Aurora Kinase

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  1. Aurora Kinase Inhibitor

    AKI-001 is a potent inhibitor of Aurora kinases, specifically targeting Aurora A and Aurora B with an IC50 of less than 100 nM. This pentacyclic compound demonstrates significant cellular efficacy, making it a valuable tool for investigating cell cycle regulation and mitotic progression. Its selective inhibitory action positions AKI-001 as an essential reagent for research in cancer biology and therapeutic development.
  2. Aurora A/PKC Inhibitor

    (Rac)-Aurora A/PKC-IN-1 is a potent inhibitor of Aurora A and protein kinase C (PKC) isoforms α, β1, β2, and θ. This compound demonstrates significant antiproliferative effects in breast cancer cell lines in vitro and exhibits antimetastatic properties in vivo. It serves as a valuable tool for researchers investigating the role of these kinases in cancer biology and therapeutic strategies.
  3. BET/Aurora kinase Inhibitor

    BET/Aurora kinase-IN-1 is a dual inhibitor targeting both BET and Aurora kinases. This compound demonstrates significant antiproliferative activity across various cancer cell lines and exhibits notable antitumor efficacy in xenograft models of renal cell cancer and colon cancer, achieving tumor growth inhibition rates of 45.99% and 53.06%, respectively. BET/Aurora kinase-IN-1 is a valuable tool for researchers investigating cancer biology and therapeutic strategies targeting these kinases.
  4. Aurora Kinase Inhibitor

    SNS-314 is a potent and selective inhibitor of aurora kinases, demonstrating IC50 values of 9 nM for Aurora A, 31 nM for Aurora B, and 6 nM for Aurora C. This compound effectively disrupts mitotic processes and is valuable in cancer research for studying cell cycle regulation and tumor growth inhibition. SNS-314 is particularly useful for investigations into therapies targeting aurora kinases in various malignancies.
  5. Aurora A Inhibitor

    MLN8054 sodium is a selective inhibitor of Aurora A kinase, which plays a critical role in cell cycle regulation. This compound enhances radiosensitivity and can activate DNA double-strand break responses in prostate cancer cells during in vitro assays. Its mechanism induces accumulation of cells in the G2/M phase and promotes polyploidy. In vivo studies demonstrate that MLN8054 sodium significantly delays tumor growth and enhances apoptosis in cancer cells when administered alongside radiotherapy, making it a valuable tool for cancer research and treatment strategies.
  6. Aurora B Inhibitor

    Aurora kinase inhibitor-10 is a potent inhibitor of Aurora B with an IC50 of 8 nM. This small molecule demonstrates significant antitumor activity, making it a valuable tool for cancer research. Its ability to selectively target Aurora B kinase supports investigations into mitotic regulation and offers potential therapeutic insights for tumor treatments.
  7. Aurora Kinase Inhibitor

    Aurora kinase inhibitor-11 is a potent inhibitor of Aurora Kinase, exhibiting an IC50 of 0.14 μM. This compound demonstrates significant anticancer activity, making it a valuable tool for research applications focused on cancer biology and therapeutic strategies targeting mitotic processes. Its efficacy in modulating kinase activity positions it as a relevant candidate for studies aimed at understanding tumorigenesis and developing novel cancer treatments.
  8. Aurora Kinase Inhibitor

    Tripolin A is a selective non-ATP competitive inhibitor of Aurora A kinase, exhibiting IC50 values of 1.5 μM for Aurora A and 7 μM for Aurora B. This compound plays a crucial role in modulating cell cycle progression by targeting Aurora kinases, making it valuable in cancer research. Tripolin A is used to investigate the mechanisms of mitotic regulation and potential therapeutic strategies in tumor cells.
  9. Aurora Kinase Inhibitor

    XMD-12 is a selective Aurora kinase inhibitor that demonstrates significant anti-tumor activity. It effectively enhances paclitaxel-induced cell death and exhibits high potency against Aurora A, B, and C kinases, with IC50 values of 5.6, 18.4, and 24.6 nM, respectively. This compound is valuable for research applications in cancer biology and therapy development.
  10. Aurora Kinases Inhibitor

