Catalog No.
Product Name
Application
Product Information
Citations
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FLT3 Inhibitor
Tandutinib sulfate is a selective inhibitor of FLT3, exerting its effects with an IC50 of 0.22 μM. It also targets c-Kit and PDGFR, with IC50 values of 0.17 μM and 0.20 μM, respectively. This compound is particularly relevant for research in acute myelogenous leukemia (AML) and is noted for its capacity to cross the blood-brain barrier, expanding its potential applications in hematological malignancies and central nervous system studies. -
FLT3 Inhibitors
FLT3-IN-32 is a highly selective, orally bioavailable inhibitor of the FLT3 receptor tyrosine kinase. It effectively targets FLT3-activating mutations, promoting apoptosis in malignant cells. In vivo studies demonstrate significant anti-tumor efficacy in MV4-11 xenograft models within NOD/SCID mice, leading to notable extensions in survival. FLT3-IN-32 is valuable for research applications focused on acute myeloid leukemia. -
FLT3 Inhibitor
HSB401 is an orally active FLT3 inhibitor with IC50 values of 28, 5, 72, and 51 nM for FLT3-WT, FLT3-D835Y, FLT3-ITD-F691L, and FLT3-ITD, respectively. It effectively downregulates FLT3 signaling, leading to cell cycle arrest and apoptosis in sensitive cells. Notably, HSB401 spares c-KIT inhibition, minimizing the risk of myelosuppression. This compound has demonstrated significant tumor growth suppression in the MV4-11 xenograft mouse model and is valuable for research in acute myeloid leukemia. -
FLT3 Inhibitor
SILA-123 is a potent FLT3 inhibitor, demonstrating IC50 values of 2.1 nM for FLT3-WT and 1.0 nM for FLT3-ITD. This compound effectively inhibits FLT3 phosphorylation and disrupts downstream signaling pathways, resulting in apoptosis through cell cycle arrest in the G0/G1 phase. SILA-123 is particularly valuable in research related to acute myeloid leukemia. -
FLT3 Inhibitor
JH-IX-179 is a potent FLT3 inhibitor with an IC50 of 4 nM for FLT3-ITD and 10 nM for FLT3-D835Y variants. This compound effectively induces cell cycle arrest in the G1 phase and promotes apoptosis in cells expressing the FLT3-ITD mutation. JH-IX-179 is primarily utilized in research focused on acute myeloid leukemia (AML), providing valuable insights into therapeutic strategies targeting FLT3 signaling pathways. -
FLT3/HDAC Inhibitor
HDAC-IN-63 is a dual inhibitor targeting both FLT3 and HDAC, with IC50 values of 0.844 nM for FLT3 and 30.0 nM for HDAC1. It demonstrates potent inhibition of MV4-11 cell proliferation, with an IC50 of 92 nM, and effectively induces apoptosis while arresting the cell cycle in MV4-11 cells. This compound serves as a valuable research tool for the study of acute myeloid leukemia (AML) and the exploration of novel therapeutic strategies. -
FLT3 Inhibitor
FLT3-IN-31 is a potent inhibitor of FLT3, exhibiting IC50 values of 0.16 nM for the wild-type FLT3 receptor and 2.4 nM for the FLT3-D835Y mutant. It demonstrates significant antiproliferative activity by decreasing the protein expression of phosphorylated FLT3, STAT5, and ERK. Additionally, FLT3-IN-31 induces apoptosis and triggers cell cycle arrest at the G1 phase, making it a valuable tool for research in targeted cancer therapies and leukemia treatment. -
FLT3/HDAC Inhibitor
