Literature DB >> 28960265

Cabozantinib is well tolerated in acute myeloid leukemia and effectively inhibits the resistance-conferring FLT3/tyrosine kinase domain/F691 mutation.

Amir T Fathi1, Traci M Blonquist2, Daniela Hernandez3, Philip C Amrein1, Karen K Ballen1, Malgorzata McMasters4, David E Avigan4, Robin Joyce4, Emma K Logan4, Gabriela Hobbs1, Andrew M Brunner1, Christelle Joseph1, Ashley M Perry1, Meghan Burke1, Tanya Behnan1, Julia Foster1, Meghan K Bergeron1, Jenna A Moran1, Aura Y Ramos1, Tina T Som1, Jessica Rae1, Kaitlyn M Fishman1, Kristin L McGregor1, Christine Connolly1, Donna S Neuberg2, Mark J Levis3.   

Abstract

BACKGROUND: Cabozantinib, a tyrosine kinase inhibitor of FMS-like tyrosine kinase 3 (FLT3), MET, AXL, vascular endothelial growth factor receptor, and KIT, is approved for use in multiple malignancies. We assessed the safety and tolerability of cabozantinib in AML, given up-regulation of multiple relevant pathways.
METHODS: Adults were eligible if they were 18 years old or older with relapsed/refractory AML or if they were 70 years old or older with newly diagnosed AML but were ineligible for conventional therapy. Cabozantinib was administered in 28-day cycles, and dose escalation occurred via cohorts. A pharmacodynamic evaluation of serial plasma samples via a plasma inhibitory assay (PIA) was used to assess FLT3-inhibitory activity in FLT3-mutant cell lines.
RESULTS: Among 18 patients enrolled, 5 were found to harbor FLT3/ITD mutations. Sixteen patients (89%) had relapsed/refractory AML, and most were treated with 2 or more lines of prior treatment. No dose-limiting toxicities (DLTs) were detected at the first dose level (40 mg daily), but 2 patients experienced DLTs at the next level (60 mg daily). The remaining patients were then dosed at 40 mg daily, the maximum tolerated dose (MTD). Additional grade 2 or higher toxicities, possibly/probably related to cabozantinib, included fatigue, nausea, transaminitis, and electrolyte imbalance. No patients had a marrow response according to formal criteria, but 4 had peripheral blast reductions; 2 of these 4 patients transiently cleared circulating blasts. One patient experienced a reduction in marrow blasts, and 1 had stable disease. The FLT3-inhibitory activity of plasma samples, as assessed with the PIA, revealed potent and sustained inhibition in FLT3/ITD and, notably, F691 tyrosine kinase domain (TKD)-mutant cells.
CONCLUSIONS: Cabozantinib is well tolerated in AML patients at an MTD of 40 mg daily and is a potent inhibitor of FLT3/ITD- and F691 TKD-altered tyrosine kinases. Cancer 2018;124:306-14.
© 2017 American Cancer Society. © 2017 American Cancer Society.

Entities:  

Keywords:  FMS-like tyrosine kinase 3 (FLT3); acute myeloid leukemia; resistance mutations; targeted therapies; tyrosine kinase inhibitors

Mesh:

Substances:

Year:  2017        PMID: 28960265      PMCID: PMC8167813          DOI: 10.1002/cncr.31038

Source DB:  PubMed          Journal:  Cancer        ISSN: 0008-543X            Impact factor:   6.860


  26 in total

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Review 2.  Cabozantinib: a MET, RET, and VEGFR2 tyrosine kinase inhibitor.

Authors:  Carsten Grüllich
Journal:  Recent Results Cancer Res       Date:  2014

Review 3.  New agents in the treatment of acute myeloid leukemia: a snapshot of signal transduction modulation.

Authors:  Ting Bao; B Douglas Smith; Judith E Karp
Journal:  Clin Adv Hematol Oncol       Date:  2005-04

4.  The presence of a FLT3 internal tandem duplication in patients with acute myeloid leukemia (AML) adds important prognostic information to cytogenetic risk group and response to the first cycle of chemotherapy: analysis of 854 patients from the United Kingdom Medical Research Council AML 10 and 12 trials.

Authors:  P D Kottaridis; R E Gale; M E Frew; G Harrison; S E Langabeer; A A Belton; H Walker; K Wheatley; D T Bowen; A K Burnett; A H Goldstone; D C Linch
Journal:  Blood       Date:  2001-09-15       Impact factor: 22.113

Review 5.  FLT3: ITDoes matter in leukemia.

Authors:  M Levis; D Small
Journal:  Leukemia       Date:  2003-09       Impact factor: 11.528

6.  Uniform sensitivity of FLT3 activation loop mutants to the tyrosine kinase inhibitor midostaurin.

Authors:  Elly V Barry; Jennifer J Clark; Jan Cools; Johannes Roesel; D Gary Gilliland
Journal:  Blood       Date:  2007-09-07       Impact factor: 22.113

7.  Analysis of FLT3 length mutations in 1003 patients with acute myeloid leukemia: correlation to cytogenetics, FAB subtype, and prognosis in the AMLCG study and usefulness as a marker for the detection of minimal residual disease.

