JB170 是一种强效且高度特异性的 PROTAC 介导的 AURORA-A 降解剂 (DC50=28 nM)，通过将 Alisertib 连接至 Cereblon配体 Thalidomide 而形成。JB170 优先结合 AURORA-A (EC50=193 nM) 而不是 AURORA-B (EC50=1.4µM)。JB170 介导的 S 期阻滞是由 AURORA-A 耗竭引起的。JB170 对 AURORA-A 激酶的非催化功能具有很好的抑制能力。
货号:ajcx36204
CAS:N/A
分子式:C48H44ClFN8O11
分子量：963.36
溶解度:DMSO : 100 mg/mL (103.80 mM; Need ultrasonic)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

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[1].

JB170 (1 μM; 24-72 hours; MV4-11 cells) mediates Aurora-A depletion inhibiting cancer cell survival[1]. JB170 (0.01-10 μM; 6 hours; MV4-11 cells) reduces AURORA-A levels [1].JB170 (0.5 μM; 12 hours; MV4-11 cells) delays/arrests S-phase progression[1].JB170 (0.5 μM; 0-72 hours; MV4-11 cells) induces apoptosis is exclusively caused by targeting AURORA-A[1].JB170 (0.1 µM; 0-9 hours; IMR5 cells) shows rapid AURORA-A depletion. JB170 (0~1 μM; 6 hours; MV4-11 cells) strongly attenuates in mutants with respect to AURORA-A. JB170 (0.1 μM; 18 hours; MV4-11 cells) does not activate AURORA-A. JB170 (0~1 µM; 24 hours; IMR5 cells) largely abrogates AURORA-AT217D depletion. JB170 (1 μM; 4 days; IMR5 cells) mediates Aurora-A depletion inhibiting cancer cell survival. JB170 (IMR5 cells) reduces AURORA-A levels by lowering AURORA-A mRNA levels[1].

[1]. Adhikari B, et al. PROTAC-mediated degradation reveals a non-catalytic function of AURORA-A kinase. Nat Chem Biol. 2020;16(11):1179-1188.