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Home / Drugs / Starting with G / Gemcitabine

Gemcitabine is a nucleoside analog used as chemotherapy. It is marketed as Gemzar® by Eli Lilly and Company. As with fluorouracil and other analogues of pyrimidines, the drug replaces one of the building blocks of nucleic acids, in this case cytidine, during DNA replication. The process arrests tumor growth, as new nucleosides cannot be attached to the "faulty" nucleoside, resulting in apoptosis (cellular "suicide"). Gemcitabine is used in various carcinomas: non-small cell lung cancer, pancreatic cancer, bladder cancer and breast cancer. It is being investigated for use in oesophageal cancer, and is used experimentally in lymphomas and various other tumor types.
Gemcitabina [INN-Spanish]
Gemcitabine HCl
Gemcitabine hydrochloride
Gemcitabinum [INN-Latin]
CategoriesAntineoplastic Agents
Antiviral Agents
Radiation-Sensitizing Agents
Enzyme Inhibitors
Immunosuppressive Agents
Antimetabolites, Antineoplastic
ManufacturersTeva parenteral medicines inc
Eli lilly and co


For the first-line treatment of patients with metastatic breast cancer, locally advanced (Stage IIIA or IIIB), or metastatic (Stage IV) non-small cell lung cancer and as first-line treatment for patients with adenocarcinoma of the pancreas.


Gemcitabine is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the "S" phase (or DNA synthesis phase of the cell cycle), stopping normal development and division. Gemcitabine blocks an enzyme which converts the cytosine nucleotide into the deoxy derivative. In addition, DNA synthesis is further inhibited because Gemcitabine blocks the incorporation of the thymidine nucleotide into the DNA strand.

mechanism of action

Gemcitabine inhibits thymidylate synthetase, leading to inhibition of DNA synthesis and cell death. Gemcitabine is a prodrug so activity occurs as a result of intracellular conversion to two active metabolites, gemcitabine diphosphate and gemcitabine triphosphate by deoxycitidine kinase. Gemcitabine diphosphate also inhibits ribonucleotide reductase, the enzyme responsible for catalyzing synthesis of deoxynucleoside triphosphates required for DNA synthesis. Finally, Gemcitabine triphosphate (diflurorodeoxycytidine triphosphate) competes with endogenous deoxynucleoside triphosphates for incorporation into DNA.


Myelosuppression, paresthesias, and severe rash were the principal toxicities, LD50=500 mg/kg (orally in mice and rats)


Transformed via nucleoside kinases to two active metabolites, gemcitabine diphosphate and gemcitabine triphosphate. Can also undergo deamination via cytidine deaminase to an inactive uracil metabolite (dFdU).



half life

Short infusions ranged from 32 to 94 minutes, and the value for long infusions vary from 245 to 638 minutes, depending on age and gender.

drug interactions

Acenocoumarol: Gemcitabine may increase the anticoagulant effect of acenocoumarol.

Anisindione: Gemcitabine may increase the anticoagulant effect of anisindione.

Bivalirudin: Gemcitabine may enhance the adverse/toxic effect of Bleomycin. The risk of pulmonary toxicity may be increased. Use extreme caution if using gemcitabine and bleomycin in combination. Monitor for the development of pulmonary toxicity.

Dicumarol: Gemcitabine may increase the anticoagulant effect of dicumarol.

Paclitaxel: Paclitaxel increases the effect/toxicity of gemcitabine

Temsirolimus: Co-administration of Temsirolimus and Gemcitabine may result in serious adverse drug reactions.

Trastuzumab: Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events.

Warfarin: Gemcitabine may increase the anticoagulant effect of warfarin.