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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Chemical Compound Review

CHEMBL327127     8-(2,6-dichlorophenyl)-3- [[3...

Synonyms: SureCN256710, NSC-735424, DNC009907, NSC735424, PD-166326, ...
 
 
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Disease relevance of PD166326

 

High impact information on PD166326

  • Furthermore, worms treated with the c-Abl inhibitor STI-571 (Gleevec; used in human cancer therapy), two newly synthesized STI-571 variants or PD166326 had a phenotype similar to that generated by abl-1(ok171) [2].
  • Both compounds potently inhibit most IM(R) variants, and in vitro drug selection demonstrates that active (AP23464) and open (PD166326) conformation-specific compounds are less susceptible to resistance than imatinib [3].
  • In mice with the CML-like disease, PD166326 rapidly inhibited Bcr/Abl kinase activity after a single oral dose and demonstrated marked antileukemic activity in vivo [1].
  • Consistent with its more potent antileukemic effect in vivo, PD166326 was also superior to imatinib mesylate in inhibiting the constitutive tyrosine phosphorylation of numerous leukemia-cell proteins, including the src family member Lyn [1].
  • Seventy percent of PD166326-treated mice achieved a white blood cell (WBC) count less than 20.0 x 10(9)/L (20,000/microL) at necropsy, compared with only 8% of imatinib mesylate-treated animals [1].
 

Anatomical context of PD166326

  • PD166326 inhibits the growth of K562 cells with IC(50) of 300 pM, leading to apoptotic G(1) arrest, whereas non-Bcr-abl cell types require >1000 times higher concentrations [4].

References

  1. PD166326, a novel tyrosine kinase inhibitor, has greater antileukemic activity than imatinib mesylate in a murine model of chronic myeloid leukemia. Wolff, N.C., Veach, D.R., Tong, W.P., Bornmann, W.G., Clarkson, B., Ilaria, R.L. Blood (2005) [Pubmed]
  2. Caenorhabditis elegans ABL-1 antagonizes p53-mediated germline apoptosis after ionizing irradiation. Deng, X., Hofmann, E.R., Villanueva, A., Hobert, O., Capodieci, P., Veach, D.R., Yin, X., Campodonico, L., Glekas, A., Cordon-Cardo, C., Clarkson, B., Bornmann, W.G., Fuks, Z., Hengartner, M.O., Kolesnick, R. Nat. Genet. (2004) [Pubmed]
  3. Activity of dual SRC-ABL inhibitors highlights the role of BCR/ABL kinase dynamics in drug resistance. Azam, M., Nardi, V., Shakespeare, W.C., Metcalf, C.A., Bohacek, R.S., Wang, Y., Sundaramoorthi, R., Sliz, P., Veach, D.R., Bornmann, W.G., Clarkson, B., Dalgarno, D.C., Sawyer, T.K., Daley, G.Q. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  4. A novel pyridopyrimidine inhibitor of abl kinase is a picomolar inhibitor of Bcr-abl-driven K562 cells and is effective against STI571-resistant Bcr-abl mutants. Huron, D.R., Gorre, M.E., Kraker, A.J., Sawyers, C.L., Rosen, N., Moasser, M.M. Clin. Cancer Res. (2003) [Pubmed]
 
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