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Not yet. Stanford researchers reported that blocking the enzyme 15-PGDH regenerated cartilage in aged mice and reduced osteoarthritis after knee injury in mice. They also saw cartilage-related changes in human tissue treated outside the body. No result shows that people can regrow cartilage, stop arthritis, or avoid joint replacement with this approach today.
What Stanford’s researchers did
The team targeted 15-PGDH, an enzyme that breaks down prostaglandin E2 and that Stanford describes as associated with aging. In mouse knee cartilage, the enzyme’s levels rose about two-fold with age, according to Stanford Medicine’s November 27, 2025 report.
Researchers used a small-molecule 15-PGDH inhibitor in aged mice, administering it either systemically or directly into the joint. Stanford reported that cartilage thickened across the joint surface and was hyaline, or articular, cartilage—not the less-functional fibrocartilage that can form during repair.
What happened in the animal studies
Aged mice
The reported cartilage thickening occurred in aged mice. The researchers attributed the response to changes in gene-expression patterns in existing chondrocytes, the cells that maintain cartilage; they did not describe stem or progenitor cells creating the new cartilage. In the mouse cartilage population analyzed, the share of cells associated with hyaline-cartilage formation rose from 22% to 42% after treatment. Stanford also reported decreases in cell populations associated with cartilage breakdown and fibrocartilage.
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Mice with knee injuries
In a separate mouse model intended to resemble injuries such as ACL tears, animals received injections twice a week for four weeks after injury. The treated mice were less likely to develop osteoarthritis, moved more typically, and bore more weight on the injured leg than untreated animals, Stanford reported. These are animal findings, not evidence that the injections prevent post-injury arthritis in people.
What the human-tissue result does—and doesn’t—show
The human evidence came from cartilage removed during total knee-replacement surgery. Researchers treated those tissue samples outside the body for one week. Compared with controls, treated samples showed lower expression of some genes associated with degradation and fibrocartilage and began to regenerate articular cartilage, according to Stanford’s account.
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That is laboratory evidence from removed tissue, not treatment of patients. It does not establish that the inhibitor can reach damaged cartilage safely in a living person, relieve pain, restore joint function, or delay surgery.
Is a cartilage treatment available or in clinical trials?
Stanford’s November 2025 report described a cartilage-regeneration clinical trial as a hoped-for next step; it did not report a trial showing cartilage benefit in patients. The same report noted that a 15-PGDH inhibitor was in clinical trials for age-related muscle weakness. That separate program is not a cartilage trial and does not demonstrate efficacy for arthritis.
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The work therefore has not established a safe or effective dose, durability of any effect, or benefit for people with osteoarthritis. It does not show that knee or hip replacement can currently be avoided.
How this differs from injections marketed as regenerative medicine
The 15-PGDH inhibitor is an experimental drug approach, not PRP, bone-marrow or adipose injections, or a stem-cell procedure. Stanford’s orthobiologics information describes those other approaches and says stem-cell therapies are not available in standard outpatient clinics and that no stem-cell therapies are FDA-approved for osteoarthritis.
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Stanford Medicine Magazine’s 2026 overview discusses several cartilage-repair research directions, including scaffolds, imaging, and patient-derived tissue models, while warning that clinics market unproven injections. These distinct approaches should not be treated as interchangeable, and the cited sources do not provide a basis for ranking their effectiveness.
Independent reader supportYour contribution helps us test, update, and keep practical guides available for everyone.Commercialization and researcher disclosure
Stanford’s report says patent applications concerning 15-PGDH inhibition in cartilage and tissue rejuvenation were licensed to Epirium Bio. It also reports that Helen Blau co-founded Myoforte/Epirium and held equity and stock options. This disclosure is relevant context for the research; the report does not establish that a cartilage product is available to patients.
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