| Quantity: | |
|---|---|
Clinically relevant – CCL4 induced cirrhosis mimics human disease with progressive fibrosis, bridging septa, and cirrhotic nodule formation.
Well-characterized endpoints – Body weight monitoring, qPCR analysis of fibrotic and inflammatory markers (Colla1, IL-6, IL-10), gross liver pathology, histopathology (H&E, Masson trichrome).
Mechanism-driven – CCL4 generates reactive metabolites causing hepatocyte necrosis, inflammation, and profibrotic cytokine release.
Translational value – Ideal for testing anti-fibrotic agents, hepatoprotective drugs, and therapies targeting inflammation and fibrosis.
IND-ready data packages – Studies can be conducted in accordance with GLP principles
CCl4 Induced Cirrhosis Rat Model
• Efficacy testing of anti-fibrotic agents (pirfenidone, nintedanib, TGF-β inhibitors, galectin-3 inhibitors)
• Evaluation of hepatoprotective drugs and anti-inflammatory compounds
• Target validation for fibrotic pathways (collagen synthesis, stellate cell activation)
• Biomarker discovery (fibrosis markers, inflammatory mediators)
• IND-enabling pharmacology and toxicology studies
Parameter | Specificatio |
Species/Strain | Wistar rat |
Induction method | Repeated oral gavage or intraperitoneal injection of carbon tetrachloride (CCL4) in olive oil vehicle, 2–3 times weekly for 8–12 weeks |
Study duration | 8–14 weeks (induction + treatment phase) |
Key endpoints | Body weight, liver gross pathology (weight, appearance), qPCR for fibrotic markers (Colla1, TIMP1, TGF-β) and inflammatory cytokines (IL-6, IL-10, TNF-α), serum biochemistry (ALT, AST, ALP, albumin, bilirubin), histopathology (H&E, Masson trichrome, Sirius Red), hydroxyproline content (optional) |
Data package | Raw data, analysis reports, qPCR data, clinical chemistry, histology slides (H&E, Masson), gross pathology images, bioinformatics (optional) |
Q: How does CCL4 induce cirrhosis in rats?
A: CCL4 is metabolically activated by cytochrome P450 in hepatocytes to produce highly reactive free radicals (trichloromethyl radical), causing lipid peroxidation, hepatocyte necrosis, and inflammation. Repeated injury leads to stellate cell activation, excessive extracellular matrix deposition, and progressive fibrosis culminating in cirrhosis.
Q: What are the key similarities with human cirrhosis?
A: The model exhibits progressive fibrosis, bridging septa, cirrhotic nodule formation, portal hypertension, and biochemical abnormalities (elevated liver enzymes, hypoalbuminemia) similar to human cirrhosis.
Q: Can this model be used for IND-enabling studies?
A: Yes. Studies can be conducted in accordance with GLP principles for regulatory submissions (FDA, EMA).
Q: Do you offer customized study protocols (e.g., different CCL4 doses, administration routes, combination with other insults)?
A: Absolutely. Our scientific team tailors CCL4 dosing regimens, treatment schedules, and endpoint analyses to your specific drug candidate.
