Catalog No.
Product Name
Application
Product Information
Citations
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FAK PROTAC degrader
FAK PROTAC B5 is a potent degrader targeting focal adhesion kinase (FAK) with an IC50 of 14.9 nM. This compound exhibits significant FAK degradation capabilities along with antiproliferative effects. Furthermore, it demonstrates notable plasma stability and moderate membrane permeability, effectively inhibiting cell migration and invasion. FAK PROTAC B5 is suitable for research applications focused on cancer biology and cellular signaling pathways. -
FAK Inhibitor
FAK-IN-23 is a selective inhibitor of focal adhesion kinase (FAK), a critical regulator of cell adhesion, migration, and survival. This compound effectively disrupts FAK activity, leading to the modulation of cellular signaling pathways associated with cancer progression and metastasis. FAK-IN-23 is primarily used in cancer research to investigate the role of FAK in tumor biology and to evaluate potential therapeutic strategies targeting FAK-related pathways. -
FAK Inhibitor
PH11 is a potent focal adhesion kinase (FAK) inhibitor that enhances TRAIL-induced apoptosis in TRAIL-resistant PANC-1 cells while sparing normal human fibroblasts. This compound operates by downregulating c-FLIP through the inhibition of FAK and the phosphatidylinositol-3-kinase (PI3K)/AKT signaling pathways, thereby reinstating the TRAIL apoptotic cascade. PH11 represents a promising therapeutic strategy for pancreatic cancer by selectively targeting the c-FLIP regulatory pathway without affecting caspase-8 processing, thus circumventing TRAIL resistance. Ongoing research will further delineate PH11's mechanism of action and its implications in overcoming resistance in TRAIL-based therapies for pancreatic cancer. -
PROTAC FAK Degarder
BSJ-04-146 is a selective PROTAC that targets focal adhesion kinase (FAK) for degradation, exhibiting an IC50 of 26 nM. It demonstrates rapid and robust degradation of FAK in cancer cells while maintaining high specificity across the proteome, and it induces prolonged degradation in murine models. The activity of BSJ-04-146 relies on the ubiquitin-proteasome system, making it a valuable tool for investigating pathways associated with pancreatic cancer and triple-negative breast cancer. -
FAK Inhibitor
FAK-IN-3 is a potent inhibitor of focal adhesion kinase (FAK), a critical regulator of cell adhesion and signaling. This compound effectively reduces migration and invasion in PA-1 ovarian cancer cells while downregulating the expression of matrix metalloproteinases MMP-2 and MMP-9. FAK-IN-3 demonstrates significant tumor growth and metastasis inhibition, making it a valuable tool for research in ovarian cancer and related fields. -
FAK Inhibitor
FAK-IN-26 is a potent inhibitor of Focal Adhesion Kinase (FAK) with an IC50 of 0.87 nM, effectively penetrating the blood-brain barrier. It has been shown to significantly reduce tumor cell viability, inhibit cancer stem cell activity, and diminish cell migration in A549 and SKOV-3 cell lines. In vivo studies demonstrate robust anti-cancer activity, achieving tumor inhibition rates of 59.15% and 57.9% in A549 and SKOV-3 mouse models, respectively, highlighting its potential for cancer research applications. -
FAK Inhibitor
FAK-IN-21 is a selective inhibitor of Focal Adhesion Kinase (FAK) with an IC50 of 37.52 nM. This compound effectively inhibits cell growth and the phosphorylation of FAK, making it a valuable tool in cancer research. FAK-IN-21 is particularly useful for studies related to diffuse gastric cancer, providing insights into the mechanistic role of FAK in tumor progression. -
FAK Ligand
FAK Ligand-5 functions as a FAK ligand, enabling the targeted modulation of focal adhesion kinase. This compound is essential for the synthesis of PROTAC molecules, particularly in the development of FAK degraders such as PROTAC FAK degrader 4. It serves as a valuable tool in cancer research, facilitating investigations into FAK signaling pathways and their implications in tumor progression. -
