SF-1670 is a specific phosphatase and tensin homolog deleted on chromosome 10 (PTEN) inhibitor. SF-1670 specifically binds to the active site of PTEN inhibiting its activity with an IC50 value of 2 μM. The innate immune responses can be enhanced and the severity of neutropenia-related infection can be alleviated by augmenting phosphatidylinositol (3, 4, 5)-trisphosphate in transfused neutrophils with PTEN inhibitor SF-1670, providing a therapeutic strategy for improving the efficacy of granulocyte transfusion.
CAS Number: 345630-40-2
Molecular Weight: 307.34
Chemical Name: N-(9,10-dihydro-9,10-dioxo-2-phenanthrenyl)-2,2-dimethyl-propanamide
Appearance: Solid Power
Purity: ≥98% (or refer to the Certificate of Analysis)
Solubility: Soluble in DMSO
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis
Storage Condition: Dry, dark and -20 oC for 1 year or refer to the Certificate of Analysis.
Shelf Life: ≥360 days if stored properly.
Stock Solution Storage: 0 - 4 oC for 1 month...
Drug Formulation: To be determined
HS Tariff Code: 382200
How to use
SF-1670 is a specific PTEN inhibitor with prolonged intracellular retention in neutrophils. SF-1670 enhances PtdIns(3, 4, 5)P3 signaling in transplanted neutrophils. SF-1670 also elevates Akt phosphorylation in murine cells. Consistent with the enhanced Akt phosphorylation, pretreatment with SF-1670 also significantly augments PtdIns(3, 4, 5)P3 level in mouse neutrophils. SF-1670-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, SF-1670 (500 nM)–pretreated neutrophils show nearly 70% higher (maximal) superoxide production than untreated neutrophils. HCT116 cells are pre-treated with the PTEN inhibitor SF-1670 (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). SF-1670 binds to the PTEN active site, resulting in elevated phosphatidylinositol (3, 4, 5) triphosphate signaling.
SF-1670 (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.
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