FLT3/HDAC-IN-3 is a dual inhibitor targeting FLT3 and HDAC, with a potent inhibitory effect on FLT3 (IC50 = 14 nM) and HDAC isoforms, including HDAC1 (IC50 = 27 nM) and HDAC6 (IC50 = 20 nM). This compound demonstrates selective inhibition, exhibiting reduced activity against HDAC8 and no activity toward HDAC4. FLT3/HDAC-IN-3 has shown anti-proliferative effects across various hematological malignancy cell lines and demonstrates efficacy in the Jeko-1 xenograft model without significant toxicity. It is suitable for research focused on hematological malignancies and the role of dual inhibition in therapeutic strategies. -
FLT3/JAK2 Inhibitor
JAK2/FLT3-IN-3 is a potent dual inhibitor of FLT3 and JAK2, exhibiting IC50 values of 2.01 nM for JAK2, 0.51 nM for FLT3, and 104.40 nM for JAK3. This compound induces apoptosis in cancer cells and demonstrates significant antitumor activity. Its ability to inhibit both FLT3 and JAK2 pathways makes it a valuable tool for research related to hematological malignancies and targeted cancer therapies. -
FLT3 Inhibitor
Tuspetinib dihydrochloride is a selective FLT3 inhibitor that demonstrates potent inhibitory activity with IC50 values of 1.1 nM for FLT3 WT, 1.8 nM for FLT3 ITD, and 1.0 nM for FLT3 D835Y kinases. As a reversible type I inhibitor, it effectively modulates downstream signaling pathways, including p-STAT5, p-ERK, SYK, JAK1/2, and TAK1. Tuspetinib dihydrochloride is utilized in research for its ability to inhibit proliferation and induce apoptosis in leukemic cells, making it significant for studies on hematological malignancies. -
FLT3/MNK2 Inhibitor
K783-0308 is a potent and selective dual inhibitor of FLT3 and MNK2, demonstrating IC50 values of 680 nM and 406 nM, respectively. This compound effectively inhibits the growth of acute myeloid leukemia (AML) cell lines, MOLM-13 and MV-4-11, with IC50 values of 10.5 µM and 10.4 µM. Additionally, K783-0308 promotes apoptosis and induces cell cycle arrest in the G0/G1 phase, making it a valuable tool for research into AML and related pathways. -
FLT3-ITD Inhibitor
FLT3-ITD-IN-3 is a potent inhibitor of FLT3-ITD (FLT3 internal tandem duplication), primarily targeting the FLT3 signaling pathway. This compound effectively disrupts FLT3 signal transduction, leading to G0/G1 cell cycle arrest and the induction of apoptosis in malignant cells. FLT3-ITD-IN-3 is valuable for research applications focused on acute myeloid leukemia (AML) and related hematological disorders. -
FLT3 Inhibitor
FLT3-IN-33 is a potent FLT3 inhibitor with an IC50 value of 7.82 nM, demonstrating significant anti-cancer activities, particularly against acute myeloid leukemia (AML) cell lines such as MV4-11 and MOLM-13. This compound effectively induces apoptosis in cancer cells and inhibits the phosphorylation of FLT3 signaling pathways. FLT3-IN-33 is suitable for research applications targeting AML and other malignancies, providing valuable insights into therapeutic strategies and cellular responses. -
RTK inhibitor
Dovitinib is a small-molecule multitargeted receptor tyrosine kinase inhibitor, which inhibits Ba/F3 cells transformed to IL3 independence by ZNF198-FGFR1 or BCR-FGFR1 with IC50 values of 150 nM and 90 nM, respectively. -
Syk Inhibitor
R406 is an orally available spleen tyrosine kinase inhibitor with an IC50 of 41 nM. -
FLT3 Inhibitor
Tandutinib (MLN518) inhibits the autophosphorylation of FLT3, c-KIT and PDGF receptor tyrosine kinases, thereby inhibiting cellular proliferation and inducing apoptosis. -
JAK2/FLT3 inhibitor
TG-101348 is an orally bioavailable, ATP-competitive and selective inhibitor of Janus-associated kinase 2 with potential antineoplastic activity. -
FLT3 inhibitor
5'-Fluoroindirubinoxime (5'-FIO, compound 13), an Indirubin derivative, is a potent FLT3 inhibitor, with an IC50 of 15 nM.
