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Breast tumor kinase

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-50895
    Gefitinib
    Maximum Cited Publications
    172 Publications Verification

    ZD1839

    EGFR Autophagy Apoptosis Cancer
    Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .
    Gefitinib
  • HY-13072
    Cenisertib
    1 Publications Verification

    AS-703569; R-763

    Aurora Kinase Bcr-Abl Akt STAT FLT3 Cancer
    Cenisertib (AS-703569) is an ATP-competitive multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3. Cenisertib induces major growth-inhibitory effects by blocking the activity of several different molecular targets in neoplastic mast cells (MC). Cenisertib inhibits tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia .
    Cenisertib
  • HY-164129

    CDK Apoptosis Cancer
    CDK4-IN-3 (Compound 389) is a potent irreversible cyclin-dependent kinase 4 (CDK4) inhibitor (IC50=25 nM, >10-fold selective over CDK6). CDK4-IN-3 arrests the cell cycle at G₁ phase, and induces tumor cell apoptosis. CDK4-IN-3 is promising for research of solid tumors such as breast and lung cancers .
    CDK4-IN-3
  • HY-50895R

    ZD1839 (Standard)

    Reference Standards EGFR Autophagy Apoptosis Cancer
    Gefitinib (Standard) is the analytical standard of Gefitinib. This product is intended for research and analytical applications. Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .
    Gefitinib (Standard)
  • HY-115514A

    BRK Cancer
    BRK inhibitor P21d hydrochloride is a potent breast tumor kinase (BRK/PTK6) inhibitor with an IC50 of 30 nM. BRK inhibitor P21d hydrochloride inhibits p-SAM68 with an IC50 of 52 nM. BRK inhibitor P21d hydrochloride can be used to evaluate the in vivo activity of BRK inhibitors in xenograft breast tumor models .
    BRK inhibitor P21d hydrochloride
  • HY-50895B

    ZD 1839 dihydrochloride

    EGFR Autophagy Apoptosis Cancer
    Gefitinib (ZD 1839) dihydrochloride is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC50 of 33 nM. Gefitinib dihydrochloride selectively inhibits EGF-stimulated tumor cell growth (IC50 of 54 nM) and blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib dihydrochloride also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .
    Gefitinib dihydrochloride
  • HY-158618

    Aurora Kinase Apoptosis Cancer
    Aurora kinase inhibitor-14 (Compound 79) is an orally active and highly selective inhibitor of Aurora kinases with IC50 values of 0.5 nM and 1.2 nM for Aurora A and Aurora B, respectively. Aurora kinase inhibitor-14 binds to the ATP-binding site of Aurora kinases to block chromosome segregation during mitosis and induce apoptosis in tumor cells. Aurora kinase inhibitor-14 is promising for research of various solid tumors and hematological malignancies, such as non-small cell lung cancer, breast cancer, and acute myeloid leukemia .
    Aurora kinase inhibitor-14
  • HY-13072B

    AS-703569 benzoate; R-763 benzoate

    Aurora Kinase Bcr-Abl Akt STAT FLT3 Cancer
    Cenisertib (AS-703569) benzoate is an ATP-competitive multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3. Cenisertib benzoate induces major growth-inhibitory effects by blocking the activity of several different molecular targets in neoplastic mast cells (MC). Cenisertib benzoate inhibits tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia .
    Cenisertib benzoate
  • HY-122844B

    BI-853520 tosylate; IN-10018 tosylate

    FAK Cancer
    Ifebemtinib (tosylate) (BI-853520 (tosylate); IN-10018 (tosylate)) is a highly selective PTK2 kinase inhibitor. Ifebemtinib (tosylate) demonstrates anti-tumor activity. Ifebemtinib (tosylate) inhibits FAK autophosphorylation in prostate carcinoma cells. Ifebemtinib (tosylate) can inhibit spheroid formation and orthotopic tumor growth in vivo. Ifebemtinib (tosylate) can be studied in anticancer research such as solid tumors, breast cancer, and malignant pleural mesothelioma .
    Ifebemtinib tosylate
  • HY-13072R

    Aurora Kinase Bcr-Abl Akt STAT FLT3 Cancer
    Cenisertib (Standard) is the analytical standard of Cenisertib. This product is intended for research and analytical applications. Cenisertib (AS-703569) is an ATP-competitive multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3. Cenisertib induces major growth-inhibitory effects by blocking the activity of several different molecular targets in neoplastic mast cells (MC). Cenisertib inhibits tumor growth in xenograft models of pancreatic, breast, colon, ovarian, and lung tumors and leukemia .
    Cenisertib (Standard)
  • HY-157396

    Aurora Kinase Apoptosis Caspase Cancer
    JAB-2485 is an orally active and selective Aurora kinase A (AURKA) inhibitor with an IC50 value of 0.327 nM. JAB-2485 exhibits inhibitory activity against various tumor cell lines such as neuroblastoma, triple-negative breast cancer, small cell lung cancer, and epithelial ovarian cancer. JAB-2485 can induce cell cycle arrest and apoptosis in tumor cells. JAB-2485 has antitumor activity .
    JAB-2485
  • HY-12964
    SGI-7079
    3 Publications Verification

    TAM Receptor Cancer
    SGI-7079 is a selective, ATP-competitive, orally active inhibitor of the receptor tyrosine kinase Axl. SGI-7079 blocks Axl-mediated signaling pathways such as NF-κB activation and MMP-9 expression, thereby inhibiting tumor cell proliferation, migration and invasion. SGI-7079 is mainly used in the research of malignant tumors such as inflammatory breast cancer and bladder cancer, as well as in combination with immunization (used in combination with PD-1 therapy)[1][2][3].
    SGI-7079
  • HY-N15340

    PKC Cancer
    1-Oleoyl-2-linoleoyl-sn-glycerol is a diacylglycerol (DG). 1-Oleoyl-2-linoleoyl-sn-glycerol can activate protein kinase C (PKC), thus triggering downstream signaling cascades and promoting tumor growth. 1-Oleoyl-2-linoleoyl-sn-glycerol is promising for research of breast cancer .
    1-Oleoyl-2-linoleoyl-sn-glycerol
  • HY-145601

    TT 00420

    Aurora Kinase FGFR VEGFR Cancer
    Tinengotinib (TT00420) is an orally active, spectrally selective small molecule kinase inhibitor targeting Aurora A/B (IC50=1.2-3.3 nM), FGFR1/2/3 (IC50=1.5-3.5 nM), VEGFRs, JAK1/2 and CSF1R. Tinengotinib blocks Aurora kinase-mediated cell cycle progression (inducing G2/M arrest), inhibits FGFR/JNK-JUN signaling pathway and activates MEK/ERK-dependent apoptotic pathway. Tinengotinib has the activity of anti-tumor proliferation, inducing apoptosis, inhibiting angiogenesis and regulating tumor microenvironment. Tinengotinib can be used in the study of triple-negative breast cancer (TNBC), gallbladder cancer and tumor immune microenvironment .
    Tinengotinib
  • HY-172737

    Polo-like Kinase (PLK) Cancer
    RP-1664 is a selective and orally active PLK4 inhibitor with an IC50 of 3 nM. RP-1664 demonstrates exquisite selectivity over related kinases, including AURKA/B and PLK1. RP-1664 disrupts centriole biogenesis in cancer cells and leads an accumulation of PLK4 and p21 protein. RP-1664 demonstrates increased sensitivity in TRIM37-high-expressing cells or tumors. RP-1664 exhibits anti-tumor activity in breast cancer and neuroblastoma research [1][2].
    RP-1664
  • HY-15150
    Bemcentinib
    50+ Cited Publications

    R428; BGB324

    TAM Receptor Cancer
    Bemcentinib (R428) is a selective and orally active Axl inhibitor with an IC50 of 14 nM. Bemcentinib retards cancer cell migration and invasion. Bemcentinib exhibits >100-fold selectivity for Axl versus Abl and 50- and >100-fold selectivity over TAM family kinases Mer and Tyro3, respectively, in cells. Bemcentinib blocks tumor spread and prolongs survival in models of metastatic breast cancer .
    Bemcentinib
  • HY-W110138

    DNA/RNA Synthesis Cytochrome P450 ROCK Cancer
    Chloroxoquinoline is an anticancer agent. Chloroxoquinoline damages the DNA templates of cancer cells, inducing DNA breaks and cell death, and inhibits cell invasion via down-regulating Rho/Rho kinase signaling pathway. Chloroxoquinoline enhances the radiation sensitivity of Lewis lung cancer cells and xenograft tumors in tumor-bearing mouse models but decreases efficacy after long term exposure in rat models by auto-induction effects on CYP1A and CYP3A. Chloroxoquinoline has a broad-spectrum anticancer activity, such as non-small-cell lung carcinoma (NSCLC), breast cancer and gastric cancer .
    Chloroxoquinoline
  • HY-E70609

    PI3K Inflammation/Immunology Cancer
    PIK3CG Recombinant Human Active Lipid Kinase belongs to PI3K enzyme family that is directly regulated by Gβγ and Ras in the G protein coupled receptor (GPCR) pathway. PIK3CG has the function of regulating cellular inflammation and immunity. PIK3CG is also a potential target for the treatment of a few malignant tumors such as acute lymphoblastic leukemia, medulloblastoma, claudin-low breast cancer (CLBC) and Kaposi sarcoma .
    PIK3CG Recombinant Human Active Lipid Kinase
  • HY-108333
    SB-633825
    3 Publications Verification

    Tie BRK Cardiovascular Disease Cancer
    SB-633825 is a potent and ATP-competitive inhibitor of TIE2, LOK (STK10) and BRK with IC50s of 3.5 nM, 66 nM, 150 nM, respectively. SB-633825 can inhibit cancer cell growth and angiogenesis .
    SB-633825
  • HY-15150R

    TAM Receptor Reference Standards Cancer
    Bemcentinib (Standard) is the analytical standard of Bemcentinib. This product is intended for research and analytical applications. Bemcentinib (R428) is a selective and orally active Axl inhibitor with an IC50 of 14 nM. Bemcentinib retards cancer cell migration and invasion. Bemcentinib exhibits >100-fold selectivity for Axl versus Abl and 50- and >100-fold selectivity over TAM family kinases Mer and Tyro3, respectively, in cells. Bemcentinib blocks tumor spread and prolongs survival in models of metastatic breast cancer .
    Bemcentinib (Standard)
  • HY-P991664

    Src Akt ERK TAM Receptor c-Met/HGFR MMP HIF/HIF Prolyl-Hydroxylase VEGFR Cancer
    AG01 is a monoclonal antibody against progranulin (GP88). AG01 inhibits triple-negative breast cancer (TNBC) cell proliferation and migration, reduces the expression of phosphorylated protein kinases p-Src, p-AKT, and p-ERK, and reduces the expression of oncogenic proteins such as Axl, c-MET, HIF-1α, and VEGF. AG01 inhibits tumor growth and Ki67 expression in a TNBC xenograft mouse model. AG01 can be used in the research of TNBC and other cancers .
    AG01
  • HY-157231A

    PERK Cancer
    HC-5404-Fu is a PERK inhibitor with an antitumor activity. HC-5404-Fu inhibits endoplasmic reticulum stress response signalling. HC-5404-Fu sensitizes renal cell carcinoma cells to vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitors (TKIs). HC-5404-Fu is promising for research of renal cell carcinoma, gastric cancer, metastatic breast cancer, small cell lung cancer, and other solid tumors .
    HC-5404-Fu
  • HY-15150G

    R428 (GMP); BGB324 (GMP)