    Aurora kinase-IN-2 is a potent inhibitor of Aurora kinases, demonstrating IC50 values of 90 nM for Aurora A and 152 nM for Aurora B. This compound effectively induces cell cycle arrest at the G2/M phase by modulating cyclin B1 and cdc2. It is primarily utilized in cancer research to explore the role of Aurora kinases in tumorigenesis and therapeutic response.
  11. Aurora A Inhibitor

    Aurora A Inhibitor 1 is a potent and selective inhibitor of the Aurora A kinase, which plays a crucial role in regulating cell division and has been implicated in various cancers. Overexpression of Aurora A is associated with oncogenic properties, making it an important target for cancer research. This compound is suitable for studies focusing on the therapeutic modulation of Aurora A in diverse cancer types.
  12. Aurora Kinase Inhibitor

    Aurora kinase inhibitor-9 is a potent dual inhibitor of Aurora A and Aurora B kinases, exhibiting IC50 values of 0.093 µM and 0.09 µM, respectively. This compound demonstrates significant anti-proliferative activity across various cancer cell lines, making it a valuable tool in cancer research. Its ability to target key regulators of cell division positions it as a candidate for studies investigating mitotic disruption and the development of novel cancer therapies.
  13. Aurora Inhibitor

    TAK-901 hydrochloride is a potent inhibitor of aurora kinases A and B, exhibiting IC50 values of 21 nM and 15 nM, respectively. This compound disrupts cell cycle progression, making it a valuable tool in cancer research and therapeutic development. Its ability to inhibit aurora kinases positions TAK-901 hydrochloride as an important reagent for studying mitotic regulation and exploring targeted cancer therapies.
  14. Aurora Kinase Inhibitor

    Tripolin B is an ATP-competitive inhibitor targeting Aurora kinases, exhibiting IC50 values of 2.5 µM and 6 µM for Aurora A and Aurora B kinases, respectively. This compound has demonstrated selectivity in its inhibition profile and is primarily utilized in cellular studies to explore the roles of Aurora kinases in cell cycle regulation and cancer progression. Tripolin B can be a valuable tool in research focused on cell division and oncogenic signaling pathways.
  15. Aurora Kinase Inhibitor

    BI 831266 is a potent and selective inhibitor of Aurora kinase B, a critical regulator of mitosis. This compound exhibits significant antitumor activity, making it valuable for cancer research. Its inhibition of Aurora B can lead to disruptions in cell division, providing insights into potential therapeutic applications for various malignancies.
  16. Aurora A/B Kinases Inhibitor

    TY-011 is a selective inhibitor of Aurora A and B kinases, disrupting normal microtubule-kinetochore attachment. This interference results in DNA damage and apoptosis, effectively inhibiting the proliferation of human gastric cancer cells, with observed IC50 values between 0.11 and 4.49 μM across various gastric cancer cell lines. TY-011 serves as a valuable tool in the study of gastric cancer and the mechanisms underlying mitotic regulation.
  17. Aurora Kinase Inhibitor

    OM137 is a potent Aurora Kinase inhibitor, demonstrating IC50 values of 21.7 μM for Aurora A kinase and 2.4 μM for Aurora B kinase. Additionally, OM137 affects cell cycle regulation by inhibiting Cdk1/cyclinB and Cdk5/p25, also with an approximate IC50 of 20 μM. This compound is notable for its ability to reduce spindle checkpoint-signaling proteins, such as Mad2 and BubR1, at the kinetochores of chromosomes, making it a valuable tool in cancer research and studies on mitotic regulation.
  18. Aurora Kinase Inhibitor

    AT9283 hydrochloride is a multi-targeted kinase inhibitor that primarily targets Aurora A and Aurora B kinases, which play critical roles in cell proliferation and survival. Its inhibitory effects extend to additional kinases such as JAK2 and Abl (T315I), enhancing its potential utility in cancer research. AT9283 hydrochloride has demonstrated significant anti-tumor activity, making it a valuable tool for investigating therapeutic strategies in various malignancies.
  19. Aurora Kinase Inhibitor

    VE-465 is a potent Aurora kinase inhibitor that promotes apoptosis in cancer cells. Its anticancer activities have been demonstrated across various tumor models, making it a valuable tool for cancer research. This compound's ability to selectively target Aurora kinases positions it as a significant candidate for investigations into tumor progression and treatment strategies.
  20. Aurora Kinase Inhibitor

