2′-Deoxycytidine (deoxyC) is one of the deoxy nucleosides, which after phosphorylation to dCTP is used to synthesize DNA via various DNA polymerases or reverse transcriptases. Deoxycytidine is phosphorylated by deoxycytidine kinase (dCK). This enzyme catalyzes the initial conversion of the nucleosides deoxyadenosine (dA), deoxyguanosine (dG), and deoxycytidine (dC) into their monophosphate forms, with subsequent phosphorylation to the triphosphate forms performed by additional enzymes.

Cordycepin, or 3'-deoxyadenosine, is a derivative of the nucleoside adenosine, differing from the latter by the absence of the hydroxy group in the 3' position of its ribose part. Cytostatic effect of cordycepin is due to incorporation of phospho-cordycepin into mRNA and inhibition of mRNA synthesis. Cordycepin exhibit rapid antidepressant effect due to potentiation of AMPA receptors

Carmofur, also known as 5-fluoro-N-hexyl-2,4-dioxo-pyrimidine-1-carboxamide and as 1-hexylcarbamoyl-5-fluorouracil, is a pyrimidine analogue which acts as an antineoplastic agent through inhibition of thymidylate synthase. It has been used in the treatment of breast and colorectal cancer. Carmofur is approved in Japan for the treatment of cancer.

Broxuridine (5-Bromo-2-deoxyuridine, BrdU) is a thymidine analogue that is incorporated into replicating DNA. BrdU taken up by cells is phosphorylated and incorporated into DNA in place of dT. Although originally designed as a chemotherapeutic agent, sublethal concentrations of BrdU have long been known to alter the growth and phenotype of a wide range of cell types. The most popular use of BrdU is as a tracer of DNA synthesis. The other well-known use of BrdU is as a DNA photosensitizer. BrdU substitution of dT in DNA sensitizes it to near-UV light, and cells with BrdU-substituted DNA cannot survive after exposure to near-UV light. BUdR has side effects on cell functions. Cell growth can be inhibited, normal development of differentiating systems be perturbed, activities of specific enzymes be reduced. Mutagenic effects of BUdR are interpreted as reflections of a mispairing of BUdR in its rare enol form. Effects of BUdR which can be reversed by addition of thymidine are not likely to be mutagenic. As another mechanism of action of BUdR has been suggested that incorporation of BUdR into DNA alters the pattern of transcription.

Buciclovir is an acyclic guanosine analog with activity against herpes simplex virus (HSV). Buciclovir is phosphorylated to its triphosphate form by HSV thymidine kinase in infected cells and acts as a specific inhibitor of the viral DNA polymerase. Buciclovir inhibited DNA synthesis, not RNA synthesis, and prevented an increase in the size of newly synthesized DNA. Topical treatment initiated early after infection was efficacious, in contrast to topical treatment delayed 24 h or more. Systemic treatment of infected mice could not prevent the spread of the virus to the brain and mortality. Systemically administered buciclovir had an effect in guinea pigs, even after the delayed onset of treatment, but this effect required high doses of the drug. Buciclovir has only a limited effect against herpesvirus infections once the virus is present in the nervous systems of infected

5-iodo-2'-deoxycytidine (IBACITABINE) is an anti-herpetic agent. Experiments with a tumor mouse model have revealed, that radioiodinated compound, (131)I-5-iodo-2'-deoxycytidine was a promising single photon emission computed tomography probe for imaging proliferation.

Brivudine (trade names Zostex, Mevir, Brivir, among others) is an antiviral drug used in the treatment of herpes zoster ("shingles"). Brivudine is an analog of the nucleoside thymidine. The active compound is brivudine 5'-triphosphate, which is formed in subsequent phosphorylations by viral (but not human) thymidine kinase and presumably by the nucleoside-diphosphate kinase. Brivudine 5'-triphosphate works because it is incorporated into the viral DNA, but then blocks the action of DNA polymerases, thus inhibiting viral replication. Brivudine is used for the treatment of herpes zoster in adult patients. It is taken orally once daily, in contrast to aciclovir, valaciclovir, and other antivirals. A study has found that it is more effective than aciclovir, but this has been disputed because of a possible conflict of interest on part of the study authors. The drug is contraindicated in patients undergoing immunosuppression (for example because of an organ transplant) or cancer therapy, especially with fluorouracil (5-FU) and chemically related (pro)drugs such as capecitabine and tegafur, as well as the antimycotic drug flucytosine, which is also related to 5-FU. It has not been proven to be safe for children and pregnant or breastfeeding women. The drug is generally well tolerated. The only common side effect is nausea (in 2% of patients). Less common side effects (<1%) include a headache, increased or lowered blood cell counts (granulocytopenia, anemia, lymphocytosis, monocytosis), increased liver enzymes, and allergic reactions. Brivudine is approved for use in a number of European countries including Austria, Belgium, Germany, Greece, Italy, Portugal, Spain, and Switzerland.

Cyclocytidine (also known as Ancitabine) is the prodrug of cytarabine, which is structurally similar to human deoxycytidine to be incorporated into human DNA and then kills the cell. Cyclocytidine was introduced as an antineoplastic agent for the treatment of lymphatic leukemia, sinus acceleration and an increase in systemic blood pressure. Cyclocytidine in combination with amsacrine were effective retrieval therapy for pediatric patients with acute nonlymphoblastic leukemia who were in relapse or unresponsive to frontline therapy.

Enocitabine is an anti-cancer nucleoside that was developed for the treatment of acute myeloid leukemia. Although the exact mechanism of its action is unknow, Enocitabine effectively inhibits tumor cell growht in vitro and the inhibition is supposed to be related to its metabolism to Ara-C, an inhibitor of DNA polymerase. The drug was approved in Japan and Korea and was marketed under the name Sunrabin, however, its current marketing status is unknown and is assumed to be discontinued.

Doxifluridine is a 5-fluorouracil prodrug that is being tested for the treatment of cancer. The cleavage into 5-fluorouracil occurs enzymatically via a nucleoside phosphorylase. Thus, doxifluridine is not active by itself and its antitumor activity is related to its metabolic conversion into 5-fluorouracil. Doxifluridine has neurotoxic adverse effects.