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CCl4 Model of Liver Fibrosis
The human NASH phenotype leading to cirrhosis and HCC can be translated into murine models of fibrosis using CCL4. The carbon tetrachloride (CCl4) model of liver fibrosis and cirrhosis is a well-established and reliable method for assessing the efficacy of anti-fibrotic compounds using a simple chemical insult. Developing similar pathology of the drivers of clinical disease, Ichor’s team is well-versed in ensuring the repeatability of this model to generate reliable data.
Administration of CCl4 is used to accelerate the development of liver damage to recapitulate the early phase effects of non-alcoholic fatty liver disease (NAFLD). Mirroring the important aspects of human disease, this model develops inflammation, fibrosis, and hepatocellular degeneration, ballooning, and necrosis.
Through the assessment of various biomarkers and end points, the inhibition of fibrosis progression can be tracked and quantified to more accurately and specifically gauge the effectiveness of potential therapeutics.
Fast and Reliable
The CCl4 model of liver fibrosis is faster at inducing hepatocellular damage than diet-only models, leading to earlier answers.
Closely Resembles Human Disease
Similar patterns of stellate cell activation, macrophage infiltration, and changes to extracellular matrix components are seen in both human disease and mouse models. This allows for a consistent translational model to evaluate your interventions.
Long Track Record
CCl4 was one of the first chemical-insults used to model toxic fatty-liver disease, so a wealth of previous data exists with which to compare and design experiments around.
Endpoints
The CCL4 model of NASH creates histopathologic changes consistent with the expected disease state. Positive controls can also be used as comparators to your treatment of interest.