Bumped-Kinase Inhibitors as Castrate-Resistant Prostate Cancer Drugs
Abstract
Recurrence through continued androgen receptor (AR) signaling remains the driver in greater than 90 percent of men who become resistant to therapy. New treatments are urgently needed for this progressive disease. Therapies that inhibit factors important in activating AR may be the most successful against these constitutively active variants and prevent further progression of CRPC. Kinase inhibitors have the potential to inhibit androgen receptor signaling and function. Purpose and Scope of Research: Establish that BKIs are specific candidates for treatment of AR-driven. BKIs work as PK inhibitors and act directly or indirectly by inhibition of AR Ser81 phosphorylation, which is necessary to activate AR to stimulate transcription. Develop new BKIs for treatment of AR- driven castrate resistant prostate cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2019
- Accession Number
- AD1086392
Entities
People
- Stephen R Plymate
Organizations
- University of Washington