Shop By
Catalog No.
Product Name
Application
Product Information
Citations
-
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. -
IRAK4 Inhibitor
IRAK4-IN-27 is a selective inhibitor of IRAK4, exhibiting an IC50 of 8.7 nM. This compound effectively inhibits cell growth and induces apoptosis in MYD88 L265P diffuse large B-cell lymphoma (DLBCL) cell lines. IRAK4-IN-27 is an important tool for studying the mechanisms underlying DLBCL and developing potential therapeutic strategies. -
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. -
TrkB Inhibitor
PC-046 is a potent multitarget inhibitor of tyrosine receptor kinase B (TrkB), IRAK-4, and Pim-1, with IC50 values of 13.4 μM, 15.4 μM, and 19.1 μM, respectively. This compound demonstrates significant cytotoxicity against BxPC3 pancreatic cancer cells, with an IC50 range of 7.5-130 nM. PC-046 effectively induces apoptosis and disrupts the cell cycle at the G2/M phase in these cells. Additionally, it showcases promising antitumor efficacy and favorable pharmacokinetic properties in murine models, making it a valuable tool for cancer research. -
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. -
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. -
IGFR Inhibitor
Cis-NVP-ADW742 is a selective inhibitor of the insulin-like growth factor 1 receptor (IGF-1R), exhibiting a potent inhibitory effect with an IC50 of 0.17 μM. This compound also demonstrates a moderate inhibition of the insulin receptor (InsR) with an IC50 of 2.8 μM. Cis-NVP-ADW742 induces significant antiproliferative and pro-apoptotic effects in tumor cells, making it a valuable tool for cancer research and the study of signaling pathways involved in cell growth and survival. -
TRK Inhibitor
IHMT-TRK-284 is a potent, orally active inhibitor targeting TRK kinases, exhibiting IC50 values of 10.5 nM, 0.7 nM, and 2.6 nM against TRKA, TRKB, and TRKC, respectively. This compound demonstrates a favorable selectivity profile within the kinome and shows promising in vivo efficacy in antitumor models. IHMT-TRK-284 is valuable for studies investigating the role of TRK signaling in various cancers and for the development of targeted therapeutic strategies. -
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. -
c-Met Inhibitor
c-Met-IN-9 is a potent c-Met kinase inhibitor with an IC50 value of 12 nM. This 4-phenoxypyridine derivative effectively induces apoptosis in cancer cells and exhibits significant antitumor activity. It is suitable for research applications focused on cancer biology and therapeutic development targeting the c-Met signaling pathway. -
IGF-1R Inhibitor
KW-2450 free base is a potent inhibitor of IGF-1 receptor (IGF-1R) and acts on multiple kinases including Aurora A and B. It demonstrates significant antitumor activity against triple-negative breast cancer (TNBC) by reducing cell viability, promoting apoptosis, and inhibiting colony and mammosphere formation in TNBC cells. In vivo studies indicate that KW-2450 free base effectively suppresses the growth of TNBC xenografts, leading to apoptotic cell death or survival of polyploid cells. Additionally, it enhances the therapeutic efficacy of combination treatments with MEK inhibitors, providing a synergistic antitumor effect in various TNBC models. -
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. -
IRAK4 Inhibitor
Emavusertib phosphate is a potent inhibitor of IRAK4, exhibiting an IC50 of 57 nM. This compound effectively disrupts NF-κB and MyD88 signaling pathways, leading to a significant reduction in pro-inflammatory cytokines such as IL-6 and IL-10. Emavusertib phosphate demonstrates both anti-inflammatory and anti-proliferative effects on cancer cells, promoting apoptosis and showcasing antitumor activity in preclinical mouse models. Its applications extend to investigating inflammatory diseases and cancer therapies. -
IRAK4 Inhibitor
Emavusertib maleate is a potent inhibitor of IRAK4, demonstrating an IC50 of 57 nM, and FLT3. This orally bioavailable compound inhibits NF-κB and MyD88 signaling pathways, effectively reducing the production of pro-inflammatory cytokines such as IL-6 and IL-10. Its anti-inflammatory and anti-proliferative properties make it a valuable tool for cancer research, promoting apoptosis in cancer cells and demonstrating antitumor activity in preclinical mouse models. -
IRAK4 Inhibitor
Emavusertib tosylate is a potent inhibitor of IRAK4, displaying an IC50 of 57 nM. By targeting IRAK4 and FLT3, it effectively disrupts NF-κB and MyD88 signaling pathways, resulting in the reduction of pro-inflammatory cytokines such as IL-6 and IL-10. This compound demonstrates significant anti-inflammatory and anti-proliferative properties against cancer cells, promoting apoptotic mechanisms. Additionally, Emavusertib tosylate has shown noteworthy antitumor activity in preclinical mouse models, making it a valuable reagent for cancer research and inflammation studies. -
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. -
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. -
IRAK4 Inhibitor
Emavusertib mesylate is a potent inhibitor of IRAK4, demonstrating an IC50 of 57 nM. This orally active compound effectively disrupts the NF-κB and MyD88 signaling pathways, leading to a reduction in pro-inflammatory cytokines such as IL-6 and IL-10. Emavusertib mesylate displays anti-inflammatory and anti-proliferative properties against cancer cells, promoting apoptosis. Additionally, it has shown significant antitumor activity in mouse models, making it valuable for cancer research and therapeutic studies targeting inflammatory 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. -
c-Met Inhibitor
LAH-1 is a potent inhibitor of c-Met, demonstrating oral bioavailability and favorable membrane permeability with an IC50 of 49 nM. It exhibits significant anticancer activity by inducing apoptosis and inhibiting cellular migration and invasion. This compound is useful in research applications focused on cancer therapeutics and the modulation of c-Met signaling pathways. -
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. -
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. -
IGF-1R Inhibitor
KW-2450 tosylate is a selective inhibitor of the insulin-like growth factor-1 receptor (IGF-1R), as well as Aurora A and B kinases. It effectively induces apoptosis in cancer cells, demonstrating significant anticancer activity, particularly against triple-negative breast cancer. This compound is valuable for research applications involving cancer biology and therapeutic targeting of kinase signaling pathways. -
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. -
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. -
TRK Inhibitor
TRK-IN-32 is a potent inhibitor of TRK proteins, effectively targeting TRKWT, TRKG595R, and TRKG667C with IC50 values of 0.08 nM, 2.14 nM, and 0.68 nM, respectively. This compound exhibits significant antiproliferative activity against Ba/F3 cell lines expressing various TRK fusion proteins, including wild type and mutant forms. TRK-IN-32 also induces apoptosis in Ba/F3-TRKAWT and Ba/F3-TRKAG667C cells, making it a valuable tool for investigating the role of TRK signaling in a range of cancers, including thyroid cancer and secretory breast carcinoma. -
c-Met Kinase Inhibitor
c-Met-IN-10 is a highly potent inhibitor of the c-Met kinase, exhibiting an IC50 value of 16 nM. This compound demonstrates significant inhibitory activity against various cancer cell lines, including A549, H460, and HT-29, with IC50 values ranging from 0.56 to 1.59 μM. c-Met-IN-10 effectively suppresses colony formation in HT-29 cells, induces apoptosis in HT-29 and A549 cells, and inhibits A549 cell motility. This reagent is valuable for research applications focused on cancer biology and therapeutic interventions targeting c-Met pathways. -
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. -
c-Met Inhibitor
c-Met-IN-14 is a selective inhibitor of the c-Met kinase, classified as an N-sulfonylamidine derivative, with an IC50 value of 2.89 nM. This compound effectively inhibits c-Met phosphorylation, leading to the arrest of the cell cycle at the G2/M phase and demonstrating significant anticancer activity. Additionally, c-Met-IN-14 induces apoptosis in A549 lung cancer cells in a dose-dependent manner, making it a valuable tool for cancer research and therapeutic studies targeting c-Met signaling pathways. -
TRK Inhibitor
TRK-IN-23 is a selective TRK inhibitor demonstrating potent biological activity with IC50 values of 0.5 nM, 9 nM, 14 nM, 4.4 nM, and 4.8 nM against TRKA, TRKC, TRKAG595R, TRKAF589L, and TRKAG667C, respectively. This compound effectively induces apoptosis in Ba/F3 cells expressing TRKAG595R and TRKAG667C. TRK-IN-23 is valuable for researchers investigating TRK signaling pathways and potential therapeutic interventions in TRK-driven malignancies. -
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. -
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. -
CSF-1R Inhibitor
CSF1R-IN-22 is a selective inhibitor of the colony-stimulating factor 1 receptor (CSF-1R) with an IC50 value of less than 6 nM. This compound enhances CXCL9 secretion from M2 macrophages and promotes CD8+ T cell infiltration, thereby amplifying anti-tumor immune responses, particularly in combination with anti-PD-1 therapies. CSF1R-IN-22 effectively reprograms M2-like tumor-associated macrophages (TAMs) to the M1 phenotype, reshaping the tumor microenvironment by increasing CD8+ T cell recruitment and decreasing immunosuppressive regulatory T cells and myeloid-derived suppressor cells (MDSCs). -
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. -
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. -
SRC Inhibitor
SI-2 is a selective inhibitor of steroid receptor coactivator-3 (SRC-3), effectively reducing both its transcriptional activity and protein levels in cells. This compound exhibits significant cytotoxicity against cancer cells and inhibits the migration of MDA-MB-468 breast cancer cells, promoting apoptosis in these cells. In vivo studies demonstrate that SI-2 suppresses tumor growth in mouse models while showing minimal toxicity to the heart and other vital organs at a dosage of 20 mg/kg. -
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. -
ALK Inhibitor
KF-20444 is a selective ALK inhibitor that effectively penetrates the blood-brain barrier. It demonstrates potent activity against ALK fusion proteins such as EML4-ALK and various ALK resistance mutations, including L1196M, G1202R, and F1174L. By inhibiting ALK phosphorylation in ALK-driven cancer cell lines, KF-20444 suppresses cell proliferation and promotes apoptosis. This compound shows significant anti-tumor efficacy in mouse models of ALK-positive non-small cell lung cancer (NSCLC) and neuroblastoma, making it a valuable tool for research on ALK-driven malignancies.
