Catalog No.
Product Name
Application
Product Information
Citations
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hTrkA Inhibitor
hTrkA-IN-2 is a selective allosteric inhibitor of human TrkA with an IC50 of 3.9 nM. This compound demonstrates the ability to modulate TrkA activity, making it valuable for studies investigating neurotrophic signaling pathways. hTrkA-IN-2 is suitable for research applications focused on neurobiology, potential therapeutic strategies for neurodegenerative diseases, and the exploration of pain mechanisms. -
TRKA Antagonist
Pegcantratinib is a selective TRKA antagonist that also exhibits activity against TRKB and TRKC. This compound is valuable for research into CYLD cutaneous syndrome (CCS) and inflammatory dermatoses, including psoriasis and associated pruritus. Its targeted inhibition of TRK receptors makes it a promising tool for studying the underlying mechanisms of these conditions. -
TRK Inhibitor
TRK-IN-28 is a potent TRK inhibitor that demonstrates IC50 values of 0.55 nM, 25.1 nM, and 5.4 nM against TRKWT, TRKG595R, and TRKG667C, respectively. This compound exhibits antiproliferative activity, with IC50 values of 9.5 nM, 3.7 nM, 205.0 nM, and 48.3 nM in various Ba/F3 cell lines expressing ETV6-TRKAWT, ETV6-TRKBWT, LMNA-TRKG595R, and LMNA-TRKAG667C, respectively. TRK-IN-28 is valuable for research focused on TRK-related tumors and signaling pathways. -
TRK Inhibitor
Trk-IN-11 is a highly effective inhibitor of tropomyosin receptor kinase (TRK), exhibiting IC50 values of 1.4 nM and 1.8 nM against TrkA and TrkAG595R, respectively. As a receptor tyrosine kinase, TRK plays a crucial role in the progression of solid tumors. This compound is valuable for studying TRK-related pathways and assessing therapeutic strategies in cancer research. -
TRK Inhibitor
(R)-Larotrectinib is a selective TRK inhibitor, demonstrating an IC50 value of 28.5 nM for TrkA. This compound is instrumental in advancing research on cancers associated with TRK fusions, offering potential insights into therapeutic strategies. Additionally, (R)-Larotrectinib may contribute to the understanding of inflammatory and certain infectious diseases, making it a valuable reagent for diverse biomedical investigations. -
Trk Receptor Inhibitor
Pan-Trk-IN-2 is a small molecule inhibitor targeting the Trk receptor family. It demonstrates potent antitumor activity by interfering with nerve growth factor signaling pathways. This compound is useful for research applications focused on cancer biology and the therapeutic exploration of neurotrophic receptor pathways. -
TrkB Agonist
TrkB-IN-1 is a potent agonist of the tropomyosin receptor kinase B (TrkB), exhibiting favorable pharmacokinetic properties. This compound has demonstrated the ability to reverse cognitive deficits in Alzheimer's disease mouse models, making it a valuable tool for investigating therapeutic strategies in neurodegenerative research. TrkB-IN-1 may facilitate the exploration of synaptic plasticity and neuroprotection, contributing to the understanding of TrkB signaling pathways in Alzheimer's disease. -
Trk Inhibitor
Trk-IN-1 is a potent inhibitor of tropomyosin-related kinases (Trk), demonstrating significant activity against TrkA with an IC50 of 3.7 nM and TrkB with an IC50 of 94 nM. This compound is useful for studying the role of Trk signaling in various biological processes, including neuronal growth and survival. Trk-IN-1 can be applied in drug discovery efforts aimed at treating conditions associated with Trk dysregulation, such as certain neurodegenerative diseases and cancers. -
TrkA Inhibitor
TrkA-IN-7 is a selective inhibitor of Tropomyosin Receptor Kinase A (TrkA), exhibiting a Kd value of 40 μM. This compound serves as a valuable tool for investigating the role of TrkA in various biological processes, including neurotrophic signaling and cancer progression. Its application in research facilitates the exploration of therapeutic strategies targeting TrkA-related pathways. -
TRK Inhibitor
Trk-IN-10 is a selective inhibitor of tropomyosin receptor kinases (TRK) with IC50 values of 0.86 nM for TrkA and 6.92 nM for the TrkAG595R variant. As a receptor tyrosine kinase, TRK plays a crucial role in the development of solid tumors. Trk-IN-10 exhibits a noteworthy selectivity profile, showing an IC50 of 350 nM against ALK, which may help mitigate potential off-target effects and toxicity in therapeutic applications. This compound is valuable for research into TRK-related pathways and the treatment of neurotrophic receptor-driven malignancies. -