    Binucleine 2 is an ATP-competitive inhibitor targeting Drosophila Aurora B kinase, displaying an inhibition constant (Ki) of 0.36 μM. This compound exhibits isoform specificity, effectively inhibiting Drosophila Aurora B in a dose-dependent manner while exhibiting minimal activity against human and Xenopus laevis Aurora B kinases at concentrations up to 100 μM. Binucleine 2 is valuable for studying mitotic processes, as it induces defects in mitosis and cytokinesis in Drosophila Kc167 cells and disrupts contractile ring assembly in Drosophila S2 cells at a concentration of 40 μM, highlighting the critical role of Aurora B kinase in cell division.
  21. Aurora A Inhibitor

    Aurora A inhibitor 4 (compound C9) is a selective inhibitor of Aurora A kinase, demonstrating a GI50 of 4.26 μM in DU 145 cells and 7.08 μM in HT-29 cells. This compound exhibits significant anti-proliferative effects, making it valuable for research focused on cell cycle regulation and cancer therapeutics. Its ability to inhibit Aurora A activity can be applied in studies investigating mitotic dysregulation in various tumor types.
  22. Aurora Kinase Inhibitor

    Aurora B inhibitor 1 is a selective inhibitor of the Aurora B kinase, exhibiting a Ki value of <0.010 µM. This compound plays a crucial role in manipulating cell division and is instrumental in research surrounding cancer biology and therapeutic development. Its ability to inhibit Aurora B activity makes it a valuable tool for studies focused on mitotic regulation and chromosomal instability.
  23. Aurora Kinase A/JAK2 Inhibitor

    AJI-100 is a dual-target inhibitor that selectively inhibits Aurora kinase A and JAK2 with IC50 values of 12.7 nM and 18.5 nM, respectively. By directly blocking Aurora kinase A, AJI-100 disrupts T cell mitosis and cell polarity, while its inhibitory effect on JAK2 activation prevents STAT3 phosphorylation. This compound is valuable for research focused on modulating immune responses and has potential applications in the prevention of graft-versus-host disease (GVHD).
  24. Aurora A Inhibitor

    Aurora A Inhibitor I is a potent and selective inhibitor of Aurora A kinase (AurA), with IC50 values to be 3.4 nM (Aurora A) and unusually high selectivity 1000 fold against Aurora B; a useful tool compound for investigating the cellular role of Aurora A kinases.

  25. Aurora Inhibitor

    CCT129202 is a representative of a structurally novel series of imidazopyridine small-molecule inhibitors of Aurora kinase activity. It shows high selectivity for the Aurora kinases over a panel of other kinases tested and inhibits proliferation in multiple cultured human tumor cell lines.

  26. Aurora Kinase inhibitor

    Aurora kinase/VEGFR 2 inhibitor CYC116 inhibits Aurora kinases A and B and vascular endothelial growth factor receptor 2 (VEGFR2), resulting in disruption of the cell cycle, rapid cell death, and the inhibition of angiogenesis.
  27. Aurora A / FLT3 Inhibitor

    ENMD-2076 has selective activity against Aurora A and Flt3 with IC50 of 14 nM and 1.86 nM, 25-fold selective for Aurora A than over Aurora B and less potent to VEGFR2/KDR and VEGFR3, FGFR1 and FGFR2 and PDGFRα. Phase 2.
  28. FLT3/FGFR/Bcr-Abl/Aurora Inhibitor

    KW-2449 is a multikinase inhibitor of FLT3, ABL, ABL-T315I, and Aurora kinase.
  29. Aurora A Inhibitor

    MLN8054 is an inhibitor of Aurora A kinase, induces senescence in human tumor cells both in vitro and in vivo.
  30. Aurora inhibitor

    PHA-680632 is potent inhibitor of Aurora A, Aurora B and Aurora C with IC50 of 27 nM, 135 nM and 120 nM, respectively. It has 10- to 200-fold higher IC50 for FGFR1, FLT3, LCK, PLK1, STLK2, and VEGFR2/3.
  31. Aurora inhibitor

