1. Signaling Pathways
  2. Cell Cycle/DNA Damage
    Epigenetics
  3. Aurora Kinase

Aurora Kinase

The Aurora kinases comprise a family of evolutionary conserved serine/threonine kinases (Aurora-A, Aurora-B, and Aurora-C). Aurora kinases control multiple events during cell cycle progression and are essential for mitotic and meiotic bipolar spindle assembly and function.

Aurora-A, Aurora-B, and Aurora-C share a highly conserved kinase domain but have quite different subcellular localizations and functions during mitosis. Aurora-A mostly controls centrosome maturation and bipolar spindle assembly, while Aurora-B and Aurora-C are required for condensation, attachment to kinetochores, and alignment of chromosomes during (pro-)metaphase and cytokinesis. In human tumors, all Aurora kinase members play oncogenic roles related to their mitotic activity and promote cancer cell survival and proliferation. Inhibitors targeting Aurora kinases have attracted attention in cancer research.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-13072
    Cenisertib
    Inhibitor 99.64%
    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-124526
    Chiauranib
    Inhibitor 99.28%
    Chiauranib (CS2164) is an orally active multi-target inhibitor against tumor angiogenesis. Chiauranib potently inhibits the angiogenesis-related kinases (VEGFR1/Flt-1, VEGFR2/KDR/Flk-1, VEGFR3/Flt-4, PDGFRα and c-Kit), mitosis-related kinase Aurora B, and chronic inflammation-related kinase CSF-1R, with IC50 values ranging from 1-9 nM. Chiauranib has strongly anticancer effects.
    Chiauranib
  • HY-137377
    TAS-119
    Inhibitor 98.03%
    TAS-119 is a potent, selective and orally active Aurora A inhibitor with an IC50 of 1.0 nM. TAS-119 shows high selectivity for Aurora A over other protein kinases, including Aurora B (IC50 of 95 nM). TAS-119 has potent antitumor activites.
    TAS-119
  • HY-107419
    NU6140
    Inhibitor 99.07%
    NU6140 is a selective CDK2-cyclin A inhibitor (IC50, 0.41 μM), exhibits 10- to 36-fold selectivity over other CDKs. NU6140 also potently inhibits Aurora A and Aurora B, with IC50s of 67 and 35 nM, respectively. Enhances the apoptotic effect, with anti-cancer activity.
    NU6140
  • HY-112273A
    CD532 hydrochloride
    Inhibitor 99.31%
    CD532 hydrochloride is a potent Aurora A kinase inhibitor with an IC50 of 45 nM. CD532 hydrochloride has the dual effect of blocking Aurora A kinase activity and driving degradation of MYCN. CD532 hydrochloride also can directly interact with AURKA and induces a global conformational shift. CD532 hydrochloride can be used for the research of cancer.
    CD532 hydrochloride
  • HY-B0712
    Ceftriaxone
    Inhibitor 98.19%
    Ceftriaxone (Ro 13-9904 free acid) is a broad spectrum β-lactam third-generation cephalosporin antibiotic, which has good antibacterial activity against a variety of gram-negative and positive bacteria. Ceftriaxone is a covalent inhibitor of GSK3β with IC50 value of 0.78 mM. Ceftriaxone is an inhibitor of Aurora B. Ceftriaxone has anti-inflammatory, antitumor and antioxidant activities. Ceftriaxone can be used in the study of bacterial infections and meningitis.
    Ceftriaxone
  • HY-148063
    DB0614
    98.80%
    DB0614 (Example 21) is a bifunctional compound targeted protein degradation of kinases. DB0614 degrades AAK1, AURKA, BMP2K, CAMKK1, CDK16, CML, CDK6, EIF2AK2, FER, GAK, LCK, LIMK2, MAP3KH, MAPK8, MAPK9, NEK9, PLK4, PTK2B, SIK2, STK17A, STK17B, ULK1, ULK3, and WEE1. DB0614 can be used for research of disease or disorder mediated by aberrant kinase activity.
    DB0614
  • HY-10987
    ENMD-2076 Tartrate
    Inhibitor 99.42%
    ENMD-2076 Tartrate is a multi-targeted kinase inhibitor with IC50s of 1.86, 14, 58.2, 15.9, 92.7, 70.8, 56.4 nM for Aurora A, Flt3, VEGFR2/KDR/Flk-1/VEGFR2/KDR/Flk-1, Flt4/VEGFR3/Flt-4, FGFR1, FGFR2, Src, PDGFRα, respectively.
    ENMD-2076 Tartrate
  • HY-18161
    CCT241736
    Inhibitor 98.09%