Trk Receptor Inhibitor
Trk-IN-6 is a selective inhibitor of Trk receptors, demonstrating remarkable in vitro potency against various TRK mutants with IC50 values ranging from 0.2 to 0.7 nM. This compound is invaluable for studying the role of Trk signaling in cancer and neurodevelopmental disorders. Its high specificity makes it a reliable tool for elucidating the biological effects of Trk inhibition in research applications. -
TRK Mutant Kinase Inhibitor
TRK-IN-34 is a potent TRK and TRKC mutant kinase inhibitor, exhibiting IC50 values of 0.75 nM and 0.96 nM against TRKAG595R and TRKAG667C, respectively. This compound effectively inhibits the kinase activities of these mutations, leading to decreased proliferation of TRKA-transfected cells and demonstrating tumor growth-inhibitory effects in xenograft models. TRK-IN-34 is valuable for investigating cancers resistant to TRK inhibitors, particularly those driven by the TRKAG667C mutation. -
TrkC Inhibitor
TrkC-IN-1 is a selective inhibitor of Tropomyosin receptor kinase C (TrkC), exhibiting IC50 values of 3.3-7.1 μM in EBC-1 cells and 7.3-10.2 μM in HT-29 cells. This compound demonstrates significant potential in cancer research, particularly in elucidating the role of TrkC in oncogenic signaling pathways. TrkC-IN-1 is a valuable tool for studying the therapeutic implications of targeting TrkC in various cancer types. -
TRK Inhibitor
Type II TRK inhibitor 1 is a selective inhibitor targeting TRK fusion proteins and wild-type TRK, demonstrating potent anti-proliferative effects in Ba/F3 cell lines that express the CD74-TRKAG667C and ETV6-TRKCG696C variants, with IC50 values of 6 nM and 1.7 nM, respectively. Additionally, this compound functions as a click chemistry reagent, featuring an alkyne group that facilitates copper-catalyzed azide-alkyne cycloaddition (CuAAc), enabling its application in bioconjugation and related chemical biology research. -
TrkA Inhibitor
D5261 is a potent allosteric inhibitor of tropomyosin-related kinase A (TrkA). It selectively targets the type III binding site, effectively modulating TrkA activity. D5261 has shown promise in biological assays for studying neuronal development and neurodegenerative diseases, making it a valuable tool for research focused on neurobiology and related therapeutic applications. -
TrkA Kinase Inhibitor
Anizatrectinib is a highly potent and orally bioavailable TrkA kinase inhibitor with an IC50 value of 1.3 nM. This compound plays an important role in the investigation of inflammatory diseases, including prostatitis and other pelvic conditions. Its mechanism of action offers valuable insights into cellular signaling pathways associated with pain and inflammation, making it a useful tool for researchers in the field of therapeutic development. -
TRKA Inhibitor
NMS-P626 is a potent inhibitor of the tropomyosin receptor kinase A (TRKA), TRKB, and TRKC, demonstrating IC50 values of 8 nM, 7 nM, and 3 nM, respectively. This compound effectively inhibits the proliferation of KM12 colorectal cancer cells by suppressing the phosphorylation of TPM3-TRKA and disrupting downstream signaling pathways, with an observed IC50 of 19 nM in these cells. NMS-P626 is valuable for research applications focused on colorectal cancer and related signaling mechanisms. -
TRK Kinase Inhibitor
(3aR)-Selitrectinib is a potent TRK kinase inhibitor, demonstrating IC50 values of 0.6 nM for TRKA and less than 2.5 nM for TRKC. This next-generation compound is designed to target TRK signaling pathways, making it a valuable tool in cancer research. Its selective inhibition of TRK kinases can aid in the investigation of tumorigenesis and the therapeutic potential in TRK fusion-positive cancers. -
TRKA Inhibitor
ONO-7579 is an orally bioavailable inhibitor targeting TRKA, primarily inhibiting its phosphorylation to reduce tumor growth. In studies with colorectal cancer cell line KM12, it exhibits an EC50 of 17.6 ng/g, indicating that this concentration effectively reduces phosphorylated TRKA activity by 50%. ONO-7579 is useful in cancer research, particularly in exploring therapeutic strategies against tumors reliant on TRKA signaling. -