    SNS-314 Mesylate is a potent and selective inhibitor of Aurora A, Aurora B and Aurora C with IC50 of 9 nM, 31 nM, and 3 nM, respectively. It is less potent to Trk A/B, Flt4, Fms, Axl, c-Raf and DDR2. Phase 1.
  32. Aurora Kinase inhibitor

    ZM 447439 is a selective and ATP-competitive inhibitor for Aurora A and Aurora B with IC50 of 110 nM and 130 nM, respectively. It is more than 8-fold selective for Aurora A/B than MEK1, Src, Lck and has little effect against CDK1/2/4, Plk1, Chk1, etc.
  33. Aurora Kinase A/B inhibitor

    TAK-901 is a novel inhibitor of Aurora A/B with IC50 of 21 nM/15 nM. It is not a potent inhibitor of cellular JAK2, c-Src or Abl. Phase 1.
  34. Aurora Kinase inhibitor

    CCT137690 is a highly selective inhibitor of Aurora A, Aurora B and Aurora C with IC50 of 15 nM, 25 nM and 19 nM. It has little effect on hERG ion-channel.
  35. ATP-competitive multitargeted kinase inhibitor

    Ilorasertib (ABT-348) is a potent and ATP-competitive multitargeted kinase inhibitor, which inhibits Aurora C, Aurora B, and Aurora A with IC50s of 1 nM, 7 nM, 120 nM, respectively.
  36. dual FLT3/Aurora kinase inhibitor

    CCT241736 is a potent and orally bioavailable dual FLT3 and Aurora kinase inhibitor.
  37. multi-targeted kinase inhibitor

    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, KDR/VEGFR2, Flt4/VEGFR3, FGFR1, FGFR2, Src, PDGFRα, respectively.
  38. Aurora inhibitor

    SCH-1473759 hydrochloride is an aurora inhibitor with IC50s of 4 and 13 nM for aurora A and B, respectively.
  39. Aurora A/B inhibitor

    Tinengotinib (TT00420) is an orally bioavailable, 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. It disrupts Aurora kinase-mediated cell cycle progression, inducing G2/M arrest, inhibits the FGFR/JNK-JUN signaling pathway, and activates the MEK/ERK-dependent apoptotic pathway. Tinengotinib exhibits potent anti-tumor proliferation, pro-apoptotic, anti-angiogenic, and tumor microenvironment-modulating activities. It is a promising candidate for research in triple-negative breast cancer (TNBC), gallbladder cancer, and tumor immune microenvironment studies.
  40. Aurora B inhibitor

    SP-96 is a highly potent, selective, and non-ATP-competitive inhibitor of Aurora B kinase, with an IC₅₀ of 0.316 nM. It exhibits exceptional selectivity, showing over 2000-fold greater specificity for Aurora B compared to off-target kinases such as FLT3 and KIT. In NCI-60 cancer cell line screening, SP-96 demonstrates selective antiproliferative activity, notably against the triple-negative breast cancer (TNBC) cell line MDA-MB-468 (GI₅₀ = 107 nM). SP-96 is a valuable tool for investigating Aurora B–driven oncogenic pathways and holds promise for the development of targeted therapies in TNBC and other malignancies.
  41. Aurora A inhibitor

    CD532 is a potent Aurora A kinase (AURKA) inhibitor with an IC₅₀ of 45 nM. It exerts a dual mechanism of action by both inhibiting AURKA enzymatic activity and promoting the degradation of the MYCN oncoprotein. CD532 directly binds to AURKA and induces a global conformational shift, disrupting its functional interactions. This unique mode of action makes CD532 a valuable tool for cancer research, particularly in MYCN-amplified tumors such as neuroblastoma.
  42. Multi-target Inhibitor

    Chiauranib (CS2164) is an orally active, multi-targeted small molecule inhibitor with potent anticancer activity. It targets key kinases involved in tumor angiogenesis, including VEGFR1, VEGFR2, VEGFR3, PDGFRα, and c-Kit, as well as mitosis-related kinase Aurora B and inflammation-associated kinase CSF-1R. Chiauranib exhibits IC₅₀ values ranging from 1 to 9 nM against these targets. Through simultaneous inhibition of angiogenesis, cell division, and inflammation pathways, Chiauranib exerts strong antitumor effects and is a promising candidate for the treatment of various solid tumors.
  43. Aurora A inhibitor

