Rodent Collagen Induced Arthritis (CIA) Models

Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by inflammatory polyarthritis, leading to cartilage and bone destruction, and can affect multiple body systems including skin, eyes, lungs, and heart. HKeyBio offers well-validated collagen induced arthritis (CIA) models in three susceptible rodent strains: C57BL/6 mice, DBA/1 mice, and Wistar rats. These models are established by immunization with type II collagen (CII), the major protein of articular cartilage, triggering an autoimmune polyarthritis that shares key clinical and histological features with human RA. All models exhibit body weight changes, elevated clinical arthritis scores, increased inflammatory markers (CRP, IL-6), and joint histopathology (pannus formation, cartilage erosion, bone destruction), providing robust platforms for preclinical efficacy testing of novel RA therapeutics including DMARDs, biologics, and JAK inhibitors.

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Product Description

Key Features & Benefits

Multiple susceptible strains – C57BL/6, DBA/1 mice and Wistar rats available to suit different genetic backgrounds and experimental needs.

Clinically relevant – Recapitulates human RA: autoimmune polyarthritis, synovial hyperplasia, pannus formation, cartilage erosion, and bone destruction.

Comprehensive endpoints – Body weight, clinical arthritis score, pedal swelling, serum inflammatory markers (CRP, IL-6), joint histopathology (HE scoring).

Translational value – Ideal for testing DMARDs (methotrexate, sulfasalazine), biologics (anti-TNF, anti-IL-6R), JAK inhibitors, and novel immunomodulators.

IND-ready data packages – Studies can be conducted in accordance with GLP principles.

Technical Data & Validation

Collagen Induced DBA/1 Arthritis Model

Collagen Induced C57BL/6 Arthritis Model

Collagen Induced Wistar Arthritis Model

Applications

• Efficacy testing of DMARDs (methotrexate, sulfasalazine, leflunomide, hydroxychloroquine)

• Evaluation of biologics (anti-TNF, anti-IL-6R, anti-IL-17, anti-CD20) and JAK inhibitors (tofacitinib, baricitinib)

• Target validation for autoimmune arthritis pathways (Th17, TNF, IL-6, RANKL)

• Biomarker discovery (anti-collagen antibodies, inflammatory mediators, acute phase proteins)

• IND-enabling pharmacology and toxicology studies

Model Specifications

Parameter	C57BL/6 CIA Model	DBA/1 CIA Model	Wistar Rat CIA Model
Species/Strain	C57BL/6 mouse	DBA/1 mouse	Wistar rat
Induction method	Immunization with type II collagen (CII) emulsified in CFA (day 0) and IFA booster (day 21)
Study duration	5–8 weeks
Key endpoints	Body weight, clinical score, IL-6, joint histopathology (HE)	Body weight, clinical score, CRP, pedal swelling, joint histopathology	Body weight, clinical score, pedal swelling, joint histopathology, larger joints for imaging
Data package	Raw data, analysis reports, clinical scores, histology slides, serum analysis (IL-6, CRP), optional: anti-CII antibodies, micro-CT imaging

❓ Frequently Asked Questions

Q1: What CIA models do you provide?

A1: We establish Collagen Induced Arthritis (CIA) models using C57BL/6 mice, DBA/1 mice and Wistar rats for rheumatoid arthritis research.

Q2: What is the modeling mechanism?

A2: Immunization with type II collagen triggers autoimmune responses in animals. It causes polyarthritis that highly resembles the clinical symptoms and histopathological features of human rheumatoid arthritis.

Q3: What evaluation indicators are used?

A3: We assess body weight and joint clinical scores. We also detect serum CRP and IL-6 levels, and conduct HE staining to analyze joint pathological changes.

Q4: What are the modeling timelines?

A4: Mice receive two injections of type II collagen on Day 0 and Day 21, with the whole experiment lasting 56 days. For Wistar rats, the procedure ends on Day 28 after two doses on Day 0 and Day 7.

Q5: What are the advantages and applications?

A5: These models feature stable inflammation and high reproducibility. They are widely applied for preclinical efficacy screening, mechanism exploration and safety assessment of anti-rheumatoid arthritis drugs.