MLN8054

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

一种有效的、选择性的、ATP 竞争性的、口服活性的 Aurora A 激酶抑制剂，IC50 为 4 nM。

A potent, selective, ATP-competitive, orally active Aurora A kinase inhibitor with IC50 of 4 nM; displays >40-fold selectivity over Aurora B, and >100-fold selectivity over a panel of kinases; causes G(2)/M accumulation and spindle defects and inhibits proliferation in multiple cultured human tumor cells lines; dramatically inhibits the growth of human tumor xenografts in nude mice.Solid Tumors Phase 1 Clinical(In Vitro):MLN8054 is an ATP-competitive, reversible inhibitor of recombinant Aurora A kinase. MLN8054 is >40-fold more selective for Aurora A compared with the family member Aurora B. MLN8054 selectively inhibits Aurora A over Aurora B in cultured human tumor cells. MLN8054 treatment results in G2/M accumulation and spindle defects and inhibits proliferation in multiple cultured human tumor cells lines. MLN8054 effectively inhibits the growth of cells from diverse tissue origins with IC50 values ranging from 0.11 to 1.43 μM. Treatment of human tumor cells grown in culture with MLN8054 shows a number of morphologic and biochemical changes associated with senescence. (In Vivo):In the HCT-116 tumor-bearing mice, MLN8054 treatment inhibits tumor growth dose dependently. MLN8054 is generally well tolerated. MLN8054 also inhibits the growth of the PC-3 tumor xenograft in nude mice. MLN8054 Treatment Results in Inhibition of Aurora A, Accumulation of Mitotic Cells, and Apoptosis in vivo. MLN8054 selectively inhibits Aurora A kinase activity when dosed at 30 mg/kg. At this dose in HCT116 tumor tissue, MLN8054 has been shown to inhibit Aurora A autophosphorylation, and induce an increase in the Aurora B substrate, pHisH3.

MLN8054 is an ATP-competitive, reversible inhibitor of recombinant Aurora A kinase. MLN8054 is >40-fold more selective for Aurora A compared with the family member Aurora B. MLN8054 selectively inhibits Aurora A over Aurora B in cultured human tumor cells. MLN8054 treatment results in G2/M accumulation and spindle defects and inhibits proliferation in multiple cultured human tumor cells lines. MLN8054 effectively inhibits the growth of cells from diverse tissue origins with IC50 values ranging from 0.11 to 1.43 μM. Treatment of human tumor cells grown in culture with MLN8054 shows a number of morphologic and biochemical changes associated with senescence.

In the HCT-116 tumor-bearing mice, MLN8054 treatment inhibits tumor growth dose dependently. MLN8054 is generally well tolerated. MLN8054 also inhibits the growth of the PC-3 tumor xenograft in nude mice. MLN8054 Treatment Results in Inhibition of Aurora A, Accumulation of Mitotic Cells, and Apoptosis in vivo. MLN8054 selectively inhibits Aurora A kinase activity when dosed at 30 mg/kg. At this dose in HCT116 tumor tissue, MLN8054 has been shown to inhibit Aurora A autophosphorylation, and induce an increase in the Aurora B substrate, pHisH3.

MLN-8054 | MLN 8054

Cell Cycle/DNA Damage

Aurora Kinase

AuroraA|AuroraB|CK2|Lck|PKA

Cancer

Solid Tumors

869363-13-3

476.862

C25H15ClF2N4O2

>98% (HPLC)

10 mM in DMSO

O=C(O)C1=CC=C(NC2=NC=C3C(C4=CC=C(Cl)C=C4C(C5=C(F)C=CC=C5F)=NC3)=N2)C=C1

Benzoic acid, 4-[[9-chloro-7-(2,6-difluorophenyl)-5H-pyrimido[5,4-d][2]benzazepin-2-yl]amino]-

(-20℃)

With Ice Pack

≥ 2 years