Auranofin Shows Promise as Adjunct Treatment for Steroid-Dependent Asthma

  • PubMed
  • May 22, 2025
  • 0 Comments

A new study highlights the potential of auranofin, a gold-derived anti-inflammatory medication, as a valuable adjunct treatment for patients with steroid-dependent asthma. Researchers have found that the drug can significantly reduce the need for oral corticosteroids, offering relief to patients who suffer from the adverse long-term effects of steroid use.

Steroid-dependent asthma remains a major challenge in respiratory medicine due to its chronic nature and the systemic side effects associated with prolonged corticosteroid therapy. These side effects include osteoporosis, hyperglycemia, and immunosuppression. Reducing their dosage while maintaining asthma control is a crucial goal in patient management.

Auranofin, traditionally prescribed for rheumatoid arthritis, has demonstrated immunomodulatory properties that are now being leveraged in asthma treatment. In recent clinical investigations, patients who included auranofin in their treatment regimen showed measurable improvement in lung function alongside a decreased dependency on systemic steroids.

According to the study’s authors, the mechanism of auranofin centers around its inhibition of specific molecular pathways involved in inflammation. By targeting these pathways, the drug helps to lower the immune system overreaction characteristic of chronic asthma.

While the findings are promising, health experts caution that more extensive clinical trials are required to confirm the drug’s long-term efficacy and safety for asthma patients. Nevertheless, this development represents a significant step in improving the quality of life for individuals affected by difficult-to-control asthma.

The introduction of auranofin as an adjunct therapy could mark a pivotal advancement in personalized asthma care, providing clinicians with an alternative strategy to manage symptoms while mitigating the health risks associated with steroid use.

Source: https:// – Courtesy of the original publisher.

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