Control of Microbial Growth via Novel Regulatory Events in the TORC Pathway

Case ID:
UA15-122
Invention:

This invention relates to systems, methods, and compositions for treating or preventing diseases associated with eukaryotic organisms, more particularly to methods and compositions for directly or indirectly triggering and/or permitting, or inhibiting Raptor/Kog1 aggregation in specific eukaryotes. This technology is a proposed class of novel drugs for the treatment of diseases caused by eukaryotic organisms, and a method of screening for such drugs. These antifungal and antiparasitic drugs will rely on a newly discovered cell signaling pathway that is present in many eukaryotes that cause infection in humans, but is not present in human cells. It is expected that these drugs could be used alone or in conjunction with other drugs to fight such infections.

Background:
Human diseases caused by eukaryotes include fungal infections and parasitic diseases. Parasitic diseases include not only those caused by helminths (parasitic worms), but also protozoans such as Plasmodium (a group of protozoans responsible for causing malaria), Leishmania (a group of protozoans responsible for causing leishmaniasis), and giardia.

 

Applications:

  • This proposed class of drugs can be used to treat infections caused by eukaryotes, including but fungal infections and infections caused by parasites such as various parasitic worms
  • May have efficacy in treating other infections caused by other eukaryotes, such as malaria, visceral leishmaniasis, giardiasis, and amebiasis

 

Advantages:

  • Because the cell signaling pathway that is the functional basis for these drugs is not present in human cells, it is expected that these drugs will potentially have a low side effect profile
  • Safe to use in conjunction with existing treatments
Patent Information:
Contact For More Information:
Jonathan Larson
Senior Licensing Manager, College of Science
The University of Arizona
jonathanlarson@arizona.edu
Lead Inventor(s):
Andrew Capaldi
Keywords: