PHPS1 sodium is a potent and selective inhibitor of Shp2, with Kis of 0.73, 5.8, 10.7, 5.8, and 0.47 μM for Shp2, Shp2-R362K, Shp1, PTP1B, and PTP1B-Q, respectively [1].

PHPS1 (30 μM; 6 days) inhibits human tumor cells proliferation[1]. PHPS1 (5-20 μM; 5-360 minutes) inhibits Erk1/2 but not Akt and Stat3 phosphorylation in a dose-dependent manner [1]. Cell Viability Assay [1] Cell Line: Human cancer cell lines MDA-MB-435, HCT-116 (colon carcinoma), HCT-15 (colon carcinoma), PC-3 (prostate carcinoma), HT-29 (colon carcinoma), NCI-H661 (lung carcinoma), and Caki-1 (kidney carcinoma) Concentration: 30 μM Incubation Time: 6 days Result: Resulted in a reduction in cell number of between 0% (Caki-1) to 74% (HT-29). Western Blot Analysis [1] Cell Line: Madin-Darby canine kidney (MDCK) cells Concentration: 5, 10, 20 μM Incubation Time: 5, 15, 60, 120, 360 minutes Result: Inhibited HGF/SF (1 unit/mL)-induced phosphorylation and thus activation of Erk1/2 over a time period of 15 min to 6 h. In contrast, transient phosphorylation of Erk1/2 after 5 min was not affected. Exhibited no effect on HGF/SF-induced activation of PI3K/Akt or Stat3.

PHPS1 (3 mg/kg; i.p. injection; every day during the last week on the high-fat diet) made Ldlr -/- mice less prone to atherosclerosis(AS)[2]. Animal Model: Ldlr -/- (005061) mice [2] Dosage: 3 mg/kg Administration: Intraperitoneal (i.p.) injection; every day during the last week on the high-fat diet. Result: Revealed a significant decrease in atherosclerotic plaque size in the aorta compared with the other two groups.