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Ref Type

Journal Article

PMID

(31310800)

Authors

Huang S, Pan J, Jin J, Li C, Li X, Huang J, Huang X, Yan X, Li F, Yu M, Hu C, Jin J, Xu Y, Ling Q, Ye W, Wang Y, Jin J

Title

Abivertinib, a novel BTK inhibitor: Anti-Leukemia effects and synergistic efficacy with homoharringtonine in acute myeloid leukemia.

Journal	Vol	Issue	Date	Pages	Journal Short Title
Cancer letters	461		2019 Oct 01	132-143	Cancer Lett

URL

Abstract Text

Ibrutinib, an inhibitor of Bruton tyrosine kinase (BTK), has shown promising pharmacologic effects in acute myeloid leukemia (AML). In this study, we report that abivertinib or AC0010, a novel BTK inhibitor, inhibits cell proliferation, reduces colony-forming capacity, and induces apoptosis and cell cycle arrest in AML cells, especially those harboring FLT3-ITD mutations. Abivertinib was also found to be more sensitive than ibrutinib in treating AML. We demonstrate that in addition to targeting the phosphorylation of BTK, abivertinib also targeted the crucial PI3K survival pathway. Furthermore, abivertinib suppressed the expression of p-FLT3 and the downstream target p-STAT5 in AML cells harboring FLT3-ITD mutations. Moreover, in vitro and in vivo data revealed synergistic activity between abivertinib and homoharringtonine (HHT), a natural plant alkaloid commonly used in China, in treating AML cells with or without FLT3-ITD mutations. Collectively, these preclinical data suggest that abivertinib may be a promising novel agent for AML, with potential for combination treatment with HHT. Clinical studies on abivertinib-involved therapy are planned.

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Molecular Profile	Treatment Approach
No data available in table

Gene Name	Source	Synonyms	Protein Domains	Gene Description	Gene Role
No data available in table

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Therapy Name	Drugs	Efficacy Evidence	Clinical Trials
Abivertinib	Abivertinib	1	1

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Drug Name	Trade Name	Synonyms	Drug Classes	Drug Description
Abivertinib		Avitinib\|AC0010\|AC0010MA	BTK inhibitor 38 EGFR Inhibitor 3rd gen 26	Abivertinib (AC0010) is a BTK inhibitor and a third-generation EGFR inhibitor that blocks the activity of mutant forms of EGFR while sparing wild-type EGFR, which potentially results in increased apoptosis and cell cycle arrest, and decreased viability and colony formation, and inhibits tumor growth (PMID: 27573423, PMID: 31310800).

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Gene	Variant	Impact	Protein Effect	Variant Description	Associated with drug Resistance
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Molecular Profile	Indication/Tumor Type	Response Type	Therapy Name	Approval Status	Evidence Type	Efficacy Evidence	References
FLT3 exon 14 ins	acute myeloid leukemia	sensitive	Abivertinib	Preclinical - Patient cell culture	Actionable	In a preclinical study, Abivertinib (AC0010) treatment inhibited PI3K signaling and phosphorylation of Btk, Flt3, and Stat5, induced apoptosis and cell cycle arrest, reduced viability, and inhibited colony formation in acute myeloid leukemia cell lines harboring FLT3-ITD mutations, and decreased viability of patient-derived acute myeloid leukemia blasts harboring FLT3-ITD mutations in culture (PMID: 31310800).	31310800
FLT3 exon 14 ins	acute myeloid leukemia	sensitive	Abivertinib + Omacetaxine mepesuccinate	Preclinical - Patient cell culture	Actionable	In a preclinical study, treatment with the combination of Abivertinib (AC0010) and Synribo (omacetaxine mepesuccinate) resulted in increased apoptosis and reduced viability of acute myeloid leukemia (AML) cell lines harboring FLT3-ITD mutations and decreased viability of patient-derived AML cells harboring FLT3-ITD mutations in culture, and reduced tumor burden and increased survival in cell line xenograft models compared to either agent alone (PMID: 31310800).	31310800
FLT3 exon 14 ins	acute myeloid leukemia	predicted - sensitive	Ibrutinib	Preclinical - Cell culture	Actionable	In a preclinical study, Imbruvica (ibrutinib) treatment reduced viability of acute myeloid leukemia cells harboring FLT3-ITD mutations, however, with decreased response compared to cells treated with Abivertinib (AC0010) in culture (PMID: 31310800).	31310800

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