New data from the open-label extension of the Phase 2b ORIGIN trial suggests that atacicept could modify the course of IgA nephropathy (IgAN). The 96-week results, presented at the American Society of Nephrology Kidney Week 2024, indicate that atacicept is associated with sustained reductions across multiple key indicators of disease progression.
Key Findings from the ORIGIN Trial
The ORIGIN trial extension data revealed a 66% mean reduction in Gd-IgA1 levels (SE, 2%) among patients treated with atacicept. Additionally, there was a 75% reduction in the percentage of patients experiencing hematuria from baseline (95% CI, -87% to -59%). The study also demonstrated a 52% mean reduction in UPCR (SE, 5%).
Notably, the annualized slope of estimated glomerular filtration rate (eGFR) was -0.6 (SE, 0.5) mL/min/1.73m2 per year, suggesting a slow decline in kidney function among patients receiving atacicept.
Expert Commentary
"We are one step closer to preventing kidney failure in the lifetime of our patients with IgA nephropathy," said Jonathan Barratt, PhD, the Mayer Professor of Renal Medicine at the University of Leicester. He highlighted the significant progress compared to the past, where the primary approach was simply monitoring the progressive decline in kidney function leading to dialysis. "A massive turnaround in terms of what we potentially could achieve with the new therapies."
Mechanism of Action and Practical Implications
Atacicept's mechanism involves targeting disease-causing cytokines. Its availability as a weekly self-administered injection enhances its practicality for long-term use. Ongoing Phase 3 trials and the sponsor's commitment to extended access programs could further redefine outcomes for IgAN patients worldwide.
IgAN Treatment Landscape
IgA nephropathy is a leading cause of kidney failure, affecting a significant portion of the global population. Current treatments often involve managing symptoms and slowing disease progression, but the new data suggests atacicept could offer a more direct approach by targeting the underlying disease mechanisms.
