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Therapy Overcoming Resistance of Refractory Prostate Cancer

Description:

 

Inhibition of cyclin-dependent-kinase 7 (CDK7) for treatment of refractory castration-resistant prostate cancer (CRPC) through reduction of androgen receptor transcriptional activity.

 

Technology

 

Prostate cancer (PCa) is the most common non-cutaneous malignancy and the second leading cause of cancer-related death in men of the western world. While effective therapies exist for clinically localized prostate cancer, progression to metastatic CRPC is essentially incurable. The Androgen receptor (AR) is the most frequent driver of resistance mechanism in CRPC patients.

 

Dr. Asangani and his team at the University of Pennsylvania have developed a new approach for the treatment of CRPC by blocking AR signaling at the transcriptional level. The researchers found that AR transcriptional activity relies on activation through a “phosphoswitch” catalyzed by CDK7. CDK7 phosphorylates the co-activator MED1 which forms a complex with AR leading to AR-mediated gene transcription. Inhibition of CDK7 disrupts the formation of this MED1-AR complex and blocks AR function. This approach allows to overcome several resistance mechanisms including AR amplification, mutation, and de novo androgen synthesis.

 

 

Applications

 

•       Treatment of advanced prostate cancer

•       Treatment of advanced prostate cancer refractory to second generation anti-androgens

•       Potential therapy for other hormonally driven cancers

 

Advantages

 

•       Treatment overcoming resistance of CRPC

 

Stage of Development

 

•       In vivo data using genetic and pharmacologic inhibition

 

Intellectual Property

 

Provisional patent application

 

Desired Partnerships

 

License

Co-development

 

Docket # 19-8898

 

 

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Patent Information:
For Information, Contact:
Linara Axanova
Associate Director, PSOM Licensing Group
University of Pennsylvania
axanova@upenn.edu
Inventors:
Irfan Asangani
Keywords: