{"id":"CU21078","slug":"reactivation-of-mtor-to-treat--CU21078","source":{"id":"CU21078","dataset":"techtransfer","title":"Reactivation of mTOR to treat acute kidney injury","description_":"<p>This technology is a method to target impaired mTOR (mammalian target of rapamycin) signaling and endocytosis to rescue kidney function following acute kidney injury.</p>\r\r<h2>Unmet Need: Therapeutic method to treat acute kidney injury by targeting impaired signaling pathways</h2>\r\r<p>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.</p>\r\r<h2>The Technology: Restoration of kidney function via amino acid replacement</h2>\r\r<p>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.</p>\r\r<h2>Applications:</h2>\r\r<ul>\r<li>Treatment of acute kidney injury, including ischemic, ischemia-reperfusion-induced, and rhabdomyolysis-induced AKI </li>\r<li>Treatment of diminished kidney function or renal failure due to AKI </li>\r<li>Research model for studying mTOR signaling and kidney function </li>\r<li>Research tool to identify different types of acute kidney injury</li>\r<li>Identification of therapeutic targets for acute kidney injury</li>\r</ul>\r\r<h2>Advantages:</h2>\r\r<ul>\r<li>Disease modifying treatment for acute kidney injury</li>\r<li>Can restore kidney function following ischemic or rhabdomyolysis-induced injury</li>\r<li>Etiology-specific amino acid selection for tailored treatment</li>\r<li>Compatible with current methods used for supportive care</li>\r<li>Amenable to intravenous infusion and other standard administration routes</li>\r</ul>\r\r<h2>Lead Inventor:</h2>\r\r<p><a href=\"https://www.pathology.columbia.edu/profile/jonathan-m-barasch-md\">Jonathan Barasch, M.D, Ph.D.</a></p>\r\r<h2>Patent Information:</h2>\r\r<p>Patent Pending(<a href=\"https://patents.google.com/patent/US20230364046A1/en?oq=18%2f223%2c810\">US18/223,810</a>)</p>\r\r<h2>Related Publications:</h2>\r\r<ul>\r<li><a href=\"https://pmc.ncbi.nlm.nih.gov/articles/PMC11563593/\">Beenken A, Shen T, Jin G, Ghotra A, Xu K, Nesanir K, Sturley RE, Vijayakumar S, Khan A, Levitman A, Stauber J, Chavez EY, Robbins-Juarez SY, Hao L, Field TB, Erdjument-Bromage H, Neubert TA, Shapiro L, Qiu A, Barasch J. “Spns1 is an iron transporter essential for megalin-dependent endocytosis” Am J Physiol Renal Physiol. 2024 Nov 1; 327(5): F775-F787.</a></li>\r</ul>\r\r<h2>Tech Ventures Reference:</h2>\r\r<ul>\r<li><p>IR CU21078</p></li>\r<li><p>Licensing Contact: <a href=\"mailto:techtransfer@columbia.edu\">Kristin Neuman</a></p></li>\r</ul>","tags":["Acid","Acute kidney injury","Amino acid","Arginine","Assessment of kidney function","Endocytosis","Etiology","Fluid replacement","Glutamine","Hemodialysis","Histidine","Intravenous therapy","Ischemia","Isoleucine","Kidney","Kidney failure","Leucine","Mortality rate","Sirolimus","Sphingolipid","Therapy","Threonine","Valine"],"file_number":"CU21078","collections":[],"meta_description":"Restore kidney function after AKI by amino-acid–driven mTOR signaling rescue, tailoring treatment to injury type.","apriori_judge_output":"{\"scores\":{\"novelty\":4.0,\"potential_impact\":4.0,\"readiness\":2.0,\"scalability\":3.0,\"timeliness\":3.0},\"weighted_score\":3.3,\"risks\":[\"Biological mechanism complexity and potential off-target effects of mTOR modulation\",\"Safety/toxicity concerns in AKI patient population\",\" translational gap from preclinical to clinical trials\",\"Regulatory uncertainty for pathway-targeted therapies in AKI\"],\"one_sentence_take\":\"Strong novelty with disease-modifying potential, but readiness and translational risk warrant cautious advancement and rigorous safety profiling.\"}","inventors":["Andong Qiu","Andrew Beenken","Jonathan M. Barasch"],"manager":"Kristin Neuman","depts":["Medicine"],"divs":["Columbia University Medical Center (CUMC)"],"date_released":"2023-04-03"},"highlight":{},"matched_queries":null,"score":0.0}