Authors:  Susanne Schnittger; Claudia Schoch; Martin Dugas; Wolfgang Kern; Peter Staib; Christian Wuchter; Helmut Löffler; Cristina Maria Sauerland; Hubert Serve; Thomas Büchner; Torsten Haferlach; Wolfgang Hiddemann
Journal:  Blood       Date:  2002-07-01       Impact factor: 22.113

8.  Prognostic significance of activating FLT3 mutations in younger adults (16 to 60 years) with acute myeloid leukemia and normal cytogenetics: a study of the AML Study Group Ulm.

Authors:  Stefan Fröhling; Richard F Schlenk; Jochen Breitruck; Axel Benner; Sylvia Kreitmeier; Karen Tobis; Hartmut Döhner; Konstanze Döhner
Journal:  Blood       Date:  2002-08-08       Impact factor: 22.113

9.  Crenolanib is a potent inhibitor of FLT3 with activity against resistance-conferring point mutants.

Authors:  Allison Galanis; Hayley Ma; Trivikram Rajkhowa; Abhijit Ramachandran; Donald Small; Jorge Cortes; Mark Levis
Journal:  Blood       Date:  2013-11-13       Impact factor: 22.113

10.  Selective FLT3 inhibition of FLT3-ITD+ acute myeloid leukaemia resulting in secondary D835Y mutation: a model for emerging clinical resistance patterns.

Authors:  A S Moore; A Faisal; D Gonzalez de Castro; V Bavetsias; C Sun; B Atrash; M Valenti; A de Haven Brandon; S Avery; D Mair; F Mirabella; J Swansbury; A D J Pearson; P Workman; J Blagg; F I Raynaud; S A Eccles; S Linardopoulos
Journal:  Leukemia       Date:  2012-02-22       Impact factor: 11.528

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  12 in total

Review 1.  FLT3-targeted treatment for acute myeloid leukemia.

Authors:  Yasuyuki Arai; SungGi Chi; Yosuke Minami; Masamitsu Yanada
Journal:  Int J Hematol       Date:  2022-05-09       Impact factor: 2.319

2.  A phase 1/2 study of the oral FLT3 inhibitor pexidartinib in relapsed/refractory FLT3-ITD-mutant acute myeloid leukemia.

Authors:  Catherine C Smith; Mark J Levis; Olga Frankfurt; John M Pagel; Gail J Roboz; Richard M Stone; Eunice S Wang; Paul L Severson; Brian L West; Mai H Le; Sabine Kayser; Bao Lam; Henry H Hsu; Chao Zhang; Gideon Bollag; Alexander E Perl
Journal:  Blood Adv       Date:  2020-04-28

Review 3.  FLT3 inhibitors in acute myeloid leukemia.

Authors:  Mei Wu; Chuntuan Li; Xiongpeng Zhu
Journal:  J Hematol Oncol       Date:  2018-12-04       Impact factor: 17.388

4.  FLT3 inhibitor design using molecular docking based virtual screening for acute myeloid leukemia.

Authors:  Padmini Gokhale; Aashish Pratap Singh Chauhan; Anushka Arora; Natasha Khandekar; Anuraj Nayarisseri; Sanjeev Kumar Singh
Journal:  Bioinformation       Date:  2019-02-28

Review 5.  From Bench to Bedside and Beyond: Therapeutic Scenario in Acute Myeloid Leukemia.

Authors:  Carmelo Gurnari; Maria Teresa Voso; Jaroslaw P Maciejewski; Valeria Visconte
Journal:  Cancers (Basel)       Date:  2020-02-04       Impact factor: 6.639

Review 6.  Mechanisms Underlying Resistance to FLT3 Inhibitors in Acute Myeloid Leukemia.

Authors:  Motoki Eguchi; Yosuke Minami; Ayumi Kuzume; Sunggi Chi
Journal:  Biomedicines       Date:  2020-07-24

7.  Repurposing cabozantinib with therapeutic potential in KIT-driven t(8;21) acute myeloid leukaemias.

Authors:  Kuan-Wei Su; Da-Liang Ou; Yu-Hsuan Fu; Hwei-Fang Tien; Hsin-An Hou; Liang-In Lin
Journal:  Cancer Gene Ther       Date:  2021-04-08       Impact factor: 5.854

Review 8.  Therapeutic Targeting of the Leukaemia Microenvironment.

Authors:  Vincent Kuek; Anastasia M Hughes; Rishi S Kotecha; Laurence C Cheung
Journal:  Int J Mol Sci       Date:  2021-06-26       Impact factor: 5.923

9.  Cabozantinib promotes erythroid differentiation in K562 erythroleukemia cells through global changes in gene expression and JNK activation.

Authors:  Yu-Hsuan Fu; Da-Liang Ou; Yi-Ru Yang; Kuan-Wei Su; Chien-Yuan Chen; Hwei-Fan Tien; Zheng-Sheng Lai; Che-Kun James Shen; Hsiung-Fei Chien; Liang-In Lin
Journal:  Cancer Gene Ther       Date:  2021-06-11       Impact factor: 5.854

10.  Cancer Drug Response Profile scan (CDRscan): A Deep Learning Model That Predicts Drug Effectiveness from Cancer Genomic Signature.

Authors:  Yoosup Chang; Hyejin Park; Hyun-Jin Yang; Seungju Lee; Kwee-Yum Lee; Tae Soon Kim; Jongsun Jung; Jae-Min Shin
Journal:  Sci Rep       Date:  2018-06-11       Impact factor: 4.379

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