{"meta":{"totalResults":10,"from":0},"results":[{"aliases":[{"type":"Synonym","name":"gemcitabine/cisplatin regimen"},{"type":"Synonym","name":"cisplatin-gemcitabine"},{"type":"Synonym","name":"cisplatin-gemcitabine regimen"},{"type":"Synonym","name":"cisplatin/gemcitabine"},{"type":"Synonym","name":"GC regimen"},{"type":"Synonym","name":"GemCis"},{"type":"Synonym","name":"gemcitabine-cisplatin"},{"type":"Synonym","name":"gemcitabine/cisplatin"},{"type":"Synonym","name":"gemcitabine-cisplatin regimen"}],"definition":{"html":"A regimen consisting of cisplatin and gemcitabine that can be used in the treatment of biliary tract, bladder, cervical, kidney, occult primary, pancreatic, ovarian, fallopian tube, primary peritoneal, and vulvar cancers, peritoneal and pleural mesothelioma, non-small cell lung cancer (NSCLC), gestational trophoblastic neoplasia (GTN), cancer of the nasopharynx, and ampullary adenocarcinoma.","text":"A regimen consisting of cisplatin and gemcitabine that can be used in the treatment of biliary tract, bladder, cervical, kidney, occult primary, pancreatic, ovarian, fallopian tube, primary peritoneal, and vulvar cancers, peritoneal and pleural mesothelioma, non-small cell lung cancer (NSCLC), gestational trophoblastic neoplasia (GTN), cancer of the nasopharynx, and ampullary adenocarcinoma."},"drugInfoSummaryLink":{"uri":"https://www.cancer.gov/about-cancer/treatment/drugs/GEMCITABINE-CISPLATIN","text":"GEMCITABINE-CISPLATIN"},"nciConceptId":"C63406","nciConceptName":"Cisplatin/Gemcitabine Regimen","termId":631940,"name":"Cisplatin/Gemcitabine Regimen","firstLetter":"c","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"cisplatin-gemcitabine-regimen"},{"aliases":[{"type":"USBrandName","name":"Acelarin"},{"type":"Synonym","name":"gemcitabine ProTide"},{"type":"CodeName","name":"NUC-1031"},{"type":"CodeName","name":"NUC 1031"}],"definition":{"html":"A pyrimidine analogue and a proprietary prodrug based on an aryloxy phosphoramidate derivative of gemcitabine with potential antineoplastic activity. Upon intravenous administration and cellular uptake, fosgemcitabine palabenamide is converted into the active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA replication; dFdCTP is incorporated into DNA, resulting in premature termination of DNA replication and eventually induction of apoptosis. With the phosphoramidate moiety on the gemcitabine monophosphate group, NUC-1031 has improved properties over its parent molecule: 1) is more lipophilic and accumulates in cancer cells by passive diffusion and does not require a nucleoside transporter, 2) as the agent is delivered in the monophosphate form, the first phosphorylation step by deoxycytidine kinase is not required, 3) this agent is not susceptible to deactivation by cytidine deaminase cleavage of the monophosphorylated form. Altogether, this may help overcome resistance to gemcitabine.","text":"A pyrimidine analogue and a proprietary prodrug based on an aryloxy phosphoramidate derivative of gemcitabine with potential antineoplastic activity. Upon intravenous administration and cellular uptake, fosgemcitabine palabenamide is converted into the active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA replication; dFdCTP is incorporated into DNA, resulting in premature termination of DNA replication and eventually induction of apoptosis. With the phosphoramidate moiety on the gemcitabine monophosphate group, NUC-1031 has improved properties over its parent molecule: 1) is more lipophilic and accumulates in cancer cells by passive diffusion and does not require a nucleoside transporter, 2) as the agent is delivered in the monophosphate form, the first phosphorylation step by deoxycytidine kinase is not required, 3) this agent is not susceptible to deactivation by cytidine deaminase cleavage of the monophosphorylated form. Altogether, this may help overcome resistance to gemcitabine."