Catalog No.
Product Name
Application
Product Information
Citations
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FGFR/HDAC Inhibitor
HDAC-IN-50 is a potent dual inhibitor targeting FGFR and HDAC with IC50 values of 0.18 nM for FGFR1, 1.2 nM for FGFR2, 0.46 nM for FGFR3, 1.4 nM for FGFR4, and varying inhibitory effects on HDAC isoforms such as HDAC1 (1.3 nM), HDAC2 (1.6 nM), HDAC6 (2.6 nM), and HDAC8 (13 nM). This compound effectively induces apoptosis and causes cell cycle arrest at the G0/G1 phase. Additionally, HDAC-IN-50 decreases the expression of phosphorylated forms of FGFR1, ERK, and STAT3, indicating its potential applications in cancer research and therapy. -
VEGFR-2 Inhibitor
VEGFR-2-IN-52 is a potent inhibitor of Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2), demonstrating an IC50 of 191.1 nM. This compound effectively downregulates the expression of phosphorylated VEGFR-2, MMP9, and key signaling proteins p-ERK1/2 and p-MEK1. In addition to its cytotoxic effects, VEGFR-2-IN-52 induces apoptosis and promotes cell cycle arrest in the G0/G1 phase. Furthermore, it enhances reactive oxygen species (ROS) levels, making it valuable for research in cancer therapeutics and angiogenesis studies. -
EGFR2 Inhibitor
EGFR-IN-105 is a selective inhibitor of the EGFR2 receptor, with an IC50 value of 0.68 μM. This compound demonstrates significant anticancer activity by inducing apoptosis in cancerous cells, making it a valuable tool for investigating therapeutic strategies in pancreatic cancer research. Its specificity and potency position it as an important reagent for studies focused on targeting EGFR-related pathways in oncology. -
VEGFR/PARP Inhibitor
VEGFR/PARP-IN-1 is a dual inhibitor targeting Vascular Endothelial Growth Factor Receptor (VEGFR) and Poly(ADP-ribose) Polymerase (PARP), with IC50 values of 191 nM and 60.9 nM, respectively. This compound inhibits DNA damage repair mechanisms, induces apoptosis, and causes G2/M phase cell cycle arrest. It demonstrates significant antiproliferative activity against BRCA wild-type breast cancer cell lines, specifically MDA-MB-231 and MCF-7, with IC50 values of 4.1 μM and 3.5 μM, respectively. VEGFR/PARP-IN-1 is an effective antitumor and anti-metastatic agent, making it valuable for cancer research applications. -
EGFR Inhibitor
EGFR-IN-45 is a potent inhibitor of the epidermal growth factor receptor (EGFR) with IC50 values of 0.4 µM for EGFR and 1.6 µM for CDK2. Additionally, it demonstrates inhibitory activity against Topoisomerase I and Topoisomerase II. This compound effectively induces apoptosis and arrests cancer cells in the pre-G1 phase, making it a valuable tool for cancer research and therapeutic studies targeting EGFR-related pathways. -
EGFR Inhibitor
Avitinib maleate dihydrate is a potent, irreversible, orally active selective inhibitor of epidermal growth factor receptor (EGFR). It exhibits high affinity, with IC50 values of 0.18 nM for both EGFR L858R and EGFR T790M mutations, as well as 7.68 nM for wild-type EGFR. In addition to its EGFR inhibition, Avitinib maleate dihydrate functions as a Bruton’s tyrosine kinase (BTK) inhibitor, promoting apoptosis in mantle cell lymphoma by inhibiting BTK phosphorylation. Its diverse targeting capabilities make it valuable for cancer research applications. -
VEGFR-2/HDAC Dual Inhibitor
VEGFR2/HDAC1-IN-1 is a potent dual inhibitor of VEGFR-2 and HDAC, demonstrating IC50 values of 57.83 nM and 9.82 nM, respectively. This compound effectively arrests the cell cycle at the S and G2 phases, leading to apoptosis in HeLa cells. Additionally, VEGFR2/HDAC1-IN-1 exhibits significant anti-angiogenic properties, making it a valuable tool for research in cancer biology and targeted therapies. -
EGFR Inhibitor
EGFR-IN-51 is a potent inhibitor of the epidermal growth factor receptor (EGFR), exhibiting IC50 values of 0.493 µM for wild-type EGFR, 102.60 µM for the L858R-TK mutation, and 461.63 µM for the T790M-TK mutation. This compound demonstrates significant cytotoxic activity against various cancer cell lines, effectively inducing apoptosis. EGFR-IN-51 is applicable in research focused on targeted cancer therapies and elucidating the role of EGFR signaling in tumorigenesis. -
ALK/EGFR Inhibitor