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FLT3 Inhibitor
AKN-028 is a potent inhibitor of FMS-like receptor tyrosine kinase 3 (FLT3), demonstrating an IC50 value of 6 nM and effectively inhibiting FLT3 autophosphorylation. This orally active compound elicits a dose-dependent cytotoxic effect, with a mean IC50 of 1 μM. AKN-028 promotes apoptosis through the activation of caspase 3, making it particularly relevant for research on acute myeloid leukemia (AML) and related hematological malignancies. -
FLT3 Inhibitor
AKN-028 TFA is a potent and orally active inhibitor of FMS-like receptor tyrosine kinase 3 (FLT3), exhibiting an IC50 value of 6 nM. This compound effectively inhibits FLT3 autophosphorylation and elicits a dose-dependent cytotoxic response with a mean IC50 of 1 μM. Additionally, AKN-028 TFA induces apoptosis through the activation of caspase 3. It is a valuable tool for research in acute myeloid leukemia (AML). -
FLT3 Inhibitor
Quizartinib dihydrochloride is a potent and selective second-generation type II FLT3 tyrosine kinase inhibitor. Demonstrating a Kd of 1.6 nM, it effectively inhibits autophosphorylation of both wild-type FLT3 and FLT3-ITD in MV4-11 cells, with IC50 values of 4.2 nM and 1.1 nM, respectively. This compound is also suitable for the development of PROTAC FLT3 degraders when linked to the VHL ligand, and it has been shown to induce apoptosis in target cells. -
Pan-FLT3/Pan-BTK Inhibitor
Luxeptinib is a first-in-class, non-covalent pan-FLT3 and pan-BTK inhibitor that exhibits potent oral activity. This compound effectively induces cell cycle arrest, apoptosis, or autophagy in acute myeloid leukemia cells, making it a significant tool for cancer research. Its dual-targeting mechanism positions Luxeptinib as a potential therapeutic candidate in the treatment of hematological malignancies. -
CDK2/JAK2/FLT3 Inhibitor
(E/Z)-Zotiraciclib hydrochloride is a potent inhibitor of CDK2, JAK2, and FLT3, exhibiting IC50 values of 13 nM, 73 nM, and 56 nM, respectively. This orally active compound demonstrates significant efficacy in inhibiting the proliferation of various cancer cell lines. It is a valuable tool for research into therapeutic strategies targeting cell cycle regulation and signal transduction pathways in cancer. -
CDK2/JAK2/FLT3 Inhibitor
(E/Z)-Zotiraciclib citrate is a potent inhibitor targeting CDK2, JAK2, and FLT3 kinases. This compound demonstrates significant biological activity in disrupting cell cycle progression and signaling pathways associated with cell proliferation and survival. It is utilized in cancer research applications, particularly for studies involving hematological malignancies and solid tumors where these kinases are dysregulated. -
JAK2/FLT3 Inhibitor
Pacritinib hydrochloride is a selective inhibitor targeting JAK2 and FLT3, demonstrating inhibitory potency against wild-type JAK2 (IC50=23 nM), the JAK2V617F mutant (IC50=19 nM), and FLT3 (IC50=22 nM) as well as the FLT3D835Y mutant (IC50=6 nM). This compound is primarily utilized in research related to acute myeloid leukemia (AML) and myelofibrosis (MF), making it a valuable tool for studying these hematological malignancies and the associated signaling pathways. -
PROTAC FLT3/JAK2/BRD4 Degrader
PROTAC FLT3/JAK2/BRD4 Degrader-1 is a potent PROTAC degrader that simultaneously targets FLT3, JAK2, and BRD4, exhibiting DC50 values of 5.23 nM, 0.678 nM, and 1.17 nM, respectively. It demonstrates significant antiproliferative activity against MV4;11 cells with an IC50 of 0.79 nM, inducing apoptosis in these cells. Additionally, PROTAC FLT3/JAK2/BRD4 Degrader-1 shows marked anti-tumor efficacy in MV4;11 xenograft models in NOD SCID mice. This compound is valuable for research into acute myeloid leukemia (AML). -
