Sclerostin Small Molecule Inhibitors Promote Osteogenesis by Activating Canonical Wnt and BMP Pathways
S. Sangadala, C. H. Kim, L. M. Fernandes, P. Makkara, S. D. Boden, G. R. Beck, H. Drissi, S. M. Presciutti
Abstract
BackgroundThe healing environment within the posterolateral lumbar spine is one of the most clinically challenging bone healing environments in all of orthopaedics due to a lack of a contained space and the need to form de novo bone in a non-bony environment. Our group has previously published data that suggests that sclerostin in expressed locally at high levels throughout the process of a spinal fusion mass maturing. MethodsWe computationally identified multiple FDA-approved drugs, as well as a novel drug, for their ability to disrupt the interaction between sclerostin and its receptor, LRP5/6. The drugs were tested in several in vitro biochemical assays using murine MC3T3 and MSCs, assessing their ability to (1) enhance canonical Wnt signaling, (2) promote the accumulation of the active (non-phosphorylated) form of {beta}-catenin, and (3) enhance the intensity and signaling duration of BMP signaling. These drugs were then tested subcutaneously in rats as standalone osteoinductive agents on plain collagen sponges. Finally, the top drug candidates (called VA1 and C07) were tested in a rabbit posterolateral spine fusion model for their ability to achieve a successful fusion. ResultsWe show that by controlling GSK3b phosphorylation, these SMIs simultaneously enhance canonical Wnt signaling and potentiate canonical BMP signaling intensity and duration. We also demonstrate that the SMIs produce dose-dependent ectopic mineralization in vivo in rats as well as significantly increase posterolateral spine fusion rates in rabbits in vivo, both as standalone osteogenic drugs and in combination with autologous iliac crest bone graft. ConclusionsFew if any osteogenic small molecules have been described that possess the osteoinductive potency of BMP itself - that is, the ability to form de novo ectopic bone as a standalone agent, particularly in stringent in vivo environments. Herein, we describe two such SMIs that have this unique ability and thus may have potential application as novel cost-effective biologic bone graft substitutes for achieving consistent spinal fusion or even or critical-sized fracture defects. FundingThis work was supported by a Veteran Affairs Career Development Award (IK2-BX003845).
02 /Specification & Classification
Click any tag to browse matching papers- Organism
- Research Focus
- Approach
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Local FK506 delivery induces osteogenesis in in vivo rat bone defect and rabbit spine fusion models
Julia Andraca Harrer, Travis M. Fulton, … Nick J. Willett·BonePeer-reviewed·Jul 11, 2024
- Combination Treatment with Sclerostin and Dkk1 Antibodies Synergizes with Tibial Loading to Stimulate Bone Formation in Aged Mice
Lisa Y. Lawson, Christopher J. Chermside‐Scabbo, … Matthew J. Silva·bioRxiv·Feb 24, 2026
- Sclerostin blockade inhibits bone resorption through PDGF receptor signaling in osteoblast lineage cells
C. Thouverey, P. Apostolides, … S. Ferrari·bioRxiv·Sep 11, 2023
- Enhancing Wnt signaling lowers fracture incidence in a severe mouse model of Osteogenesis Imperfecta
Giulia Montagna, Stephanie Lee, … Christina M. Jacobsen·BonePeer-reviewed·Jan 1, 2026
- Suppression of sost/sclerostin and dickkopf-1 promote intervertebral disc structure in mice
T. M. Kroon, P. Niziolek, … N. Holguin·bioRxiv·Jul 1, 2021
- A non-ligand surrogate agonist antibody that enhances canonical Wnt signaling and bone regeneration
N.-K. Lee, S. Bidlingmaier, … B. Liu·bioRxiv·Sep 25, 2022