    TAM Receptor Cancer
    Bemcentinib (R428) GMP is Bemcentinib (HY-15150) in GMP grade. GMP-grade small molecules can be used as auxiliary reagents in cell therapy.Bemcentinib (R428) is a selective and orally active Axl inhibitor with an IC50 of 14 nM. Bemcentinib retards cancer cell migration and invasion. Bemcentinib exhibits >100-fold selectivity for Axl versus Abl and 50- and >100-fold selectivity over TAM family kinases Mer and Tyro3, respectively, in cells. Bemcentinib blocks tumor spread and prolongs survival in models of metastatic breast cancer .
    Bemcentinib (GMP)
  • HY-N7694

    TGF-β Receptor JAK STAT Apoptosis Inflammation/Immunology Cancer
    Isotoosendanin is an orally active TGFβR1 inhibitor and abrogating its kinase activity (IC50 = 6732 nM). Isotoosendanin inhibits the JAK/STAT3 signaling pathway by directly targeting SHP-2, enhancing its stability, and reducing its ubiquitination. Isotoosendanin inhibits TGF-β-induced reduces the migration, invasion, and metastasis in triple-negative breast cancer (TNBC) cells. Isotoosendanin exhibits anti-tumor efficacy in TNBC xenograft models and A549 xenograft tumors. Isotoosendanin exhibits significant anti-inflammatory effects in acetic acid-induced vascular permeability and λ-carrageenan-induced hind paw edema tests. Isotoosendanin can be used for the study of non-small cell lung cancer (NSCLC), TNBC and inflammation .
    Isotoosendanin
  • HY-176561

    Casein Kinase HDAC Cancer
    IOR-160 is a dual inhibitor of casein kinase 2 (CK2) and HDACs. IOR-160 exhibits high selectivity for CK2 (IC50 = 1.7 nM) and broad inhibitory activity against HDAC (HDAC 1, 2, 3, and 6 with IC50s of 3.3 nM, 24.0 nM, 3.9 nM, and 13.0 nM, respectively, with low activity for HDAC8). IOR-160 modulates key cellular signaling pathways by inhibiting AKT phosphorylation and increasing acetylated α-tubulin. IOR-160 inhibits tumor growth and reduces tumor burden through dual CK2/HDAC inhibition. IOR-160 is indicated for use in triple-negative breast cancer research .
    IOR-160
  • HY-164530

    Src VEGFR Raf p38 MAPK Cancer
    SKLB646 is an orally active multi-target kinase inhibitor. SKLB646 shows significant inhibitory effects on SRC and VEGFR2 with IC50 values ??of 0.002 μmol/L and 0.012 μmol/L, respectively. SKLB646 also shows significant inhibitory effects on B-Raf and C-Raf with IC50 values ??of 0.022 μmol/L and 0.019 μmol/L, respectively. SKLB646 inhibits the activation of the SRC signaling pathway and blocks the MAPK signaling pathway by inhibiting Raf kinase. In addition, SKLB646 can inhibit the proliferation, migration and invasion of human umbilical vein endothelial cells (HUVEC) to inhibit tumor-induced angiopoietic formation. SKLB646 shows significant anti-proliferative and anti-survival activities against triple-negative breast cancer (TNBC) cell lines .
    SKLB646
  • HY-167854

    Aurora Kinase Apoptosis IGF-1R Cancer
    KW-2450 Free base is a potent multikinase inhibitor targeting Aurora A and B kinases, demonstrating significant antitumor activity against triple-negative breast cancer (TNBC). KW-2450 Free base effectively reduces cell viability, promotes apoptosis, and inhibits colony formation and mammosphere formation in TNBC cells. KW-2450 Free base significantly suppresses the growth of TNBC xenografts, leading to tetraploid accumulation followed by apoptosis or the survival of octaploid cells. KW-2450 Free base enhances the efficacy of combination therapy with the MEK inhibitor selumetinib, resulting in a synergistic antitumor effect in TNBC models. KW-2450 Free base also acts as an orally bioavailable inhibitor of IGF-1R and IR tyrosine kinases, contributing to its potential antineoplastic activity by inhibiting tumor cell proliferation and inducing apoptosis.
    KW-2450 free base

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