A nucleotide analogue synthesized by Zalcitabine is a human immunodeficiency virus reverse transcriptase inhibitor. After absorption, this product is converted into zetacitabine monophosphate by the action of deoxycytidine kinase in cells, and further metabolized into active dodeoxycytidine triphosphate under the action of other cellular enzymes to competitively inhibit HIV. Reverse transcriptase, thereby terminating the extension of viral DNA, impedes the process by which HIV reverses from RNA to DNA. In addition, ddCTP is more susceptible to binding to the nucleoside binding site of the viral reverse transcriptase to competitively inhibit endogenous 5' triphosphate, thereby further impeding the elongation of viral DNA. Zalcitabine has a higher affinity with viral reverse transcriptase and is currently the strongest anti-HIV infection in dideoxynucleosides. Clinically often combined with AZT or used interchangeably. The toxicity of Zalcitabine and AZT is manifested in different organs, and the myelosuppression of AZT occurs more frequently in 4-6 weeks. The peripheral neurotoxicity of this product is mostly in the larger dose and occurs after 6 weeks of administration. Combination or alternation enhances efficacy and reduces toxicity, and there is no cross-resistance between the two. Some in vitro assays have shown that Zalcitabine is the most potent nucleotide analogue in clinical applications and can completely inhibit HIV replication in human T lymphocytes at a concentration of 0.5 μmol/L. Since endogenous cytidine triphosphate competes for the active site of the reverse transcriptase, the in vitro activity of the product varies with different cell culture media, and the small cell level can regulate the antiviral activity of the product. When combined with recombinant α-interferon αA, dextran sulfate or dipyridamole, Zalcitabine has synergistic antiviral activity in vitro. When combined with zidovudine, there is additive effect in addition to synergistic effect.