ALK/EGFR-IN-1-d5 is a deuterated dual-target inhibitor that specifically targets ALK and EGFR, exhibiting IC50 values of 1.08 nM for EGFR and 2.395 nM for ALK. This compound effectively inhibits phosphorylated proteins within the EGFR, ALK, and BRK signaling pathways, disrupting the cell cycle and subsequently promoting apoptosis through a decrease in mitochondrial membrane potential. Furthermore, ALK/EGFR-IN-1-d5 shows significant anti-tumor activity in preclinical animal models, indicating its potential for advancing research in cancer therapeutics. -
ALK Inhibitor
ALK-IN-22 is a potent inhibitor of Anaplastic Lymphoma Kinase (ALK), demonstrating IC50 values of 2.3 nM, 3.7 nM, and 2.9 nM against ALK, ALKL1196M, and ALKG1202R, respectively. This compound effectively down-regulates the phosphorylation of ALK and its downstream signaling proteins, thereby inducing apoptosis in tumor cells. ALK-IN-22 is suitable for various research applications, particularly in the study of tumors associated with ALK dysregulation. -
JAK2/Bcr-Abl/FLT3 Inhibitor
LS-104 is a non-ATP-competitive inhibitor targeting JAK2, Bcr-Abl, and FLT3. It effectively induces apoptosis in JAK2V617F-positive cells while inhibiting JAK2 autophosphorylation and downstream signaling pathways. Additionally, LS-104 demonstrates significant cytotoxic effects and inhibits the proliferation of FLT3-expressing leukemic cells. This hydroxystyryl-acrylonitrile compound holds potential for research into myeloproliferative disorders and refractory or relapsed hematologic malignancies. -
EGFR Inhibitor
EGFR-IN-141 is a potent inhibitor of the epidermal growth factor receptor (EGFR), demonstrating an IC50 of 2.67 nM. This compound exhibits significant cytotoxicity in A549 lung cancer cells, with an IC50 of 13.75 μM. EGFR-IN-141 has been shown to induce apoptosis and cause mitochondrial membrane depolarization, highlighting its potential for antitumor efficacy in cancer research applications. -
VEGFR Inhibitor
VEGFR-IN-3 is a selective VEGFR inhibitor that demonstrates significant antiproliferative activity against OVCAR-4 and MDA-MB-468 cancer cell lines, with IC50 values of 0.29 μM and 0.35 μM, respectively. This compound is valuable for research applications focused on cancer biology, particularly in studies investigating angiogenesis and tumor growth modulation. Its efficacy makes it a suitable candidate for exploring therapeutic strategies targeting vascular endothelial growth factor receptor pathways. -
HIF-1α Inhibitor
GEM-5 is a gemcitabine-based conjugate that functions as a potent HIF-1α inhibitor, with an IC50 value of 30 nM. This compound effectively down-regulates HIF-1α expression while promoting the up-regulation of the tumor suppressor protein p53. GEM-5 has demonstrated the ability to induce apoptosis in A2780 cancer cells and inhibit tumor growth, making it a valuable tool for cancer research and therapeutic studies targeting hypoxia-driven tumor progression. -
EGFR Inhibitor
EGFR-IN-172 is a selective epidermal growth factor receptor (EGFR) inhibitor that effectively disrupts the proliferation of non-small cell lung cancer (NSCLC) cells harboring L858R, T790M, and C797S drug-resistant mutations. This compound acts by inhibiting EGFR phosphorylation, leading to cell cycle arrest and apoptosis in affected cells. EGFR-IN-172 serves as a valuable tool for research focused on NSCLC treatment and the development of targeted cancer therapies. -
PI3K/VEGFR2 Inhibitor
PI3K/VEGFR2-IN-1 is a highly effective dual inhibitor of PI3K and VEGFR2, exhibiting IC50 values of 2.21 μM and 68 μM, respectively. This compound has been shown to induce apoptosis in various cancer cell lines. It is suitable for research applications focused on cancer biology and therapy development targeting the PI3K/VEGFR2 signaling pathways. -
FLT3 Inhibitor
AFG206 is a first-generation ATP-competitive "type II" inhibitor of FLT3. This compound effectively inhibits cell proliferation with an IC50 of approximately 0.1 µM by inducing apoptosis in FLT3-ITD-Ba/F3 and D835Y-Ba/F3 cell lines. AFG206 holds significant promise for research applications related to acute myeloid leukemia. -
Bcr-Abl1 Inhibitor
Radotinib dihydrochloride is a selective Bcr-Abl1 tyrosine kinase inhibitor with an IC50 of 34 nM, demonstrating oral bioavailability and the ability to penetrate the blood-brain barrier. This compound exhibits significant anti-tumor activity by inhibiting cell proliferation, inducing cell cycle arrest, and promoting apoptosis in tumor cells. Radotinib dihydrochloride is utilized in research related to chronic myeloid leukemia, multiple myeloma, and neurodegenerative disorders, particularly those involving prion diseases. -
BCR-ABL Inhibitor
CHMFL-48 is a potent BCR-ABL kinase inhibitor that effectively targets both wild-type and imatinib-resistant mutants. With IC50 values of 1 nM for ABL wild-type and 0.8 nM for the ABL T315I mutant, CHMFL-48 inhibits autophosphorylation of BCR-ABL, disrupting downstream signaling pathways involving STAT5 and CRKL. This mechanism results in cell cycle arrest and the induction of apoptosis, making CHMFL-48 a valuable tool for research focused on chronic myeloid leukemia (CML). -
FLT3 Inhibitor
BPR1J-340 is a potent inhibitor of FLT3, exhibiting an IC50 of approximately 25 nM. It effectively inhibits the phosphorylation of FLT3 and STAT5, inducing apoptosis in FLT3-ITD positive acute myeloid leukemia (AML) cells. This compound demonstrates considerable anti-tumor activities, making it a valuable tool for research in cancer biology and therapeutic strategies targeting FLT3 dysregulation. -
BCR-ABL Inhibitor
HS-438 is a potent and selective inhibitor of BCR-ABL, a fusion protein associated with chronic myeloid leukemia (CML). This compound exhibits significant antiproliferative effects, leading to reduced phosphorylation of BCR-ABL at Tyr177, and promotes apoptosis alongside G0/G1 cell cycle arrest. HS-438 demonstrates substantial antitumor activity, making it a valuable tool for investigations into CML and related therapeutic strategies. -
VEGFR2 Inhibitor
YLL545 is a potent inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), effectively blocking VEGF-induced phosphorylation of VEGFR2 and preventing the activation of downstream signaling mediators such as phosphorylated STAT3 and phosphorylated ERK1/2 in human umbilical vein endothelial cells (HUVEC). This compound demonstrates significant anti-angiogenic properties by suppressing the proliferation, migration, and invasion of HUVEC. Furthermore, YLL545 has shown the capability to induce apoptosis in breast cancer models and inhibit tumor growth, making it a valuable tool for cancer research and the study of angiogenesis. -
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. -
FAK Signaling Inhibitor
FAK-IN-5 is a potent inhibitor of focal adhesion kinase (FAK) signaling. It effectively induces apoptosis and autophagy in various cell types, making it a valuable tool for studying cellular responses to FAK modulation. This compound is utilized in cancer research and investigations related to cell migration and survival pathways. -
VEGFR2 Inhibitor
VEGFR-2-IN-18 is a potent inhibitor of the vascular endothelial growth factor receptor 2 (VEGFR-2) with an IC50 of 60 nM. This compound induces apoptosis in targeted cells and exhibits significant antitumor activity. It is a valuable reagent for research applications focused on angiogenesis, cancer biology, and the development of targeted therapies. -
EGFR/FAK Inhibitor
EGFR-IN-46 is a potent dual inhibitor targeting the epidermal growth factor receptor (EGFR) and focal adhesion kinase (FAK), with IC50 values of 20.17 nM and 14.25 nM, respectively. This compound effectively inhibits cancer cell proliferation and induces apoptotic pathways in these cells. EGFR-IN-46 is designed for research applications focused on cancer biochemistry and therapeutic development. -
FGFR Inhibitor
FGFR-IN-8 is a potent pan-FGFR inhibitor that targets both wild-type and mutant forms of fibroblast growth factor receptors (FGFRs). With impressive inhibitory potency, it demonstrates IC50 values of less than 0.5 nM against FGFR1, V564F-FGFR2, and FGFR3, alongside 22.6 nM for V555M-FGFR3, and 7.30 nM for FGFR4. This compound induces apoptosis in cancer cells and exhibits notable anticancer properties, making it a valuable reagent for cancer research and therapeutic studies involving FGFR signaling pathways. -
EML4-ALK PROTAC Degrader
Pro-PEG3-BA is a targeted PROTAC degrader that specifically degrades EML4-ALK and EGFR mutants, with DC50 values of 0.42 μM and 13.50 μM, respectively. It effectively inhibits proliferation and induces cell cycle arrest and apoptosis in non-small cell lung cancer (NSCLC) cell lines in vitro. In vivo studies reveal that Pro-PEG3-BA rewires the ubiquitin-proteasome system, leading to a reduction in EML4-ALK protein levels while demonstrating a favorable safety profile. This reagent is suitable for research focused on non-small cell lung cancer treatments. -
EGFRvIII Epitope
EGFRvIII peptide is a synthetic epitope derived from the EGFRvIII variant, specifically designed to bind to MHC I molecules. This peptide is known to induce apoptosis and elicit targeted immune responses against glioblastoma, particularly when used in conjunction with Flagellin B. It is a valuable tool for research in cancer immunotherapy and the development of personalized medicine approaches for glioblastoma treatment. -
EGFR Inhibitor
EGFR-IN-60 is a potent inhibitor of the epidermal growth factor receptor (EGFR), specifically targeting EGFRWT, EGFRT790M, EGFRL858R, and JAK3 with IC50 values of 83, 26, 53, and 69 nM, respectively. This compound effectively suppresses the proliferation of H1975 cells with the EGFRT790M mutation (IC50=1.32 µM) while yielding less potency against A431 cells expressing EGFRWT (IC50=4.96 µM). With favorable oral bioavailability, EGFR-IN-60 demonstrates significant antitumor activity, promoting cell death via apoptosis as indicated by an increased Bax/Bcl-2 ratio. This makes it a valuable candidate for research into targeted therapies for EGFR-related cancers. -
EGFR Inhibitor
EGFR-IN-62 is a potent and reversible inhibitor of the epidermal growth factor receptor (EGFR) kinase, demonstrating IC50 values of 10 nM for the L858R/T790M mutation, 29 nM for wild-type EGFR, and 242 nM for the L858R/T790M/C797S mutation. This compound exhibits significant antiproliferative effects on human lung cancer cell lines A549 and H1975, with IC50 values of 2.53 μM and 1.56 μM, respectively. Furthermore, EGFR-IN-62 promotes dose-dependent apoptosis, induces G1/G0 phase arrest, and inhibits cell motility, making it a valuable tool for research in cancer biology and targeted therapies. -
EGFR Inhibitor
EGFR-IN-52 is a potent inhibitor of the epidermal growth factor receptor (EGFR) with IC50 values of 0.358 µM for wild-type EGFR, 86.02 µM for the L858R-TK variant, and 432.67 µM for the T790M-TK resistance mutant. This compound exhibits significant cytotoxicity against various cancer cell lines and is known to induce apoptosis. EGFR-IN-52 is valuable for research applications focusing on targeted cancer therapies and the study of EGFR signaling pathways. -
FAK Inhibitor
FAK-IN-4 is a potent inhibitor of focal adhesion kinase (FAK), a key regulator of cellular adhesion and signaling pathways in cancer. This compound exhibits significant anti-cancer properties, including the induction of apoptosis in various cancer cell lines. FAK-IN-4 is valuable for research applications focused on cancer biology, particularly in studying the modulation of FAK-related signaling pathways and their role in tumor progression. -
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. -
EGFR Inhibitor
EGFR-IN-3 is a selective inhibitor of the epidermal growth factor receptor (EGFR), demonstrating an IC50 of 0.32 µM against EGFR wild-type kinase. This compound exhibits significant cytotoxic effects on various cancer cell lines and promotes apoptosis, making it a valuable tool for studies related to cancer biology and therapeutic development targeting EGFR signaling pathways. -
VEGFR-2 Inhibitor
VEGFR-2-IN-23 is a highly selective inhibitor of the vascular endothelial growth factor receptor 2 (VEGFR-2), exhibiting an IC50 value of 0.34 nM. This compound demonstrates significant antitumor activity by inducing apoptosis and causing cell cycle arrest at the G1 phase. VEGFR-2-IN-23 is particularly relevant for research focused on oncology and angiogenesis, providing valuable insights into therapeutic strategies targeting vascular growth pathways. -
NF-κB/MAPK/FAK/Akt Inhibitor
Ephemeranthol A is an inhibitor of NF-κB, MAPK, FAK, and Akt signaling pathways. This phenanthrene compound demonstrates notable anti-inflammatory effects through the inhibition of NF-κB and MAPK pathways in macrophages. Additionally, Ephemeranthol A induces apoptosis and inhibits metastasis in non-small cell lung cancer by suppressing FAK/Akt signaling and epithelial-mesenchymal transition (EMT) processes. It is applicable for research into acute and chronic inflammatory diseases as well as non-small cell lung cancer. -