FAK Inhibitor
Defactinib-d6 is a deuterium-labeled derivative of Defactinib, a potent inhibitor of focal adhesion kinase (FAK). It exhibits antiangiogenic and antineoplastic properties, making it valuable for cancer research. This reagent is suitable for studies investigating FAK-related signaling pathways and their role in tumor growth and metastasis. -
FAK Activator
FAK activator-1 is a selective activator of Focal Adhesion Kinase (FAK) that enhances phosphorylation at Tyr-397, thereby promoting FAK activation. This reagent is particularly effective in advancing mucosal healing processes. FAK activator-1 is applicable in research focused on NSAID-associated gastrointestinal mucosal injury, providing valuable insights into cellular mechanisms involved in tissue repair and integrity. -
FAK Inhibitor
FAK-IN-9 is a potent inhibitor of focal adhesion kinase (FAK) with an IC50 of 27.44 nM. This compound has demonstrated the ability to induce apoptosis in triple-negative breast cancer (TNBC) cells, highlighting its potential as a therapeutic agent in cancer research. FAK-IN-9 can be utilized to explore the role of FAK in cell signaling and its implications in various cancer types. -
FAK Inhibitor
FAK-IN-6 is a potent inhibitor of focal adhesion kinase (FAK), exhibiting an IC50 value of 1.415 nM. This compound demonstrates significant anti-proliferative activity against various cancer cell lines, making it valuable for in vitro studies. FAK-IN-6 is particularly relevant for research focused on pancreatic cancer, providing a tool for elucidating the role of FAK in tumor progression and potential therapeutic strategies. -
FAK Inhibitor
FAK Inhibitor 6 specifically targets focal adhesion kinase (FAK) and is recognized for its potent inhibitory effects, with an IC50 of 28.2 nM. This compound demonstrates reduced cytotoxicity (IC50 = 3.32 µM) while effectively inducing apoptosis in MDA-MB-231 breast cancer cells in a dose-dependent manner. Additionally, FAK Inhibitor 6 effectively halts the cell cycle progression of MDA-MB-231 cells at the G0/G1 phase, making it a valuable tool for research in cancer biology and therapeutic development. -
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. -
FAK Inhibitor
FAK Inhibitor 5 is a novel allosteric inhibitor of focal adhesion kinase (FAK) that exhibits efficient modulation of FAK activity with IC50 values in the low micromolar range. This compound is utilized in research focusing on cancer biology, cell adhesion, and migration, making it a valuable tool for studying pathways involving FAK signaling. Its specificity allows for detailed investigations into the role of FAK in various cellular processes and disease states. -
PTK2/FAK PROTAC Degrader
BI-0319 is a selective PROTAC degrader targeting PTK2/FAK, effectively promoting the degradation of these proteins. This compound has demonstrated the ability to reduce cancer cell viability, inhibit cellular proliferation, and curtail invasion, making it a valuable tool for cancer research, particularly in studies related to liver cancer. BI-0319 provides insights into therapeutic strategies focused on protein degradation in oncology. -
FAK Inhibitor
FAK-IN-16 is a selective inhibitor of focal adhesion kinase (FAK) that exhibits an exceptionally low IC50 of 1.2 pM. This compound effectively inhibits FAK phosphorylation at both pFAK[Y397] and pFAK[Y861], resulting in decreased tumor growth and reduced vascularity and invasiveness. Additionally, FAK-IN-16 enhances the effects of Cisplatin on tumor cell proliferation and apoptosis in vitro, as well as its anti-tumor properties in murine models. This reagent is valuable for researchers focusing on cancer therapy and tumor biology. -
FAK Inhibitor
FAK-IN-8 is a potent inhibitor of Focal Adhesion Kinase (FAK) with an IC50 value of 5.32 µM. It exhibits significant anti-proliferative activity, making it a valuable tool for cancer research. This compound can be utilized to explore the role of FAK in tumor progression and metastasis, as well as in the development of targeted therapies. -