},"drugInfoSummaryLink":null,"nciConceptId":"C102752","nciConceptName":"Fosgemcitabine Palabenamide","termId":735822,"name":"fosgemcitabine palabenamide","firstLetter":"f","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"fosgemcitabine-palabenamide"},{"aliases":[{"type":"CodeName","name":"CP-4126"},{"type":"Synonym","name":"gemcitabine elaidate"},{"type":"CodeName","name":"CO-1.01"}],"definition":{"html":"A lipophilic, unsaturated fatty acid ester derivative of gemcitabine (dFdC), an antimetabolite deoxynucleoside analogue, with potential antineoplastic activity. Upon hydrolysis intracellularly by esterases, the prodrug gemcitabine is converted into the active metabolites difluorodeoxycytidine di- and tri-phosphate (dFdCDP and dFdCTP) by deoxycytidine kinase. dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis; dFdCTP is incorporated into DNA, resulting in DNA strand termination and apoptosis. Due to its lipophilicity, gemcitabine 5'-elaidic acid ester exhibits an increased cellular uptake and accumulation, resulting in an increased conversion to active metabolites, compared to gemcitabine. In addition, this formulation of gemcitabine may be less susceptible to deamination and deactivation by deoxycytidine deaminase.","text":"A lipophilic, unsaturated fatty acid ester derivative of gemcitabine (dFdC), an antimetabolite deoxynucleoside analogue, with potential antineoplastic activity. Upon hydrolysis intracellularly by esterases, the prodrug gemcitabine is converted into the active metabolites difluorodeoxycytidine di- and tri-phosphate (dFdCDP and dFdCTP) by deoxycytidine kinase. dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis; dFdCTP is incorporated into DNA, resulting in DNA strand termination and apoptosis. Due to its lipophilicity, gemcitabine 5'-elaidic acid ester exhibits an increased cellular uptake and accumulation, resulting in an increased conversion to active metabolites, compared to gemcitabine. In addition, this formulation of gemcitabine may be less susceptible to deamination and deactivation by deoxycytidine deaminase."},"drugInfoSummaryLink":null,"nciConceptId":"C79803","nciConceptName":"Gemcitabine Elaidate","termId":624375,"name":"gemcitabine 5'-elaidic acid ester","firstLetter":"g","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"gemcitabine-elaidate"},{"aliases":[{"type":"USBrandName","name":"Infugem"},{"type":"USBrandName","name":"Gemzar"},{"type":"Synonym","name":"difluorodeoxycytidine hydrochloride"},{"type":"ChemicalStructureName","name":"1-(2-oxo-4-amino-1,2-dihydropyrimidin-1-yl)-2-deoxy-2,2-difluororibose hydrochloride"},{"type":"ChemicalStructureName","name":"2'-deoxy-2',2'-difluorocytidine hydrochloride"},{"type":"ChemicalStructureName","name":"2'deoxy-2',2'-difluorocytidine hydrochloride"},{"type":"CodeName","name":"LY-188011"},{"type":"Abbreviation","name":"dFdCyd"},{"type":"CodeName","name":"LY188011"},{"type":"NSCNumber","name":"613327"},{"type":"CASRegistryName","name":"122111-03-9"},{"type":"ChemicalStructureName","name":"1-(2-oxo-4-amino-1,2-dihydropyrimidin-1-yl)-2-deoxy-2,2-difluororibose, hydrochloride"},{"type":"ChemicalStructureName","name":"2'deoxy-2',2'-difluorocytidine, hydrochloride"},{"type":"Synonym","name":"gemcitabine HCI"}],"definition":{"html":"The hydrochloride salt of an analogue of the antimetabolite nucleoside deoxycytidine with antineoplastic activity. Gemcitabine is converted intracellularly to the active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis; dFdCTP is incorporated into DNA, resulting in DNA strand termination and apoptosis.","text":"The hydrochloride salt of an analogue of the antimetabolite nucleoside deoxycytidine with antineoplastic activity. Gemcitabine is converted intracellularly to the active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis; dFdCTP is incorporated into DNA, resulting in DNA strand termination and apoptosis."},"drugInfoSummaryLink":{"uri":"https://www.cancer.gov/about-cancer/treatment/drugs/gemcitabinehydrochloride","text":"Gemcitabine Hydrochloride"},"nciConceptId":"C961","nciConceptName":"Gemcitabine Hydrochloride","termId":41213,"name":"gemcitabine hydrochloride","firstLetter":"g","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"gemcitabine-hydrochloride"},{"aliases":[{"type":"Synonym","name":"gemcitabine HCl oral"},{"type":"CodeName","name":"D07001-F4"}],"definition":{"html":"An orally available nanoparticle-based formulation containing the hydrochloride salt form of gemcitabine, a broad-spectrum antimetabolite and deoxycytidine analogue, with antineoplastic activity. The formulation consists of an oil-in-water emulsion in which gemicitabine is solubilized in the excipient matrix containing a mixture of oil and (co)surfactants. Upon oral administration, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA, resulting in premature termination of DNA replication and the induction of apoptosis. Further, dFdCDP inhibits ribonucleotide reductase and reduces the deoxynucleotide pool available for DNA