Catalog No.
Product Name
Application
Product Information
Citations
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PROTAC ALK Degrader
TL13-112 is a potent and selective PROTAC degrader targeting ALK, with an IC₅₀ of 0.14 nM for ALK inhibition. In addition to ALK, TL13-112 also induces degradation of Aurora A (IC₅₀: 8550 nM), FER (42.4 nM), PTK2 (25.4 nM), and RPS6KA1 (677 nM), supporting its utility in kinase signaling and cancer research. -
PROTAC ALK Degrader
TL13-12 is a selective PROTAC degrader targeting anaplastic lymphoma kinase (ALK), exhibiting an IC50 of 0.69 nM for ALK inhibition. In addition to its primary action, TL13-12 induces degradation of several other kinases, including Aurora A (IC50 = 13.5 nM), FER (IC50 = 5.74 nM), PTK2 (IC50 = 18.4 nM), and RPS6KA1 (IC50 = 65 nM). This compound is designed through the conjugation of TAE684 and the Cereblon ligand derived from Pomalidomide, making it a valuable tool for studying kinase biology and developing targeted therapies. -
RIPK2/ALK2 Inhibitor
OD36 hydrochloride is a potent inhibitor of receptor-interacting protein kinase 2 (RIPK2) and an effective modulator of activin receptor-like kinase 2 (ALK2), exhibiting an IC50 of 5.3 nM against RIPK2. This macrocyclic compound demonstrates strong binding affinity for the ALK2 kinase ATP pocket, with a Kd of 37 nM. OD36 hydrochloride is suitable for research applications focused on signaling pathways involving RIPK2 and ALK2, relevant in studying various diseases, including inflammation and cancer. -
RIPK2/ALK2 Inhibitor
OD36 is a selective inhibitor of RIPK2 with an IC50 of 5.3 nM, demonstrating potent binding affinity to the ATP pocket of the ALK2 kinase, with a KD of 37 nM. This macrocyclic compound exhibits specific ALK2-directed activity, making it a valuable tool for investigating the roles of these kinases in various biological pathways. Research applications include the exploration of inflammatory signaling and potential therapeutic interventions in related diseases. -
RIPK2/ALK2 Inhibitor
RIPK2-IN-1 is a selective inhibitor targeting RIPK2 and ALK2, with an IC50 of 51 nM and 5 nM, respectively. This compound demonstrates substantial efficacy in modulating RIPK2/NOD2 pathways, exhibiting an IC50 of 390 nM in cellular assays. RIPK2-IN-1 is suitable for research applications investigating pathways related to inflammation and immune response mechanisms. -
ALKBH5 Inhibitor
ALKBH5-IN-5 is a selective inhibitor of ALKBH5 with an IC50 of 0.62 μM and a Kd of 804 nM. This compound disrupts the interaction between ALKBH5 and its substrates, m6A-RNA and 6mA-DNA, leading to enhanced differentiation and apoptosis in cancer cells, as well as G2-M phase arrest. Notably, ALKBH5-IN-5 reduces the protein levels of TACC3 and MYC while increasing cleaved caspase-3 levels, demonstrating significant antiproliferative effects. Furthermore, it exhibits antitumor activity in xenograft mouse models and is relevant for research into acute myeloid leukemia. -
ALK Inhibitor
ALK-IN-26 is a selective inhibitor of the anaplastic lymphoma kinase (ALK) with an IC50 value of 7.0 μM for ALK tyrosine kinase. This compound exhibits favorable pharmacokinetic properties and demonstrates permeability across the blood-brain barrier. ALK-IN-26 has been shown to induce apoptosis, autophagy, and necrosis, making it a valuable tool in the study of glioblastoma and related malignancies. -
ALK Inhibitor
ALK/PI3K/AKT-IN-1 is a selective ALK inhibitor that demonstrates significant anti-proliferative effects on A549, H1975, and PC9 cancer cell lines with IC50 values of 0.44, 0.83, and 1.51 μM, respectively. This compound induces cell cycle arrest at the G1 phase by enhancing p21 and p27 expression while inhibiting CDK2 and phosphorylated Rb activity. Additionally, ALK/PI3K/AKT-IN-1 disrupts the ALK/PI3K/AKT signaling pathway, leading to mitochondrial membrane depolarization and apoptosis in A549 cells. It also effectively inhibits spheroid formation and growth in A549 cells, making it a valuable tool for cancer research. -
ALK Inhibitor
ALK-IN-31 is an orally active inhibitor of anaplastic lymphoma kinase (ALK), with an IC50 of 1135 nM. This compound demonstrates significant antiproliferative activity against H2228 lung cancer cells, showing an IC50 of 1.35 μM. ALK-IN-31 induces apoptosis and halts cell cycle progression in the G0/G1 phase by modulating mitochondrial function. Furthermore, it attenuates tumor growth by downregulating p-AKT and p-mTOR within the PI3K-AKT-mTOR signaling pathway, making it a valuable tool for research in non-small cell lung cancer (NSCLC). -
EML4-ALK PROTAC Degrader
Gly-PEG3-BA is an EML4-ALK PROTAC degrader that targets the EML4-ALK fusion protein. This compound exhibits a DC50 of 0.50 μM for EML4-ALK in H3122 cells and a DC50 of 20.15 μM for EGFR mutant (L858R/T790M) levels in H1975 cells. Gly-PEG3-BA demonstrates notable antiproliferative effects, with IC50 values of 0.84 μM against H3122 cells and 20.74 μM against H1975 cells. It is a valuable tool for research in non-small cell lung cancer. -
EML4-ALK/EGFR PROTAC Degrader
Lys-PEG3-BA is a novel EML4-ALK/EGFR PROTAC degrader that influences target proteins through the ubiquitin-proteasome pathway. With DC50 values of 1.32 μM against H3122 (EML4-ALK) cells and 19.66 μM for H1975 (EGFR-L858R/T790M) cells, it effectively inhibits cell proliferation. This compound serves as a valuable tool for research into non-small cell lung cancer and the mechanisms underlying targeted protein degradation. -
EGFR/ALK Inhibitor
DA-0157 is a selective inhibitor of the epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), designed to address drug-resistant mutations, specifically EGFR C797S and ALK mutations in non-small cell lung cancer (NSCLC) models. It demonstrates potent antiproliferative activity in cells bearing EGFR Del19/T790M/C797S (IC50 = 6.9 nM), as well as in various ALK mutant forms, including Ba/F3-EML4-ALK-L1196M (IC50 = 5.5 nM). Additionally, DA-0157 has been shown to inhibit CYP2D6 with an IC50 of 5.26 μM, and exhibits promising antitumor efficacy in preclinical mouse models, making it a valuable tool for cancer research. -
ALK/EGFR Degrader
SIAIS164018 is a PROTAC-based degrader targeting ALK and EGFR, demonstrating IC50 values of 2.5 nM and 6.6 nM against ALK and ALK G1202R, respectively. This compound exhibits potent inhibitory effects on cancer cell migration and invasion, induces G1 cell cycle arrest, and promotes apoptosis. SIAIS164018 is a valuable tool for research applications investigating targeted degradation mechanisms in oncology. -
ALK/ROS1 Inhibitor
Lorlatinib acetate is a selective and orally active inhibitor targeting ROS1 and ALK pathways. This compound exhibits potent anticancer activity with Kis of less than 0.025 nM for ROS1 and less than 0.07 nM for wild-type ALK, establishing it as a promising therapeutic candidate for ALK-driven cancers. Additionally, Lorlatinib acetate effectively inhibits ALK phosphorylation, demonstrated by IC50 values ranging from 15-43 nM for ALKL1196 and varying efficacy against multiple resistant mutations, making it a valuable tool for cancer research and drug discovery. -
ALK/EGFR Inhibitor
ALK/EGFR-IN-1 is a potent dual inhibitor targeting ALK and EGFR, effectively blocking their phosphorylation. This compound demonstrates high inhibitory activity against EGFR L858R T790M mutants in H1975 cells, with an IC50 of 4.3 nM, and EML4-ALK in BaF3 cells, with an IC50 of 3.6 nM. ALK/EGFR-IN-1 is particularly valuable for research in non-small cell lung cancer (NSCLC) and provides insights into the mechanisms of resistance in targeted therapies. -
ALKBH5 Inhibitor
DDO-2728 is a selective inhibitor of AlkB homologue 5 (ALKBH5), demonstrating an IC50 of 2.97 μM. This compound enhances the levels of N6 methyladenosine (m6A) modifications, leading to increased cell apoptosis and cell cycle arrest. DDO-2728 has shown efficacy in suppressing tumor growth in the MV4 11 xenograft model, highlighting its potential application in cancer research and therapeutic strategies targeting ALKBH5. -
ALK Inhibitor
Neladalkib is a potent oral selective inhibitor of anaplastic lymphoma kinase (ALK) with an IC50 of 2.8 nM. This compound induces apoptotic cell death and demonstrates anti-tumor activity, making it a valuable tool for cancer research. Neladalkib is particularly relevant in studies focused on ALK-driven malignancies and therapeutic resistance mechanisms. -
ALK/FAK/ROS1 Multikinase Inhibitor
APG-2449 is an orally active inhibitor targeting BCL-2 and multikinase pathways, specifically ALK, FAK, and ROS1. It demonstrates potent antitumor activity by reducing cell viability and enhancing apoptosis in acute myeloid leukemia cells in vitro. APG-2449 effectively decreases the activation of FAK and its downstream signaling effectors. This compound is suitable for research applications in various malignancies, including mesothelioma, non-small cell lung cancer, ovarian cancer, and other hematologic and solid tumors. -
ALKBH5 Inhibitor
W23-1006 is a selective and covalent inhibitor of ALKBH5, targeting the C200 residue with an IC50 of 3.848 μM. This compound exhibits approximately 30-fold and 8-fold greater inhibitory activity against ALKBH5 compared to FTO and ALKBH3, respectively. W23-1006 is particularly valuable for research applications focusing on triple-negative breast cancer (TNBC), enabling studies on the role of ALKBH5 in tumor biology and potential therapeutic strategies. -
ALK Tyrosine Kinase Inhibitor
Ceritinib-d7 is a deuterium-labeled derivative of Ceritinib, which functions as a selective and ATP-competitive inhibitor of the ALK (anaplastic lymphoma kinase) tyrosine kinase. This compound is utilized in research to explore mechanisms of ALK-mediated oncogenesis and to evaluate the therapeutic efficacy of targeted treatments in malignancies such as non-small cell lung cancer. Its deuterium labeling allows for advanced studies in pharmacokinetics and metabolism, making it a valuable tool for chemical biology investigations. -
ALK Inhibitor
ALK-IN-24 is a potent, orally active inhibitor of anaplastic lymphoma kinase (ALK) with an IC50 value of 1.7 nM, also exhibiting inhibition of insulin receptor kinase with an IC50 value of 6 nM. It effectively suppresses the proliferation of lung adenocarcinoma cells and has demonstrated the ability to inhibit ALK-driven tumor growth in xenograft mouse models. This compound is applicable for research focused on non-small cell lung cancer and other ALK-related malignancies. -
ALK/IR/VEGFR2/TIE2/DLK Inhibitor
CEP-14083 is an ATP-competitive inhibitor targeting ALK, with IC50 values of 2 nM in enzymatic assays. This compound also inhibits other kinases, including the insulin receptor (IR), vascular endothelial growth factor receptor 2 (VEGFR2), angiopoietin-1 receptor (TIE2), and dual leucine zipper kinase (DLK). CEP-14083 has been shown to suppress CD274 mRNA expression and the function of NPM/ALK in NPM/ALK-positive T cell lymphoma cells. It is a valuable tool for research focused on lymphoma and related signaling pathways. -
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. -
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. -
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. -
ALK/c-Met/ROS1 Inhibitor
Crizotinib acetate is an orally bioavailable inhibitor targeting ALK, c-Met, and ROS1 through ATP competition. It demonstrates potent inhibition of tyrosine phosphorylation in cell-based assays, with IC50 values of 20 nM for ALK, 8 nM for c-Met, 24 nM for NPM-ALK, and 11 nM for c-Met. The compound has shown significant efficacy in inhibiting tumor growth, making it a valuable tool in cancer research and therapeutic applications targeting these pathways. -
c-Met/ALK Inhibitor
CM-118 is a selective inhibitor of c-Met and ALK, targeting the HGF-induced c-Met phosphorylation and impairing ALK phosphorylation in key variants including EML4-ALKv1, ALK F1174L, and EML4-ALKv1 L1196M. With IC50 values of 0.92, 1.25, 1.9, and 3.5 μM respectively, CM-118 demonstrates significant anticancer activity against tumors reliant on c-Met or ALK oncogenic pathways. This compound is useful for investigating therapeutic strategies in cancers driven by these targets. -
ALK Inhibitor
SMU-B is a potent orally active inhibitor of anaplastic lymphoma kinase (ALK) with an IC50 of less than 0.5 nM, along with c-ros oncogene 1 (ROS1) and c-MET, exhibiting IC50 values of 1.87 nM and 28.9 nM for AXL. This compound demonstrates significant antiproliferative activity against MKN45, H1993, and H441 cell lines, with IC50s of 0.02 μM, 1.58 μM, and 2.82 μM, respectively. Additionally, SMU-B has shown promising antitumor efficacy in various mouse models, highlighting its potential for cancer research applications. -
Stable Isotope
Crizotinib-d8 is a deuterated analog of Crizotinib, functioning as an ATP-competitive inhibitor of ALK and c-Met. This compound exhibits potent biological activity, with IC50 values of 20 nM and 8 nM, respectively, and effectively inhibits tyrosine phosphorylation of NPM-ALK and c-Met in cellular assays. Additionally, Crizotinib-d8 serves as an inhibitor of ROS1. This stable isotope is primarily utilized in pharmacokinetic studies and metabolic research involving Crizotinib to enhance understanding of its therapeutic mechanisms. -
PROTAC ALK Degrader
SIAIS001 is a potent PROTAC degrader targeting anaplastic lymphoma kinase (ALK) with a DC50 of 3.9 nM. This compound induces G1/S phase cell cycle arrest and effectively inhibits the proliferation of SR cells with an IC50 of 0.9 nM. SIAIS001 is suitable for research in non-small cell lung cancer (NSCLC) and anaplastic large-cell lymphomas (ALCLs). -
NPM-ALK PROTAC Degrader
MS99-β-Gal is a galactose-modified PROTAC degrader targeting the NPM-ALK fusion protein. This compound is selectively hydrolyzed by SA-β-gal and esterase in senescent cancer cells, allowing the release of MS99, which effectively degrades the NPM-ALK protein. MS99-β-Gal demonstrates an IC50 of 454.8 nM in aging Karpas 299 cells, showing improved potency compared to normal Karpas 299 cells with an IC50 of 2.162 μM. This reagent is valuable for cancer research, particularly in studies focused on targeted protein degradation. -
ALKBH5 Inhibitor
ALKBH5-IN-3 is a selective inhibitor of the ALKBH5 enzyme, exhibiting an IC50 of 0.021 μM. This compound effectively stabilizes ALKBH5 in HepG2 cells, resulting in an elevated level of m6A in intact cells. ALKBH5-IN-3 serves as a valuable chemical probe for investigating the biological functions of ALKBH5, with significant applications in cancer research. -
ALK Inhibitor
CPD-1224 is a potent ALK inhibitor that specifically targets the EML4-ALK oncogenic fusion protein. This compound promotes the degradation of both ALK and its mutant forms, including L1196M and G1202R. CPD-1224 demonstrates significant potential in slowing tumor growth, making it a valuable reagent for cancer research and therapeutic development focused on ALK-driven malignancies. -
ALK Inhibitor