FAK/Aurora Kinase Inhibitor
FAK/Aurora kinase-IN-1 is a dual inhibitor targeting focal adhesion kinase (FAK) and Aurora kinase, exhibiting IC50 values of 6.61 nM and 0.91 nM, respectively. This compound demonstrates significant anticancer activity, making it a valuable tool for research applications focused on cancer biology and therapeutic development. Its efficacy in inhibiting both kinases positions it as a promising candidate for further studies in tumor proliferation and treatment strategies. -
FAK Inhibitor
FAK-IN-10 is a potent inhibitor of focal adhesion kinase (FAK) with an IC50 of 76.3 µM. This compound demonstrates significant antitumor activity, particularly against the MCF-7 and A431 cell lines, exhibiting IC50 values of 4.23 µM and 0.78 µM, respectively. FAK-IN-10 is valuable for research focused on cancer therapeutics and the modulation of signaling pathways associated with tumor growth and metastasis. -
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. -
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. -
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. -
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. -
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. -
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. -
BTK Inhibitor
Pirtobrutinib is a highly selective, non-covalent inhibitor of Bruton's tyrosine kinase (BTK). It effectively targets diverse BTK C481 substitution mutations, demonstrating strong antitumor activity in BTK-dependent lymphoma models in vivo. Pirtobrutinib exhibits over 300-fold selectivity for BTK compared to a panel of 370 other kinases and shows minimal inhibition of non-kinase off-targets at 1 μM. This specificity makes it a valuable tool for studying BTK-related signaling pathways and therapeutic applications in hematological malignancies. -
BTK Inhibitor
2-(Bromomethyl)acrylic acid functions as a selective inhibitor of Bruton's tyrosine kinase (BTK). It covalently modifies the cysteine 481 residue of BTK through a nucleophilic addition-elimination mechanism, leading to the inhibition of the B-cell receptor signaling pathway. This compound promotes immunogenic cell death in BTK-expressing B-cell lymphoma cells by triggering the release of damage-associated molecular patterns like extracellular ATP and HMGB1. It exhibits significant cytotoxicity against BTK-expressing cells while demonstrating minimal toxicity to BTK-negative counterparts, making it valuable for research into B-cell lymphoma. -
BTK Inhibitor
Acalabrutinib maleate is an oral, irreversible, and highly selective BTK inhibitor targeting cysteine residue Cys481 in the ATP-binding pocket of BTK. This compound exhibits potent activity against chronic lymphocytic leukemia (CLL) in mouse models, making it a valuable tool for CLL research. Additionally, Acalabrutinib maleate features an alkyne group, enabling it to participate in copper-catalyzed azide-alkyne cycloaddition (CuAAc), facilitating its use in click chemistry applications. -
BTK Inhibitor
Tolebrutinib, a selective inhibitor of Bruton tyrosine kinase (BTK), demonstrates potent activity with IC50 values of 0.4 nM in Ramos B cells and 0.7 nM in HMC microglia cells. Its ability to penetrate the blood-brain barrier underscores its relevance in studying central nervous system immunity. Tolebrutinib is a valuable tool for research into multiple sclerosis (MS) and other neurological conditions influenced by BTK activity. -
BTK Degrader
Catadegbrutinib is a selective chimeric degradation activator compound targeting Bruton's tyrosine kinase (BTK), with an IC50 of 0.69 nM. By facilitating the recruitment of BTK to E3 ubiquitin ligase, Catadegbrutinib promotes polyubiquitination and subsequent proteasomal degradation of BTK, effectively reducing its activity. This compound is valuable for investigating B-cell malignancies, including chronic lymphocytic leukemia, small lymphocytic lymphoma, and mantle cell lymphoma. -
