At a glance
ClinicalIndex Comparison Record- ✓Histologically or cytologically confirmed high-grade (grade 2 or 3) serous ovarian, fallopian tube, or primary peritoneal cancer; mixed histology eligible if serous is dominant
- ✓Measurable disease by RECIST 1.1 criteria
- ✓Evidence of PI3K/AKT pathway defect: PTEN loss by immunohistochemistry OR PIK3CA/AKT mutation, both in CLIA-certified assay
- ✓Prior first-line platinum-based chemotherapy
- ✕Known brain metastases
- ✕Prior Akt or PI3K pathway inhibitors including mTOR inhibitors
- ✕Chemotherapy or radiotherapy within 4 weeks (6 weeks for nitrosoureas or mitomycin C) prior to study entry, or unrecovered toxicity >grade 1 from earlier agents
- ✕Diabetes or hyperglycemia not well controlled; fasting glucose >130 mg/dL or HgbA1c >7.5 mg/dL; insulin-dependent diabetes excluded
Standardized by ClinicalIndex from the ClinicalTrials.gov record · verify against the source.
A Phase II Study of MK-2206 in the Treatment of Recurrent High-Grade Serous Platinum-Resistant Ovarian, Fallopian Tube, or Primary Peritoneal Cancer
In Brief
A Phase 2 clinical trial evaluating Akt Inhibitor MK2206 and Laboratory Biomarker Analysis for Ovarian Sarcoma and 3 related conditions. Completed, enrolled 6 participants across 6 sites.
Detailed Summary
Akt inhibitor MK2206 is a drug that may stop cancer cells from growing by blocking a protein called protein kinase B (AKT) inside the cell. AKT interacts with other proteins in the cell that are part of the P13K/AKT pathway, a pathway that is know to play a role in the growth of cancer cells. Mutations in P13K or in AKT, or changes in another protein called phosphatase and tensin homolog (PTEN) in this pathway can lead it to become more active than is normal. This study investigates how effective MK-2206 is in treating ovarian, fallopian tube, or primary peritoneal cancer where there are mutations in P13K or AKT or low levels of PTEN.
Study Details
Timeline
Interventions
Given PO
Correlative studies