synthesis. Compared to gemcitabine alone, the emulsion allows for increased oral bioavailability and decreases its susceptibility to deamination and deactivation by cytidine deaminase.","text":"An orally available nanoparticle-based formulation containing the hydrochloride salt form of gemcitabine, a broad-spectrum antimetabolite and deoxycytidine analogue, with antineoplastic activity. The formulation consists of an oil-in-water emulsion in which gemicitabine is solubilized in the excipient matrix containing a mixture of oil and (co)surfactants. Upon oral administration, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA, resulting in premature termination of DNA replication and the induction of apoptosis. Further, dFdCDP inhibits ribonucleotide reductase and reduces the deoxynucleotide pool available for DNA synthesis. Compared to gemcitabine alone, the emulsion allows for increased oral bioavailability and decreases its susceptibility to deamination and deactivation by cytidine deaminase."},"drugInfoSummaryLink":null,"nciConceptId":"C105613","nciConceptName":"Gemcitabine Hydrochloride Emulsion","termId":747250,"name":"gemcitabine hydrochloride emulsion","firstLetter":"g","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"gemcitabine-hydrochloride-emulsion"},{"aliases":[{"type":"CodeName","name":"FF-10832"},{"type":"CodeName","name":"FF10832"},{"type":"CodeName","name":"FF 10832"},{"type":"Synonym","name":"liposomal gemcitabine FF-10832"}],"definition":{"html":"A liposomal formulation in which gemcitabine, a broad-spectrum antimetabolite and deoxycytidine analogue, is encapsulated in liposomes, with potential antineoplastic activity. Upon administration of gemcitabine liposome FF-10832, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA, resulting in premature termination of DNA replication and the induction of tumor cell apoptosis. In addition, dFdCDP inhibits ribonucleotide reductase (RNR) and reduces the deoxynucleotide pool available for DNA synthesis. This inhibits tumor cell proliferation.","text":"A liposomal formulation in which gemcitabine, a broad-spectrum antimetabolite and deoxycytidine analogue, is encapsulated in liposomes, with potential antineoplastic activity. Upon administration of gemcitabine liposome FF-10832, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA, resulting in premature termination of DNA replication and the induction of tumor cell apoptosis. In addition, dFdCDP inhibits ribonucleotide reductase (RNR) and reduces the deoxynucleotide pool available for DNA synthesis. This inhibits tumor cell proliferation."},"drugInfoSummaryLink":null,"nciConceptId":"C200252","nciConceptName":"Gemcitabine Liposome FF-10832","termId":813598,"name":"gemcitabine liposome FF-10832","firstLetter":"g","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"gemcitabine-liposome-ff-10832"},{"aliases":[{"type":"CodeName","name":"LY2334737"}],"definition":{"html":"An orally available valproic acid ester of gemcitabine, a broad-spectrum antimetabolite with antineoplastic activity. Upon administration, gemcitabine prodrug LY2334737 is hydrolyzed by carboxylesterase 2 (CES2) and releases gemcitabine systemically over a period of time consistent with formation rate-limited kinetics. In turn, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate and triphosphate (dFdCDP and dFdCTP) by deoxycytidine kinase. dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA replication; dFdCTP is incorporated into DNA, resulting in premature termination of DNA replication and eventually the induction of apoptosis. Compared to gemcitabine, this prodrug is able to avoid hydrolysis in enterocytes and the portal circulation thus avoiding first pass metabolism and increasing systemic gemcitabine availability. In addition, the slow release of gemcitabine may enhance efficacy while lowering toxicity. CES2, a serine ester hydrolase, is expressed in certain tumors which may allow for increased conversion of gemcitabine at the tumor site, thus increasing cytotoxicity.","text":"An orally available valproic acid ester of gemcitabine, a broad-spectrum antimetabolite with antineoplastic activity. Upon administration, gemcitabine prodrug LY2334737 is hydrolyzed by carboxylesterase 2 (CES2) and releases gemcitabine systemically over a period of time consistent with formation rate-limited kinetics. In turn, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate and triphosphate (dFdCDP and dFdCTP) by deoxycytidine kinase. dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA replication; dFdCTP is incorporated into DNA, resulting in premature termination of DNA replication and eventually the induction of apoptosis. Compared to gemcitabine, this prodrug is able to avoid hydrolysis in enterocytes and the portal circulation thus avoiding first pass metabolism and increasing systemic gemcitabine availability. In addition, the slow release of gemcitabine may enhance efficacy while lowering toxicity. CES2, a serine ester hydrolase, is expressed in certain tumors which may allow for increased conversion of gemcitabine at the tumor site, thus increasing cytotoxicity."