1 rogated by the PDGFRalpha-specific inhibitor
crenolanib.
2 Crenolanib (
100 mg thrice a day) was given from day 9 un
3 Using biochemical assays, we determined that
crenolanib,
a novel TKI, demonstrates type I properties
4 Crenolanib,
a potent type I pan-FLT3 inhibitor, is effec
5 We tested
crenolanib against a panel of D835 mutant cell lines and
6 was to examine the therapeutic potential of
crenolanib,
an inhibitor of PDGF receptor signaling, in
7 cy: ruxolitinib, baricitinib, silmitasertib,
crenolanib,
and abemaciclib.
8 Treatment with
crenolanib attenuated the skin and heart fibrosis.
9 any resistant colonies in the presence of a
crenolanib concentration well below what has been safely
10 Crenolanib delayed the outgrowth of MV4-11 cells in a xe
11 eting mutant FLT3, including Quizartinib and
Crenolanib,
develop resistance to these drugs.
12 Unlike other FLT3 inhibitors,
crenolanib does not induce FLT3 secondary mutations, and
13 Crenolanib effectively inhibited proliferation and migra
14 ate that the tyrosine kinase inhibitor (TKI)
crenolanib effectively suppresses growth of leukemic cel
15 The remaining patients exhibit post-
crenolanib expansion of mutations associated with epigen
16 Crenolanib has significant promise for achieving deep an
17 n safely achieved in humans, suggesting that
crenolanib has the potential to suppress KD mutation-med
18 Treatment with the PDGFRA inhibitor,
crenolanib,
improved contractile function of patient iPS
19 ondrial fission and mitophagy in response to
crenolanib in FLT3-ITD(+) AML cells expressing stable sh
20 In addition,
crenolanib inhibited drug-resistant AML primary blasts w
21 Crenolanib is a highly selective and potent FLT3 tyrosin
22 onstrate that the investigational type I TKI
crenolanib is a potent inhibitor of Fms tyrosine kinase-
23 Crenolanib is a second-generation tyrosine kinase inhibi
24 These preclinical data demonstrate that
crenolanib is effective against FLT3-ITD containing seco
25 Additionally, co-treatment of HPA-12 and
Crenolanib is effective in FLT3-ITD(+) and FLT3-TKD(+) A
26 Moreover,
crenolanib is highly selective for FLT3 relative to the
27 Another potential advantage of
crenolanib is its reduced inhibition of c-Kit compared w
28 Crenolanib is thus an important next-generation FLT3 TKI
29 ning secondary KD mutations, suggesting that
crenolanib may be a useful therapeutic agent for TKI-nai
30 Second-generation FLT3 inhibitors such as
crenolanib may overcome the resistance of these mutation
31 While
crenolanib monotherapy has demonstrated clinical benefit
32 Crenolanib plus intensive chemotherapy in adults with ne
33 We conducted a trial of
crenolanib plus intensive chemotherapy in adults with ne
34 with FLT3-mutant clones and are enriched in
crenolanib poor-responders.
35 Crenolanib represents the first TKI to exhibit both kina
36 Here, to investigate the mechanisms of
crenolanib resistance, we perform whole exome sequencing
37 ing diverse genetic/epigenetic mechanisms of
crenolanib resistance.
38 Moreover, activating FLT3-ITD signaling in
crenolanib-
resistant AML cells suppressed ceramide-depen
39 combinations in experimental models restore
crenolanib sensitivity.
40 Importantly, the PDGFR-specific inhibitor
crenolanib significantly reduced intracranial growth of
41 ia patients can achieve sufficient levels of
crenolanib to inhibit both FLT3/ITD and resistance-confe
42 cing of AML patient samples before and after
crenolanib treatment.
43 A randomized trial of
crenolanib versus midostaurin plus chemotherapy in young
44 Crenolanib was active against Ba/F3 cells harboring FLT3
45 In progenitor cell assays,
crenolanib was less disruptive of erythroid colony growt
46 death in response to FLT3-ITD inhibition by
crenolanib,
which was restored by wild-type (WT)-LC3, bu