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1 rogated by the PDGFRalpha-specific inhibitor crenolanib.
2 Using biochemical assays, we determined that crenolanib, a novel TKI, demonstrates type I properties
3                                    We tested crenolanib against a panel of D835 mutant cell lines and
4  was to examine the therapeutic potential of crenolanib, an inhibitor of PDGF receptor signaling, in
5                               Treatment with crenolanib attenuated the skin and heart fibrosis.
6  any resistant colonies in the presence of a crenolanib concentration well below what has been safely
7                                              Crenolanib delayed the outgrowth of MV4-11 cells in a xe
8                                              Crenolanib effectively inhibited proliferation and migra
9 ate that the tyrosine kinase inhibitor (TKI) crenolanib effectively suppresses growth of leukemic cel
10                                              Crenolanib has significant promise for achieving deep an
11 n safely achieved in humans, suggesting that crenolanib has the potential to suppress KD mutation-med
12 ondrial fission and mitophagy in response to crenolanib in FLT3-ITD(+) AML cells expressing stable sh
13                                 In addition, crenolanib inhibited drug-resistant AML primary blasts w
14                                              Crenolanib is a highly selective and potent FLT3 tyrosin
15 onstrate that the investigational type I TKI crenolanib is a potent inhibitor of Fms tyrosine kinase-
16      These preclinical data demonstrate that crenolanib is effective against FLT3-ITD containing seco
17                                    Moreover, crenolanib is highly selective for FLT3 relative to the
18               Another potential advantage of crenolanib is its reduced inhibition of c-Kit compared w
19                                              Crenolanib is thus an important next-generation FLT3 TKI
20 ning secondary KD mutations, suggesting that crenolanib may be a useful therapeutic agent for TKI-nai
21    Second-generation FLT3 inhibitors such as crenolanib may overcome the resistance of these mutation
22                                              Crenolanib represents the first TKI to exhibit both kina
23   Moreover, activating FLT3-ITD signaling in crenolanib-resistant AML cells suppressed ceramide-depen
24 ia patients can achieve sufficient levels of crenolanib to inhibit both FLT3/ITD and resistance-confe
25                                              Crenolanib was active against Ba/F3 cells harboring FLT3
26                   In progenitor cell assays, crenolanib was less disruptive of erythroid colony growt
27  death in response to FLT3-ITD inhibition by crenolanib, which was restored by wild-type (WT)-LC3, bu

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