Laflunimus (HR325) is a DHODH inhibitor that inhibits immunoglobulin IgM and IgG secretion in vitro and in vivo, with an IC50=2.5 μm, and exerts an immunosuppressive effect by interfering with pyrimidine metabolism, and is used in the study of neuralgia.

IgM secretion from LPS-stimulated mouse splenocytes: 2.5 μM, IgG secretion with 50 μM uridine:60 μM, IgM secretion with 50 μM uridine: 70 μM, IgG secretion from LPS-stimulated mouse splenocytes: 2.0 μM

Laflunimus (HR325) inhibited LPS-induced IgM and IgG secretion from mouse splenocytes, with IC₅₀ values of 2.5 μM and 2 μM, respectively.[1]
The addition of exogenous uridine (50 μM) reversed this effect, increasing the IC₅₀ values to 70 μM for IgM and 60 μM for IgG, suggesting a pyrimidine depletion mechanism.[1]
Laflunimus also suppressed LPS-induced κ light-chain surface expression in 70Z/3 cells, which was similarly reversed by uridine.[1]

Laflunimus inhibited the secondary antibody response to sheep red blood cells (SRBC) in mice, with an ID₅₀ of 38 mg/kg orally.[1]
Co-administration of uridine reversed immunosuppression induced by Laflunimus (50 mg/kg), whereas uridine alone had no effect and did not reverse immunosuppression caused by cyclophosphamide (10 mg/kg).[1]