SRT 1720 is a selective activator of human SIRT1 (EC1.5: 0.16 μM) and is >230-fold less potent for SIRT2 and SIRT3.

SIRT1:0.16 μM (EC1.5, cell free), SIRT2:37 μM (EC1.5, cell free)

SRT1720对最接近的sirtuin同源蛋白SIRT2（EC1.5 = 37 μM）和SIRT3（EC1.5 > 300 μM）的最大激活比率高达781%。SRT1720通过与SIRT1酶-肽底物复合物的异源位点结合，该位点位于催化域的氨基末端，能够降低乙酰化底物的米氏常数。SRT1720高浓度（15 μM）对正常细胞活性产生轻微下降（10-20%）。此外，SRT1720显著抑制依赖VEGF的MM细胞迁移[1]。

SRT 1720（10、30、100 mg/kg，p.o.）在4周后显著降低高胰岛素血症，部分地将升高的胰岛素水平恢复至接近罗格列酮治疗的水平。SRT 1720治疗在Lepob/ob小鼠中显著减少空腹血糖至接近正常水平[1]。SRT 1720能够抵抗饮食诱导的肥胖在小鼠中的负面效果，并通过SIRT1的下游靶点如PGC1α和FOXO1与脂肪酸及氧化代谢的代谢适应性连接[2]。在肺气肿发展期间，SRT 1720（50-100 mg/kg，p.o.）减缓了由弹性酶引起的气腔扩大和肺功能衰竭，并降低了WT小鼠的动脉氧饱和度[3]。

Nine-week-old C57BL/6 male mice are fed a high-fat diet (60% calories from fat) until their mean body weight reaches approximately 40 g. The mice are then divided into test groups (6-10 per group). SRT1460 (100 mg/kg), SRT1720 (100 mg/kg), SRT501 (500 mg/kg) and rosiglitazone (5 mg/kg) are administered once daily via oral gavage. The vehicle used is 2% HPMC + 0.2% DOSS. Individual mouse body weights are measured twice weekly. At 2, 4, 6, 8 and 10 weeks of dosing a fed blood glucose measurement are taken and after 5 weeks of treatment, an IPGTT is conducted on all mice from each of the groups. After 10 weeks of treatment, an ITT is conducted. Statistical analysis is completed using the JMP program. Data are analyzed by a one way ANOVA with a comparison to control using a Dunnett's Test. A p-value < 0.05 indicates a significant difference between groups.