JAK2/FLT3 Inhibitor
SB1578 is a selective inhibitor of JAK2 and FLT3, exhibiting IC50 values of 46 nM and 60 nM, respectively. This compound demonstrates high selectivity for other kinase targets, making it a valuable tool for research. SB1578 is particularly useful in studying non-oncological indications, such as rheumatoid arthritis, offering insights into potential therapeutic applications in inflammatory diseases. -
CDK2/JAK2/FLT3 Inhibitor
Zotiraciclib hydrochloride is a novel small molecule inhibitor targeting cyclin-dependent kinase 2 (CDK2), Janus kinase 2 (JAK2), and Fms-like tyrosine kinase 3 (FLT3). This reagent demonstrates anti-tumor activity by downregulating the Myc oncogene through CDK9 inhibition, contributing to reduced tumor growth. Zotiraciclib hydrochloride is particularly relevant for research into cancers capable of crossing the blood-brain barrier, and elevated levels of the MCL-1 protein may indicate its potential as a prognostic marker and therapeutic target in cancer studies. -
FLT3/JAK2/BRD4 Ligand
FLT3/JAK2/BRD4 ligand-1 is a specific ligand for the FLT3, JAK2, and BRD4 proteins. This compound facilitates the design and synthesis of proteolysis-targeting chimeras (PROTACs), specifically PROTAC FLT3/JAK2/BRD4 Degrader-1. It demonstrates potential applications in targeted protein degradation and cancer research, enabling innovative therapeutic strategies against malignancies associated with these targets. -
FLT3 Inhibitor
JI6 is a potent and selective FLT3 inhibitor, exhibiting IC50 values of approximately 40 nM for FLT3-WT, 8 nM for FLT3-D835Y, and 4 nM for FLT3-D835H. Additionally, JI6 demonstrates inhibitory activity against JAK3 and c-Kit, with IC50 values of around 250 nM and 500 nM, respectively. This compound serves as a valuable tool for research applications focused on acute myeloid leukemia. -
BET/JAK2/FLT3 Inhibitor
SG3-179 is a selective inhibitor of BET bromodomain proteins, with additional activity against JAK2 and FLT3. This compound effectively reduces HOXB13 protein expression, demonstrating potential relevance in the study of multiple myeloma (MM1.S). SG3-179 is a valuable tool for research involving epigenetic regulation and signaling pathways associated with hematological malignancies. -
FLT3/FGFR Inhibitor
MAX-40279 is a dual inhibitor targeting FLT3 and FGFR kinases, exhibiting potent activity against both wild-type and FLT3 mutants, including FLT3D835Y. This compound effectively inhibits NDRG1 phosphorylation at Ser330 and suppresses endothelial-to-mesenchymal transition (EndMT). MAX-40279 is valuable for research applications in acute myelogenous leukemia (AML), particularly in studying resistance mechanisms to existing therapies. -
FLT3/FGFR Inhibitor
MAX-40279 hemiadipate is a dual inhibitor of FLT3 and FGFR kinases, exhibiting oral bioactivity. This compound effectively targets multiple FLT3 mutants, including FLT3D835Y, and has the potential to overcome resistance against existing treatments. Inhibition of NDRG1 phosphorylation at Ser330 and suppression of endothelial-to-mesenchymal transition (EndMT) further characterize its biological activity. MAX-40279 hemiadipate is a valuable tool for research into acute myelogenous leukemia (AML). -
FLT3/FGFR Inhibitor
