x

Liver Fibrosis Rodent Models

Conventional nutritional- or chemical-induced preclinical liver fibrosis rodent models for NASH and anti-fibrotic agent evaluation

ccl4-banner

Conventional Liver Fibrosis Preclinical Models for NASH and Anti-Fibrosis Drug Development

Rapidly and cost-effectively evaluate your NASH and anti-fibrotic agent effects on acute liver injury, advanced fibrosis, and fibrosis reversal. Choose from models with liver fibrosis rapidly induced by carbon tetrachloride (CCl4) or a cholesterol added choline deficient fibrosis diet (CCDF) to:

  • Effectively evaluate the efficacy of anti-fibrosis agents
  • Accurately identify improvements in fibrosis over time
  • Understand the effects of combination regimens on key model endpoints
  • Benchmark your preclinical agents against leading anti-fibrosis compounds
  • Study fat accumulation in the liver using the CCDF-induced liver fibrosis model

Carbon Tetrachloride (CCl4) Induction Mouse Models

carbon tetrachloride induction of fibrosis in liver fibrosis rodent model
  • Rapid compound testing with severe fibrosis induced in as little as 4 weeks
  • Save time and money on studies, without waiting for delayed fibrosis development in overnutrition or nutritional deficit models
  • Evaluate agents for the severe fibrotic component of advanced NASH
  • Choose from standard mouse models including Balb/c and C57BL/6
  • Conventional models of liver fibrosis induced through CCl4 administration i.p. twice per week

Cholesterol Added, Choline Deficient Fibrosis (CCDF) Diet Induction Rodent Models

Cholesterol Added, Choline Deficient Fibrosis (CCDF) Diet induction of fibrosis in liver fibrosis rodent model
  • L-amino acid diet with 46% fat, reduced methionine, no added choline, and 1% cholesterol
  • Added cholesterol contributes to more severe liver injury and hepatic steatosis compared to current industry standard choline deficient, L-amino acid defined, high fat diet (CDAHFD)
  • Study agent effects on rapid moderate to severe liver fibrosis induced in only 6-9 weeks
  • Use models with maintained body weight, unlike the severe weight loss typical of other nutritional deficit models
  • Study multiple targets for hepatic fat accumulation
  • Choose from Wistar rat or C57BL/6 mouse models

CCDF-Induced Liver Fibrosis Model Data

liver cholesterol and fibrosis comparison with elafibranor treatment in wistar rat liver fibrosis rodent model

Figure 1: Liver cholesterol and liver fibrosis percentage in Wistar
rats on normal control diet vs CCDF diet with/without elafibranor

liver histopathology images for wistar rat ccdf liver fibrosis rodent model plus elafibranor treatment

Figure 2: Histology images of livers from Wistar rats on
normal control diet vs CCDF diet with/without elafibranor

histology images for C57BL/6 ccdf liver fibrosis rodent model plus elafibranor treatment

Figure 3: Representative histology images and group means of liver fibrosis from C57BL/6
mice on CCDF diet at 4, 6, and 12 weeks, and 12 weeks under administration of elafibranor

Liver Fibrosis Rodent Model Endpoints

Evaluate a range of endpoints using our liver fibrosis rodent models. Key study endpoints include:

  • Liver weight
  • Liver enzymes (ALT, AST, ALP)
  • Livery hydroxyproline
  • Liver injury panel (Meso Scale Diagnostics assay kit)
  • Histopathology
  • Compare your agent with anti-fibrotic compounds such as sorafenib, obeticholic acid, and elafibranor, which lower inflammation, serum liver enzymes, liver fibrosis, and other endpoints across all models