Inducing Chemotherapeutic Sensitivity in Hyper-Transcription Diseases

Tech ID:
HSC-1494

This discovery is a method for the induction of sensitivity in tumor cells to a synergistic combination of PARP1 and ATR inhibition. It is applicable to hyper-transcription diseases , primarily cancers, including: Ewing sarcoma, acute myeloid leukemia, breast cancer, myelodysplastic syndrome, and possibly even Alzheimers and ALS.

 

Background:

Modern treatment options for cancer are multi-modal, involving varying combinations of chemotherapy regimens, surgical resection procedures, and radiation. However, these treatment options are often limited in their efficacy due to side-effect and toxicity driven dosage limits of the chemotherapy drugs, acquired resistance to the drugs used, and failure to control the growth or spread of the tumor.

 

The ability of this new technology to render tumor cells sensitive to both PARPA1 and ATR inhibitors provides a synergistic therapeutic approach that can increase efficacy while reducing the required dosages and associated side effects.  It may provide a new treatment option for diseases that currently lack a truly effective therapeutic regimen.

 

Commercial Applications & Advantages:

This new technology is primarily applicable to the field of oncology, specifically cancers marked by hyper-transcription.  However, it may also prove beneficial in Alzheimers and ALS.  It provides the following advantages over the current standard of care:

  • New therapeutic target which may provide higher efficacy
  • Ability to increase sensitivity to existing chemotherapeutics
  • Synergism of therapeutic combination may reduce effective dosage needed, thus reducing toxic side effects
  • Diagnostic assay to determine applicability of treatments

 

For information contact:
John Fritz
Sr. Business Development Manager
FRITZJA@UTHSCSA.EDU
210-562-4033
Inventors:
Alexander Bishop
Aparna Gorthi
Carolina Romero
Liesl Lawrence
Patent Information:

United States - Provisional

Patent No.

Status: Pending

Keywords: