| Quantity: | |
|---|---|
Clinical relevance —CCl4-induced fibrosis recapitulates human liver fibrosis with progressive extracellular matrix deposition and liver dysfunction.
Comprehensive endpoint - body weight, serum ALT and AST (liver injury markers), liver histopathology (HE, Masson trichrome, Sirius Red), fibrosis score.
Reproducible and well characterized - widely used model with established protocols and high reproducibility across experiments.
Translational value – ideal for testing anti-fibrotic drugs (nintedanib, pirfenidone), antioxidants and hepatoprotective compounds.
IND Ready Packet – Research can be conducted in accordance with GLP principles.
CCl4-induced C57BL/6 liver fibrosis model
• Efficacy testing of antifibrotic drugs (nintedanib, pirfenidone, TGF-β inhibitors, galectin-3 inhibitors)
• Evaluation of hepatoprotective drugs, antioxidants and anti-inflammatory compounds
• Target validation of fibrotic pathways (collagen synthesis, stellate cell activation)
• Biomarker discovery (collagen markers, liver enzymes, inflammatory mediators)
• Pharmacology and toxicology studies to support IND
scope | Specification |
Species/Strain | C57BL/6 mouse |
induction method | Intraperitoneal injection of carbon tetrachloride (CCl4, 0.5–1.0 mL/kg, dissolved in olive oil) twice weekly for 4–8 weeks |
study time | 4–10 weeks (induction + treatment phase) |
critical endpoint | Body weight, serum ALT and AST levels (clinical chemistry), liver histopathology (HE, Masson's trichrome, Sirius red fibrosis score), optional: hydroxyproline content, serum albumin/bilirubin, immunohistochemistry (α-SMA, collagen I) |
| positive control | Nintedanib or pirfenidone may be used as reference antifibrotic compounds |
packet | Raw data, analysis reports, clinical chemistry, histology slides (HE, Masson, Sirius Red), bioinformatics (optional) |
Question: How does CCl4 induce liver fibrosis?
Answer: CCl4 is metabolized by cytochrome P450 enzymes in liver cells to produce highly active trichloromethyl free radicals, which cause lipid peroxidation, hepatocyte necrosis and inflammation. Repeated injury leads to stellate cell activation, excessive extracellular matrix deposition, and progressive liver fibrosis.
Q: What are the key similarities to human liver fibrosis?
A: This model exhibits progressive collagen deposition, elevated serum aminotransferases (ALT, AST), and histopathological changes that are very similar to human liver fibrosis (bridging fibrosis, pseudolobule formation).
Q: Can this model be used for IND support studies?
Answer: Yes. Studies can be conducted according to GLP principles for regulatory submissions (FDA, EMA).
Q: Do you offer customized study protocols (e.g., different CCl4 doses, administration routes, treatment times)?
Answer: Of course. Our scientific team customizes CCl4 dosing regimens, dosing schedules, and endpoint analyzes based on your specific drug candidate.
Q: What is the typical timeline for a pilot efficacy study?
A: Pilot studies typically involve 4-8 weeks of CCl4 induction with treatment concurrently or after fibrosis is established.