    CCT241736 is a potent and orally bioavailable dual FLT3 and Aurora kinase inhibitor, which inhibits Aurora kinases (Aurora-A Kd, 7.5 nM, IC50, 38 nM; Aurora-B Kd, 48 nM), FLT3 kinase (Kd, 6.2 nM), and FLT3 mutants including FLT3-ITD (Kd, 38 nM) and FLT3(D835Y) (Kd, 14 nM).
    CCT241736
  • HY-137344A
    dAURK-4 hydrochloride
    Inhibitor 99.44%
    dAURK-4 hydrochloride, an Alisertib derivative, is a potent and selective AURKA (Aurora A) degrader. dAURK-4 hydrochloride has anticancer effects.
    dAURK-4 hydrochloride
  • HY-N0110B
    Palmatine hydroxide
    Inhibitor 99.64%
    Palmatine hydroxide is an orally active and irreversible indoleamine 2,3-dioxygenase 1 (IDO-1) inhibitor with IC50s of 3 μM and 157μM against HEK 293-hIDO-1 and rhIDO-1, respectively. Palmatine hydroxide can also inhibit West Nile virus (WNV) NS2B-NS3 protease in an uncompetitive manner with an IC50 of 96 μM. Palmatine hydroxide shows anti-cancer, anti-oxidation, anti-inflammatory, neuroprotection, antibacterial, anti-viral activities.
    Palmatine hydroxide
  • HY-112809
    GSK2646264
    Inhibitor 98.39%
    GSK2646264 (Compound 44) is a potent and selective spleen tyrosine kinase (SYK) inhibitor with a pIC50 of 7.1. GSK2646264 also inhibits other kinases with pIC50 values of 5.4, 5.4, 5.3, 5, 4.5, <4.6 and <4.3 against LCK, LRRK2, GSK3β, JAK2, VEGFR2/KDR/Flk-1, Aurora B and Aurora A, respectively. GSK2646264 is penetrable into the epidermis and dermis of the skin.
    GSK2646264
  • HY-145601
    Tinengotinib
    Modulator 98.45%
    Tinengotinib is the modulator of one or more protein kinases such as Aurora kinase and VEGFR kinase. Tinengotinib has the potential for the research of these kinase abnormalities diseases mediated, especially cancer-related diseases (extracted from patent WO2018108079A1).
    Tinengotinib
  • HY-112373
    Aurora kinase inhibitor-3
    Inhibitor 99.34%
    Aurora kinase inhibitor-3 is a strong and selective Aurora A kinase inhibitor with an IC50 of 42 nM, and weakly inhibits EGFR with an IC50 of >10 μM. Aurora kinase inhibitor-3 has a binding mode with the cyclopropanecarboxylic acid moiety directed towards the solvent exposed region of the ATP-binding pocket.
    Aurora kinase inhibitor-3
  • HY-123159
    AKI603
    Inhibitor 98.03%
    AKI603 is an inhibitor of Aurora kinase A (AurA), with an IC50 of 12.3 nM. AKI603 is developed to overcome resistance mediated by BCR-ABL-T315I mutation. AKI603 exhibits strong anti-proliferative activity in leukemic cells.
    AKI603
  • HY-112273
    CD532
    Inhibitor 98.78%
    CD532 is a potent Aurora A kinase inhibitor with an IC50 of 45 nM. CD532 has the dual effect of blocking Aurora A kinase activity and driving degradation of MYCN. CD532 also can directly interact with AURKA and induces a global conformational shift. CD532 can be used for the research of cancer.
    CD532
  • HY-112355
    Aurora kinase inhibitor-2
    Inhibitor 99.19%
    Aurora kinase inhibitor-2 is a selective and ATP-competitive Aurora kinase inhibitor with IC50s of 310 nM and 240 nM for Aurora A and Aurora B, respectively.
    Aurora kinase inhibitor-2
  • HY-144991
    Aurora kinase inhibitor-8
    Inhibitor 98.10%
    Aurora kinase inhibitor-8 is a highly selective inhibitor of the Aurora kinases.
    Aurora kinase inhibitor-8
  • HY-103266
    TC-A 2317 hydrochloride
    Inhibitor
    TC-A 2317 hydrochloride is an orally active Aurora A kinase inhibitor (Ki=1.2 nM). TC-A 2317 hydrochloride exhibits excellent selectivity to Aurora B kinase (Ki=101 nM) and other 60 kinases, good cell permeability and good PK profile. Antitumor activity.
    TC-A 2317 hydrochloride
  • HY-151971
    Aurora Kinases-IN-3
    Inhibitor 98.47%
    Aurora Kinases-IN-3 (Compound 15a) is an orally active AURKB inhibitor that elicits an AURKB-suppressive activity by disrupting the mitotic localization of AURKB, rather than inhibiting its phosphorylation of H3 at Ser10.
    Aurora Kinases-IN-3
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