Literature DB >> 20517635

Kit inhibitor APcK110 extends survival in an AML xenograft mouse model.

Stefan Faderl1, Carlos Bueso-Ramos, Zhiming Liu, Ashutosh Pal, William Bornmann, Diana V Ciurea, David Harris, Inbal Hazan-Halevy, Hagop M Kantarjian, Zeev Estrov.   

Abstract

BACKGROUND: Constitutive activation of kit contributes to pathogenesis of acute myeloid leukemia (AML) and targeting Kit may be of therapeutic benefit. APcK110, a novel inhibitor of Kit, has potent proapoptotic and antiproliferative activity in AML cell lines and primary AML samples. Here we extend our studies to the activity of APcK110 in a xenograft mouse model.
METHODS: After sub-lethal whole body radiation, OCI/AML3 cells were injected intravenously in NOD-SCID mice. Ten days later, either APcK110 or phosphate buffered saline (PBS) was injected intraperitoneally every other day. Kaplan-Meier estimates were used to calculate survival.
RESULTS: We show that 1) all mice injected with OCI/AML3 cells developed a clinical and histological picture consistent with myelomonocytic AML; and 2) survival of APcK110-treated mice was significantly longer compared with mice injected with PBS (p = .02).
CONCLUSIONS: APcK110 is a novel kit kinase inhibitor with anti-AML activity in vitro and in vivo. Further evaluation in toxicology and clinical studies is warranted.

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Year:  2010        PMID: 20517635      PMCID: PMC4251765          DOI: 10.1007/s10637-010-9459-6

Source DB:  PubMed          Journal:  Invest New Drugs        ISSN: 0167-6997            Impact factor:   3.850


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