SP-96 is a highly selective and non-ATP-competitive Aurora A/B inhibitor with IC50 values of 0.316nM 18.975 nM for Aurora A and Aurora B, respectively.
SP-96 is a potent, selective, and non-ATP-competitive inhibitor of Aurora B (IC50=0.316 nM), with >2000 fold selectivity against FLT3 and KIT. It demonstrates selective growth inhibition in NCI60 screening, including MDA-MD-468 (GI50=107 nM). SP-96 is a valuable tool for researching triple negative breast cancer (TNBC)[1].
体外研究
SP-96 is a potent, selective, and non-ATP-competitive inhibitor of Aurora B (IC50=0.316 nM), exhibiting over 2000-fold selectivity against FLT3 (IC50=1475.6 nM) and KIT (IC50=1307.6 nM)[1].
SP-96 (0-1 µM; 24 hours) exhibits selectivity rather than promiscuity towards specific cell lines. It inhibits the growth of MDA-MB-468, CCRF-CEM, COLO 205, and A498 cells with GI50 values of 107 nM, 47.4 nM, 50.3 nM, and 53.2 nM, respectively[1].
SP-96 (63.2 nM) suppresses Aurora B activity in H460 cells, leading to increased DNA content and enlarged cell volume with enlarged nuclei[1].
SP-96 (0-2 µM) suppresses Aurora B enzymatic activity with an IC50 of 0.316 nM and Aurora A with an observed IC50 value of 18.975 nM. It demonstrates over 2000-fold selectivity against FLT3 (IC50=1475.6 nM) and KIT (IC50=1307.6 nM). Additionally, it inhibits other receptor tyrosine kinases (RTKs) such as EGFR, RET, and HER2, with IC50 values ≥2 µM[1].
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