Pharmacological inhibition of FAP reduces weight, improves glucose and lipid metabolism in obese, but not lean mice.

FAP inhibitor Talabostat at higher doses lessens food intake, without any apparent adverse effects in short term studies.

Obese FGF21 deficient mice did not exhibit meaningful change in metabolic regulation when treated with Talabostat.

The mechanism of Talabostat in vivo action appears to center on an increase in total and active levels of plasma FGF21.

FAP inhibition alone, or in combination with DPP4 is proposed as a novel approach to treat metabolic diseases.