|PD173955Dual Src/Abl kinase inhibitor, ATP-competitive,|
Sample solution is provided at 25 µL, 10mM.
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|Description||PD173955 is an ATP-competitive, dual inhibitor of Src/Abl kinase.|
|IC50||1-2 nM||22 nM|
|Cas No.||260415-63-2||SDF||Download SDF|
|Solubility||Limited solubility||Storage||Store at -20° C|
|General tips||For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.|
|Shipping Condition||Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
PD173955 is a potent inhibitor of Bcr-Abl, Src and Yes with IC50 value of 1-2 nM, 300 nM and 175 nM, respectively [1-3].
Bcr-Abl is a protein tyrosine kinase which has oncogenic potential. Src is an enzyme and plays an important role in a variety of cancer cells survival, angiogenesis, proliferation and invasion pathways. Yes is a proto-oncogene tyrosine-protein kinase smf belongs to the Src kinase family [1-3].
PD173955 is a potent Bcr-Abl, Src and Yes inhibitor. When tested with CML CD34+ GM progenitors, PD173955 inhibited KL-dependent proliferation at an IC50 value of 50 nM and GM-CSF-dependent cell growth at an IC50 value of 1μM and the maximum inhibition was achieved at the dose of 25 nM. It was shown that PD173955 reduced the fractions of cells in G2-M phase and increased the cells in G1 phase with significant difference . In HT29 cells, PD173955 treatment inhibited Src auot-phosphorylation in a dose dependent manner. Further, PD173955 showed inhibition on cell growth with IC50 value of 800 nM without morphologic changes and high concentrations arrested cell cycle at the M phase . When tested with Bcr-Abl-depedent cell lines K562 and RWLeu4, PD173955 showed inhibition on cell proliferation with the IC50 value of 35 and 10 nM, respectively and arrested cell cycle in G1 phase at the low nanomolar .
. Windham, T.C., et al., Src activation regulates anoikis in human colon tumor cell lines. Oncogene, 2002. 21(51): p. 7797-807.
. Strife, A., et al., Direct evidence that Bcr-Abl tyrosine kinase activity disrupts normal synergistic interactions between Kit ligand and cytokines in primary primitive progenitor cells. Mol Cancer Res, 2003. 1(3): p. 176-85.
. Wisniewski, D., et al., Characterization of potent inhibitors of the Bcr-Abl and the c-kit receptor tyrosine kinases. Cancer Res, 2002. 62(15): p. 4244-55.