[(2R)-1-[(2S)-2-氨基-3-甲基丁酰基]吡咯烷-2-基]硼酸

IC50: < 4 nM (DPP-IV), 4/11 nM (DPP8/9), 310 nM (QPP), 560 nM (FAP)
Ki: 0.18 nM (DPP-IV), 1.5/0.76 nM (DPP8/9)

By cleaving N-terminal Xaa-Pro or Xaa-Ala residues, Talabostat (Val-boroPro) inhibits dipeptidyl peptidases, such as FAP, resulting in the stimulation of cytokine and chemokine production and specific T-cell immunity and T-cell dependent activity.
Talabostat (Val-boroPro) competitively inhibits the dipeptidyl peptidase (DPP) activity of FAP and CD26/DPP-IV, and there is a high-affinity interaction with the catalytic site.

Talabostat (Val-boroPro; PT100) can stimulate immune responses against tumors involving both the innate and adaptive branches of the immune system.In WEHI 164 fibrosarcoma and EL4 and A20/2J lymphoma models, Talabostat (Val-boroPro) causes regression and rejection of tumors. The antitumor effect appears to involve tumor-specific CTL and protective immunological memory.Talabostat (Val-boroPro) treatment of WEHI 164-inoculated mice increases mRNA expression of cytokines and chemokines known to promote T-cell priming and chemoattraction of T cells and innate effector cells.