Novel Mechanism Anti-Fungal with High Specificity

Case ID:

University of Arizona researchers have discovered a novel approach for treating fungal or yeast infections using a previously unstudied GPCR-like protein, which is integral to the regulation of cell growth in yeast cells. This protein and metabolic pathway is absent in higher-order animals, which provides a novel pathway for drugs to stop the growth of deadly fungal pathogens, such as drug resistant Candida glabrata. This technology may also provide a route to improved control of yeast growth in manufacturing.

This invention builds on a previous UArizona discovery of a novel cell signaling pathway/mechanism regulating cell growth and metabolism via TORC1, that is present in simple eukaryotes, such as fungi, yeast, and some parasites, but is not present in higher-order animals. To function correctly, cells set their growth rate based on a wide array of factors, such as nutrient, stress, and hormone signals. In eukaryotes, this fine-tuned control depends, in a large part, on a single, highly-conserved, signaling hub called the Target of Rapamycin kinase Complex I (TORC1). In the presence of pro-growth hormones and abundant nutrients, TORC1 drives growth by activating protein, ribosome, lipid, and nucleotide synthesis. In contrast, when nutrient or hormone levels drop, TORC1 is repressed, causing cells to switch from anabolic to catabolic metabolism, and eventually enter a quiescent state.

  • Solution to address drug resistant fungal infections
  • Treatment to slow or stop the growth of fungal infections
  • Control the growth/metabolism of yeast in an industrial setting


  • Selective mode of action for controlling yeast or fungal growth
  • Novel approach to address drug resistant fungal infection
Patent Information:
Contact For More Information:
Jonathan Larson
Senior Licensing Manager, College of Science
The University of Arizona
Lead Inventor(s):
Andrew Capaldi
Ryan Wallace
Eric Lu