TrkA Inhibitor
TrkA-IN-8 is a potent TrkA inhibitor with a Kd value of 3.3 µM. This compound demonstrates concentration-dependent inhibition of cell proliferation in lung cancer cell lines, particularly in non-small cell lung cancer. TrkA-IN-8 is valuable for research applications aimed at understanding the role of TrkA signaling in oncogenesis and therapeutic resistance. -
Ligands for Target Protein for PROTAC
GNF-8625 is a potent TRK inhibitor that functions by targeting TRK receptor tyrosine kinases, specifically TRKA, TRKB, and TRKC, with IC50 values of 0.8 nM, 22 nM, and 5.4 nM, respectively. This compound can be utilized in conjunction with Thalidomide to create a PROTAC degrader, enabling targeted protein degradation. GNF-8625 is valuable in research applications investigating TRK-mediated pathways and offers potential in therapeutic strategies for cancers involving aberrant TRK signaling. -
TrkA Inhibitor
VMD-928 is an orally active, allosteric, and irreversible inhibitor targeting tropomyosin receptor kinase A (TrkA). By blocking the downstream signaling pathways initiated by nerve growth factor (NGF) binding, VMD-928 inhibits cell proliferation and invasion while promoting cancer cell apoptosis. This compound is of significant interest in research related to various cancers, including prostate cancer, thymic carcinoma, mesothelioma, squamous cell carcinoma of the head and neck, lung squamous cell carcinoma, ovarian cancer, and hepatocellular carcinoma. -
Src-FAK-Paxillin Inhibitor
JP-153 is a Src-FAK-Paxillin signaling inhibitor that specifically targets the Src-dependent phosphorylation of paxillin at tyrosine 118, leading to downstream inhibition of Akt activation at serine 473. This compound effectively reduces VEGF-induced migration and proliferation in retinal endothelial cells, making it a valuable tool for studying neovascular eye diseases. Researchers can utilize JP-153 to explore the molecular mechanisms underlying angiogenesis and potential therapeutic interventions. -
VEGFR2/FAK Inhibitor
ZINC09875266 is a dual inhibitor that specifically targets Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) and Focal Adhesion Kinase (FAK). This compound demonstrates potent inhibitory activity that can suppress angiogenesis and cancer cell proliferation. Research applications include studying tumor growth and metastasis in various cancer models. -
Anti-c-MET ADC
Telisotuzumab vedotin is an antibody-drug conjugate targeting c-MET, comprised of the anti-c-MET monoclonal antibody Telisotuzumab and the cytotoxic agent Monomethyl Auristatin E. This compound demonstrates antitumor efficacy in vivo while maintaining acceptable toxicity levels. It is primarily utilized in research focusing on non-small cell lung cancer (NSCLC), making it a valuable tool for investigating therapeutic approaches in this area. -
c-Met Agonist
Fosgonimeton is a c-Met agonist known to activate the hepatocyte growth factor receptor. This compound exhibits neuroprotective properties, demonstrating efficacy in models of neuroinflammation induced by LPS as well as in Alzheimer's disease models characterized by amyloid-beta pathology. Its potential applications extend to research aimed at understanding neurodegenerative diseases and therapeutic interventions. -
c-Met Receptor Activator
Terevalefim is a mimetic of hepatocyte growth factor (HGF) that selectively activates the c-Met receptor. This compound demonstrates significant biological activity in modulating cell proliferation, survival, and migration, making it a crucial tool in cancer research. Terevalefim is particularly relevant for studies focused on tumor microenvironment interactions and therapeutic targets in various malignancies. -
TAM/c-Met Inhibitor
PF-07265807 is a potent inhibitor of TAM receptors and the c-Met kinase, exhibiting IC50 values of 6.1 nM for AXL, 13.2 nM for MER, and 21.6 nM for TYRO3. This compound is primarily utilized in research focused on cancer biology, particularly in understanding tumor progression and metastasis. Its selective inhibition of specific tyrosine kinases offers valuable insights into therapeutic strategies targeting these pathways in oncology. -
C-Met Inhibitor
