A bispecific antibody targeting sclerostin and DKK-1 promotes bone mass accrual and fracture repair

نویسندگان

  • Monica Florio
  • Kannan Gunasekaran
  • Marina Stolina
  • Xiaodong Li
  • Ling Liu
  • Barbara Tipton
  • Hossein Salimi-Moosavi
  • Franklin J. Asuncion
  • Chaoyang Li
  • Banghua Sun
  • Hong Lin Tan
  • Li Zhang
  • Chun-Ya Han
  • Ryan Case
  • Amy N. Duguay
  • Mario Grisanti
  • Jennitte Stevens
  • James K. Pretorius
  • Efrain Pacheco
  • Heidi Jones
  • Qing Chen
  • Brian D. Soriano
  • Jie Wen
  • Brenda Heron
  • Frederick W. Jacobsen
  • Emil Brisan
  • William G. Richards
  • Hua Zhu Ke
  • Michael S. Ominsky
چکیده

Inhibition of the Wnt antagonist sclerostin increases bone mass in patients with osteoporosis and in preclinical animal models. Here we show increased levels of the Wnt antagonist Dickkopf-1 (DKK-1) in animals treated with sclerostin antibody, suggesting a negative feedback mechanism that limits Wnt-driven bone formation. To test our hypothesis that co-inhibition of both factors further increases bone mass, we engineer a first-in-class bispecific antibody with single residue pair mutations in the Fab region to promote efficient and stable cognate light-heavy chain pairing. We demonstrate that dual inhibition of sclerostin and DKK-1 leads to synergistic bone formation in rodents and non-human primates. Furthermore, by targeting distinct facets of fracture healing, the bispecific antibody shows superior bone repair activity compared with monotherapies. This work supports the potential of this agent both for treatment and prevention of fractures and offers a promising therapeutic approach to reduce the burden of low bone mass disorders.

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عنوان ژورنال:

دوره 7  شماره 

صفحات  -

تاریخ انتشار 2016