Silver sulfadiazine (CF-100) binds to deoxyribonucleic acid (DNA) but not to ribonucleic acid (RNA). DNA degradation is not observed. Nucleic acid and protein synthesis are not inhibited by silver sulfadiazine in cell-free systems. Conformational changes in the DNA are observed as evidenced by altered thermal transition, suggesting that silver sulfadiazine is inhibiting DNA replication.

Silver chelates of uracil and uracil derivatives yield biologically active compounds effective against several strains of bacteria including P. aeruginosa with minimal toxicity to the host in vitro. Toxicity studies conducted in tissue culture revealed comparative toxicity equal to that of the control containing penicillin and streptomycin. In vivo studies indicated no apparent toxicity. These silver uracil derivatives do not react with chlorides, hydroxides or iodides and are extremely toxic to Protozoa such as Paramecium and Euglena in vitro. One of thesecompounds (AgBU) was studied by Cs₂SO₄ density gradient ultracentrifugationwhich revealed no combination with the DNA of B. subtilis.

Mice infected with Trypanosoma rhodesiense were treatment concurrently with cis-diamminedichloroplatinum (II) (DDP), disulfiram, and hydration. Most of the mice (92.5 percent) were cured; inoculation of blood or suspensions of brain or heart from these animals did not produce disease in recipient mice. The dose of DDP needed to eliminate the trypanosomes, 3 milligrams per kilogram of body weight per day for 7 days, was lethally toxic unless the animals received disulfiram orally and subcutaneous injections of physiologic saline, which reduced the acute renal necrosis caused by DDP alone. Some mild to moderate reversible renal damage was noted upon pathologic examination of the treated mice.

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