Blocking Axl may open a new path for osteoporosis treatment

Researchers in Germany say the AXL receptor tyrosine kinase acts as a brake on bone-building cells, and blocking it increased bone formation and bone mass in mice. The findings, published July 6 in Bone Research, could point to a more accessible anabolic approach for osteoporosis if future human studies confirm the effect.

Why it matters: - Osteoporosis weakens bones, raises fracture risk and affects millions of people worldwide. - Current bone-building therapies can be expensive and often require regular injections. - A treatment approach based on a small-molecule inhibitor could be easier to deploy than biologic drugs if it proves safe and effective in people.

What happened: - Researchers identified AXL receptor tyrosine kinase as a previously unrecognized regulator of osteoblasts, the cells that build new bone. - The study was published online July 6, 2026, in Volume 14 of Bone Research. - The work was led by Dr. Mubashir Ahmad with Prof. Dr. Jan Tuckermann at Ulm University’s Institute of Molecular Endocrinology and Physiology, and continued by Ahmad as a postdoctoral researcher with Prof. Dr. Anita Ignatius at Ulm University Hospital. - Blocking Axl increased bone formation and bone mass in mice.

The details: - The team used a kinome-wide RNA interference screen to search for genes that control bone formation. - Screening hundreds of protein kinases pointed to Axl as a new regulator of osteoblast function. - Researchers then reduced Axl activity with genetic methods and with BGB324, a small-molecule inhibitor. - In cell studies and in mice, Axl inhibition promoted osteoblast maturation and increased mineralized bone tissue production. - Mice treated with BGB324 showed greater bone mass in long bones and vertebrae because of increased bone formation. - The treatment also increased osteocyte numbers, which suggests support for normal bone development. - The mice showed no evidence of significant toxicity during the study period. - Blocking Axl increased the activity of interferon-stimulating gene 15, which helped activate signals needed for osteoblast maturation. - BGB324 has already been studied in clinical trials for certain cancers because Axl is involved in tumor growth and immune regulation. - The original paper is titled “Inhibition of AXL receptor tyrosine kinase increases osteoblast function and bone mass.” - The paper’s DOI is https://doi.org/10.1038/s41413-026-00554-0.

Between the lines: - The result is still preclinical, so the key question is whether Axl blockade will work the same way and remain safe in people. - The fact that an existing Axl inhibitor already has cancer-trial experience could shorten the path for follow-up osteoporosis research. - The study adds a new molecular target to a field where better anabolic options are still needed.

What's next: - Researchers say further studies are needed to determine whether targeting Axl can be translated into a safe and effective treatment for osteoporosis and other bone disorders. - Clinical research will have to test dosing, safety and whether the bone-building effect seen in mice carries over to humans.

The bottom line: - Blocking Axl may offer a new strategy to boost bone formation, but the approach still needs human testing before it can be considered a treatment for osteoporosis.