MIV-711

  • Mechanism

    Cathepsin K inhibitor

  • Disease areas

    Osteogenesis Imperfecta

    Osteoarthritis

    LCPD

MIV-711 - for the treatment of Osteogenesis Imperfecta (OI) and other bone-related disorders

Osteogenesis Imperfecta is a hereditary skeletal disorder characterized by bone fragility and deformity, affecting an estimated 1 in 15,000–20,000 people worldwide.

MIV-711 has the potential of becoming the first, approved treatment option for patients with Osteogenesis Imperfecta.

MIV-711 has been granted Orphan Drug Designation (ODD) from the FDA for the treatment of OI. A disease for which there are currently no approved treatment options.

About Osteogenesis Imperfecta

Osteogenesis imperfecta (OI), also known as brittle bone disease, is a rare and hereditary disorder characterised by fragile bones with a high susceptibility to fractures. The disease is caused by various genetic mutations that affect the structure or production of the bone matrix. The severity varies from mild to very severe forms. The most severe cases can involve repeated fractures, skeletal deformities, pain and short stature, and in the most severe form, children do not survive infancy. Globally, an estimated 500,000 people are affected, of whom around 135,000 are children. OI often requires lifelong medical assistance, with the aim of improving quality of life and reducing the risk of fractures. 

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Dual effect to help rebalance bone remodelling in OI

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Dual effect to help rebalance bone remodelling in OI

Cathepsin K - a protease highly expressed in osteoclasts that efficiently degrades type I collagen - plays a central role in bone matrix breakdown. Inhibiting cathepsin K has been shown to reduce excessive bone resorption while uniquely preserving or even promoting aspects of bone formation by enhancing osteoclast/osteoblast communication and supporting the initiation of osteogenesis. This dual effect suggests that a cathepsin K inhibitor could help rebalance bone remodelling in OI by slowing collagen degradation, improving bone microarchitecture, and potentially reducing fracture rates - addressing a core pathological driver of the disease rather than only its symptoms.

Medivir’s research in preclinical models has demonstrated that inhibition of cathepsin K can improve both bone quantity and quality in OI

Supporting evidence for positive effect on bone remodeling

Additional support for the disease-modifying effects of MIV-711 comes from a phase II study demonstrating positive effects on both bone and cartilage in the knee joints of osteoarthritis patients after only six months of treatment. The study showed a significant difference in preservation of cartilage and reduction of bone erosion in patients treated with MIV-711 compared with placebo.

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Publications

Analgesic effects of the cathepsin K inhibitor L-006235 in the monosodium iodoacetate model of osteoarthritis pain

Safety and Efficacy of Six Months´ Open Label Extension Post-RCT Using the Novel Cathepsin K Inhibitor MIV-711 in Patients with Osteoarthritis

The-potential-clinical-relevance-of-imaging-biomarker-data-from-short-term-interventional-trials-in-osteoarthritis

The selective cathepsin K inhibitor MIV‑711 attenuates joint pathology in experimental animal models of osteoarthritis


MIV-711, a novel cathepsin K inhibitor demonstrates evidence of osteoarthritis structure modification