flt3-in-3

FLT3-IN-3 is an effective FLT3 inhibitor, and the IC50s of FLT3 WT and FLT3 D835Y are 13 and 8 nM, respectively.

JAK2/FLT3-IN-3 (11r) is a dual inhibitor of FLT3 and JAK2, with IC50 values respectively at 0.51 nM for FLT3, 2.01 nM for JAK2, and 104.40 nM for JAK3. It can induce apoptosis and exhibits anticancer activity.

FLT3-IN-38 (Flt-3 Inhibitor II) is a compound that acts as an FLT3 inhibitor. It also exhibits off-target effects by inhibiting the serine/threonine kinase haspin, a mitotic signaling coordinator. FLT3-IN-38 has potential applications in cancer research.

FLT3-IN-32 is a potent FLT3 inhibitor with high selectivity, effectively suppressing FLT3 activating mutations and inducing apoptosis. It demonstrates good tolerance in non-tumor-bearing mice. In NOD/SCID mice loaded with MV4-11 cells, FLT3-IN-32 exhibits outstanding antitumor efficacy, significantly extending mouse survival. FLT3-IN-32 is applicable for acute myeloid leukemia research.

FLT3-IN-31 (compound 10q) is a potent FLT3 inhibitor, with IC50 values of 0.16 nM for FLT3 and 2.4 nM for FLT3-D835Y, exhibiting antiproliferative activity. It reduces protein expression of p-FLT3, P-STAT5, and P-ERK. Additionally, FLT3-IN-31 induces apoptosis and causes cell cycle arrest at the G1 phase, displaying antitumor properties.

FLT3-IN-33 (Compound 7r) is a potent FLT3 inhibitor with an IC50 of 7.82 nM. It exhibits excellent anticancer activity against acute myeloid leukemia (AML) cells, such as MV4-11 and MOLM-13 cells. FLT3-IN-33 significantly induces apoptosis and inhibits the phosphorylation of the FLT3 pathway, making it useful for research in AML and other cancers.

FLT3-IN-32 TFA is a potent FLT3 inhibitor with IC50 values of 2.40 nM and 3.83 nM against FLT3-ITD and FLT3-D835Y, respectively. It effectively inhibits the proliferation/survival of human MV4-11 cells with an IC50 of 0.07 nM. FLT3-IN-32 TFA is applicable in acute myeloid leukemia (AML) research.

FLT3-IN-32 hydrochloride is a potent, orally active FLT3 inhibitor with IC50 values of 0.29 nM for FLT3-ITD, 0.77 nM for FLT3-D835Y, and 2.07 nM for FLT3-N676K. It induces apoptosis in FLT3-mutant Ba/F3 cells by reducing the phosphorylation of FLT3 and its downstream signaling molecules (STAT5, MAPK, AKT). In MV4-11 xenograft models, it demonstrates significant antitumor effects. This compound is suitable for research in acute myeloid leukemia (AML).

FLT3-IN-34 is an FLT3 inhibitor with an IC50 value of 1.4 nM. It inhibits the phosphorylation of FLT3 and downstream signaling molecules AKT and ERK1/2. In FLT3-ITD positive MV4-11 cells, FLT3-IN-34 induces concentration-dependent G0/G1 phase arrest and mild apoptosis (apoptosis). It exhibits potent antiproliferative activity against FLT3-ITD positive MV4-11 cells (IC50 = 14.95 nM) and MOLM-13 cells (IC50 = 18.5 nM). FLT3-IN-34 is useful for research on FLT3-positive acute myeloid leukemia (AML).

FLT3-IN-35 (Compound 4K) is an orally active, covalent, irreversible FLT3 inhibitor. It suppresses the phosphorylation of FLT3 and its downstream signaling factors, inducing cell cycle arrest and apoptosis. FLT3-IN-35 has potential applications in the research of acute myeloid leukemia (AML).

FLT3-IN-37 (Compound 6z) is a potent inhibitor of FLT3-ITD, with IC50 values of 1.5 nM for FLT3-ITD and 3.4 nM for TEL-VEGFR2. It exhibits high selectivity for FLT3 wild-type (WT) and c-Kit. The compound inhibits FLT3 phosphorylation and downregulates the expression of p-Akt, p-STAT5, and p-ERK. By causing cell cycle arrest and inducing apoptosis, FLT3-IN-37 demonstrates anti-leukemic activity, making it suitable for research into acute myeloid leukemia (AML).

