Hansa Biopharma AB has announced that GOOD-IDES-02, a global pivotal phase 3 trial in anti-glomerular basement membrane (anti-GBM) disease, did not meet its primary endpoint. The endpoint was renal function at six months, evaluated by estimated glomerular filtration rate (eGFR).
Approximately 60% of patients treated with imlifidase followed by the standard of care (SoC) protocol defined in the trial did not require dialysis at six months, which represented a substantial improvement and clinical benefit compared to what has been observed in historical control cohorts. Outcomes generally observed in these patients reflect only 20-25% who do not require dialysis at six months, which also was the basis for powering the trial. However, the treatment response was similar in patients in the control arm treated with the defined SoC alone.
In the trial, SoC was defined as immediate and intense plasma exchange (PLEX) together with cyclophosphamide (CYC) and glucocorticoids.
The administration of imlifidase in combination with SoC proved to be well tolerated with an acceptable safety profile, in keeping with what has been observed in other imlifidase clinical trials.
A total of 50 adult patients were enrolled in the trial, with 25 randomised to receive imlifidase in combination with SoC and 25 receiving SoC treatment only.
GOOD-IDES-02 (Trial ID: 21-HMedIdeS-24) is an open label, multi-centre phase 3 trial involving over 50 sites in 14 countries in the EU, US and the UK. The primary objective of the study was to assess the effect on kidney function of imlifidase in combination with SoC versus SoC alone in the treatment of patients with severe anti-GBM disease. The primary and key secondary endpoints were assessed at 6 months through the evaluation of renal function as measured by estimated glomerular filtration rate (eGFR) and need for dialysis. Other outcomes include effects of treatment on anti-GBM antibody and ANCA levels, other measures of kidney function, health-related quality of life and safety. Patients continue to be followed up until 24 months after randomisation; long-term outcomes will be reported separately.
References
1. Canney M, et al. Spatial and Temporal Clustering of Anti-Glomerular Basement Membrane Disease. Clin J Am Soc Nephrol. 2016 Aug 8;11(8):1392-1399. doi: 10.2215/CJN.13591215.
2. McAdoo SP, Pusey CD. Anti-Glomerular Basement Membrane Disease. Clin J Am Soc Nephrol. 2017 Jul 7;12(7):1162-1172. doi: 10.2215/CJN.01380217
3. Kluth DC, Rees AJ. Anti-glomerular basement membrane disease. J Am Soc Nephrol. 1999 Nov;10(11):2446-53. doi: 10.1681/ASN.V10112446.
4. Hellmark T, Segelmark M. Diagnosis and classification of Goodpasture’s disease (anti-GBM). J Autoimmun. 2014 Feb-Mar;48-49:108-12. doi: 10.1016/j.jaut.2014.01.024.
5. European Medicines Agency. Idefirix® summary of product characteristics. Available at: https://www.ema.europa.eu/en/documents/product-information/idefirix-epar-product-information_en.pdf.
6. Angum F, et al. The Prevalence of Autoimmune Disorders in Women: A Narrative Review. Cureus. 2020 May 13;12(5):e8094. doi: 10.7759/cureus.8094.
7. Wang L, et al. Human autoimmune diseases: a comprehensive update. J Intern Med. 2015 Oct;278(4):369-95. doi: 10.1111/joim.12395.
8. Ma H, Murphy C, Loscher CE and O’Kennedy R (2022) Autoantibodies – enemies, and/or potential allies? Front. Immunol. 13:953726. doi: 10.3389/fimmu.2022.953726