    JAB-2485 is a highly potent and selective inhibitor of Aurora kinase A (AURKA), with an IC₅₀ of 0.33 nM. It exhibits exceptional selectivity, showing approximately 1700-fold preference for AURKA over Aurora kinase B (AURKB). JAB-2485 induces cell cycle arrest and apoptosis, making it a promising candidate for cancer research, particularly in tumors driven by dysregulated mitotic signaling.
  44. Aurora A inhibitor

    Aurkin A is an allosteric inhibitor that disrupts the interaction between Aurora A kinase (AURKA) and its co-activator TPX2 by selectively targeting the TPX2 binding site on Aurora A. It binds with a dissociation constant (K\_d) of 3.77 μM, thereby interfering with Aurora A activation and its downstream mitotic functions. Aurkin A offers a unique mechanism of action compared to ATP-competitive inhibitors and serves as a valuable tool for studying Aurora A–TPX2–mediated signaling in cell division and cancer progression.
  45. Aurora A-TPX2 interaction inhibitor

    CAM2602 is a selective inhibitor targeting the interaction between Aurora A kinase and its co-activator TPX2, with a high binding affinity of 19 nM for Aurora A. It effectively inhibits the growth of pancreatic cancer cells and demonstrates antitumor activity in solid tumor transplant models. Mechanistically, CAM2602 increases the proportion of phospho-histone H3 (PH3) positive cells—indicative of mitotic arrest—while decreasing the levels of Aurora A phosphorylated at threonine 288 (P-Thr288), a marker of Aurora A activation. These effects collectively contribute to its ability to disrupt mitosis and suppress tumor progression.
  46. Aurora kinase inhibitor

    DBPR728 is an acyl prodrug of 6K465, engineered to improve pharmacokinetic properties by reducing the number of hydrogen bond donors, thereby enhancing membrane permeability and stability. As a prodrug of 6K465, DBPR728 functions as an Aurora kinase inhibitor that destabilizes MYC family oncoproteins, including c-MYC and N-MYC. It exhibits potent antitumor activity, particularly in cancers characterized by MYC overexpression. Notably, DBPR728 offers a 10-fold increase in oral bioavailability compared to 6K465, making it a promising candidate for the development of orally administered therapies targeting MYC-driven malignancies.
  47. Aurora Kinase A/JAK2 Inhibitor

    AJI-214 is a dual-target inhibitor that simultaneously inhibits Aurora kinase A and Janus kinase 2 (JAK2). It directly blocks Aurora A activity, disrupting T cell mitotic progression and polarity, while also inhibiting JAK2-mediated STAT3 phosphorylation, thereby suppressing the differentiation of pro-inflammatory TH1 and TH17 cells. AJI-214 holds therapeutic potential for modulating immune responses and is being investigated for the prevention and treatment of graft-versus-host disease (GVHD).
  48. Aurora A inhibitor.

    6K465 is a pyrimidine-based small molecule inhibitor selectively targeting Aurora A kinase (AURKA). By inhibiting AURKA activity, 6K465 effectively reduces the expression levels of the oncogenic transcription factors c-MYC and N-MYC, contributing to its anticancer effects. This compound shows promise as a therapeutic agent for MYC-driven cancers by disrupting mitotic regulation and oncogene stabilization.
  49. Aurora kinase inhibitor

    Derrone is a prenylated isoflavone that functions as an Aurora kinase inhibitor, exhibiting IC₅₀ values of 6 μM for Aurora B and 22.3 μM for Aurora A. By targeting these key mitotic kinases, Derrone disrupts cell cycle progression and displays notable antitumor activity, making it a promising compound for cancer research focused on mitotic regulation.
  50. Aurora-A Inhibitor

    PHA-680626 is a selective inhibitor of Aurora-A kinase, disrupting its interaction with N-Myc. This compound effectively inhibits the kinase activities of both AURKA and Bcr-Abl, leading to the degradation of N-Myc. Additionally, PHA-680626 reduces phosphorylation levels of CrkL and histone H3. Its anti-proliferative and pro-apoptotic effects have been demonstrated in Imatinib-resistant chronic myeloid leukemia cell lines and primary CD34+ hematopoietic stem cells, making it a valuable tool for research in cancer therapeutics.

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