Inflammatory Pain
Inflammation is a protective response to tissue injury, infection, or irritation involving immune cells, blood vessels and molecular mediators to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged by the original insult, and initiate tissue repair.
Among the five cardinal signs of inflammation, pain is prominent. Inflammatory pain results from the increased excitability of peripheral nociceptive sensory fibers produced by the action of inflammatory mediators. This mechanism is central to many clinically relevant conditions, including acute inflammatory states as well as chronic diseases such as osteoarthritis and rheumatoid arthritis.
Transpharmation offers validated acute and chronic inflammatory pain models that reproduce key patient-relevant features and support robust assessment of new analgesic candidates.
Models
Intraplantar injection of CFA in mice and rats produces an acute inflammatory response associated with non-evoked pain that can persist for several days. In Transpharmation’s model, weight bearing is measured post-CFA injection to reveal analgesic potency. Compounds can be tested acutely (day 1 post-CFA) or over a longer time course, the latter more closely reflecting the pathophysiology of chronic inflammatory conditions such as rheumatoid arthritis or osteoarthritis. This flexibility makes the CFA model a versatile, well-validated tool for screening novel analgesic and anti-inflammatory candidates across both acute and chronic inflammatory pain indications.
Osteoarthritis (OA) is a degenerative joint disease that affects a majority of the elderly population causing chronic pain and joint disability. In the model proposed by Transpharmation in mice and rats, a single intra-articular injection of monoiodoacetate (MIA) into the femorotibial joint produces progressive joint degeneration through inhibition of glycolysis and subsequent chondrocyte death that develops over several weeks. Weight bearing is assessed to reveal the analgesic potency of your drugs during both early and late phases of the development of the model.
The sodium urate-induced synovitis model is a reproducible, rapidly induced and reversible model of acute inflammatory joint pain for evaluating analgesic and anti-inflammatory therapeutics in dogs. Intra-articular administration of sodium urate into the stifle produces localized synovitis, joint effusion, edema, and pain-associated functional impairment within hours, with the response resolving over 2 days. The model has demonstrated pharmacological sensitivity to established anti-inflammatory treatments, including oral meloxicam, and is well suited to dose-ranging, proof-of-concept and comparative efficacy studies in the target species.
The kaolin-induced inflammatory pain model is a robust and reproducible transient model of acute peripheral pain and inflammation used to evaluate the pharmacodynamic activity of analgesic and anti-inflammatory compounds in companion animals. Subcutaneous administration of kaolin into the paw induces a localized inflammatory response characterized by edema, pain-related behaviors, and functional impairment. The model has been established in both feline and canine species, with species-specific endpoint selection including lameness scoring, paw circumference, grimace scoring, creeping test performance, Glasgow Pain Scale assessment, and modified Canine Brief Pain Inventory (mCBPI) measures.
Platforms used
Molecular Biomarkers & Histology Molecular biomarkers and tissue biomarker expression
Electroencephalography (EEG) In-vivo rodent telemetry
MoSeq AI-powered motion sequencing
Operant Platform Motivation, impulsivity, attention, cognition, memory
PK/PD Studies Endpoints for lead optimization
PK-Bridge PK studies for discovery budgets
Humanized Models PXB humanized-liver mice
SPIDAR Rapid analgesic screening
Transgenics Genetically modified mice
Have a program in mind?
Talk to a Transpharmation researcher about your study design and timelines.