TPI-1 is a SHP-1 inhibitor.

SHP1:40 nM.

SHP-1被认为是潜在的癌症治疗靶标。TPI-1在10 ng/mL的浓度开始有效地增加SHP-1磷酸化底物pLck-pY394。TPI-1在Jurkat T细胞中选择性地增加SHP-1磷酸化底物（pLck-pY394、pZap70和pSlp76），对pERK1/2或pLck-pY505的影响较小。TPI-1诱导小鼠脾脏产生IFNγ+细胞，并在人类外周血中诱导IFNγ+细胞[1]。

TPI-1通过口服可耐受剂量在T细胞依赖的方式下抑制小鼠中B16黑素瘤肿瘤的生长，但对体外培养的B16细胞生长影响不大。同时，TPI-1在小鼠体内增加了pLck-pY394和IFNγ+细胞的数量。TPI-1还作为一个可耐受的皮下(s.c.)药剂，抑制了B16肿瘤的生长并延长了肿瘤小鼠的生存时间[1]。

Jump-In TI CHO-K cells stably expressing WT or mutant S1P3 are serum-starved for 4 hrs. They are then incubated at 4 °C for 30 min in the binding buffer containing 20 mM Tris-HCl (pH 7.5), 100 mM NaCl, 15 mM NaF, 0.5 mM EDTA, 1 mM Na3VO4, 0.5% fatty acid-free bovine serum albumin, and protease inhibitor mixture with 0.1 nM [33P]S1P and increasing concentrations of S1P, SPM-242, or CYM-5541. Cells are washed three times with cold binding buffer. Cell-bound radioactivity is measured by lysing the cells with 0.5% SDS followed by liquid scintillation counting. The raw data is normalized so that the level of [33P]S1P bound to each cell line (WT or mutant) in the absence of competing ligand is referenced as 100% for its own cell line[1].