MAX-40279 hydrochloride is a dual inhibitor targeting FLT3 and FGFR kinases. This compound demonstrates efficacy against FLT3 mutants, including FLT3D835Y, potentially overcoming resistance to existing therapies. MAX-40279 hydrochloride has been shown to inhibit NDRG1 phosphorylation at Ser330 and suppress endothelial-to-mesenchymal transition (EndMT). It is suited for research focused on acute myelogenous leukemia (AML) and related pathways. -
FLT3/FGFR Inhibitor
MAX-40279 hemifumarate is an orally active dual inhibitor of FLT3 and FGFR kinases, demonstrating efficacy against FLT3 mutant variants, including FLT3D835Y. This compound effectively inhibits NDRG1 phosphorylation at Ser330 and suppresses endothelial-to-mesenchymal transition (EndMT). MAX-40279 hemifumarate is relevant for research in acute myelogenous leukemia (AML) and offers potential therapeutic insights into overcoming resistance associated with traditional FLT3 inhibitors. -
JAK2/FLT3 Inhibitor
Flonoltinib sulfate is a potent, orally active dual inhibitor targeting JAK2 and FLT3. It demonstrates significant biological activity with IC50 values of 0.7 nM for JAK2 and 4 nM for FLT3, along with activity against JAK1 and JAK3 at 26 nM and 39 nM, respectively. This compound is primarily utilized in cancer research, particularly in the study of hematological malignancies influenced by aberrant JAK2 and FLT3 signaling pathways. -
FLT3 Inhibitor
Tuspetinib hydrate is a selective FLT3 inhibitor that demonstrates IC50 values of 1.1 nM, 1.8 nM, and 1.0 nM against FLT3 wild-type, FLT3 internal tandem duplication (ITD), and FLT3 D835Y kinases, respectively. As a reversible type I inhibitor, Tuspetinib hydrate effectively modulates key signaling pathways, including p-STAT5, p-ERK, SYK, JAK1/2, and TAK1. This compound exhibits potent anti-leukemic activity by inhibiting cell proliferation and inducing apoptosis in leukemic cells, making it a valuable tool for research in leukemia and related hematological malignancies. -
FLT3-PROTAC Degrader
PROTAC FLT-3 degrader 4 is a CRBN-based degrader that selectively targets FLT3-ITD mutants by harnessing the ubiquitin-proteasome system for degradation. This compound demonstrates potent activity against FLT3-ITD mutant acute myeloid leukemia (AML) cells, offering a focused approach for research applications in cancer therapeutics. Its oral bioavailability positions it as a valuable tool for investigating FLT3-related signaling pathways and potential treatment strategies in AML. -
FLT3 Inhibitor
HI042 is a selective inhibitor of FMS-like Tyrosine Kinase 3 (FLT3), demonstrating potent activity with IC50 values of 0.62 μM in MOLM-13, 0.33 μM in MV4-11, and 0.89 μM in OCI-AML3 cell lines. This compound effectively reduces the viability of FLT3-internal tandem duplication (FLT3-ITD) mutation-positive cells, induces apoptosis, disrupts cell cycle progression, and diminishes clonogenic potential. HI042 serves as a valuable reagent in the research of acute myeloid leukemia (AML). -
Menin-KMT2A inhibitor
Bleximenib (JNJ-75276617) is an orally active and highly selective menin–KMT2A (MLL) interaction inhibitor, with IC50 values of 0.1 nM in humans, 0.045 nM in mice, and ≤0.066 nM in dogs. It effectively inhibits the proliferation of tumor cells and induces apoptosis and differentiation, particularly in malignancies driven by KMT2A rearrangements. Bleximenib is a promising therapeutic candidate for the study and treatment of leukemia and other menin-dependent cancers. -
Menin-KMT2A inhibitor
