This technology describes ILDR2 as a target that can be used to develop first-in-class therapeutics for the treatment of non-alcoholic steatohepatitis (NASH) and other metabolic diseases.
Unmet Need: Effective targets for treatment of fatty liver disease
Non-alcoholic steatohepatitis (NASH) is an advanced form of fatty liver disease which is common in individuals with metabolic syndrome such as obesity or diabetes. NASH can progress to cirrhosis and hepatocellular carcinoma. There is currently no approved treatment for NASH and patients rely on dietary and lifestyle changes for managing the disease, but these approaches are hard to sustain and ineffective for many patients. There remains an urgent need to identify appropriate molecular targets and develop efficacious therapeutics for treating NASH.
The Technology: ILDR2 as a therapeutic target for NASH and other metabolic disorders
This technology describes ILDR2 as a potential therapeutic target to treat metabolic disease. ILDR2 regulates lipid metabolism in the liver and maintains lipoprotein homeostasis. Vector-mediated overexpression of ILDR2 in a preclinical animal model of obesity rescues hepatic steatosis. In view of this, expression of ILDR2 offers a promising strategy for therapeutic intervention against a range of metabolic diseases, including NASH, dyslipidemia, and obesity.
This technology has been validated in vivo using ILDR2 knockdown and overexpression techniques.
Applications:
- ILDR2 vector-based therapies for metabolic disease
- Biological and pharmacological methods for ILDR2 upregulation
- Combinatorial therapies for metabolic disease
Advantages:
- Offers vector and non-vector methods for increasing ILDR2 expression
- Treats a variety of metabolic diseases (e.g. NASH, dyslipidemia, obesity, etc.)
- Effective in reducing liver fat content
Lead Inventor:
Rudolph L. Leibel, MD
Patent Information:
Patent Status
Related Publications:
Millings EJ, De Rosa MC, Fleet S, Watanabe K, Rausch R, Egli D, Li G, Leduc CA, Zhang Y, Fischer SG, Leibel RL. “ILDR2 has a negligible role in hepatic steatosis” PLoS One. 2018 May 30; 13(5).
Watanabe K, Watson E, Cremona ML, Millings EJ, Lefkowitch JH, Fischer SG, LeDuc CA, Leibel RL. “ILDR2: an endoplasmic reticulum resident molecule mediating hepatic lipid homeostasis” PLoS One. 2013 Jun 24; 8(6).
Dokmanovic-Chouinard M, Chung WK, Chevre JC, Watson E, Yonan J, Wiegand B, Bromberg Y, Wakae N, Wright CV, Overton J, Ghosh S, Sathe GM, Ammala CE, Brown KK, Ito R, LeDuc C, Solomon K, Fischer SG, Leibel RL. “Positional cloning of “Lisch-Like”, a candidate modifier of susceptibility to type 2 diabetes in mice” PLoS Genetics. 2008 Jul 25; 4(7).
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