Cabozantinib hydrochloride is a potent and orally active inhibitor of VEGFR2 and MET, with IC50 values of 0.035 and 1.3 nM, respectively. Cabozantinib hydrochloride displays strong inhibition of KIT, RET, AXL, TIE2, and FLT3 (IC50=4.6, 5.2, 7, 14.3, and 11.3 nM, respectively). Cabozantinib hydrochloride shows antiangiogenic activity. Cabozantinib hydrochloride disrupts tumor vasculature and promotes tumor and endothelial cell apoptosis[1].
Gilteritinib hemifumarate is a potent FLT3/AXL inhibitor with IC50 of 0.29 nM/0.73 nM, respectively.
Ruserontinib (SKLB1028) is an orally active multikinase inhibitor of EGFR, FLT3 and Abl, with an IC50 value of 55 nM for human FLT3, and has antitumor activity[1].
AST 487 is a RET kinase inhibitor with IC50 of 880 nM, inhibits RET autophosphorylation and activation of downstream effectors, also inhibits Flt-3 with IC50 of 520 nM.
CCT241736 is a potent and orally bioavailable dual FLT3 and Aurora kinase inhibitor, which inhibits Aurora kinases (Aurora-A Kd, 7.5 nM, IC50, 38 nM; Aurora-B Kd, 48 nM), FLT3 kinase (Kd, 6.2 nM), and FLT3 mutants including FLT3-ITD (Kd, 38 nM) and FLT3(D835Y) (Kd, 14 nM).
HDAC-IN-63 (Compound 63) is a dual FLT3/HDAC inhibitor (IC50: 0.844 and 30.0 nM for FLT3 and HDAC1 respectively). HDAC-IN-63 inhibits MV4-11 cell proliferation (IC50: 92 nM. HDAC-IN-63 induces apoptosis and arrests cell cycle in MV4-11 cells. HDAC-IN-63 can be used for research of acute myeloid leukemia (AML)[1].
MAX-40279 hemiadipate is a dual and potent inhibitor of FLT3 kinase and FGFR kinase. MAX-40279 hemiadipate has the potential for the research of acute myelogenous leukemia (AML) (extracted from patent WO2021180032)[1].
MAX-40279 hemifumarate is a dual and potent inhibitor of FLT3 kinase and FGFR kinase. MAX-40279 hemifumarate has the potential for the research of acute myelogenous leukemia (AML) (extracted from patent WO2021180032)[1].
LT-540-717 (compound 32) is a potent FLT3 inhibitor (IC50=0.62 nM) with antiproliferative activity. LT-540-717 also inhibits several acquired FLT3 mutations, FLT3 (ITD, D835V), FLT3 (ITD, F691L), FLT3 (D835Y) and FLT3 (D835V). LT-540-717 has potential to be an anti-AML agent[1].
3-Hydroxy Midostaurin (CGP 52421), a metabolite of PKC412, effectively inhibits FMS-like tyrosine kinase-3 (FLT3) autophosphorylation with IC50s of approximately 132 nM and 9.8 μM in culture medium and plasma, respectively. 3-Hydroxy Midostaurin is less selective but more cytotoxic than PKC412[1].
SB1317 is a potent inhibitor of CDK2, JAK2, and FLT3 for the treatment of cancer, with IC50 of 13, 73, and 56 nM for CDK2, JAK2 and FLT3, respectively.
Emavusertib (CA-4948) hydrochloride is a selective, potent and orally active IRAK4/FLT3 inhibitor. Emavusertib hydrochloride has an IC50 of 57 nM for IRAK4 in a FRET kinase assay. Emavusertib hydrochloride shows anti-tumor activity[1][2][3].
Pacritinib is a potent inhibitor of both wild-type JAK2 (IC50=23 nM) and JAK2V617F mutant (IC50=19 nM). Pacritinib also inhibits FLT3 (IC50=22 nM) and its mutant FLT3D835Y (IC50=6 nM).
c-Met-IN-14 (compound 26af) is a selective inhibitor of c-Met kinase from N-sulfonylamidine-based derivatives, with an IC50 value of 2.89 nM. c-Met-IN-14 shows anticancer activity by blocking phosphorylation of c-Met, and arrests cell cycle at G2/M phase. c-Met-IN-14 induces apoptosis of A549 cells in a dose-dependent manner[1].
FLT3-IN-2 is a FLT3 inhibitor with IC50 of ＜ 1 μM, detailed information refer to WO 2012158957 A2 and WO 2007013896.
PDGFRα/FLT3-ITD-IN-1 (Compound 12d) is a potent inhibitor of PDGFRα/FLT3 with IC50s of more than 0.036 and 0.003 μM, respectively. PDGFRα/FLT3-ITD-IN-1 has the potential for the research of acute myeloid leukemia or chronic eosinophilic leukemia[1].
Gilteritinib-d8 is deuterium labeled Gilteritinib. Gilteritinib (ASP2215) is a potent and ATP-competitive FLT3/AXL inhibitor with IC50s of 0.29 nM/0.73 nM, respectively.
