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Items: 1 to 20 of 113

1.

Crenolanib is a selective type I pan-FLT3 inhibitor.

Smith CC, Lasater EA, Lin KC, Wang Q, McCreery MQ, Stewart WK, Damon LE, Perl AE, Jeschke GR, Sugita M, Carroll M, Kogan SC, Kuriyan J, Shah NP.

Proc Natl Acad Sci U S A. 2014 Apr 8;111(14):5319-24. doi: 10.1073/pnas.1320661111. Epub 2014 Mar 12.

2.

Crenolanib is active against models of drug-resistant FLT3-ITD-positive acute myeloid leukemia.

Zimmerman EI, Turner DC, Buaboonnam J, Hu S, Orwick S, Roberts MS, Janke LJ, Ramachandran A, Stewart CF, Inaba H, Baker SD.

Blood. 2013 Nov 21;122(22):3607-15. doi: 10.1182/blood-2013-07-513044. Epub 2013 Sep 17.

3.

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

Galanis A, Ma H, Rajkhowa T, Ramachandran A, Small D, Cortes J, Levis M.

Blood. 2014 Jan 2;123(1):94-100. doi: 10.1182/blood-2013-10-529313. Epub 2013 Nov 13.

4.

Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD.

Smith CC, Lasater EA, Zhu X, Lin KC, Stewart WK, Damon LE, Salerno S, Shah NP.

Blood. 2013 Apr 18;121(16):3165-71. doi: 10.1182/blood-2012-07-442871. Epub 2013 Feb 21.

5.

Reversal of acquired drug resistance in FLT3-mutated acute myeloid leukemia cells via distinct drug combination strategies.

Zhang W, Gao C, Konopleva M, Chen Y, Jacamo RO, Borthakur G, Cortes JE, Ravandi F, Ramachandran A, Andreeff M.

Clin Cancer Res. 2014 May 1;20(9):2363-74. doi: 10.1158/1078-0432.CCR-13-2052. Epub 2014 Mar 11.

6.

The FLT3 and PDGFR inhibitor crenolanib is a substrate of the multidrug resistance protein ABCB1 but does not inhibit transport function at pharmacologically relevant concentrations.

Mathias TJ, Natarajan K, Shukla S, Doshi KA, Singh ZN, Ambudkar SV, Baer MR.

Invest New Drugs. 2015 Apr;33(2):300-9. doi: 10.1007/s10637-015-0205-y. Epub 2015 Jan 20.

PMID:
25597754
7.

Quizartinib (AC220) is a potent second generation class III tyrosine kinase inhibitor that displays a distinct inhibition profile against mutant-FLT3, -PDGFRA and -KIT isoforms.

Kampa-Schittenhelm KM, Heinrich MC, Akmut F, Döhner H, Döhner K, Schittenhelm MM.

Mol Cancer. 2013 Mar 7;12:19. doi: 10.1186/1476-4598-12-19.

8.

Emergence of crenolanib for FLT3-mutant AML.

Fathi AT.

Blood. 2013 Nov 21;122(22):3547-8. doi: 10.1182/blood-2013-10-528992.

9.

FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro.

von Bubnoff N, Engh RA, Aberg E, Sänger J, Peschel C, Duyster J.

Cancer Res. 2009 Apr 1;69(7):3032-41. doi: 10.1158/0008-5472.CAN-08-2923. Epub 2009 Mar 24.

10.

Investigational FMS-like tyrosine kinase 3 inhibitors in treatment of acute myeloid leukemia.

Pemmaraju N, Kantarjian H, Andreeff M, Cortes J, Ravandi F.

Expert Opin Investig Drugs. 2014 Jul;23(7):943-54. doi: 10.1517/13543784.2014.911839. Epub 2014 Apr 21. Review.

11.

FLT3 kinase inhibitor TTT-3002 overcomes both activating and drug resistance mutations in FLT3 in acute myeloid leukemia.

Ma HS, Nguyen B, Duffield AS, Li L, Galanis A, Williams AB, Brown PA, Levis MJ, Leahy DJ, Small D.

Cancer Res. 2014 Sep 15;74(18):5206-17. doi: 10.1158/0008-5472.CAN-14-1028. Epub 2014 Jul 24.

12.

FLT3 D835 mutations confer differential resistance to type II FLT3 inhibitors.

Smith CC, Lin K, Stecula A, Sali A, Shah NP.

Leukemia. 2015 Dec;29(12):2390-2. doi: 10.1038/leu.2015.165. Epub 2015 Jun 25.

PMID:
26108694
13.

Emergence of polyclonal FLT3 tyrosine kinase domain mutations during sequential therapy with sorafenib and sunitinib in FLT3-ITD-positive acute myeloid leukemia.

Baker SD, Zimmerman EI, Wang YD, Orwick S, Zatechka DS, Buaboonnam J, Neale GA, Olsen SR, Enemark EJ, Shurtleff S, Rubnitz JE, Mullighan CG, Inaba H.

Clin Cancer Res. 2013 Oct 15;19(20):5758-68. doi: 10.1158/1078-0432.CCR-13-1323. Epub 2013 Aug 22.

14.

Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia.

Smith CC, Wang Q, Chin CS, Salerno S, Damon LE, Levis MJ, Perl AE, Travers KJ, Wang S, Hunt JP, Zarrinkar PP, Schadt EE, Kasarskis A, Kuriyan J, Shah NP.

Nature. 2012 Apr 15;485(7397):260-3. doi: 10.1038/nature11016.

15.

Ponatinib may overcome resistance of FLT3-ITD harbouring additional point mutations, notably the previously refractory F691I mutation.

Zirm E, Spies-Weisshart B, Heidel F, Schnetzke U, Böhmer FD, Hochhaus A, Fischer T, Scholl S.

Br J Haematol. 2012 May;157(4):483-92. doi: 10.1111/j.1365-2141.2012.09085.x. Epub 2012 Mar 13.

PMID:
22409268
16.

Prolonged exposure to FLT3 inhibitors leads to resistance via activation of parallel signaling pathways.

Piloto O, Wright M, Brown P, Kim KT, Levis M, Small D.

Blood. 2007 Feb 15;109(4):1643-52. Epub 2006 Oct 17.

17.

FLT3-mutant allelic burden and clinical status are predictive of response to FLT3 inhibitors in AML.

Pratz KW, Sato T, Murphy KM, Stine A, Rajkhowa T, Levis M.

Blood. 2010 Feb 18;115(7):1425-32. doi: 10.1182/blood-2009-09-242859. Epub 2009 Dec 10.

18.

The role of quizartinib in the treatment of acute myeloid leukemia.

Ostronoff F, Estey E.

Expert Opin Investig Drugs. 2013 Dec;22(12):1659-69. doi: 10.1517/13543784.2013.842973. Epub 2013 Sep 26. Review.

PMID:
24070241
19.

Mechanisms of resistance against PKC412 in resistant FLT3-ITD positive human acute myeloid leukemia cells.

Stölzel F, Steudel C, Oelschlägel U, Mohr B, Koch S, Ehninger G, Thiede C.

Ann Hematol. 2010 Jul;89(7):653-62. doi: 10.1007/s00277-009-0889-1. Epub 2010 Jan 30.

PMID:
20119833
20.

Mutant FLT3: a direct target of sorafenib in acute myelogenous leukemia.

Zhang W, Konopleva M, Shi YX, McQueen T, Harris D, Ling X, Estrov Z, Quintás-Cardama A, Small D, Cortes J, Andreeff M.

J Natl Cancer Inst. 2008 Feb 6;100(3):184-98. doi: 10.1093/jnci/djm328. Epub 2008 Jan 29.

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