SF1670

Research use only, not for human use.

SF1670 is a highly potent and specific PTEN inhibitor with IC50 of 2 μM.

SF1670 is a highly potent and specific PTEN inhibitor with IC50 of 2 μM.

SF1670 is a specific PTEN inhibitor with prolonged intracellular retention in neutrophils. SF1670 enhances PtdIns(3,4,5)P3 signaling in transplanted neutrophils. SF1670 also elevates Akt phosphorylation in murine cells. Consistent with the enhanced Akt phosphorylation, pretreatment with SF1670 also significantly augments PtdIns(3,4,5)P3 level in mouse neutrophils. SF1670-induced Akt hyperactivation is abolished in PTEN-null neutrophils, further demonstrating that this effect is mediated by specific inhibition of PTEN activity. At 500 nM fMLP stimulation, SF1670 (500 nM)–pretreated neutrophils show nearly 70% higher (maximal) superoxide production than untreated neutrophils. HCT116 cells are pre-treated with the PTEN inhibitor SF1670 (2 μM) for 24 h (untreated HCT116 cells served as control); treated cells are subsequently plated under non-adherent conditions with added MET (60 μM), Lun (2 μM), or Gen (2 μM). SF1670 binds to the PTEN active site, resulting in elevated phosphatidylinositol (3,4,5) triphosphate signaling.

SF1670 (3 mg/kg; i.p.) triggers postconditioning after inducing cerebral global ischaemia (17 min) and reperfusion (24 h)‐induced injury via occlusion of both carotid arteries in mice. Animal Model:Swiss albino male mice (bodyweight 25-30 g) Dosage:3 mg/kg Administration:Treatment with i.p.Result:Lead to attenuation of cerebral I/R-induced increase in thiobarbituric acid reactive substances (TBARS).

SF1670 | SF-1670 | SF 1670

Others

PTEN

PTEN

Cancer

——

345630-40-2

307.34

C19H17NO3

>98% (HPLC)

DMSO:29 mg/mL warmed (94.35 mM); Ethanol:1 mg/mL warmed (3.25 mM); Water:<1 mg/mL (<1 mM)

CC(C)(C)C(NC(C=C1C2=O)=CC=C1C3=C(C2=O)C=CC=C3)=O

N-(9,10-dihydro-9,10-dioxo-2-phenanthrenyl)-2,2-dimethyl-propanamide

(-20℃)

With Ice Pack

≥ 2 years