Catalog No.
Product Name
Application
Product Information
Citations
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HGF/c-Met Inhibitor
Norleual is a hepatocyte growth factor (HGF) and c-Met inhibitor with an IC50 of 3 pM. As an angiotensin IV analog and AT4 receptor antagonist, Norleual demonstrates significant antiangiogenic properties. This compound is utilized in research focused on cancer biology, vascular biology, and angiogenesis-related studies. -
c-Met Inhibitor
c-Met-IN-12 is a potent and selective type II c-Met kinase inhibitor, exhibiting an IC50 of 10.6 nM. This compound effectively inhibits c-Met as well as AXL, Mer, and TYRO3 kinases, demonstrating an inhibition rate exceeding 80% at 1 μM concentration. c-Met-IN-12 shows promising antitumor efficacy and serves as a valuable scaffold for the development of further kinase selectivity enhancements in cancer research applications. -
c-Met Inhibitor
c-Met-IN-17 is a potent inhibitor of c-Met kinase, exhibiting an IC50 of 0.031 μM. This compound demonstrates significant biological activity and serves as a valuable tool in anticancer research. Additionally, c-Met-IN-17 features an alkyne group, facilitating its use as a click chemistry reagent through copper-catalyzed azide-alkyne cycloaddition (CuAAc) with azide-containing molecules. -
c-Met Inhibitor
AC-386 is a potent c-Met inhibitor with an IC50 value of 7.42 nM. It demonstrates significant antiproliferative effects against specific cancer cell lines, making it a valuable tool for investigating mechanisms of anti-cancer resistance. This compound is particularly useful for research in cancer biology and therapeutic development targeting c-Met pathways. -
EGFR/c-Met Inhibitor
EGFR/c-Met-IN-2 is a dual inhibitor targeting the epidermal growth factor receptor (EGFR) and c-Met. This compound effectively inhibits cell proliferation by inducing a G2/M cell cycle arrest, demonstrating significant antitumor activity. It is suitable for research applications investigating cancer biology and therapeutic responses in tumors driven by EGFR and c-Met signaling pathways. -
PROTAC c-Met Degrader
PROTAC c-Met degrader-2 is a PROTAC-based degrader that selectively targets c-Met for degradation through the ubiquitin-proteasome pathway, exhibiting a DC50 of 50 nM. This compound employs a unique linkage incorporating a CRBN ligand derived from Thalidomide, facilitating targeted protein degradation. It serves as a valuable tool for researching c-Met-related pathways and their implications in various cancers, enhancing the understanding of therapeutic strategies involving c-Met modulation. -
c-Met Inhibitor
c-Met-IN-13 is a potent inhibitor of the c-Met receptor with an IC50 value of 2.43 nM. This compound exhibits significant cytotoxic effects against cancer cells, demonstrating antiproliferative activity that is both concentration- and time-dependent. c-Met-IN-13 is valuable for research applications focused on cancer biology and therapeutic development targeting c-Met signaling pathways. -
c-MET Inhibitor
c-Met-IN-11 is a selective inhibitor of c-MET and VEGFR-2. It demonstrates potent biological activity with IC50 values of 41.4 nM for c-MET and 71.1 nM for VEGFR-2, making it a valuable tool for studying signaling pathways in cancer. This compound is suitable for applications in cancer research, particularly in exploring the role of c-MET in tumor growth and metastasis. -
VEGFR-2/c-Met Inhibitor
VEGFR-2/c-Met-IN-2 is a selective inhibitor targeting VEGFR-2 and c-Met, demonstrating IC50 values of 83 nM and 48 nM, respectively. This compound exhibits significant cytotoxicity against the HCT-116 cell line, with an IC50 of 3.403 µM. Its potent inhibitory effects make it a valuable tool for research into angiogenesis and cancer metastasis. -
Type-III c-MET Inhibitor
c-Met-IN-18 is an ATP-competitive type-III c-MET inhibitor that effectively targets both wild-type and D1228V mutant forms of c-MET, with IC50 values of 0.013 µM and 0.20 µM, respectively. This compound is primarily utilized in research focused on c-MET-driven cancers. Additionally, c-Met-IN-18 features an alkyne moiety, enabling it to participate in copper-catalyzed azide-alkyne cycloaddition (CuAAc) reactions, allowing for diverse applications in chemical biology. -
c-Met Inhibitor
