NCT02581501

Prospective Phase I Study of GAX for Metastatic Pancreatic Cancer

Prospective Phase I Study of Gax (Gemcitabine, ABRAXANE, and Xeloda) for Metastatic Pancreatic Cancer Protocol # TSH - APG - 2015-01

• Status: Withdrawn
• Phase: Phase 1
• Study type: Interventional
• Enrollment: 0 (actual)
• Sponsor: Stamford Hospital · Academic / Other
• Sex: All
• Age: 18 Years
• Healthy volunteers: Not accepted

Summary

GAX represents a novel approach to the development of cancer chemotherapy agents in pancreatic cancer and is based upon extensive laboratory investigations for the induction of apoptosis in pancreatic carcinoma cells.

Detailed description

It is the investigators expectation that this combination will induce apoptotic pathways downstream of biochemical mechanisms of resistance and synergistically induce pathways for apoptosis that are non-p53 dependent, which have not been previously explored in chemotherapy trials for this cancer. ABRAXANE® is novel in that it induces apoptosis to the same degree in mutant and wt p53 cancers. Mutant p53 tumors occur in 80-90% of PC and mutant p53 is thought of as one of the major mechanisms of drug resistance. Furthermore, the investigators will be starting Xeloda and gemcitabine at slightly lower doses than the initial GTX studies. This is because the investigators have found that the efficacy is maintained at these slightly lower doses while side effects are minimized. The reason that GTX works at lower doses, as well as higher doses, is the synergy between drugs. Drug regimens that are synergistic can maintain their antitumor effect at doses lower than in non-synergistic regimens, but must maintain their dose intensity to achieve their anti-tumor effect. RECIST 1.1 criteria will be utilized for judging response, progression and stable disease. Overall assessment of the data will be by intention to treat analysis (ITT).

Conditions

• Pancreatic Cancer

Interventions

Type	Name	Description
DRUG	GAX - Gemcitabine, Abraxane and Xeloda	GAX represents a novel approach to the development of cancer chemotherapy agents in pancreatic cancer and is based upon extensive laboratory investigations for the induction of apoptosis in pancreatic carcinoma cells. It is our expectation that this combination will induce apoptotic pathways downstream of biochemical mechanisms of resistance and synergistically induce pathways for apoptosis that are non-p53 dependent, which have not been previously explored in chemotherapy trials for this cancer.

Timeline

• Start date: 2016-02-01
• Primary completion: 2016-12-01
• Completion: 2016-12-01
• First posted: 2015-10-21
• Last updated: 2019-04-18

Locations

1 site across 1 country: United States