This technology is a method to target impaired mTOR (mammalian target of rapamycin) signaling and endocytosis to rescue kidney function following acute kidney injury.
Current methods to treat acute kidney injury primarily target symptoms via supportive care such as dialysis, medications like diuretics, and fluid replacement. Furthermore, there are no pharmacological therapies to treat acute kidney injury and there is a high incidence and mortality rate for patients in intensive care units. Understanding the underlying molecular mechanisms of impaired kidney function can indicate relevant therapeutic targets and further differentiate the various types of acute kidney injury.
This technology describes the use of specific amino acids to target dysfunctional mTOR signaling and endocytosis to restore kidney function. Defective mTOR signaling, mediated by altered Sphingolipid Transporter 1 (Spns1) activity, can result in impaired endocytosis in the kidney. Administration of one or more amino acids, including leucine, isoleucine, threonine, histidine, valine, arginine, glutamine, or aspartic acid, can restore mTOR signaling and rescue the kidney from acute kidney injury, with the optimal amino acid selection dependent on injury etiology (ischemia-reperfusion-induced or rhabdomyolysis-induced AKI). By targeting the molecular mechanisms of acute kidney injury, this technology can help restore kidney function following injury, inform patient treatment decisions, and further inform pharmacological development in the treatment of acute kidney injury.
Patent Pending(US18/223,810)
IR CU21078
Licensing Contact: Kristin Neuman
