Its mode of action is as a reversible inhibitor of inosine monophosphate dehydrogenase  (IMPDH) in purine biosynthesis. MMF is selective for the de novo pathway critical to lymphocytic proliferation and activation. In the de novo purine synthesis pathway, IMPDH is the first of two enzymes responsible for the conversion of inosine monophosphate (IMP) to guanosine monophosphate (GMP), which is normally converted to GDP, GTP, and dGTP. IMPDH is not involved in the salvage pathway of purine biosynthesis. It has been proposed that, since lymphocytes are relatively independent of the salvage pathway of nucleotide biosynthesis, MPA treatment should reduce guanine nucleotide pools in lymphocytes. Other cells are able to recover purines via a separate, scavenger, pathway and are thus able to escape the effect. Measurements show that MPA causes a reduction of GTP and GTP in lymphocytes but not neutrophils. The consequences of the reduction in guanine nucleotides in lymphocytes, such as the inhibition of DNA synthesis, and GTP-dependent metabolic events, are discussed.
The drug also seems to augment the absorption of Tacrolimus & hence MMF is administered along with Tacrolimus.