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. -
EGFRT790M/L858R Inhibitor
EGFR T790M/L858R-IN-2 is a selective inhibitor of the EGFR T790M and L858R mutants, exhibiting IC50 values of 3.5 nM and 1290 nM for these targets, respectively. This compound effectively reduces the phosphorylation of EGFR, AKT, and ERK1/2, subsequently inducing apoptosis and causing cell cycle arrest in the G1 phase. EGFR T790M/L858R-IN-2 demonstrates significant anti-cancer activity, making it a valuable tool for research in targeted therapies for lung cancer and other malignancies associated with these mutations. -
EGFR-TKI
TAS-121 is a selective, covalent third-generation mutant EGFR-tyrosine kinase inhibitor (EGFR-TKI) that targets various EGFR mutations, including L858R (IC50=1.7 nM), Ex19del (IC50=2.7 nM), L858R/T790M (IC50=0.56 nM), and Ex19del/T790M (IC50=1.1 nM), as well as wild-type EGFR (IC50=8.2 nM). It also exhibits inhibitory activity against HER2 and HER4 with IC50s of 110 and 2.6 nM, respectively. TAS-121 effectively inhibits EGFR phosphorylation and downstream signaling pathways, leading to reduced cell proliferation and induction of apoptosis. Its antitumor efficacy has been demonstrated in xenograft models utilizing SW48 (EGFR G719S) and NCI-H1975 (EGFR L858R/T790M) cell lines. -
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. -
VEGFR2 Inhibitor
VEGFR-2-IN-19 is a potent inhibitor of Vascular Endothelial Growth Factor Receptor 2 (VEGFR2). This compound has been shown to induce apoptosis in cancer cells and elevate intracellular levels of reactive oxygen species. VEGFR-2-IN-19 is primarily utilized in cancer research, offering potential therapeutic insights into tumor progression and vascularization. -
FAK Inhibitor
FAK-IN-24 is a potent inhibitor of focal adhesion kinase (FAK) with an IC50 of 0.815 nM. This compound induces DNA damage and apoptosis, demonstrating significant anti-glioblastoma activity. FAK-IN-24 effectively inhibits the proliferation of glioblastoma cell lines U87-MG and U251, with IC50 values of 15 nM and 20 nM, respectively, and has shown the ability to suppress tumor growth in U87-MG xenograft models. -
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. -
Bcr-AblT315 PROTAC Degrader
PROTAC BCR-ABL Degrader-2 is a selective degrader targeting the Bcr-AblT315 mutant, with a DC50 of 108.7 nM in Ba/F3 Bcr-AblT315I cells. This compound demonstrates a notable degradation efficacy, achieving degradation rates of 69.89% and 94.23% at concentrations of 100 nM and 300 nM, respectively. Additionally, it shows promising in vivo anti-tumor effects including significant tumor regression and induction of apoptosis in tumor cells, while maintaining a favorable safety profile. PROTAC BCR-ABL Degrader-2 is suitable for research focused on chronic myeloid leukemia (CML). -
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. -
EGFR Inhibitor
EGFR-IN-117 is a potent EGFR inhibitor designed to target mutated forms of the epidermal growth factor receptor. It exhibits significant inhibitory activity against a range of EGFR mutant cell lines, including H1975, PC-9, BaF3-EGFRL858R/T790M/C797S, and BaF3–C797S/Del19/T790M, with IC50 values of 13 nM, 19 nM, 1.2 nM, and 1.3 nM, respectively. In addition to its antiproliferative effects, EGFR-IN-117 induces apoptosis and demonstrates antitumor efficacy in preclinical mouse models, making it a valuable tool for cancer research. -
VEGFR-2 Inhibitor
VEGFR-2-IN-13 is a potent inhibitor of the vascular endothelial growth factor receptor-2 (VEGFR-2), demonstrating an IC50 value of 3.4 nM. This compound effectively disrupts the cell cycle in HepG2 cells by inducing G2/M phase arrest and triggering apoptosis. VEGFR-2-IN-13 is valuable for research applications focusing on angiogenesis, cancer development, and therapeutic interventions targeting tumor growth. -
VEGFR-2 Inhibitor
VEGFR-2-IN-28 is a selective inhibitor of the vascular endothelial growth factor receptor 2 (VEGFR-2) with an IC50 value of 0.83 µM. This compound has been shown to induce apoptosis in cancer cells, highlighting its potential as an anticancer agent. VEGFR-2-IN-28 is suitable for research applications focused on tumor vascularization and the mechanisms of cancer cell survival signaling. -
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.
