Romosozumab (Evenity) exerts its bone-forming effect by binding to which protein to activate the Wnt signaling pathway?

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Multiple Choice

Romosozumab (Evenity) exerts its bone-forming effect by binding to which protein to activate the Wnt signaling pathway?

Explanation:
Romosozumab works by neutralizing sclerostin, a protein produced by osteocytes that normally inhibits the Wnt/β-catenin signaling pathway. When sclerostin is blocked, Wnt signaling is unleashed, promoting osteoblast differentiation and activity, which increases bone formation and bone mineral density. Other drugs in this area act through different mechanisms—denosumab blocks RANKL to reduce bone resorption, alendronate inhibits osteoclasts as a bisphosphonate, and teriparatide is a PTH analog that stimulates bone formation with indirect effects on Wnt—so the direct action that explains the bone-forming effect is binding to sclerostin to lift its inhibition of Wnt signaling.

Romosozumab works by neutralizing sclerostin, a protein produced by osteocytes that normally inhibits the Wnt/β-catenin signaling pathway. When sclerostin is blocked, Wnt signaling is unleashed, promoting osteoblast differentiation and activity, which increases bone formation and bone mineral density. Other drugs in this area act through different mechanisms—denosumab blocks RANKL to reduce bone resorption, alendronate inhibits osteoclasts as a bisphosphonate, and teriparatide is a PTH analog that stimulates bone formation with indirect effects on Wnt—so the direct action that explains the bone-forming effect is binding to sclerostin to lift its inhibition of Wnt signaling.

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