Aurora A Inhibitor

Alisertib (MLN 8237) is an orally active and selective Aurora A kinase inhibitor (IC₅₀=1.2 nM), which binds to Aurora A kinase resulting in mitotic spindle abnormalities, mitotic accumulation. Alisertib (MLN 8237) induces apoptosis and autophagy through targeting the AKT/mTOR/AMPK/p38 pathway in leukemic cells. Antitumor activity.

Reversine is a novel class of ATP-competitive Aurora kinase inhibitor with IC₅₀s of 400, 500 and 400 nM for Aurora A, Aurora B and Aurora C, respectively.

Tozasertib (VX 680; MK-0457) is an inhibitor of Aurora A/B/C kinases with K_is of 0.6, 18, 4.6 nM, respectively.

JNJ-7706621 is a potent aurora kinase inhibitor, and also inhibits CDK1 and CDK2, with IC₅₀s of 9 nM, 3 nM, 11 nM, and 15 nM for CDK1, CDK2, aurora-A and aurora-B, respectively.

ZM-447439 is an aurora kinase inhibitor with IC₅₀s of 110 and 130 nM for aurora A and B, respectively.

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.

Aurora kinase-IN-10 is an Aurora kinase inhibitor. Aurora kinase-IN-10 exhibits IC₅₀ values of 5.94 nM and 86.06 nM against Aurora A and Aurora B, respectively. Aurora kinase-IN-10 has anti-tumor activity and can be used in the research of tumors such as triple-negative breast cancer.

Danusertib is a pyrrolo-pyrazole and aurora kinase inhibitor with IC₅₀ of 13, 79, and 61 nM for Aurora A, B, and C, respectively.

AMG 900 is a potent and highly selective pan-Aurora kinases inhibitor with IC₅₀ of 5 nM, 4 nM and 1 nM for Aurora A, B and C, respectively.

KW-2449 is a multi-targeted kinase inhibitor of FLT3, ABL, ABL^T315I and Aurora kinase with IC₅₀s of 6.6, 14, 4 and 48 nM, respectively.

AT9283 is a multi-targeted kinase inhibitor with potent activity against Aurora A/B, JAK2/3, Abl (T315I) and Flt3 (IC₅₀s ranging from 1 to 30 nM). AT9283 inhibits growth and survival of multiple solid tumors in vitro and in vivo.

LY3295668 (AK-01) is a highly specific and orally active inhibitor of Aurora-A kinase with a K_i values for AurA and AurB of 0.8 nM and 1038 nM respectively. LY3295668 can effectively inhibit the autophosphorylation of AurA, induce mitotic arrest and apoptosis. LY3295668 avoids the formation of polyploids related to AurB inhibition. LY3295668 can be used for the study of small cell lung cancer.

MK-5108 is a highly potent and specific inhibitor of Aurora A kinase with an IC₅₀ value of 0.064 nM.

GRK6-IN-1 (Compound 18) is the inhibitor for G protein-coupled receptorkinase 6 (GRK6) with an IC₅₀ of 3.8-8 nM. GRK6-IN-1 also inhibits GRK7, GRK5, GRK4 and GRK1 with IC₅₀s of 6.4, 12, 22 and 52 nM, respectively. GRK6-IN-1 has the potential for the research of multiple myeloma.

PF 477736 (PF 00477736) is a potent, selective and ATP-competitive inhibitor of Chk1, with a K_i of 0.49 nM, it is also a Chk2 inhibitor, with a K_i of 47 nM. PF 477736 shows <100-fold selectivity for Chk1 over VEGFR2, Fms, Yes, Aurora-A, FGFR3, Flt3, and Ret (IC₅₀=8 (K_i), 10, 14, 23, 23, 25, and 39 nM, respectively). PF 477736 can enhance Gemcitabine antitumor activity in vitro and in vivo.

MLN8054 is a potent, selective and orally available aurora A kinase inhibitor with an IC₅₀ of 4 nM.

PF-03814735 is a potent, orally available, ATP-competitive and reversible aurora A and aurora B inhibitor with IC₅₀s of 0.8 and 0.5 nM, respectively.

ENMD-2076 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.

GRK2 Inhibitor 2 is an orally active and selective G protein-coupled receptor kinase 2 (GRK) inhibitor with an IC₅₀ of 19 nM. GRK2 Inhibitor 2 also inhibits Aurora-A with an IC₅₀ of 137 nM. GRK2 Inhibitor 2 can be used in the study of congestive heart failure (HF).

JB170 is a potent and highly specific PROTAC-mediated AURORA-A (Aurora Kinase) degrader (DC₅₀=28 nM) by linking Alisertib, to the Cereblon-binding molecule Thalidomide. JB170 preferentially binds AURORA-A (EC₅₀=193 nM) over AURORA-B (EC₅₀=1.4 µM). JB170-mediated S-phase arrest is caused specifically by AURORA-A depletion. JB170 has excellent ability to inhibit non-catalytic function of AURORA-A kinase.