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|Therapy Name||Gemcitabine + Nimotuzumab|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|Gemcitabine||Gemzar||Difluorodeoxycytidine Hydrochlorothiazide|LY-188011||Chemotherapy - Antimetabolite 11||Gemzar (gemcitabine) is converted in cells to difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP), which act to inhibit ribonucleoside reductase and as a deoxynucleotide analog respectively, resulting in DNA strand termination and apoptosis (NCI Drug Dictionary).|
|Nimotuzumab||Theraloc|hR3||EGFR Antibody 29||Nimotuzumab is a humanized anti-EGFR antibody that blocks EGFR signaling, resulting in anti-tumor activity (PMID: 25842083).|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|Unknown unknown||pancreatic cancer||not applicable||Gemcitabine + Nimotuzumab||Phase II||Actionable||In a Phase IIb trial, the combination of Nimotuzumab and Gemzar (gemcitabine) resulted in improved median overall survival (8.6 mo vs. 6.0 mo), overall survival rate at 12 months (34% vs. 19%) and median progression-free survival (5.1 mo vs. 3.4 mo) compared to Gemzar (gemcitabine) plus placebo in pancreatic cancer patients, with patients with wild-type KRAS demonstrating an overall survival rate at 12 months of 53.8% vs. 27.8% in patients harboring KRAS mutations (PMID: 28961832).||28961832|
|Clinical Trial||Phase||Therapies||Title||Recruitment Status|