SF-1670 is a specific phosphatase and tensin homolog deleted on chromosome 10 (PTEN) inhibitor. SF1670 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 SF1670, providing a therapeutic strategy for improving the efficacy of granulocyte transfusion.
Chemical Formula: C19H17NO3
Exact Mass: 307.1208
Molecular Weight: 307.349
Elemental Analysis: C, 74.25; H, 5.58; N, 4.56; O, 15.62
Appearance: Solid powder
Purity: >98% (or refer to the Certificate of Analysis)
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Solubility: Soluble in DMSO
Shelf Life: >2 years if stored properly
Drug Formulation: This drug may be formulated in DMSO
Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).
HS Tariff Code: 2934.99.9001
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.
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