New White Paper: NAFLD/NASH: Accelerating Drug Discovery with an Improved Metabolic Dysregulation Model

Enhance NASH Drug Development with More Translational Preclinical Models, Better Recapitulating Complex Human Disease

New White Paper NAFLD/NASH: Accelerating Drug Discovery with an Improved Metabolic Dysregulation Model

Nonalcoholic steatohepatitis (NASH) is an increasing public health issue, with no currently approved treatment options. Preclinical development of new agents is hindered by the complexity of NASH, with no standout preclinical model that captures of clinical aspects of the disease. It is therefore important to develop more translatable animal models to accelerate NASH drug development.

The MS-NASH (formerly called FATZO) mouse is a polygenic model featuring an intact leptin pathway. The model closely mimics human metabolic disease progression, spontaneously developing obesity, dyslipidemia, and diabetes.

Through the administration of a Western diet plus fructose, the MS-NASH mouse develops liver steatosis leading to NAFLD/NASH. This provides an inherently dysmetabolic model combined with NASH pathological features for a more translational drug development choice.

Download This White Paper to Understand:

  • How current NASH drug development is limited by preclinical models lacking both pathological (e.g. fibrosis) and dysmetabolic features of NASH

  • The establishment of a more translational NAFLD/NASH mouse model, developed from an inherently dysmetabolic and hyperglycemic background which also displays fibrosis, ballooning, inflammation, steatosis, and elevations in liver enzymes

  • How this model has been validated for preclinical drug development, with clinically relevant agents inducing improvements in liver function

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