Lift(Artivila)

Methods for pharmacokinetic modulation of the plasma 5‐fluorouracil (5‐FU) level to increase antitumor activity during continuous venous infusion (CVI) of low doses of 5‐FU were examined in Yoshida sarcoma‐bearing rats. These methods were additional infusion of 5‐FU for a short period (4 h) or oral administration of LIFT or Tegafur during long‐term CVI of 5‐FU that alone gave a plasma 5‐FU level of about 50 ng/ml. The antitumor effect on Yoshida sarcoma was markedly potentiated when an additive dose of 5‐FU combined with 3‐cyano‐2,6‐dihydroxypyridine (CNDP), a potent inhibitor of 5‐FU degradation, giving a plasma level of about 500 ng/ml, was infused for 4 h. A similar increase in the antitumor effect was observed with oral administration of a conventional dose of UFT during CVI of 5‐FU without CNDP, giving a plasma level of 30 to 60 ng/ml. These results suggest that the antitumor effect of CVI of 5‐FU can be potentiated by pharmacokinetic modulation of the 5‐FU concentration in the blood.

The lymphocyte‐inhibiting factor extracted from the thymus (LIFT) is effective in decreasing several immune responses. The aim of this study was to determine whether LIFT is able to depress humoral immune reactions and if so, whether it acts on T lymphocytes, B lymphocytes, or both.Simultaneous administration of LIFT and antigen severely impairs the IgG antibody formation against dinitrophenylated human IgG (DNP‐HGG(a highly T lymphocyte‐dependent response) and, to a lesser extent, the IgM antibody formation against sheep red blood cells (a partly T lymphocyte‐dependent response). In contrast, the IgM anti‐DNP‐polymerized flagellin response (which does not require T lymphocyte collaboration) is not depressed at all by such treatment. These results demonstrate a LIFT action specificity on T lymphocytes only, and strongly argue for the assimilation of LIFT with a T lymphocyte chalone. The existence of a lymphocyte‐inhibiting factor specific for B lymphocytes, or B lymphocyte chalone, is discussed.