Anti-WISP2/CCN5 Therapy Against Bone Loss
Tech ID: 34600 / UC Case 2026-391-0
Abstract
Researchers at the University of California, Davis have
developed a novel nanobody specific for WISP2 that restores skeletal stem cell
function to treat bone loss and promote bone growth in age-related bone
diseases.
Full Description
This technology involves the
development of nanobodies—small antigen-binding fragments—targeted against
WISP2, a protein upregulated in aged skeletal stem cells (SSCs) that impairs
bone repair. These nanobodies can be formulated as pharmaceuticals for topical
or injectable use to treat bone diseases by restoring SSC function, inhibiting
bone loss, promoting new bone growth, and accelerating fracture healing. The
approach addresses intrinsic stem cell aging and skeletal regeneration failures
linked to age-related conditions such as osteoporosis, osteonecrosis, and
osteoarthritis.
Applications
- Treatment of osteoporosis and other age-related bone diseases such as osteonecrosis and osteoarthritis.
- Therapies to promote bone growth and increase bone density in elderly patients.
- Accelerated healing solutions for bone fractures including bicortical fractures.
- Pharmaceutical formulations for regenerative medicine and orthopedics.
- In vitro applications to restore or study skeletal stem cell function.
Features/Benefits
- Targets intrinsic aging mechanisms in skeletal stem cells to enhance bone regeneration.
- Decoupled from bone resorption mechanisms.
- Compared to available anabolic therapies it acts at stem cell level, potentially enabling long-term efficacy (without limited use requirement).
- Restores stem cell osteogenic capacity and differentiation ability.
Reduces inflammatory microenvironments that contribute to bone loss.
- Supports both local and systemic administration with flexible formulations (gel or injectable).
- Promotes bone density, strength, and accelerates fracture healing.
- Achieves high specificity for WISP2, minimizing off-target effects.
- Addresses the root causes of bone loss rather than just alleviating symptoms.
- Counteracts the age-related decline in skeletal stem cell function, improving bone repair.
- Reduces excessive osteoclast activity responsible for bone resorption.
- Overcomes limitations of treatments that ignore local skeletal microenvironment factors.
- Reduces the high incidence of fractures and skeletal disorders in aging populations.
Patent Status
Patent Pending