Bleximenib (JNJ-75276617) oxalate is an orally active and highly selective inhibitor of the menin–KMT2A (MLL) interaction, with IC50 values of 0.1 nM in humans, 0.045 nM in mice, and ≤0.066 nM in dogs. It effectively inhibits tumor cell proliferation and induces apoptosis and differentiation, particularly in cancers driven by KMT2A rearrangements. Bleximenib oxalate is a promising candidate for research in leukemia and other menin–KMT2A-dependent malignancies. -
JAK2/FLT3 inhibitor
Flonoltinib is a potent and orally active dual JAK2/FLT3 inhibitor with IC50 values of 0.7 nM for JAK2, 4 nM for FLT3, 26 nM for JAK1, and 39 nM for JAK3. It exhibits strong anti-cancer activity and is a promising candidate for the treatment of hematologic malignancies and other JAK/FLT3-driven cancers. -
FLT3/CHK2 inhibitor
Lasmotinib (PHI-101) is a dual inhibitor of FLT3 and CHK2 with potent activity against FLT3 single activating mutations (ITD or TKD), as well as double (ITD/D835Y or ITD/F691L) and triple (ITD/D835Y/F691L) resistance mutations. It synergizes with Venetoclax or Azacytidine to enhance anti-leukemic effects and also demonstrates anticancer activity in ovarian and breast cancer models. -
FLT3 Inhibitor
FLT3-IN-32 hydrochloride is a potent and orally bioavailable inhibitor of FLT3, demonstrating IC50 values of 0.29 nM, 0.77 nM, and 2.07 nM against the FLT3-ITD, FLT3-D835Y, and FLT3-N676K mutations, respectively. This compound effectively reduces FLT3 phosphorylation and inhibits downstream signaling pathways such as STAT5, MAPK, and AKT, ultimately leading to apoptosis in FLT3-mutated Ba/F3 cells. Additionally, FLT3-IN-32 hydrochloride exhibits significant anti-tumor efficacy in the MV4-11 xenograft model, making it a valuable tool for investigations into acute myeloid leukemia (AML). -
FLT3 Inhibitor
FLT3-IN-34 is a selective FLT3 inhibitor, exhibiting an IC50 value of 1.4 nM. It effectively blocks FLT3 phosphorylation and disrupts downstream signaling pathways involving AKT and ERK1/2. FLT3-IN-34 induces a concentration-dependent G0/G1 phase arrest and promotes mild apoptosis in FLT3-ITD-positive MV4-11 cells, demonstrating potent anti-proliferative effects with IC50 values of 14.95 nM and 18.5 nM against MV4-11 and MOLM-13 cell lines, respectively. This compound is suitable for investigating FLT3-positive acute myeloid leukemia (AML) and understanding FLT3-related signaling mechanisms. -
FLT3-ITD Inhibitor
Clifutinib is a selective inhibitor of the FLT3-ITD mutation, exhibiting an IC50 of 15.1 nM. This compound demonstrates potent antiproliferative effects against FLT3-ITD acute myeloid leukemia (AML) cell lines, with IC50 values of 1.5 nM and 1.4 nM for MV-4-11 and MOLM-13, respectively. Clifutinib disrupts FLT3-ITD kinase activity, subsequently inhibiting downstream RAS/MAPK, PI3K/AKT, and JAK/STAT5 signaling pathways, leading to apoptosis in FLT3-ITD-positive AML cells. Additionally, it shows significant antitumor efficacy in mouse models bearing MV-4-11 or MOLM-13 xenografts, making it a valuable tool for investigating relapsed/refractory FLT3-ITD-positive AML. -
FLT3 Inhibitor
Dovitinib lactate hydrate is a multi-targeted tyrosine kinase inhibitor primarily targeting FLT3. It exhibits potent inhibitory activity with IC50 values of 1 nM for FLT3, making it a valuable tool for research in hematological malignancies. In addition to FLT3, it also inhibits c-Kit, FGFR1/3, VEGFR1/2/3, and PDGFRα/β, facilitating studies focused on various signaling pathways and cancer therapeutics.
