Ropidoxuridine is a thymidine analogue and an oral prodrug of iododeoxyuridine that is easier to administer and less toxic with a more favorable therapeutic index in preclinical studies. Iododeoxyuridine demonstrated a survival advantage in Phase II studies in anaplastic astrocytoma, a type of brain tumor. Ropidoxuridine may help radiation therapy work better by making tumor cells more sensitive to the radiation therapy. In 2019, phase I clinical trials were ongoing to study the best dose of ropidoxuridine and its side effects in patients with metastatic malignant neoplasm in the brain and in patients with metastatic gastrointestinal cancer. First results showed that ropidoxuridine, combined with radiation therapy, was well-tolerated in patients with metastatic gastrointestinal cancer.

Ribavirin is a synthetic nucleoside analogue, which was first discovered and developed in 1970 by researchers from the International Chemical & Nuclear Corporation (ICN), today known as Valeant Pharmaceuticals. Ribavirin was initially approved for use in humans to treat pediatric respiratory syncytial virus infections (RSV). In cell cultures the inhibitory activity of ribavirin for RSV is selective. The mechanism of action is unknown. Reversal of the in vitro antiviral activity by guanosine or xanthosine suggests ribavirin may act as an analogue of these cellular metabolites. There were no other significant advancements in the treatment of hepatitis C until 1998, when the combination of ribavirin and interferon-alpha gained approval. Clinically, ribavirin showed a small, additive antiviral effect in combination with interferon, but its main effect was dose-dependent prevention of virological relapse. The mechanism by which the combination of ribavirin and an interferon product exerts its effects against the hepatitis C virus has not been fully established. However, it could be thorough the inhibition of inosine monophosphate dehydrogenase (IMPDH), which is the key step in de novo guanine synthesis, a requirement for viral replication.

Acyclovir is a synthetic antiviral nucleoside analogue. A screening program for antiviral drugs begun at Burroughs Wellcome in the 1960s resulted in the discovery of acyclovir in 1974. Preclinical investigation brought the drug to clinical trials in 1977 and the first form of the drug (topical) was available to physicians in 1982. Activity of acyclovir is greatest against herpes 1 and herpes 2, less against varicella zoster, still less against Epstein-Barr, and very little against cytomegalovirus. Acyclovir is an antiviral agent only after it is phosphorylated in infected cells by a viral-induced thymidine kinase. Acyclovir monophosphate is phosphorylated to diphosphate and triphosphate forms by cellular enzymes in the infected host cell where the drug is concentrated. Acyclovir triphosphate inactivates viral deoxyribonucleic acid polymerase.

Azathioprine remains one of the most important and widely prescribed drugs for immunosuppression/immunomodulation in autoimmune disease over 30 years after its introduction. Azathioprine is licensed for the treatment of only a limited range of autoimmune disorders, which is probably a reflection on the age of the drug. Widening the license for a drug is both costly and time consuming, and it would make no commercial sense for manufacturers to do so, at this late stage of life, for azathioprine. However, azathioprine is now so well established as an immunomodulating drug in autoimmune disorders that it represents the gold standard by which other drugs are compared. Azathioprine is indicated as an adjunct for the prevention of rejection in renal homotransplantation. It is also indicated for the management of active rheumatoid arthritis to reduce signs and symptoms. The combined use of azathioprine tablets with disease modifying anti-rheumatic drugs (DMARDs) has not been studied for either added benefit or unexpected adverse effects. The use of azathioprine tablets with these agents cannot be recommended. Azathioprine is a pro-drug, converted in the body to the active metabolite 6-mercaptopurine. Azathioprine acts to inhibit purine synthesis necessary for the proliferation of cells, especially leukocytes and lymphocytes. It is a safe and effective drug used alone in certain autoimmune diseases, or in combination with other immunosuppressants in organ transplantation. Its most severe side effect is bone marrow suppression, and it should not be given in conjunction with purine analogues such as allopurinol. The enzyme thiopurine S-methyltransferase (TPMT) deactivates 6-mercaptopurine. Genetic polymorphisms of TPMT can lead to excessive drug toxicity, thus assay of serum TPMT may be useful to prevent this complication. Azathioprine is metabolized to 6-mercaptopurine (6-MP). Both compounds are rapidly eliminated from blood and are oxidized or methylated in erythrocytes and liver; no azathioprine or mercaptopurine is detectable in urine after 8 hours. Activation of 6-mercaptopurine occurs via hypoxanthine-guanine phosphoribosyltransferase (HGPRT) and a series of multi-enzymatic processes involving kinases to form 6-thioguanine nucleotides (6-TGNs) as major metabolites.

Ropidoxuridine is a thymidine analogue and an oral prodrug of iododeoxyuridine that is easier to administer and less toxic with a more favorable therapeutic index in preclinical studies. Iododeoxyuridine demonstrated a survival advantage in Phase II studies in anaplastic astrocytoma, a type of brain tumor. Ropidoxuridine may help radiation therapy work better by making tumor cells more sensitive to the radiation therapy. In 2019, phase I clinical trials were ongoing to study the best dose of ropidoxuridine and its side effects in patients with metastatic malignant neoplasm in the brain and in patients with metastatic gastrointestinal cancer. First results showed that ropidoxuridine, combined with radiation therapy, was well-tolerated in patients with metastatic gastrointestinal cancer.

Ropidoxuridine is a thymidine analogue and an oral prodrug of iododeoxyuridine that is easier to administer and less toxic with a more favorable therapeutic index in preclinical studies. Iododeoxyuridine demonstrated a survival advantage in Phase II studies in anaplastic astrocytoma, a type of brain tumor. Ropidoxuridine may help radiation therapy work better by making tumor cells more sensitive to the radiation therapy. In 2019, phase I clinical trials were ongoing to study the best dose of ropidoxuridine and its side effects in patients with metastatic malignant neoplasm in the brain and in patients with metastatic gastrointestinal cancer. First results showed that ropidoxuridine, combined with radiation therapy, was well-tolerated in patients with metastatic gastrointestinal cancer.