SF1670

• CAT Number: I003262
• CAS Number: 345630-40-2
• Molecular Formula: C₁₉H₁₇NO₃
• Molecular Weight: 307.34
• Purity: ≥95%
• Target: PTEN
• Solubility: 10 mM in DMSO
• Storage: Desiccate at -20C
• InChI: InChI=1S/C19H17NO3/c1-19(2,3)18(23)20-11-8-9-13-12-6-4-5-7-14(12)16(21)17(22)15(13)10-11/h4-10H,1-3H3,(H,20,23)
• InChIKey: VZQDDSYKVYARDW-UHFFFAOYSA-N
• SMILES: CC(C)(C)C(=O)NC1=CC2=C(C=C1)C3=CC=CC=C3C(=O)C2=O

SF1670（Cat No.:I003262） is a highly potent and specific inhibitor of PTEN (phosphatase and tensin homolog deleted on chromosome 10) with an IC50 value of 2 μM. By targeting PTEN, SF1670 disrupts its phosphatase activity, which is involved in regulating cell growth, survival, and metabolism. As a specific PTEN inhibitor, SF1670 offers a valuable tool for studying the function of PTEN in cellular processes and disease models.

Reference

1:Blood. 2011 Jun 16;117(24):6702-13. doi: 10.1182/blood-2010-09-309864. Epub 2011 Apr 26. Pretreatment with phosphatase and tensin homolog deleted on chromosome 10 (PTEN) inhibitor SF1670 augments the efficacy of granulocyte transfusion in a clinically relevant mouse model.Li Y,Prasad A,Jia Y,Roy SG,Loison F,Mondal S,Kocjan P,Silberstein LE,Ding S,Luo HR, PMID: 21521784 PMCID: PMC3123029 DOI: 10.1182/blood-2010-09-309864 Abstract: The clinical outcome of granulocyte transfusion therapy is often hampered by short ex vivo shelf life, inefficiency of recruitment to sites of inflammation, and poor pathogen-killing capability of transplanted neutrophils. Here, using a recently developed mouse granulocyte transfusion model, we revealed that the efficacy of granulocyte transfusion can be significantly increased by elevating intracellular phosphatidylinositol (3,4,5)-trisphosphate signaling with a specific phosphatase and tensin homolog deleted on chromosome 10 (PTEN) inhibitor SF1670. Neutrophils treated with SF1670 were much sensitive to chemoattractant stimulation. Neutrophil functions, such as phagocytosis, oxidative burst, polarization, and chemotaxis, were augmented after SF1670 treatment. The recruitment of SF1670-pretreated transfused neutrophils to the inflamed peritoneal cavity and lungs was significantly elevated. In addition, transfusion with SF1670-treated neutrophils led to augmented bacteria-killing capability (decreased bacterial burden) in neutropenic recipient mice in both peritonitis and bacterial pneumonia. Consequently, this alleviated the severity of and decreased the mortality of neutropenia-related pneumonia. Together, these observations demonstrate that 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.