IPD-1151T: a prototype drug for IgE antibody synthesis modulation.

IPD-1151T [(+/-)-[2-[4-(3-ethoxy-2-hydroxypropoxy)phenylcarbamoyl]-ethyl] dimethylsulfonium p-toluenesulfonate] inhibits not only antigen-induced histamine release from mast cells but also IgE antibody formation. The present paper describes the inhibitory effect of IPD-1151T on the IgE antibody formation. The IgE antibody formation in BALB/c mice which had been immunized with dinitrophenylated ascaris extract (DNP.As) plus alum was inhibited dose-dependently by IPD-1151T given p.o. The formations of anti-DNP.IgM and IgG antibodies, however, were unaffected in this case. Ongoing IgE antibody formation was also inhibited by this agent. The total IgE in sera of atopic patients including asthma and atopic dermatitis showed a tendency to decrease when IPD-1151T was given p.o. for 6 to 12 weeks, though the titer of specific IgE antibody against Dermatophagoides pteronyssinus or D. farinae clearly decreased. In these cases, the ratio of B cell expressing low-affinity Fc receptor for IgE (Fc epsilon RII) also decreased. Antigen-induced production of interleukin 4 (IL-4) from a helper T-cell line (TCL) prepared from peripheral blood lymphocytes of an allergic patient sensitive to Japanese cedar pollen was reduced with the addition of IPD-1151T. This agent also decreased antigen-induced IgE synthesis by autologous B cell concomitant with the TCL and antigen presenting cell. The consideration was done on the mechanism regarding the inhibition of IgE antibody formation by IPD-1151T.