Vera Therapeutics reported that its kidney drug Trutakna (atacicept) delivered strong final results in a two-year Phase 3 trial for IgA nephropathy — essentially stopping the decline in kidney function that the disease normally causes. The data strengthen Vera’s bid to convert an existing accelerated approval into a full one.

The disease

IgA nephropathy (IgAN), sometimes called Berger’s disease, is a chronic kidney disorder in which a faulty antibody — a poorly formed version of immunoglobulin A (IgA) — builds up in the kidneys’ filtering units, triggering inflammation and scarring. It is a leading cause of kidney failure in young adults, and many patients progress to dialysis or transplant over time. The core problem is measured by two markers: proteinuria (protein leaking into the urine) and declining eGFR, a measure of how well the kidneys filter blood.

How atacicept works

Atacicept is a biologic that targets the disease upstream. It blocks two signaling proteins, BLyS and APRIL, that drive the B cells responsible for producing the harmful IgA antibodies. By turning down that production at the source, the drug aims to reduce the antibody buildup that damages the kidneys — rather than just managing symptoms downstream.

The results

The final analysis of the ORIGIN 3 trial hit all its prespecified goals. The headline: through 52 weeks, kidney function was essentially stable — mean eGFR changed by just -0.1 with Trutakna versus -5.7 with placebo, a placebo-adjusted benefit of 5.6. Over 104 weeks, the drug reduced kidney-disease-progression events by 76% versus placebo. It also produced statistically significant reductions in proteinuria, in the harmful galactose-deficient IgA1 antibody, and in hematuria (blood in the urine). Safety was described as favorable and generally comparable to placebo.

Why nearly flat eGFR is a big deal

In a progressive kidney disease, the goal isn’t just to slow the slide — it’s to stop it. An eGFR decline of essentially zero over a year, against a placebo group that lost 5.7 points, suggests the drug is preserving the kidney’s working capacity rather than merely delaying failure. Because lost kidney function generally doesn’t come back, keeping it stable is exactly what patients and nephrologists want.

The regulatory path

The FDA granted Trutakna accelerated approval for IgA nephropathy in July 2026 (typically based on the proteinuria signal). Vera plans to file a supplemental BLA in the fourth quarter of 2026 seeking full approval, with a potential FDA decision in 2027. The two-year eGFR and progression data are the kind of hard, long-term evidence regulators want to see to convert an accelerated approval into a full one.

Why it matters — and the context

IgA nephropathy has become a competitive field, with several new therapies arriving after years of few options. Strong, durable data like these help a drug stand out — and, more importantly, offer patients a real prospect of preserving kidney function and avoiding dialysis. As always, trial results describe averages; individual outcomes vary, and treatment decisions rest with a nephrologist. This is business and clinical news, not investment or medical advice.