Two-Year Phase 3 Data Confirms Trutakna's Efficacy in IgA Nephropathy, Intensifying Race for Full Approval

The regulatory framework for kidney disease is caught between two competing pressures. On one side, patient advocates and drug developers argue that relying on early reductions in urine protein is the only ethical way to rush new therapies to market, as patients facing renal failure cannot wait years for definitive proof. On the other, clinical nephrologists and insurance payers caution that fixing a surrogate marker does not guarantee the kidney itself is saved from long-term structural decline.[5]

That tension now has a definitive data point for one of the newest entrants in the immunology market. Two-year results from the Phase 3 ORIGIN 3 trial show that Vera Therapeutics' Trutakna (atacicept-vymj) does more than just clear protein from the urine—it fundamentally stabilizes the kidney's filtration rate in adults with primary immunoglobulin A nephropathy (IgAN).[1][3][4]

The final efficacy analysis, released this week, demonstrated that patients receiving the once-weekly subcutaneous injection saw their estimated glomerular filtration rate (eGFR) decline by just 0.6 mL/min/1.73m² annually over 104 weeks. In contrast, those receiving a placebo experienced a drop of 5.6 mL/min/1.73m² per year.[2][3][4]

By holding the loss of kidney function to a rate comparable to normal age-related decline, the treatment met the stringent targets set by the KDIGO 2025 Clinical Practice Guidelines. The clinical consequences of that stabilization translated directly into hard outcomes for the 428 adults enrolled in the trial.

Over the two-year study period, 11 patients in the Trutakna group experienced a composite kidney disease progression event, compared to 38 in the placebo group. That difference represents a 76 percent relative risk reduction for those on the active therapy.[1][3]

Most notably, zero patients on the active drug required dialysis for 30 days or more, received a kidney transplant, or died from kidney-related causes. In the placebo cohort, eight patients reached those critical endpoints.[3]

"Prevention of kidney failure or kidney-related death is the ultimate goal," said Richard Lafayette, M.D., a principal investigator for ORIGIN 3 and director of the Glomerular Disease Center at Stanford University Medical Center. "We now have evidence suggesting that TRUTAKNA may help patients avoid dialysis, transplantation, or kidney-related death over the long term."[3]

Trutakna operates by inhibiting two specific immune-system signaling proteins: B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL). By blocking both pathways, the drug suppresses the production of the abnormal galactose-deficient IgA1 antibodies that clump in the kidneys and drive the disease's destructive inflammation.[1][5]

The drug previously secured accelerated approval from the Food and Drug Administration in July 2026, a decision based entirely on its ability to reduce proteinuria by 46 percent at 36 weeks. The new two-year eGFR data fulfills the agency's requirement for confirmatory evidence of long-term clinical benefit.[5]

With the ORIGIN 3 endpoints met, Vera Therapeutics plans to submit a supplemental Biologics License Application in the fourth quarter of 2026, seeking to convert the accelerated nod into a full traditional approval. The company reported that more than 350 patient start forms were generated in the first ten weeks following the initial July clearance.[3]

The results also intensify a brewing market rivalry. Trutakna is competing directly with other recently approved targeted therapies in the rapidly evolving IgAN space. Market analysts note that Trutakna's 76 percent reduction in progression risk provides a compelling differentiator as multiple companies vie for a foundational role in kidney care.

For patients, the immediate takeaway is practical: the early promise of dual BAFF/APRIL inhibition translates into durable protection against dialysis. The drug does carry an immunosuppressive profile, with infections reported in 32 percent of treated patients compared to 28 percent on placebo across clinical trials, requiring careful screening before initiation and monitoring throughout the treatment course.[1][5]