SF2523 is a highly selective and potent inhibitor (SF2523) with improved physicochemical properties, excellent aqueous solubility, and biological efficacy. It is typically used in genome editing [CRISPR/Cas Solution] technology and can effectively enhance the efficiency of this process.

DNA-PK:9 nM, BRD4:241 nM, PI3Kα:34 nM, mTOR:280 nM, PI3Kγ:158 nM

Treatment with SF2523 leads to a reduction in the protein levels of MYCN and Cyclin D1, targets of MYCN. It also impedes AKT activation by preventing the phosphorylation at Ser473 and results in the removal of BRD4 from MYCN promoter sites. SF2523 exhibits a strong interaction with full-length BRD4 (Kd=140 nM), showing a similar affinity for BRD4's first bromodomain (BD1) (Kd=150 nM) but a weaker affinity for its second bromodomain (BD2) (Kd=710 nM). When comparing the binding affinities of SF2523 to bromodomains (BDs) of different proteins, it demonstrates equal binding to BDs of BRD4, BRD2, and BRD3; a moderate binding to BDs of CECR2 and BRDT; and significantly weaker binding to other BDs[1].

Treatment with SF2523 significantly reduces tumor volume without causing gross toxicity in mice, as evidenced by stable body weight. Furthermore, tumors in mice treated with SF2523 exhibit notably lower levels of MYCN, pAKT, and Cyclin D1 compared to those in mice treated with the vehicle[1].