Dalmelitinib is a selective c-Met kinase inhibitor with an IC50 of 2.9 nM, targeting the ATP-binding region of the c-Met receptor. This compound effectively induces phosphorylation of MET while partially or completely inhibiting the phosphorylation of downstream signaling proteins AKT and ERK. Dalmelitinib demonstrates potent anti-proliferative effects on cancer cells with c-Met oncogene amplification, making it a valuable reagent for research applications in cancers such as human non-small cell lung cancer (NSCLC). -
Tyrosine Kinase Inhibitor
Zurletrectinib is a potent tyrosine kinase inhibitor that selectively targets TRK kinases (TRKA IC50 = 0.81 nM; TRKB IC50 = 0.145 nM; TRKC IC50 = 0.184 nM). Its enhanced binding affinity results in superior efficacy, especially against various resistance mutations (effectively targeting 13 out of 18 known mutations). This compound is particularly useful for research applications related to glioma and exploring TRK signaling pathways in tumor biology. -
c-Met/AXL Inhibitor
BPI-9016M is a potent, orally active dual inhibitor of c-Met and AXL tyrosine kinases. It demonstrates significant biological activity by suppressing tumor cell growth, migration, and invasion in lung adenocarcinoma. This compound is valuable for research applications targeting cancer signaling pathways and metastasis. -
c-MET Inhibitor
(rel)-Tivantinib is a potent and selective inhibitor of the receptor tyrosine kinase c-MET. This compound also targets GSK3α and GSK3β, which are involved in the cellular mechanisms associated with non-small cell lung cancer (NSCLC). Its inhibition of c-MET signaling pathways and modulation of GSK3 activity position (rel)-Tivantinib as a valuable tool for researching therapeutic strategies in cancer biology. -
c-Met PROTAC Degrader
PROTAC c-Met degrader-1 is a selective and orally active degrader targeting c-Met, exhibiting a DC50 of 6.21 nM. This compound promotes CRBN-dependent ubiquitination and subsequent proteasomal degradation of c-Met, effectively inducing G0/G1 phase arrest in c-Met-dependent cancer cells. Furthermore, PROTAC c-Met degrader-1 demonstrates significant anticancer activity by killing c-Met-dependent cells and inhibiting tumor growth in animal models, making it a valuable tool for research in gastric cancer. -
JNK/c-Met Inhibitor
JNK-IN-16 is a potent inhibitor of both JNK and c-Met, exhibiting IC50 values of 72 nM and 120 nM, respectively. This compound demonstrates significant anti-cancer activity, making it valuable for research in cancer biology and therapeutic development. Its dual inhibition profile allows for exploration in signaling pathways associated with tumor progression and metastasis. -
c-Met/HGFR Inhibitor
Meleagrin is a potent c-Met/HGFR inhibitor derived from the alkaloid roquefortine C, produced by fungi of the genus Penicillium. This compound exhibits significant antimicrobial and anti-proliferative activities, making it valuable in research focused on cancer biology. Meleagrin serves as a promising lead compound for targeting c-Met-dependent metastatic and invasive breast cancers, contributing to the development of novel therapeutic strategies. -
c-Met/TRK Inhibitor
1D228 is a potent c-Met/TRK inhibitor that exhibits significant antitumor activity. By inhibiting cyclin D1, 1D228 induces G0/G1 cell cycle arrest and effectively reduces cancer cell proliferation and migration. This compound is relevant for research applications focused on gastric, liver, and vascular tumors. -
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 inhibitor
PF-04217903 phenolsulfonate is a potent ATP-competitive inhibitor of the c-Met kinase with a Ki value of 4.8 nM for human c-Met. It demonstrates over 1,000-fold selectivity against a profile of 208 kinases, highlighting its specificity. This compound possesses antiangiogenic properties and is useful in research applications related to cancer therapy and the modulation of tumor microenvironments. -
c-Met Inhibitor
Tepotinib hydrochloride is a highly selective, reversible, ATP-competitive inhibitor of c-Met, exhibiting an IC50 of 3 nM and over 200-fold selectivity for c-Met compared to other kinases such as IRAK4, TrkA, Axl, IRAK1, and Mer. This compound effectively inhibits c-Met phosphorylation and promotes autophagy. Tepotinib hydrochloride demonstrates significant antitumor activity and is applicable in cancer research targeting c-Met-driven pathways. -
