SF1670 is a potent and specific PTEN (phosphatase and tensin homolog deleted on chromosome 10) inhibitor[1]. SF1670 protects cells from oxygen-glucose deprivation-induced cell death[2]. SF1670 helps maintain the pluripotency of mouse embryonic stem cells (ESCs)[3].
In vitro, treatment of nucleus pulposus (NP) cells with SF1670 (0-5µM) for 3h significantly increased cell viability, inhibited PTEN expression, and activated Akt activity[4]. Pretreatment of neutrophils with SF1670 (125-500nM) for 30min dose-dependently enhanced fMLP-induced neutrophil polarization[5]. Treatment of MCF-7 cells with SF1670 (200nM) for 48h significantly inhibited curcumin-induced cell apoptosis and significantly upregulated p-AKT protein expression[6].
In vivo, SF1670 (3mg/kg) was intraperitoneally injected into mice with cerebral ischemia-reperfusion (I/R) injury, which attenuated the increase in thiobarbituric acid reactive substances (TBARS) induced by I/R and reversed the decrease in GSH levels and SOD activity[7].
References:
[1] Li F Q, Chen W B, Luo Z W, et al. Bone marrow mesenchymal stem cell-derived exosomal microRNAs target PI3K/Akt signaling pathway to promote the activation of fibroblasts[J]. World Journal of Stem Cells, 2023, 15(4): 248.
[2] Farajdokht F, Mohaddes G, Karimi-Sales E, et al. Inhibition of PTEN protects PC12 cells against oxygen-glucose deprivation induced cell death through mitoprotection[J]. Brain research, 2018, 1692: 100-109.
[3] Wang W, Lu G, Su X, et al. Pten-mediated Gsk3β modulates the naïve pluripotency maintenance in embryonic stem cells[J]. Cell Death & Disease, 2020, 11(2): 107.
[4] Fu H Y, Shen L, Gao X S, et al. SF1670 inhibits apoptosis and inflammation via the PTEN/Akt pathway and thus protects intervertebral disc degeneration[J]. European Review for Medical & Pharmacological Sciences, 2020, 24(17).
[5] Li Y, Prasad A, Jia Y, et al. 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[J]. Blood, The Journal of the American Society of Hematology, 2011, 117(24): 6702-6713.
[6] Li M Z, Wang C R, Lin C L. Curcumin promotes apoptosis of breast cancer cells by down-regulating DJ-1-PTEN/PI3K/AKT signaling pathways[J]. Int. J. Clin. Exp. Med, 2019, 12: 8992-8998.
[7] Grewal A K, Singh N, Singh T G. Neuroprotective effect of pharmacological postconditioning on cerebral ischaemia–reperfusion-induced injury in mice[J]. Journal of Pharmacy and Pharmacology, 2019, 71(6): 956-970.
SF1670是一种有效的特异性PTEN(第10号染色体上缺失的磷酸酶和张力蛋白同源物)抑制剂[1]。SF1670能够保护细胞免受氧-葡萄糖剥夺诱导的细胞死亡[2]。SF1670有助于维持小鼠胚胎干细胞(ESC)的多能性[3]。
在体外,SF1670(0-5µM)处理髓核(NP)细胞3h,显著提高了细胞活力,抑制了PTEN的表达,激活了Akt活性[4]。SF1670(125-500nM)预处理中性粒细胞30min,剂量依赖性地增强了fMLP诱导的中性粒细胞极化[5]。SF1670(200nM)处理MCF-7细胞48h,显著抑制了姜黄素引起的细胞凋亡,显著上调了p-AKT蛋白表达[6]。
在体内,SF1670(3mg/kg)通过腹腔注射治疗脑缺血再灌注(I/R)损伤小鼠,减弱了I/R引起的硫代巴比妥酸反应物质(TBARS)的增加,逆转了GSH水平和SOD活性的下降[7]。
















