FLT3 Inhibitor

c-Fms-IN-3 is an orally active c-Fms (CSF1R) kinase inhibitor (IC₅₀ = 0. 8 nM). c-Fms-IN-3 inhibits CSF1R kinase activity and reduces macrophage populations. c-Fms-IN-3 reduces bone erosion, pannus invasion, cartilage damage, and inflammation in collagen (HY-NP003)-induced arthritis mouse model. c-Fms-IN-3 is useful for arthritis research.

FLT3-IN-16 is a potent FLT3 inhibitor with an IC₅₀ of 1.1 μM. FLT3-IN-16 can be used for researching acute myeloid leukemia.

IRAK1/4/pan-FLT3 Kinase-IN-1 hydrochloride is an orally active, potent and selective IRAK/pan-FLT3 kinase inhibitor with IC₅₀s of 5 nM, 0.6 nM and <0.5 nM against IRAK1, IRAK4 and FLT3, respectively. IRAK1/4/pan-FLT3 Kinase-IN-1 hydrochloride can be used for research on AML.

FLT3-IN-10 (compound 7c) is a potent inhibitor of FMS-like tyrosine kinase 3 (FLT3). FLT3-IN-10 has the potential for the research of FLT3-mutated acute myeloid leukemia (AML).

AMG 925 HCl is a potent, selective, and orally available FLT3/CDK4 dual inhibitor with IC₅₀s of 2±1 nM and 3±1 nM, respectively.

FLT3-IN-19 (Comp 50) is a potent and selective FLT3 inhibitor with IC₅₀ of 0.213 nM. FLT3-IN-19 can be used in AML disease research.

BPR1J-097 is a novel potent FLT3 inhibitor with an IC₅₀ of 11 nM.

AC710 is a potent PDGFR inhibitor with K_ds of 0.6, 1.57, 1, 1.3, 1.0 nM for FLT3, CSF1R, KIT, PDGFRα and PDGFRβ, respectively.

Crenolanib (Standard) is the analytical standard of Crenolanib. This product is intended for research and analytical applications. Crenolanib is a potent and selective inhibitor of wild-type and mutant isoforms of the class III receptor tyrosine kinases FLT3 and PDGFRα/β with Kds of 0.74 nM and 2.1 nM/3.2 nM, respectively.

Cenisertib (Standard) is the analytical standard of Cenisertib. This product is intended for research and analytical applications. Cenisertib (AS-703569) is an ATP-competitive multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3. Cenisertib induces major growth-inhibitory effects by blocking the activity of several different molecular targets in neoplastic mast cells (MC). Cenisertib inhibits tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia.

Sitravatinib malate (MGCD516 malate) is an orally bioavailable receptor tyrosine kinase (RTK) inhibitor with IC₅₀s of 1.5 nM, 2 nM, 2 nM, 5 nM, 6 nM, 6 nM, 8 nM, 0.5 nM, 29 nM, 5 nM, and 9 nM for Axl, MER, VEGFR3, VEGFR2, VEGFR1, KIT, FLT3, DDR2, DDR1, TRKA, TRKB, respectively. Sitravatinib malate shows potent single-agent antitumor efficacy and enhances the activity of PD-1 blockade through promoting an antitumor immune microenvironment.

TAK-659 is a highly potent, selective, reversible and orally available dual inhibitor of spleen tyrosine kinase (SYK) and fms related tyrosine kinase 3 (FLT3), with an IC₅₀ of 3.2 nM and 4.6 nM for SYK and FLT3, respectively. TAK-659 induces cell death in tumor cells but not in nontumor cells, and with potential for the treatment of chronic lymphocytic leukemia (CLL).

Dovitinib lactate hydrate (TKI258 lactate hydrate) is a multi-targeted tyrosine kinase inhibitor with IC₅₀s of 1, 2, 8/9, 10/13/8, 27/210 nM for FLT3, c-Kit, FGFR1/3, VEGFR1/2/3 and PDGFRα/β, respectively.

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.

Sorafenib-d4 (Bay 43-9006-d4) is the deuterated-labeled Sorafenib (HY-10201). Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.

Flonoltinib maleate is a potent and orally active dual JAK2/FLT3 inhibitor with IC₅₀ values of 0.7 nM, 4 nM, 26 nM and 39 nM for JAK2, FLT3, JAK1 and JAK3, respectively. Flonoltinib maleate has anti-cancer activity.

Emavusertib hydrochloride (CA-4948 tosylate) is the hydrochloride salt form of Emavusertib (HY-135317). Emavusertib hydrochloride is an orally active inhibitor for IRAK4 (IC₅₀=57 nM) and FLT3. Emavusertib hydrochloride inhibits NF-κB and MyD88 signaling pathways, reduces the generation of pro-inflammatory cytokines like IL-6 and IL-10, thereby exhibiting anti-inflammatory and anti-proliferative activities against cancer cells, leading to cell apoptosis. Emavusertib hydrochloride exhibits antitumor activity in mouse model.

FLT3/TrKA-IN-1 is a potent FLT3/TrKA dual kinase inhibitor with the IC₅₀s of 43.8 nM, 97.2 nM, 92.5 nM and 23.6 nM for FLT3, FLT3-ITD, FLT3-TKD and TrKA, respectively. FLT3/TrKA-IN-1 induces cell cycle arrest at the G0/G1 phase as well as apoptosis and shows antiproliferative activity in vitro. FLT3/TrKA-IN-1 has the potential for the research of Acute myeloid leukemia (AML).

Amuvatinib hydrochloride (MP470 hydrochloride) is an orally bioavailable multi-targeted tyrosine kinase inhibitor with potent activity against mutant c-Kit, PDGFRα, Flt3, c-Met and c-Ret. Amuvatinib hydrochloride (MP470 hydrochloride) is also a DNA repair suppressor through suppression of DNA repair protein RAD51, thereby disrupting DNA damage repair. Antineoplastic activity.

MAX-40279 hydrochloride is a dual and orally active inhibitor of FLT3 kinase and FGFR kinase. MAX-40279 hydrochloride is also effective against the FLT3 mutants such as FLT3^D835Y, suggesting that it can overcome resistance to Quizartinib (HY-13001) and Sorafenib (HY-10201). MAX-40279 hydrochloride inhibits NDRG1 phosphorylation at Ser330 and suppresses endothelial-to-mesenchymal transition (EndMT). MAX-40279 hydrochloride can be used for the research of acute myelogenous leukemia (AML).