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Aurora kinase inhibitors block Aurora A, Aurora B and Aurora C, three serine/threonine kinases that coordinate mitosis. The founding aurora gene was described in Drosophila in 1995, where its mutations prevented centrosome separation and produced monopolar spindles. In human cells Aurora A acts at centrosomes and spindle poles during spindle assembly. Aurora B belongs to the chromosomal passenger complex, which moves from centromeres to the spindle midzone during division. Alisertib preferentially inhibits Aurora A, whereas barasertib-HQPA and hesperadin mainly target Aurora B. Work with hesperadin in 2003 linked Aurora B to correcting kinetochore-microtubule attachments and maintaining the spindle assembly checkpoint. Tozasertib and AMG 900 inhibit all three family members and are used as pan-Aurora tools.
Synonyms: AS-703569; R-763
Cenisertib (AS-703569) is a multi-kinase inhibitor that blocks the activity of Aurora-kinase-A/B, ABL1, AKT, STAT5 and FLT3.
XL228 is a protein kinase inhibitor targeting IGF1R, the AURORA kinases, FGFR1-3, ABL and SRC family kinases. XL228 is an Aurora A inhibitor (IC50, f3 nmol/L) that has shown potent biochemical activity against ABL1 (Ki, 5 nmol/L), as well as the BCR-ABL1 T315I (Ki, 1.4 nmol/L) kinases.
MK-8745 is a novel Aurora-A specific inhibitor. It induces apoptotic cell death in a p53-dependent manner when tested in vitro in cell lines of multiple lineages.
Synonyms: TCA2317
TC-A-2317 hydrochloride is a potent Aurora kinase A inhibitor (Ki = 1.2 nM compared to 101 nM for inhibition of Aurora kinase B). Selective over 60 other kinases (IC50 values > 1000 nM). Exhibits good cell permeability and antitumor activity.
SCH-1473759 is a novel sub-nanomolar Aurora A/B inhibitor with IC50 of 4 nM and 13 nM, respectively.
SAR156497 is an exquisitely selective Aurora A, B, and C inhibitor with in vitro and in vivo efficacy with IC50 = 0.5 nM (Aurora A), 1 nM (Aurora B / incenp), 3 nM (Aurora C / incenp) respectively SAR156497 combines high in vitro potency with satisfactory metabolic stability and limited CYP3A4 and PDE3 inhibition.
Synonyms: Barasertib
AZD1152 is a pro-drug that rapidly undergoes phosphatase-mediated cleavage in serum to release barasertib-hQPA, a selective Aurora B kinase inhibitor that has shown preliminary activity in clinical studies of patients with acute myeloid leukemia (AML).
Synonyms: AK-01
LY3295668, also known as AK-01, is potent Aurora-A kinase inhibitor.
AAPK-25 is a potent and selective Aurora/PLK dual inhibitor with anti-tumor activity, which can cause mitotic delay and arrest cells in a prometaphase, reflecting by the biomarker histone H3Ser10 phosphorylation and followed by a surge in apoptosis.
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>10 μM.
Aurora inhibitor 1 is a potent Aurora inhibitor with an IC50 of ?? 4 nM and ??13 nM for Aurora A and Aurora B kinase, respectively.
Synonyms: ABT-348
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.
CCT241736 is a potent and orally bioavailable dual FLT3 and Aurora kinase inhibitor.
Synonyms: ENMD2076
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.
Synonyms: SCH1473759
SCH-1473759 hydrochloride is an aurora inhibitor with IC50s of 4 and 13 nM for aurora A and B, respectively.
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.
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.
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).
Phthalazinone pyrazole is a potent, selective, and orally bioavailable inhibitor of Aurora-A kinase, with an IC₅₀ of 0.031 μM. It exerts antitumor effects by arresting mitosis and inducing apoptosis in proliferating cells, leading to inhibition of tumor growth. Additionally, phthalazinone pyrazole suppresses epithelial-mesenchymal transition (EMT) during the differentiation of hepatocyte-like cells (HLCs) derived from human embryonic stem cells, indicating potential applications in both cancer therapy and stem cell biology.
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.
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.
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.
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.
Synonyms: Chiauranib; CS2164
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.
