serine), CHK1 (site 345 serine), and SMC1 (serine at position 966), the addition of KU-55933 had no significant effect. Upon UV treatment, KU-55933 cleaves the substrate of ATM phosphorylation induced by ionizing radiation. KU-55933 HeLa cells were sensitive to ionizing radiation. In cancer cells, KU-55933 inhibited growth factor-induced phosphorylation of Akt. KU-55933 inhibition of cancer cell proliferation. KU-55933 inhibition of ATM, by blocking the activation of downstream TAp63α, improve the viability. |
In vivo study | KU-55933 inhibits the activation of STAT3 in ATM-dependent and enhances TRAIL-regulated apoptosis by up-regulating the expression of DR5. Both inhibition of STAT3 and NF-κB are associated with down-regulation of cFLIP, accompanied by an increase in the level of apoptosis. ATM inhibitor KU-55933 had a greater effect on TRAIL-regulated apoptosis than either the JAK2 inhibitor AG490 or STAT3β overexpression. KU-55933 inhibits ATM-dependent STAT3 activation and enhances TRAIL-regulated apoptosis by up-regulating DR5 expression. Both inhibition of STAT3 and NF-κB are associated with down-regulation of cFLIP, accompanied by increased levels of apoptosis. ATM inhibitor KU-55933 had a greater effect on TRAIL-regulated apoptosis than either the JAK2 inhibitor AG490 or STAT3β overexpression. |
WGK Germany | 3 |
Reference Show more | Liang Yan, Jia Zhen, Chen Zhong Hai, a Liang De. Effect of ATM on lung ischemia-reperfusion injury in rats SEVOFRANE (Sevoflurane) [J]. Chin J Gerol 2018 38(15):3756-3759. |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 2.529 ml | 12.643 ml | 25.285 ml |
5 mM | 0.506 ml | 2.529 ml | 5.057 ml |
10 mM | 0.253 ml | 1.264 ml | 2.529 ml |
5 mM | 0.051 ml | 0.253 ml | 0.506 ml |
biological activity | KU-55933 (ATM Kinase Inhibitor) is an effective, specific ATM inhibitor with IC50/Ki of 12.9 nM/2.2 nM. Compared with DNA-PK, PI3K/PI4K, ATR and mTOR, ATM is highly selective. KU-55933 (ATM Kinase Inhibitor) is an effective and specific ATM inhibitor. IC50/Ki is 12.9 nM/2.2 nM in cell-free test. Compared with DNA-PK, PI3K/PI4K, ATR and mTOR, it is highly selective for ATM. KU -55933 (ATM Kinase Inhibitor) can inhibit the activation of autophagy-initiating kinase ULK1, resulting in a significant reduction in autophagy. |
in vitro studies | KU-55933 are effective specific ATM inhibitors with IC50 of 13 nM and Ki value of 2.2 nM. KU-55933 also inhibited DNA-PK and PI3K with IC50 of 2.5 and 16.6 μM, respectively. KU-55933 also inhibited mTOR activity with IC50 of 9.3 μM. KU-55933 effectively acts on ATM-dependent phosphorylation. KU-55933 inhibited ATM-dependent phosphorylation in a dose-dependent manner with an IC50 of 300 nM. At less than 30 μM, KU-58050 cannot inhibit ATM-dependent phosphorylation of p53 (serine at position 15). In UV-induced H2AX (serine at site 139), NBS1 (serine at site 343), CHK1 (serine at site 345), and SMC1 (serine at site 966), the addition of KU-55933 had no obvious effect. During UV treatment, ATM phosphorylated substrates induced by ionizing radiation were KU-55933 excised. KU-55933 sensitize HeLa cells to ionizing radiation. In cancer cells, KU-55933 inhibits the phosphorylation of Akt induced by growth factors. KU-55933 inhibit the proliferation of cancer cells. KU-55933 inhibit ATM and improve the viability by blocking the activation of downstream TAp63α. KU-55933 is an effective specific ATM inhibitor with IC50 of 13 nM and K I value of 2.2 nM. KU-55933 also inhibited DNA-PK and PI3K with IC50 of 2.5 and 16.6 μM, respectively. KU-55933 also inhibited mTOR activity with IC50 of 9.3 μM. KU-55933 effectively acts on ATM-dependent phosphorylation. KU-55933 inhibited ATM-dependent phosphorylation in a dose-dependent manner with an IC50 of 300 nM. At less than 30 μM, KU-58050 cannot inhibit ATM-dependent phosphorylation of p53 (serine at position 15). In UV-induced H2AX (serine at site 139), NBS1 (serine at site 343), CHK1 (serine at site 345), and SMC1 (serine at site 966), the addition of KU-55933 had no obvious effect. During UV treatment, ATM phosphorylated substrates induced by ionizing radiation were KU-55933 excised. KU-55933 sensitize HeLa cells to ionizing radiation. In cancer cells, KU-55933 inhibits the phosphorylation of Akt induced by growth factors. KU-55933 inhibit the proliferation of cancer cells. KU-55933 inhibit ATM and improve the viability by blocking the activation of downstream TAp63α. |
in vivo studies | KU-55933 inhibit ATM-dependent STAT3 activation, enhance TRAIL-regulated apoptosis by up-regulating DR5 expression, and inhibit STAT3 and NF-κB both related to down-regulating cFLIP, accompanied by an increase in apoptosis level. ATM inhibitors KU-55933 affect TRAIL-regulated apoptosis than JAK2 inhibitors AG490 or STAT3β overexpression. KU-55933 inhibits ATM-dependent STAT3 activation, enhances TRAIL-regulated apoptosis by up-regulating DR5 expression, and inhibits STAT3 and NF-κB both related to down-regulating cFLIP, accompanied by an increase in apoptosis level. ATM inhibitors KU-55933 affect TRAIL-regulated apoptosis than JAK2 inhibitors AG490 or STAT3β overexpression. |
target | TargetValue ATM (Cell-free say) 12.9 nM |
Target | Value |
ATM (Cell-free assay) | 12.9 nM |