SKLB1028, a novel oral multikinase inhibitor of EGFR, FLT3 and Abl, displays exceptional activity in models of FLT3-driven AML and considerable potency in models of CML harboring Abl mutants

Leukemia

Volumn 26, Issue 8, 2012, Pages 1892-1895

  Cao, Z X ^a   Liu, J J ^a   Zheng, R L ^a   Yang, J ^a   Zhong, L ^a   Xu, Y ^a   Wang, L J ^a   Zhang, C H ^a   Wang, B L ^a   Ma, S ^a   Wang, Z R ^a   Xie, H Z ^a   Wei, Y Q ^a   Yang, S Y ^a  

^a SICHUAN UNIVERSITY   (China)

Author keywords

[No Author keywords available]

Indexed keywords

ABELSON KINASE; ANTINEOPLASTIC AGENT; CD135 ANTIGEN; IMATINIB; SKLB 1028; UNCLASSIFIED DRUG;

ACUTE GRANULOCYTIC LEUKEMIA; ANTINEOPLASTIC ACTIVITY; AREA UNDER THE CURVE; CHRONIC MYELOID LEUKEMIA; CONCENTRATION RESPONSE; DRUG HALF LIFE; DRUG POTENCY; GROWTH INHIBITION; HUMAN; IC 50; LETTER; MAXIMUM PLASMA CONCENTRATION; NONHUMAN; PRIORITY JOURNAL; SURVIVAL TIME; WESTERN BLOTTING;

EID: 84864865391     PISSN: 08876924     EISSN: 14765551     Source Type: Journal    
DOI: 10.1038/leu.2012.67     Document Type: Letter

References (15)

1. Jongen-Lavrencic M, Sun SM, Dijkstra MK, Valk PJM, Löwenberg B. MicroRNA expression profiling in relation to the genetic heterogeneity of acute myeloid leukemia. Blood 2008; 11: 5078-5085.
2. Tyner JW, Walters DK, Willis SG, Luttropp M, Oost J, Loraux M et al. RNAi screening of the tyrosine kinome identifies therapeutic targets in acute myeloid leukemia. Blood 2008; 111: 2238-2245.
3. Loriaux MM, Levine RL, Tyner JW, Frö hling S, Scholl C, Stoffregen EP et al. Highthroughput sequence analysis of the tyrosine kinome in acute myeloid leukemia. Blood 2008; 111: 4788-4796.
4. Kantarjian HM, Giles F, Quintás-Cardama AQ, Cortes J. Important therapeutic targets in chronic myelogenous leukemia. Clin Cancer Res 2007; 13: 1089-1097.
5. Gilliland DG, Griffin JD. The roles of FLT3 in hematopoiesis and leukemia. Blood 2002; 100: 1532-1542.
6. Kiyoi H, Towatari M, Yokota S, Hamaguchi M, Ohno R, Saito H et al. Internal tandem duplication of the FLT3 gene is a novel modality of elongation mutation which causes constitutive activation of the product. Leukemia 1998; 12: 1333-1337.
7. Kiyoi H, Yanada M, Ozekia K. Clinical significance of FLT3 in leukemia. Int J Hematol 2005; 82: 85-92.
8. Cloos J, Goemans BF, Hess CJ, Oostveen JW, Waisfisz Q, Corthals S et al. Stability and prognostic influence of FLT3 mutations in paired initial and relapsed AML samples. Leukemia 2006; 20: 1217-1220.
9. Schlenk RF, Dohner K, Krauter J, Frö hling S, Corbacioglu A, Bullinger L et al. Mutations and treatment outcome in cytogenetically normal acute myeloid leukemia. N Engl J Med 2008; 358: 1909-1918.
10. Levis M, Brown P, Smith BD, Stine A, Pham R, Stone R et al. Plasma inhibitory activity (PIA): a pharmacodynamic assay reveals insights into the basis for cytotoxic response to FLT3 inhibitors. Blood 2006; 108: 3477-3483.
11. Knapper S, Mills KI, Gilkes AF, Austin SJ, Walsh V, Burnett AK. The effects of lestaurtinib (CEP701) and PKC412 on primary AML blasts: the induction of cytotoxicity varies with dependence on FLT3 signaling in both FLT3-mutated and wild-type cases. Blood 2006; 108: 3494-3503.
12. Zarrinkar PP, Gunawardane RN, Cramer MD, Gardner MF, Brigham D, Belli B et al. AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML). Blood 2009; 114: 2984-2992.
13. Renneville A, Roumier C, Biggio V, Nibourel O, Boissel N, Fenaux P et al. Cooperating gene mutations in acute myeloid leukemia: a review of the literature. Leukemia 2008; 22: 915-931.
14. Boehrer S, Adè s L, Braun T, Galluzzi L, Grosjean J, Fabre C et al. Erlotinib exhibits antineoplastic off-target effects in AML and MDS: a preclinical study. Blood 2008; 111: 2170-2180.
15. Stegmaier K, Corsello SM, Ross KN, Wong JS, DeAngelo DJ, Golub TR. Gefitinib induces myeloid differentiation of acute myeloid leukemia. Blood 2005; 106: 2841-2848.