PF 04254644 is an orally active inhibitor of the c-Met receptor, also known as mesenchymal-epithelial transition factor (MET). It selectively targets the hepatocyte growth factor receptor, leading to significant biological effects, including myocardial degeneration in animal models. This compound serves as a valuable tool for research into cardiovascular diseases and cancer, facilitating the exploration of c-Met signaling pathways and therapeutic interventions. -
c-MET Inhibitor
Zgwatinib (SOMG-833) is a highly selective and ATP-competitive inhibitor of c-MET, exhibiting an IC50 of 0.93 nM. It demonstrates over 10,000-fold selectivity against 19 related tyrosine kinases, including c-MET family members. Zgwatinib effectively inhibits c-MET-mediated cell proliferation, making it a promising candidate for research focused on c-MET-driven human cancers. -
c-Met Inhibitor
KRC-00715 is a potent oral inhibitor of c-Met with an IC50 of 9.0 nM, exhibiting high selectivity for gastric cancer cells. This compound effectively induces G1/S phase arrest in c-Met-overexpressing cell lines, resulting in diminished downstream signaling through Akt and Erk pathways as well as reduced c-Met activity. In the gastric cancer cell line Hs746, KRC-00715 demonstrates an IC50 of 39 nM and shows significant efficacy in reducing tumor size in Hs746T xenograft mouse models, highlighting its potential application in cancer research and therapeutics. -
c-Met Inhibitor
SOMCL-863 is a selective and orally bioavailable c-Met inhibitor, demonstrating significant antitumor activity in both in vitro and in vivo models. This compound serves as a valuable tool in cancer research, aiding in the exploration of pathways involving c-Met and its role in tumor progression. -
c-Met Inhibitor
EMD 1204831 is a potent and selective inhibitor of the c-Met receptor tyrosine kinase, exhibiting an IC50 of 9 nM. This compound effectively suppresses c-Met activity, making it a valuable tool for investigating the role of c-Met in cancer biology. Its application can lead to insights into tumor growth, metastasis, and potential therapeutic strategies targeting c-Met dysregulation. -
c-Met/VEGFR-2 Inhibitor
T-1840383 is a highly potent ATP-competitive inhibitor targeting c-Met and VEGFR-2, demonstrating IC50 values of 1.9 nM for c-Met, 7.7 nM for VEGFR1, 2.2 nM for VEGFR2, and 5.5 nM for VEGFR3. This compound effectively inhibits key signaling pathways associated with cancer progression and angiogenesis. It is suitable for research applications focused on tumor growth and vascular development, making it a valuable tool in oncology and vascular biology studies. -
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. -
RON Kinase/c-Met Inhibitor
LCRF-0004 is a potent inhibitor of RON kinase, exhibiting an IC50 value of 10 nM. Additionally, LCRF-0004 also demonstrates significant inhibitory activity against c-Met, with an IC50 of 12 nM. This compound is valuable for research in cancer biology, particularly in studies focusing on RON kinase and c-Met signaling pathways. -
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. -
ALK/ROS1 Dual Inhibitor
ALK/ROS1-IN-1 is a potent and selective dual inhibitor targeting ALK and ROS1, demonstrating IC50 values of 0.174 μM for ALK and 0.530 μM for ROS1. This compound is particularly effective against crizotinib-resistant variants, making it valuable for research applications focusing on cancer therapeutics and drug resistance mechanisms. Its ability to modulate these key oncogenic pathways makes it a significant tool for studying the therapeutic potential in various cancer models. -
EML4-ALK PROTAC Degrader
PROTAC EML4-ALK Degrader-2 is an advanced degrader specifically targeting the EML4-ALK fusion protein. With an IC50 of 1.6 nM, it exhibits potent selective inhibitory activity against ALK while maintaining selectivity over IGF1R, INSR, FLT3, and FGFR2. This compound demonstrates significant anti-cancer effects in both in vitro and in vivo models and is particularly relevant for research applications involving non-small cell lung cancer (NSCLC), as well as liver and cervical cancers. -
ALK2 Inhibitor
ALK2-IN-5 is a pyrazolopyrimidine compound that selectively inhibits ALK2 activity, as well as FGFR activity. This compound demonstrates significant potential in research applications related to disorders influenced by dysregulated ALK2 and FGFR, including various cancer types. Its ability to modulate these key pathways makes it a valuable tool for investigating the molecular mechanisms underlying ALK2 and FGFR-related pathologies. -