Btk Inhibitor
BIIB091 is a selective and potent reversible Bruton’s tyrosine kinase (BTK) inhibitor, demonstrating an IC50 of less than 0.5 nM. By binding to the BTK protein and inducing an inactive conformation via sequestering of TYR-551, BIIB091 effectively obstructs BTK signaling pathways. This compound is valuable for research applications in multiple sclerosis and other immune-mediated disorders. -
PROTAC BTK Degrader
PROTAC BTK Degrader-1 is an innovative PROTAC-based compound designed for the selective degradation of Bruton's tyrosine kinase (BTK), exhibiting IC50 values of 34.51 nM for wild-type BTK and 64.56 nM for the BTK-481S mutant. This compound effectively lowers BTK protein levels, thereby inhibiting tumor growth. Additionally, PROTAC BTK Degrader-1 features an alkyne group facilitating its application in copper-catalyzed azide-alkyne cycloaddition (CuAAc) for advanced chemical research and targeted therapies. -
BTK Inhibitor
Elsubrutinib is a potent and selective irreversible inhibitor of Bruton's tyrosine kinase (BTK). With an IC50 value of 0.18 μM for the BTK catalytic domain, it demonstrates strong inhibitory activity. Elsubrutinib is utilized in research related to inflammatory diseases, providing valuable insights into BTK's role in various cellular processes. -
HCK/BTK Inhibitor
KIN-8194 is an orally active dual inhibitor targeting HCK and BTK, exhibiting IC50 values of 0.915 nM and <0.495 nM, respectively. It effectively disrupts growth and integrin-mediated adhesion in BTK inhibitor-resistant mantle cell lymphoma (MCL). KIN-8194 demonstrates the ability to overcome ibrutinib resistance, providing a survival advantage in TMD-8 ABC DLBCL xenograft models, making it a valuable tool for research in hematologic malignancies and therapeutic resistance mechanisms. -
BTK Inhibitor
PF-06658607 is an alkynylated irreversible inhibitor of Bruton's tyrosine kinase (BTK), designed to covalently bind to active site cysteines in the ATP-binding pocket. This compound effectively serves as a research tool for identifying off-target effects of covalent kinase inhibitors in cancer cell models. Its unique alkyne functionality facilitates the use of azide-based detection probes through copper-catalyzed click chemistry, enhancing the study of BTK-related signaling pathways. -
BTK/MNK Dual Inhibitor
QL-X-138 is a selective dual inhibitor of Bruton's tyrosine kinase (BTK) and MAPK-interacting kinase (MNK), demonstrating potent covalent binding to BTK and non-covalent binding to MNK. It exhibits IC50 values of 9.4 nM for BTK, and 107.4 nM and 26 nM for MNK1 and MNK2, respectively. Additionally, QL-X-138 displays antiviral activity against dengue virus serotype 2, with an IC50 of 3.5 μM. This compound is valuable for research involving B-cell malignancies and related therapeutic investigations. -
PROTAC
L18I is a PROTAC designed to target Bruton’s tyrosine kinase (Btk), facilitating the degradation of this protein and thereby mitigating inflammation associated with autoimmune diseases, such as lupus erythematosus induced by BM12 splenocytes. This compound comprises the IBT6A ligand, a linker moiety (Propargyl-PEG3-alcohol), and an E3 ubiquitin ligase ligand (Lenalidomide-Br), effectively promoting the destruction of Btk. L18I serves as a valuable tool for investigating Btk's role in autoimmunity and offers potential pathways for therapeutic intervention. -
BTK Degrader
BTK degrader-1 is a bifunctional degrader targeting Bruton’s tyrosine kinase (BTK) through its conjugation with CD79b. This compound facilitates the targeted degradation of BTK, leading to significant anti-tumor effects. It serves as a valuable tool for research applications focused on therapeutic strategies for hematological malignancies. -
BLK Inhibitor
BLK-IN-2 is a potent and selective irreversible inhibitor of B-Lymphoid tyrosine kinase (BLK), exhibiting an IC50 of 5.9 nM. In addition, it inhibits Bruton’s tyrosine kinase (BTK) with an IC50 of 202 nM. This compound demonstrates strong antiproliferative activity against various lymphoma cell lines, making it a valuable tool for research in B-cell malignancies and related signaling pathways. -
