Trutakna (atacicept)

A weekly injection that blocks two immune signals (BAFF and APRIL) driving B-cell activity, resulting in major reductions in pathogenic IgA antibodies. The Phase 3 ORIGIN 3 trial showed a 42% placebo-adjusted reduction in proteinuria at week 36 (46% with atacicept vs 7% with placebo). The FDA granted accelerated approval on July 7, 2026 under the brand name Trutakna, to reduce protein in the urine in adults with primary IgA nephropathy who are at risk of their disease getting worse.

Atacicept blocks two proteins (BAFF and APRIL) that tell immune cells to make harmful antibodies. By stopping these signals, the drug prevents your immune system from attacking your kidneys, addressing the root cause of IgA nephropathy.

The most common side effects in the main trial were infections (32% vs 28% on placebo), most often upper respiratory infections such as colds (12% vs 9%), and injection site reactions such as redness or pain (30% vs 5% on placebo). Most were mild or moderate. Because Trutakna lowers antibody production, it may raise your risk of infection. Tell your doctor if you have signs of infection such as fever. Live vaccines are not recommended within 30 days before starting or during treatment.

Trutakna is given as a 150 mg injection under the skin once a week, using a single-dose autoinjector in the belly or thigh. Patients inject themselves or have a caregiver do it at home. Take the autoinjector out of the refrigerator 15 to 30 minutes before the shot, and use a different spot each time. If a dose is missed, take it as soon as possible, then go back to once a week counting from that dose.

Yes, Atacicept (Trutakna) is FDA approved (2026) for the treatment of IgA Nephropathy.

BAFF and APRIL are cytokines that signal B cells to survive and produce antibodies. In IgA nephropathy, they drive production of harmful galactose-deficient IgA1. Atacicept blocks both signals simultaneously, providing broader immune modulation than targeting just one.

The Phase 3 ORIGIN 3 trial showed atacicept reduced proteinuria by 46% from baseline at Week 36, compared to a 7% reduction with placebo (a 42% placebo-adjusted reduction, p<0.0001). It also reduced harmful Gd-IgA1 antibody by 68% and resolved blood in urine in 81% of patients with baseline hematuria.

Atacicept (Trutakna) is given as a 150 mg injection under the skin once a week with a single-dose autoinjector, in the belly or thigh. Patients can self-inject at home or have a caregiver do it. The autoinjector needs to sit at room temperature for 15 to 30 minutes before each shot.

Yes. The FDA granted accelerated approval on July 7, 2026 under the brand name Trutakna, for adults with primary IgA nephropathy who are at risk of their disease getting worse. Accelerated approval was based on how much the drug lowered protein in the urine. In September 2026, Vera reported that the final 2-year ORIGIN 3 results showed kidney function stayed about stable on Trutakna. Vera plans to ask the FDA for full approval in the last quarter of 2026. Until then, Trutakna remains on accelerated approval.

It means the FDA cleared the drug based on a marker that is expected to predict real benefit, in this case, less protein in the urine, rather than waiting for the full 2-year kidney function results. The drug is available to prescribe now. If the confirmatory results do not hold up, the FDA can revisit the approval.

Both block BAFF and APRIL with a decoy built from the TACI receptor. Atacicept contains the human TACI receptor, is FDA approved as Trutakna, and is injected once a week. Povetacicept (ALPN-303, from Vertex) carries an engineered TACI domain, was given every 4 weeks in its Phase 3 RAINIER trial, and is under FDA review with a decision due November 30, 2026. No trial has compared the 2 directly, and atacicept is the only one with 2-year kidney function results so far.

Vera Therapeutics makes and sells atacicept as Trutakna in the US. Vera licensed the drug from Ares Trading, an affiliate of Merck KGaA, and developed it for IgA nephropathy. It represents a targeted approach to reducing pathogenic IgA production.