5'-Fluoroindirubinoxime (5’-FIO, compound 13), an Indirubin (HY-N0117) derivative, is a potent FLT3 inhibitor, with an IC50 of 15 nM[1].
UNC2025 is a potent and orally bioavailable Mer/Flt3 dual inhibitor with IC50 of 0.8/0.74 nM for Mer/Flt3.IC50 value: 0.8/0.74 nM(MER/FLT3)Target: Mer/Flt3 inhibitorUNC2025 was capable of inhibiting Mer phosphorylation in vivo, following oral dosing as demonstrated by pharmaco-dynamic (PD) studies examining phospho-Mer in leukemic blasts from mouse bone marrow. Kinome pro ling versus more than 300 kinases in vitro and cellular selectivity assessments demonstrate that 11 has similar subnanomolar activity against Flt3, an additional important target in acute myelogenous leukemia (AML), with pharmacologically useful selectivity versus other kinases examined.
PHI-101 is an orally active FLT3 inhibitor that overcomes resistance to multiple drug-resistant mutations. PHI-101 potently inhibits FLT3 single activating mutations (ITD or TKD mutants) and has inhibitory activity against FLT3 double (ITD/D835Y or ITD/F691L) and triple (ITD/D835Y/F691L) resistance mutations. PHI-101 has potential for research in relapsed or refractory acute myeloid leukemia (AML)[1].
ENMD-2076 is a multi-targeted kinase inhibitor with IC50s of 1.86, 14, 58.2, 15.9, 92.7, 70.8, 56.4 nM for Aurora A, Flt3, KDR/VEGFR2, Flt4/VEGFR3, FGFR1, FGFR2, Src, PDGFRα, respectively.
FLT3/ITD-IN-4 (Compound 16) is a selective FMS-like tyrosine kinase 3 internal tandem duplications (FLT3-ITD) inhibitor with an IC50 of 2.3 nM. FLT3/ITD-IN-4 can be used for acute myeloid leukemia research[1].
PDGFRα/FLT3-ITD-IN-2 (Compound 13d) is a potent inhibitor of PDGFRα/FLT3 with IC50s of more than 20 and 1.654 μM, respectively. PDGFRα/FLT3-ITD-IN-2 has the potential for the research of acute myeloid leukemia or chronic eosinophilic leukemia[1].
Hypothemycin, a fungal polyketide, is a multikinase inhibitor with Kis of 10/70 nM, 17/38 nM, 90 nM, 900 nM/1.5 μM, and 8.4/2.4 μM for VEGFR2/VEGFR1, MEK1/MEK2, FLT-3, PDGFRβ/PDGFRα, and ERK1/ERK2, respectively[1][2].
FLT3/ITD-IN-3 (Compound 19) is a potent FLT3 internal tandem duplications (FLT3-ITD) inhibitor with IC50 values of 0.3, 0.4 and 0.9 nM against FLT3D835Y, FLT3 and FLT3-ITD, respectively. FLT3/ITD-IN-3 potently inhibits the phosphorylation of FLT3 and displays excellent antiproliferative activities against acute myeloid leukemia cell lines[1].
(S)-3-Hydroxy Midostaurin ((S)-CGP52421) is a potent kinases inhibitor with IC50 values of <400 nM for 13 kinases (VEGFR-2, TRK-A, FLT3, et). (S)-3-Hydroxy Midostaurin is a minor metabolite of midostaurin (PKC412; HY-10230) undergoing by the hepatic CYP3A4 enzyme. (S)-3-Hydroxy Midostaurin has the potential for acute myeloid leukemia (AML)[1].
FLT3-IN-11 (compound 30) is a potent, selective and orally active FLT3 kinase inhibitor with IC50s of 7.22 nM and 4.95 nM for wild-type FLT3 and FLT3-D835Y, respectively. FLT3-IN-11 high selectivity for FLT3 over c-KIT (>1000-fold). FLT3-IN-11has excellent anti-acute myeloid leukemia (AML) activity (MV4-11 cells, IC50 of 3.2 nM)[1].
Gilteritinib is a potent FLT3/AXL inhibitor with IC50s of 0.29 nM/0.73 nM, respectively.
UNC4203 (UNC-4203) is a potent, highly selective MerTK with IC50 of 2.4 nM, displays >30- and 4 -foldfold selectivity over Alx (IC50=80 nM) and Tyro3 (IC50=9.1 nM); display IC50 of 39 nM for FLT-3, inhibits MERTK phosphorylation in cell-based assays with IC50 of 13.8 nM, inhibits MERTK phosphorylation in vivo in mice with advanced leukemia (30 mg/kg, ip injection).
(R)-3-Hydroxy Midostaurin ((R)-CGP52421) is a potent kinases inhibitor. (R)-3-Hydroxy Midostaurin is a major metabolite of midostaurin (PKC412; HY-10230) undergoing by the hepatic CYP3A4 enzyme. (R)-3-Hydroxy Midostaurin has the potential for acute myeloid leukemia (AML)[1].