Covalent Probe/Btk Inhibitor
CNX-500 is a covalent probe that targets Bruton's tyrosine kinase (Btk) through a potent inhibitor (CC-292) chemically linked to biotin. With an IC50 of 0.5 nM, CNX-500 exhibits strong inhibitory activity against Btk while forming a stable covalent bond. The compound demonstrates low off-target effects on epidermal growth factor receptor and upstream Src-family kinases such as Syk and Lyn, making it suitable for research applications focused on Btk-related pathways in cellular signaling and disease models. -
BTK Inhibitor
N-piperidine Ibrutinib hydrochloride is a reversible derivative of Ibrutinib, functionally acting as a potent Bruton Tyrosine Kinase (BTK) inhibitor. It demonstrates IC50 values of 51.0 nM for wild-type BTK and 30.7 nM for the C481S mutant. This compound serves as a valuable BTK ligand in the synthesis of PROTACs, including SJF620, which has shown a DC50 of 7.9 nM, highlighting its potential utility in targeted protein degradation research applications. -
BTK Inhibitor
BIIB129 is a covalent and selectively targeting inhibitor of Bruton's tyrosine kinase (BTK), designed to penetrate the blood-brain barrier effectively. By covalently binding to Cys481 in BTK, BIIB129 disrupts the signaling pathways in B cells and myeloid cells. This compound is particularly relevant for research applications in multiple sclerosis (MS), providing insights into the modulation of immune responses associated with the disease. -
BTK Inhibitor
ACP-5862 is a potent Bruton tyrosine kinase (BTK) inhibitor, exhibiting an IC50 of 5.0 nM. As a major circulating metabolite of Acalabrutinib, it maintains high selectivity for BTK, which is critical for the modulation of B-cell signaling pathways. ACP-5862 is also a weak time-dependent inactivator of CYP3A4 and CYP2C8. This compound is widely utilized in research focused on hematological malignancies and B-cell related disorders, facilitating insights into targeted therapies. -
PROTAC BTK Degrader
DD-03-171 is a selective PROTAC BTK degrader that targets Bruton's tyrosine kinase (BTK) for degradation. This compound demonstrates significant anti-proliferative effects on mantle cell lymphoma (MCL) cells with an IC50 of 5.1 nM and enhances survival in murine models bearing patient-derived xenograft (PDX) lymphoma. Additionally, DD-03-171 inhibits platelet function and thrombosis, making it a valuable tool for research in cancer and hematological disorders. -
Stable Isotope
Acalabrutinib-d4 is a deuterated derivative of Acalabrutinib, an orally active and irreversible second-generation Bruton Tyrosine Kinase (BTK) inhibitor. This stable isotope labeled compound serves as a valuable tool for studying BTK inhibition in biological systems. Additionally, Acalabrutinib-d4 features an alkyne group, facilitating its use as a click chemistry reagent through copper-catalyzed azide-alkyne cycloaddition (CuAAc). Its applications extend to exploring therapeutic potential and pharmacokinetic properties in research settings. -
BTK Degrader
(R)-Zelebrudomide is a Bruton’s Tyrosine Kinase (BTK) degrader synthesized as an isomer of the PROTAC compound Zelebrudomide. It selectively induces the degradation of BTK, a crucial target in the treatment of various hematological malignancies. This compound is utilized in research to investigate its potential therapeutic applications in autoimmune diseases and cancers where BTK is implicated. -
Ibrutinib Derivative
Ibrutinib-MPEA is an Ibrutinib derivative targeting Bruton's tyrosine kinase (BTK), a key regulator in B cell receptor signaling. As a covalent and irreversible inhibitor, Ibrutinib-MPEA demonstrates significant biological activity against various hematological malignancies. This compound is primarily utilized in research applications focusing on cancer biology and the study of BTK-related signaling pathways.
