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1. Phenothiazines and structurally related drugs are effective in eliminating bacterial plasmids. 2. Charge transfer complex formation between chlorpromazine and xanthine dyes with different electron acceptor activities (e.g. fluorescein, eosin, erythrosin and rose bengal) was detected by differential spectrophotometry. Charge transfer complexes were formed between the strong electron acceptor rose bengal and various tricyclic drugs. 3. On the basis of the wavelength shift, the binding energies of drugs and dyes were estimated. 4. The temperatures dependence of the reaction indicates charge transfer complex formation rather than a chemical reaction between drugs and dyes. 5. The anti-plasmid action of the phenothiazines was decreased in the presence of xanthine dyes. As a consequence of competitive inhibition between bacterial binding sites and xanthine dyes, the binding energy of drugs in the plasmid replication system could be determined in the presence of dyes. 6. Drugs with binding energies in the range of 0.23-2.31 kcal/mol can inactivate the plasmid replication system.

A newly synthetized rutin derivative, rutin-N-mustard, showed a marked antiproliferative effect on NK/Ly ascites tumour cells in vivo. When administered i.p. or i.v., this compound increased the survival time of the animals, but oral administration had no such effect. The drug was not able to kill the tumour cells, since the chromium release from the rutin-N-mustard-treated tumour cells was the same as in the case of the controls. Tumour growth was completely inhibited in the animals when the cells were pretreated with 100 mg/kg rutin-N-mustard before transplantation. The results also showed that rutin-N-mustard has little effect on the xenogenization of NK/Ly tumour cells. We presume that the antiproliferative action of rutin-N-mustard is due to its alkylating activity.

The binding between the HIV surface protein, gp120, and the CD4 coreceptor is known to be initiated by electrostatic interactions. Because of the ability of chlorpromazine to interact with proteins by charge transfer, we tested several derivatives for their ability to block binding of HIV to CD4+ cells. We have shown that 7,8-dioxo-chlorpromazine blocks binding of fluorescein isothiocyanate-labeled anti-Leu3a and rgp120 to peripheral human blood T4 cells and blocks syncytia formation between gp120- and CD4-expressing cells. We also found that 7,8-dioxo-chlorpromazine blocks HIV infectivity of H9 cells and acts synergistically with zidovudine.

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