Nucleoside antimetabolite that undergoes intracellular phosphorylation to activated diphosphate and triphosphate forms.
A nucleoside analog of deoxycytidine.
Undergoes metabolic activation by kinases to form a cytotoxic trinucleotide in the cell.
Metabolic inactivation is by deamination is catalyzed by cytidine deaminase or after phosphorylation by deoxycytidylate deaminase.
Structure similar to cytarbrine.
Exerts effects by interacting with genomic DNA.
A nucleoside analogue that when incorporated into DNA inhibits DNA polymerase during cell replication or repair.
Gemcitabine is a pyrimidine analogue that is metabolized intracellularly to an active nucleotide.
It inhibits ribonucleotide reductase and competes with deoxycytidine triphosphate for incorporation into DNA.
It is cell-cycle specific for the S phase.
Gemcitabine, in combination with paclitaxel, is indicated as a first-line treatment for metastatic breast cancer after the failure of prior anthracycline-containing adjuvant chemotherapy.
Induces an S-phase arrest and triggers apoptosis.
Fixed dose rate of 10mg/m2/min allows maximum intracellular accumulation of the active triphosphate form of the drug.
Phase II studies reveal response rates of 4-18% in soft tissue sarcomas.
A potent radiation sensitizer in vitro and in vivo.
In a phase III randomized study og the addition of gemcitabine to concurrent cisplatin chemoradiotherapy in locally advanced cervical cancer: 515 treatment naive stage IIB to IVA disease patients-3 year PFS significantly improved in gemcitabine arm, as was time to progression, and overall survival (Duenas-
May be associated with posterior reversible encephalopathy syndrome.