​
H&E staining of mice liver sections showing protection against high blood triglyceride and MASLD induced by a high-fat diet in knockout mice.
Invention Summary:
Diabetes and obesity are the major contributors to the pathological accumulation of triglyceride (TAG) in the blood and liver, resulting in metabolic syndrome, myocardial infarction, stroke, vascular occlusive diseases, and metabolic dysfunction-associated steatotic liver disease (MASLD). MASLD has surpassed alcoholic liver disease as the most common chronic liver disease worldwide and can progress to hepatitis, cirrhosis, and hepatocellular carcinoma. Current treatment options for hypertriglyceridemia and MASLD are limited.
Unexpectedly, Rutgers researchers discovered that blocking hepatic glycerol metabolism by genetically deleting a key enzyme in the metabolic pathway, dramatically reduced fatty acid and TAG synthesis, protecting mice from diet-induced hypertriglyceridemia and liver steatosis. Novel synthetic GalNAc-siRNA conjugates were then developed that reproduced these effects found in gene ‘knockout’ animals. Based on these findings, new GalNAc-siRNA conjugates are being developed as a potential therapeutic strategy for hypertriglyceridemia and MASLD in humans.
Market Applications:
- A new drug class for management of hypertriglyceridemia associated with metabolic syndrome, myocardial infarction, stroke, and vascular occlusive diseases.
- A more effective treatment for MASLD and its complications.
- A safe treatment using GalNAc-siRNA conjugates that specifically target the liver.
Advantages:
- Novel approach to target specifically glycerol metabolism pathway in the liver.
- GalNAc-siRNA conjugates targets both fatty acid and substrate required for TAG synthesis.
Intellectual Property & Development Status: Provisional patent application filed. Available for licensing and/or research collaboration. For any business development and other collaborative partnerships contact: marketingbd@research.rutgers.edu