Zotizalkib is a potent and selective inhibitor of anaplastic lymphoma kinase (ALK) with a low IC50 of 1.4 nM for wild-type ALK and 0.3 nM for key ALK-resistant mutations such as G1202R and L1196M. This CNS-penetrant compound demonstrates significant antitumor activity, making it valuable for research in cancer biology and treatment strategies for ALK-driven tumors. Its oral bioavailability and ability to target resistant ALK mutations further enhance its potential in therapeutic applications. -
ALK1/2 Inhibitor
M4K2234 is a potent and selective inhibitor of ALK1 and ALK2, with IC50 values of 7 nM and 14 nM, respectively. This compound effectively disrupts BMP signaling by inhibiting the phosphorylation of SMAD1/5/8, thereby reducing BMP7-stimulated reporter activity (IC50 = 16 nM). M4K2234 is suitable for studying ALK1/2-mediated biological pathways and investigating diseases such as diffuse midline glioma (DMG) and fibrodysplasia ossificans progressiva (FOP). -
ALK5/VEGFR2 Inhibitor
Tosposertib is a dual inhibitor targeting ALK5 and VEGFR2, with IC50 values of 1.2 nM and 4.9 nM, respectively. This compound effectively restores the functionality of cytotoxic T lymphocytes (CTLs) and natural killer cells that are suppressed by TGFβ, while concurrently inhibiting the activity and viability of regulatory T cells. Tosposertib is valuable for research applications related to melanoma and colon cancer. -
ALK Inhibitor
CEP-28122 mesylate salt is a potent and selective inhibitor of Anaplastic Lymphoma Kinase (ALK), exhibiting an IC50 value of 1.9 nM. This diaminopyrimidine derivative demonstrates significant antitumor activity in preclinical models of ALK-positive human cancers. Its favorable pharmacodynamic and pharmacokinetic profiles support its use in research related to ALK-positive anaplastic large-cell lymphoma (ALCL), non-small cell lung cancer (NSCLC), and neuroblastoma. -
Trk/ROS1/ALK Inhibitor
Entrectinib-d8 is a deuterated derivative of Entrectinib, targeting TrkA/B/C, ROS1, and ALK receptors. This compound exhibits potent inhibitory effects with IC50 values of 1 nM for TrkA, 3 nM for TrkB, 5 nM for TrkC, and 12 nM for ROS1 and ALK. Entrectinib-d8 is effective in inducing apoptosis and cell cycle arrest in various cancer cell lines, demonstrating significant anti-tumor activity. Additionally, it has been shown to alleviate bleomycin-induced pulmonary fibrosis in murine models, making it a valuable tool for research in cancer and fibrosis therapies. -
ALK Inhibitor
Ficonalkib is a potent anaplastic lymphoma kinase (ALK) inhibitor that targets the tyrosine kinase receptor. It exhibits significant antineoplastic activity and is utilized in research to explore therapeutic strategies for ALK-driven malignancies. Its mechanism of action provides valuable insights into cancer biology and potential treatment pathways. -
Anaplastic lymphoma kinase (ALK) Inhibitor
ALK-IN-28 is a selective inhibitor of anaplastic lymphoma kinase (ALK), a critical target in various cancers, including non-small cell lung cancer and neuroblastoma. This compound effectively blocks ALK activity, demonstrating significant anti-proliferative effects in ALK-driven tumor models. ALK-IN-28 is suitable for research applications focused on elucidating ALK signaling pathways and exploring potential therapeutic strategies for ALK-positive malignancies. -
ALKBH5 Inhibitor
Ena15 is an inhibitor of the ALKBH5 enzyme, which plays a critical role in m6A RNA methylation. This compound enhances the demethylase activity of FTO, leading to increased levels of m6A-modified RNA and stabilization of FOXM1 mRNA. Ena15 demonstrates potent antitumor activity by suppressing the growth of glioblastoma multiforme, making it a valuable tool for research in cancer biology and therapeutic development. -