c-Met Inhibitor
c-Met-IN-16 is a potent inhibitor of the c-Met receptor tyrosine kinase, known to play a crucial role in tumor growth and metastasis. This compound demonstrates significant biological activity in targeting aberrant c-Met signaling pathways associated with various cancers. c-Met-IN-16 is primarily used in cancer research to explore therapeutic strategies and mechanisms of resistance in c-Met-driven malignancies. -
c-Met Kinase Inhibitor
c-Met-IN-15 is a selective inhibitor of c-Met kinase, a critical regulator of cell proliferation and survival. At a concentration of 10 μM, c-Met-IN-15 demonstrates 21.1% inhibition of c-Met kinase activity, making it a valuable tool for studying c-Met signaling pathways. This compound is suitable for research applications related to cancer biology, particularly in contexts involving c-Met dysregulation. -
c-Met Inhibitor
c-Met-IN-26 is a potent c-Met inhibitor, exhibiting an IC50 of 1.6 nM. This compound plays a crucial role in cancer research, targeting the c-Met signaling pathway to disrupt tumor proliferation and metastasis. Its high specificity makes it a valuable tool for studying the molecular mechanisms underlying c-Met-related oncogenesis and for evaluating potential therapeutic interventions. -
VEGFR-2/c-Met Inhibitor
Taligantinib is a selective dual inhibitor of vascular endothelial growth factor receptor 2 (VEGFR-2) and hepatocyte growth factor receptor (c-Met). This orally active compound effectively suppresses tumor angiogenesis and cell proliferation. Taligantinib is of particular interest in the research of solid tumors, including non-small cell lung cancer and hepatocellular carcinoma, making it a valuable tool for cancer biology studies. -
Type IIb c-Met Inhibitor
KIN-8741 is a highly selective Type IIb c-Met inhibitor that targets the c-Met kinase, effectively addressing various mutations associated with this oncogenic pathway. Demonstrating significant antitumor activity, KIN-8741 is particularly effective in models of non-small cell lung cancer characterized by MET gene amplification and exon 14 deletions. This reagent is suitable for research applications focusing on c-Met-driven cancers, especially in advanced tumors with MET exon 14 jump mutations and acquired drug resistance. -
c-Met Inhibitor
c-Met-IN-19 is a potent c-Met inhibitor with an IC50 of 1.99 nM. This compound exhibits significant cytotoxic effects on various cancer cell lines, including A549, HT-29, SGC-7901, and MDA-MB-231, demonstrating IC50 values of 0.25, 0.36, 0.98, and 0.76 μM, respectively. c-Met-IN-19 is valuable for research applications focused on cancer therapies targeting the c-Met pathway. -
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. -
c-Met Inhibitor
c-Met-IN-21 is a highly potent c-Met inhibitor, exhibiting an IC50 value of 0.45 nM. This compound demonstrates significant anti-tumor efficacy in vivo, making it a valuable tool for research in cancer biology and therapeutic applications targeting c-Met signaling pathways. Its potent inhibitory activity offers the potential for studying tumor proliferation and metastasis mechanisms. -
c-MET Inhibitor
(3S,4S)-Tivantinib is a selective inhibitor of the receptor tyrosine kinase c-MET. In addition to its primary target, (3S,4S)-Tivantinib also inhibits glycogen synthase kinase 3 alpha (GSK3α) and glycogen synthase kinase 3 beta (GSK3β), which are critical in the pathogenesis of non-small cell lung cancer (NSCLC). This compound is utilized in research focused on understanding c-MET-related signaling pathways and evaluating therapeutic strategies for NSCLC. -
MET/VEGFR2/KDR Inhibitor
Foretinib phosphate is a potent inhibitor of the c-MET and VEGFR2 receptors, which play crucial roles in tumor growth and angiogenesis. By selectively targeting hepatocyte growth factor receptor c-MET and vascular endothelial growth factor receptor 2, Foretinib phosphate exhibits significant anti-tumor activity, potentially reducing tumor cell proliferation and metastasis. Its unique mechanism offers distinct advantages over other treatments, making it a valuable tool for research in oncology, particularly in studies related to lung cancer and the pathways involving MEK1/2, FER, and AURKB. -
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.
