Osteoarthritis Drug by Suppressing R-Spondin2 Pathway in Chondrocyte

This repurposing drug specifically suppresses R-Spondin2-dependent abnormal activation of Wnt/β-catenin signaling in OA chondrocytes

Advantages

  • This drug shows higher OA therapeutic effect and lower adverse effect than existing experimental drug candidates which suppress whole Wnt/β-catenin signal pathway.
  • This drug has been used for entirely different chronic disease from OA for more than 30 years and its repositioning dosage form and method for OA are different from those of the conventional indication.

Background and Technology

  •   Osteoarthritis (OA) is the most common form of arthritis affecting approximately 27 million persons in the US.
  •   Chondrocyte hypertrophy in OA is not under the strict control of a single pathway but appears to be regulated by an intricately regulated network of multiple signaling pathways. Wnt/β-catenin signaling is one of the most important pathways and its abnormal activation causes chondrocyte hypertrophy.
  •   R-Spondins are secretory proteins found as Wnt agonists in 2004. Especially, R-spondin2 (Rspo2) was found to facilitate differentiation of proliferating chondrocytes into hypertrophic chondrocytes by enhancing Wnt/β-catenin signaling in endochondral ossification.
  •   Here, we found a repurposing drug specifically suppressing Rspo2-dependent abnormal activation of Wnt/β-catenin signaling. This drug improves OA symptoms without side-effect by specific suppression of excessive Wnt/β-catenin signal in hypertrophic chondrocytes.
 Osteo 1

Our Target Mechanism and Data

Osteo 2 Osteo 3

 Patent

Patent pending (unpublished)

Researcher

Dr. Toshiaki Okura (Nagoya University)

Product No:TP-00784

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