Osteoarthritis (OA) is a serious disease, characterized by chronic joint pain and functional impairment.
Articular cartilage is a connective tissue composed of chondrocytes and an extracellular matrix essentially formed from water, high molecular weight proteoglycans and type II collagen.
The good health of cartilage depends on continuous complex exchanges between chondrocytes and the matrix and is continually subjected to a balance between degradation (catabolism) and synthesis (anabolism).
Destruction of articular cartilage is a result of chondrocyte failure to maintain balance between synthesis (anabolism) and degradation (catabolism) of cartilage matrix.
This imbalance essentially results in an increase of pro-degradative enzymes and a decrease of anabolic factors.
Moreover, proinflammatory cytokines, coming from the synovial tissue and produced by macrophages, monocytes, and synovial cells play an important role for the development of the disease.
Today, there is no available therapy that effectively alters the disease progression by stopping or even delaying joint structural damages while easing pain.
Current osteoarthritis treatments only focus on symptoms (pain and joint function). A recent review (Katz et al., JAMA, 2021) shows that just a few of these symptomatic treatments are strongly recommended by national and international medical organizations, the others being not, or only conditionally recommended mainly due to lack of efficacy and/or safety concerns.
As a last resort, surgical joint replacement, an invasive procedure, is proposed to patients with end-stage OA. Unfortunately, around 20% of patients with knee OA still experience chronic pain after surgery, highlighting the importance of finding new effective and long-acting disease-modifying treatments for OA patients.
“Today, there is a pressing need to bring curative treatment delaying the structural damage of the joints or restoring the cartilage. At 4Moving Biotech, our aim is to provide this long-term solution for patients through the development of 4P004, our disease-modifying treatment for OA (DMOAD).“