Gilteritinib (ASP2215) is a potent inhibitor of FMS-related tyrosine kinase 3 (FLT3) and AXL tyrosine kinase receptors (IC50 = 0.29 nM and <1 nM, respectively). In preclinical studies, gilteritinib demonstrated strong antileukemic and antitumor effects. Gilteritinib is currently in several Phase 3 clinical trials for acute myeloid leukemia.

JAK3-IN-14 is a potent, selective and orally active FLT3 inhibitor, with IC50s of ∼40, 8, and 4 nM for FLT3-WT, FLT3-D835Y, and FLT3-D835H, respectively.

Cediranib (AZD2171) (AZD2171) is a highly potent (IC50 < 1 nmol/L) ATP-competitive inhibitor of recombinant KDR tyrosine kinase in vitro, also inhibits Flt1/4 (IC50: 5 nM/≤3 nM), similar activity against PDGFRβ and c-Kit, selective more for VEGFR than PDGFR-α (36-fold), CSF-1R (110-fold), and Flt3 (1000-fold) in HUVEC cells.

LY2457546 is a highly potent, orally bioavailable multi-target anti-angiogenic tyrosine kinase inhibitor. It shows strong inhibitory activity against multiple targets including VEGFR2, PDGFRβ, FLT-3, Tie-2, and Eph family receptors, and is applied in cancer research such as leukemia.

FLT3-IN-10 (2-Oxazolamine, 5-(4-fluorophenyl)-N-phenyl-) (compound 7c) is a potent inhibitor of FMS-like tyrosine kinase 3 (FLT3). FLT3-IN-10 shows the potential for the treatment of FLT3-mutated acute myeloid leukemia (AML).

FLT3-IN-4 (FLT3 inhibitor 9u) is a potent and orally effective Fms-like tyrosine receptor kinase 3 (FLT3; IC50=7 nM) inhibitor ,for treating acute myelogenous leukemia.

FLT3-IN-6 is a potent and selective inhibitor of FLT3-ITD [FLT3 mutation], with an IC50 of 1.336 nM.

PIM1-IN-1 is a potent and highly selective PIM kinase inhibitor with strong preference for PIM1 and PIM3 over PIM2, effectively inhibiting BAD phosphorylation without detectable effects on FLT3 or hERG binding, and exhibiting antiproliferative and anticancer activity suitable for mechanistic studies of PIM-driven oncogenic signaling.

3-Hydroxy Midostaurin (CGP 52421), a PKC412 metabolite, inhibits FMS-like tyrosine kinase-3 (FLT3) autophosphorylation with IC50 values of approximately 132 nM in culture medium and 9.8 μM in plasma. Although less selective, it shows greater cytotoxicity compared to PKC412[1].

Lestaurtinib (CEP 701) is an orally available and selective inhibitor of FMS-like tyrosine kinase-3 (FLT3, IC50: 0.9 nM), which inhibits FLT3 autophosphorylation in vitro.Lestaurtinib promotes the expression of c-MYC, inhibits the phosphorylation of RPTKs, and has high affinity for TrkA and JAK2. Lestaurtinib promotes c-MYC expression, inhibits phosphorylation of RPTKs, has a high affinity for TrkA and JAK2, induces apoptosis and cell growth arrest, and can be used to study leukemia.

3-Hydroxy Midostaurin-D5 is a deuterium-labeled 3-Hydroxy Midostaurin (T12610L) which is a metabolite of PKC412. PKC412 effectively inhibits FMS-like tyrosine kinase-3 (FLT3) autophosphorylation (IC50s: 132 nM and 9.8 μM in culture medium and plasma).

FLT3-IN-2 is an FLT3 inhibitor (IC50<1 μM).

FLT3/HDAC-IN-1 is a dual inhibitor targeting FLT3 and HDAC, with IC50 values of 30.4 nM for FLT3 and 52.4, 14.7 nM for HDAC1/3, respectively. It induces apoptosis in MV-4-11 cells and exhibits antiproliferative effects against BaF3 cells transformed by FLT3 mutations. FLT3/HDAC-IN-1 is useful for research on refractory solid tumors and hematological malignancies.