Additionally, SF1670 administered at 3 mg/kg intraperitoneally induces protective postconditioning effects following cerebral global ischemia (induced by 17 minutes of occlusion) and subsequent reperfusion (24 hours) injury in mice, highlighting its potential in modulating ischemic injury responses^[1].

F1670 is identified as a potent and specific inhibitor of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), demonstrating prolonged intracellular retention in neutrophils and enhancing phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) signaling and Akt phosphorylation within these cells. Such SF1670-mediated Akt hyperactivation and PtdIns(3,4,5)P3 elevation are absent in PTEN-null neutrophils, confirming the specificity of SF1670's action on PTEN. Notably, SF1670 pre-treatment at 500 nM increases superoxide production in neutrophils stimulated with fMLP by nearly 70% compared to untreated cells^[1].

In vitro, HCT116 cells pre-treated with SF1670 (2 μM) for 24 hours, followed by plating under non-adherent conditions with added MET (60 μM), Lun (2 μM), or Gen (2 μM), exhibit elevated phosphatidylinositol (3,4,5) triphosphate signaling due to SF1670 binding to PTEN's active site^[2].