Talabostat (Val-boroPro; PT100) is an orally active and nonselectivedipeptidyl peptidaseIV (DPP-IV)inhibitor (IC₅₀< 4 nM;K_i= 0.18 nM) and the first clinical inhibitor of fibroblast activation protein(FAP)(IC₅₀= 560 nM), inhibits DPP8/9 (IC₅₀= 4/11 nM;K_i= 1.5/0.76 nM), quiescent cell proline dipeptidase (QPP) (IC₅₀= 310 nM), DPP2, and some other DASH family enzymes. Antineoplastic and hematopoiesis- stimulating activities^[1][2][3].

IC50:< 4 nM (DPP-IV), 4/11 nM (DPP8/9), 310 nM (QPP), 560 nM (FAP)^[1]
Ki: 0.18 nM (DPP-IV), 1.5/0.76 nM (DPP8/9)^[2]

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^[3].
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^[4].

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^[4].

214.07

C₉H₁₉BN₂O₃

149682-77-9

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

DMSO : ≥ 40 mg/mL(186.85 mM)

*"≥" means soluble, but saturation unknown.