},"drugInfoSummaryLink":null,"nciConceptId":"C102856","nciConceptName":"Gemcitabine Prodrug LY2334737","termId":737787,"name":"gemcitabine prodrug LY2334737","firstLetter":"g","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"gemcitabine-prodrug-ly2334737"},{"aliases":null,"definition":{"html":"A first-line chemotherapy regimen consisting of gemcitabine and erlotinib used for the treatment of locally advanced and metastatic pancreatic cancer.","text":"A first-line chemotherapy regimen consisting of gemcitabine and erlotinib used for the treatment of locally advanced and metastatic pancreatic cancer."},"drugInfoSummaryLink":null,"nciConceptId":"C63503","nciConceptName":"Erlotinib/Gemcitabine Regimen","termId":657337,"name":"gemcitabine-erlotinib regimen","firstLetter":"g","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"erlotinib-gemcitabine-regimen"},{"aliases":[{"type":"Synonym","name":"GEM-OX regimen"},{"type":"Synonym","name":"GEMOX regimen"}],"definition":{"html":"A regimen consisting of gemcitabine and oxaliplatin used for the treatment of biliary adenocarcinoma,  pancreatic cancer, hepatocellular cancer, and testicular cancer. This regimen is currently being studied in a variety of other cancers.","text":"A regimen consisting of gemcitabine and oxaliplatin used for the treatment of biliary adenocarcinoma,  pancreatic cancer, hepatocellular cancer, and testicular cancer. This regimen is currently being studied in a variety of other cancers."},"drugInfoSummaryLink":{"uri":"https://www.cancer.gov/about-cancer/treatment/drugs/GEMCITABINE-OXALIPLATIN","text":"GEMCITABINE-OXALIPLATIN"},"nciConceptId":"C64833","nciConceptName":"GemOx Regimen","termId":751389,"name":"gemcitabine-oxaliplatin regimen","firstLetter":"g","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"gemox-regimen"},{"aliases":[{"type":"USBrandName","name":"GemRIS"},{"type":"CodeName","name":"TAR-200"},{"type":"CodeName","name":"TAR 200"}],"definition":{"html":"A controlled-release intravesical system consisting of a small flexible tube-like device with a solid core composed of gemcitabine, a broad-spectrum antimetabolite and deoxycytidine analogue, with antineoplastic activity. Upon placement of the gemcitabine-releasing intravesical system (GemRIS) into the bladder, gemcitabine is gradually and continuously released from the system over an extended period of time before being removed from the bladder. Upon release, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA, resulting in premature termination of DNA replication and the induction of apoptosis of bladder tumor cells. In addition, dFdCDP inhibits ribonucleotide reductase (RNR) and reduces the deoxynucleotide pool available for DNA synthesis.","text":"A controlled-release intravesical system consisting of a small flexible tube-like device with a solid core composed of gemcitabine, a broad-spectrum antimetabolite and deoxycytidine analogue, with antineoplastic activity. Upon placement of the gemcitabine-releasing intravesical system (GemRIS) into the bladder, gemcitabine is gradually and continuously released from the system over an extended period of time before being removed from the bladder. Upon release, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA, resulting in premature termination of DNA replication and the induction of apoptosis of bladder tumor cells. In addition, dFdCDP inhibits ribonucleotide reductase (RNR) and reduces the deoxynucleotide pool available for DNA synthesis."},"drugInfoSummaryLink":null,"nciConceptId":"C150807","nciConceptName":"Gemcitabine-Releasing Intravesical System","termId":793540,"name":"gemcitabine-releasing intravesical system","firstLetter":"g","type":"DrugTerm","termNameType":"PreferredName","prettyUrlName":"gemcitabine-releasing-intravesical-system"}],"links":null}