ALK Inhibitor
ALK-IN-23 is a selective ALK inhibitor exhibiting IC50 values of 1.6 nM, 0.71 nM, and 1.3 nM against ALKWT, ALKL1196M, and ALKG1202R respectively. It effectively arrests the cell cycle in the G2 phase and promotes apoptosis in cancer cells. Additionally, ALK-IN-23 demonstrates the ability to inhibit cancer cell migration and colony formation in vitro, while revealing promising antitumor efficacy in H2228 xenograft models with low toxicity. This reagent is suitable for studies focused on ALK-related pathways and cancer therapeutics. -
Brigatinib-PROTAC Degrader
SIAIS117 is a potent Brigatinib-PROTAC degrader that targets the ALK protein, specifically effective against the ALK G1202R point mutation. By utilizing a VHL-1 conjugation, SIAIS117 exhibits significant capability to induce protein degradation, leading to inhibited growth of SR and H2228 cancer cell lines. This compound holds potential for applications in anti-proliferative research, particularly in small cell lung cancer contexts. -
ALK Inhibitor
Con B-1 is a potent and selective inhibitor of anaplastic lymphoma kinase (ALK), exhibiting low toxicity towards normal cells. This compound effectively modulates ALK activity, making it valuable for research into ALK-driven cancers. It is suitable for use in studies related to targeted therapies and evaluation of cancer cell proliferation and survival pathways. -
ALK Inhibitor
(E)-Belizatinib is a potent and selective anaplastic lymphoma kinase (ALK) inhibitor, exhibiting an enzymatic IC50 of 0.005 μM and a cellular IC50 of 0.048 μM. Demonstrating over 61-fold selectivity for ALK over JAK2, SRC, and IGF1R, (E)-Belizatinib possesses favorable pharmacokinetic properties in both rats and dogs. This compound is valuable for research focused on ALK-driven cancers, offering significant potential for therapeutic development in this area. -
ALK5 Inhibitor
ALK5-IN-79 is a selective ALK5 inhibitor that interferes with TGF-β1/SMAD signaling pathways, exhibiting significant anticancer activity. This compound reduces extracellular matrix production and collagen deposition, making it pertinent for studies focused on fibrosis and cancer progression. ALK5-IN-79 demonstrates favorable pharmacokinetic properties and good in vivo tolerance, supporting its potential as a therapeutic agent in various research applications. -
Anaplastic lymphoma kinase (ALK) Inhibitor
KRCA-0713 is a potent inhibitor of anaplastic lymphoma kinase (ALK), demonstrating robust anti-ALK activity in both enzyme and cell-based assays. This compound effectively suppresses ALK-driven tumor growth, as evidenced by studies conducted in H3122 xenograft models. KRCA-0713 serves as a valuable tool for researchers investigating ALK-related oncogenesis and therapeutic responses in cancer treatment. -
ALK Inhibitor
ALK5-IN-26 is a potent inhibitor of Activin receptor-like kinase 5 (ALK5), exhibiting an IC50 value of ≤10 nM. This compound is valuable for research applications investigating the role of ALK5 in cancer progression and related pathways. Its high specificity and efficacy make it a useful tool for elucidating the mechanistic underpinnings of tumor biology. -
ALK Inhibitor
WZH-15-125 is a potent anaplastic lymphoma kinase (ALK) inhibitor, showing significant activity against compound ALK mutations that contribute to drug resistance. With an IC50 of 101.7 nM, it effectively targets the G1202R/L1196M mutation, which demonstrates resistance to Lorlatinib. WZH-15-125 serves as a valuable ligand for PROTAC synthesis, specifically for the development of PROTAC WZH-17-002. This compound is particularly relevant for research in non-small cell lung cancer, offering new avenues for therapeutic exploration. -
ALK inhibitor
ALK-IN-13 is a selective inhibitor of anaplastic lymphoma kinase (ALK), targeting key pathways involved in oncogenesis. This compound exhibits potent anti-tumor activity, making it valuable for research focused on ALK-driven cancers, including non-small cell lung cancer. Its mechanism of action allows for detailed studies of ALK signaling and the development of targeted therapeutic strategies.