ALK Inhibitor
ALK Kinase Inhibitor-1 is a selective anaplastic lymphoma kinase (ALK) inhibitor, identified as compound I-202 from patent US20130261106A1. This compound exhibits potent inhibitory activity against ALK, a crucial target in various cancers, particularly those driven by ALK mutations such as non-small cell lung cancer. It is suitable for research applications aimed at studying ALK-related signaling pathways and evaluating potential therapeutic strategies in oncological contexts. -
EML4-ALK Inhibitor
EML4-ALK kinase inhibitor 1 is a potent inhibitor targeting the echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK), demonstrating an IC50 value of 1 nM. This compound effectively disrupts EML4-ALK signaling pathways, which are implicated in certain types of cancer, particularly non-small cell lung cancer. It serves as a valuable tool for research focused on understanding EML4-ALK-mediated oncogenic processes and exploring therapeutic strategies for EML4-ALK-positive malignancies. -
ALKBH5 Inhibitor
ALKBH5-IN-2 is a selective inhibitor of the ALKBH5 enzyme, demonstrating a potent inhibitory effect with an IC50 value of 0.79 µM. This compound has been shown to significantly reduce cell viability, making it a valuable tool for studying the role of ALKBH5 in various biological processes. Applications include investigations into cellular responses to RNA demethylation and exploring its implications in cancer research and epigenetic regulation. -
ALK Inhibitor
TL13-22 is a potent anaplastic lymphoma kinase (ALK) inhibitor with an IC50 of 0.54 nM. As a negative control for TL13-12, it serves as a valuable tool in research involving ALK pathways without inducing degradation of the ALK protein in cells. This compound can be utilized in studies focused on ALK-related cancers and signaling mechanisms. -
ALK Degreder
AP-1 is a PROTAC designed to target anaplastic lymphoma kinase (ALK) for selective degradation. This compound comprises the target protein ligand CS-1243648, the E3 ligase ligand Pomalidomide, and a linker derived from 2-(Tert-Butoxy)-2-oxoacetic acid. AP-1 is valuable for research applications focused on studying ALK-related signaling pathways and the therapeutic potential of targeted protein degradation in cancer treatment. -
ALK Inhibitor
ALK-IN-5 is a highly potent and selective inhibitor of anaplastic lymphoma kinase (ALK), demonstrating an IC50 value of 2.9 nM. This compound effectively crosses the blood-brain barrier, making it suitable for research applications related to ALK-driven malignancies, particularly in neurological contexts. ALK-IN-5 serves as a valuable tool for investigating ALK signaling pathways and developing targeted therapies in cancer research. -
ALK Inhibitor
CJ-2360 is a highly selective and orally bioavailable inhibitor of anaplastic lymphoma kinase (ALK), demonstrating IC50 values of 2.2 nM against wild-type ALK and various mutant forms, including F1197M, G1269A, L1196M, and S1206Y. This compound exhibits significant inhibitory activity against clinically relevant ALK mutants such as C1156Y and L1196M, as well as selectivity towards other kinases, including LTK, MERTK, CLK1, DAPK1, and DAPK2. CJ-2360 is suitable for studies focused on ALK-related cancers and the development of targeted therapies. -
ALK/EGFR Inhibitor
ALK/EGFR-IN-3 is a potent dual inhibitor targeting both ALK and EGFR. It demonstrates significant anti-proliferative effects on H1975, PC9, and Baf3-EML4-ALK cancer cell lines, with IC50 values of 0.1360, 0.0332, and 0.0339 μM, respectively. This compound is valuable for research in cancer biology, specifically for studying treatment resistance and therapeutic strategies in tumors characterized by ALK and EGFR alterations.
