--- title: "Atacicept | PepTracker Pro" url: https://peptrackerpro.com/peptides/atacicept description: "Atacicept (brand name Trutakna) is a recombinant soluble TACI-Fc fusion protein and the first dual BAFF/APRIL inhibitor approved for IgA nephropathy (IgAN). It fuses the extracellular ligand-binding domain of the TACI receptor to the Fc region of human IgG1, letting it soak up two B-cell survival cytokines at once - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). By starving autoreactive B cells and plasma cells of both signals, atacicept lowers production of galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody that drives immune-complex deposition and kidney injury in IgAN. It is given as a 150 mg once-weekly subcutaneous self-injection with an autoinjector at home. On July 7, 2026 the FDA granted atacicept accelerated approval (as Trutakna) to reduce proteinuria in adults with primary IgAN at risk of progression - the first and only BAFF-and-APRIL inhibitor cleared for the disease - based on the Phase 3 ORIGIN 3 trial (NCT04716231, 431 adults), in which it cut urine protein (UPCR) 46% from baseline and 42% versus placebo at week 36 (p<0.0001), reduced Gd-IgA1 by 68%, resolved hematuria in 81% of those with baseline blood in the urine, and produced serious adverse events in only 0.5% of patients (versus 5% on placebo). Originated at ZymoGenetics and developed by Merck KGaA (Merck Serono) before being out-licensed to Vera Therapeutics, atacicept sits alongside the anti-APRIL antibody sibeprenlimab and the engineered dual BAFF/APRIL inhibitor povetacicept in the fast-moving IgAN pipeline." lang: en --- Skip to main content **Educational information only.** This site does not provide medical advice. Read full disclaimer (https://peptrackerpro.com/disclaimer) **Research-only content.** This page is for educational purposes and does not constitute medical advice. Read full disclaimer → (https://peptrackerpro.com/research-disclaimer) # Atacicept High Evidence Atacicept (brand name Trutakna) is a recombinant soluble TACI-Fc fusion protein and the first dual BAFF/APRIL inhibitor approved for IgA nephropathy (IgAN). It fuses the extracellular ligand-binding domain of the TACI receptor to the Fc region of human IgG1, letting it soak up two B-cell survival cytokines at once - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). By starving autoreactive B cells and plasma cells of both signals, atacicept lowers production of galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody that drives immune-complex deposition and kidney injury in IgAN. It is given as a 150 mg once-weekly subcutaneous self-injection with an autoinjector at home. On July 7, 2026 the FDA granted atacicept accelerated approval (as Trutakna) to reduce proteinuria in adults with primary IgAN at risk of progression - the first and only BAFF-and-APRIL inhibitor cleared for the disease - based on the Phase 3 ORIGIN 3 trial (NCT04716231, 431 adults), in which it cut urine protein (UPCR) 46% from baseline and 42% versus placebo at week 36 (p<0.0001), reduced Gd-IgA1 by 68%, resolved hematuria in 81% of those with baseline blood in the urine, and produced serious adverse events in only 0.5% of patients (versus 5% on placebo). Originated at ZymoGenetics and developed by Merck KGaA (Merck Serono) before being out-licensed to Vera Therapeutics, atacicept sits alongside the anti-APRIL antibody sibeprenlimab and the engineered dual BAFF/APRIL inhibitor povetacicept in the fast-moving IgAN pipeline. Aliases Atacicept +8 more Evidence High Evidence Last Updated 2026-09-29 Reading Time 9 min ## What It Is Atacicept is a soluble recombinant fusion protein built from the extracellular, ligand-binding portion of the TACI receptor (transmembrane activator and calcium-modulating cyclophilin ligand interactor) joined to the Fc region of human IgG1. TACI is one of three receptors that normally sit on B cells and bind the cytokines BAFF and APRIL. As a soluble decoy, atacicept captures BAFF and APRIL in the circulation before they can deliver survival and maturation signals through BAFF-R, TACI or BCMA - so unlike antibodies that hit a single target, it neutralizes BOTH B-cell survival factors at once. That dual blockade is aimed squarely at the biology of IgA nephropathy. IgAN is described by a 'four-hit' model: (1) B cells and plasma cells overproduce galactose-deficient IgA1 (Gd-IgA1); (2) the immune system makes autoantibodies against it; (3) these form immune complexes; and (4) the complexes deposit in the kidney's mesangium, triggering inflammation, proteinuria and progressive loss of filtering function that can end in kidney failure. BAFF and APRIL sit upstream of hit #1 - they keep the antibody-producing cells alive - so soaking them up is intended to turn down Gd-IgA1 production at the source rather than mopping up damage downstream. The pivotal evidence is ORIGIN 3 (NCT04716231), a global Phase 3 randomized, double-blind, placebo-controlled trial in 431 adults with IgAN. At the week-36 primary analysis atacicept reduced urine protein-to-creatinine ratio (UPCR) by 46% from baseline and by 42% relative to placebo (p<0.0001), lowered Gd-IgA1 by about 68%, and resolved hematuria (blood in the urine) in roughly 81% of participants who had it at baseline. Safety looked clean in the trial: serious adverse events occurred in just 0.5% of atacicept patients versus 5% on placebo, with no deaths in either arm and an overall profile the sponsor described as comparable to placebo. The results were presented as a late-breaker at ASN Kidney Week 2025 and published in the New England Journal of Medicine (November 2025). On the strength of that data - plus FDA Breakthrough Therapy Designation and Priority Review - the FDA granted atacicept ACCELERATED approval on July 7, 2026 under the brand name Trutakna, to reduce proteinuria in adults with primary IgAN at risk of disease progression. Accelerated approval is important context: it rests on proteinuria as a reasonably-likely-to-predict surrogate, not yet on proven long-term preservation of kidney function. Continued approval is expected to hinge on confirmatory two-year kidney-function (eGFR) data from ORIGIN 3; Vera Therapeutics aligned with the FDA on an earlier eGFR analysis expected in Q3 2026 and has signaled a supplemental BLA in Q4 2026 seeking full approval, with a full-approval decision possible in 2027. Atacicept is self-administered as a 150 mg once-weekly subcutaneous injection. Atacicept's road to the kidney was long and instructive. It originated at ZymoGenetics, was developed by Merck KGaA (Merck Serono), and was out-licensed to Vera Therapeutics in 2020. Earlier programs targeted other autoimmune diseases with mixed results: in systemic lupus erythematosus (the APRIL-SLE and ADDRESS II programs) a high-dose arm was halted over serious infections even as signals of reduced severe flares emerged, and - most strikingly - in the Phase 2 ATAMS multiple sclerosis trial atacicept UNEXPECTEDLY INCREASED relapses versus placebo, leading to early termination. Those results are a lasting reminder that manipulating the BAFF/APRIL axis can help or harm depending on the disease. In IgAN, the pipeline is now crowded and complementary: atacicept (dual BAFF/APRIL) arrives alongside the anti-APRIL monoclonal antibody sibeprenlimab (VOYXACT), the engineered dual BAFF/APRIL inhibitor povetacicept, the plasma-cell-depleting anti-CD38 antibody felzartamab, the complement factor B inhibitor iptacopan (Fabhalta), and targeted-release budesonide (Tarpeyo). What still isn't known for atacicept is the most important thing of all: whether cutting proteinuria this much translates into durably slower loss of kidney function over years - the question the confirmatory eGFR readout is meant to answer. Also known as: Atacicept, Trutakna, TACI-Ig, TACI-Fc fusion protein, recombinant TACI-Fc, soluble TACI receptor fusion protein, dual BAFF and APRIL inhibitor, BAFF/APRIL blocker, Vera Therapeutics atacicept ## Why Researchers Study It Researchers study atacicept because it tests a clean, upstream idea: if the antibody-producing cells that drive an autoimmune disease depend on two survival cytokines - BAFF and APRIL - then soaking up both at once should quiet the disease at its source. In IgA nephropathy that source is galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody at the top of the 'four-hit' cascade, and atacicept's TACI-Fc decoy design lets it capture BAFF and APRIL together rather than blocking a single downstream messenger. The IgAN results have been compelling - large, durable reductions in proteinuria and Gd-IgA1 with a placebo-like safety profile - making atacicept a proof of concept for dual BAFF/APRIL blockade and a natural comparator to single-target agents like the anti-APRIL antibody sibeprenlimab and the engineered dual inhibitor povetacicept. Just as important is what atacicept teaches about the LIMITS of the idea: the same mechanism that helps in kidney disease unexpectedly WORSENED multiple sclerosis in the ATAMS trial and raised infection concerns in lupus, a vivid lesson that immune-axis manipulation is context-dependent. That combination - strong efficacy in the right disease, cautionary signals in the wrong one - makes atacicept a case study in target biology, surrogate endpoints (proteinuria) versus hard outcomes (eGFR/kidney survival), and how a decades-old molecule can find its indication. ## Proposed Mechanisms - Dual cytokine capture: atacicept is a soluble TACI-Fc decoy that binds and neutralizes both BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand) in the circulation before they can signal through the B-cell receptors BAFF-R, TACI and BCMA. - B-cell and plasma-cell suppression: withdrawing BAFF and APRIL removes key survival and maturation signals from autoreactive B cells, plasmablasts and long-lived plasma cells, reducing output of pathogenic antibodies. - Lowering galactose-deficient IgA1: fewer and less-active IgA-producing plasma cells means less Gd-IgA1 - the abnormal antibody at the top of the IgA nephropathy 'four-hit' cascade - observed as roughly a 68% Gd-IgA1 reduction in ORIGIN 3. - Upstream, source-level control: by acting on antibody production itself rather than on downstream complement activation or FcRn-mediated IgG recycling, atacicept aims to reduce the immune-complex formation and mesangial deposition that cause proteinuria and kidney injury. - Broad immunoglobulin reduction: BAFF/APRIL blockade lowers total IgA, IgG and IgM - the intended pharmacodynamic effect that also underlies its infection-risk profile. - TACI-Fc versus alternatives: as a wild-type TACI-Fc fusion it captures both ligands, contrasting the engineered TACI variant povetacicept and the APRIL-only monoclonal antibody sibeprenlimab - a design bet that hitting both BAFF and APRIL yields deeper suppression of pathogenic antibody production. ## Evidence Snapshot High Evidence Low Medium High | Study Type | Model | Outcome | Link | | --- | --- | --- | --- | | Phase 3 randomized, double-blind, placebo-controlled trial ORIGIN 3 (NCT04716231) in adults with primary IgA nephropathy; week-36 primary analysis published in the New England Journal of Medicine (2025) and presented at ASN Kidney Week 2025. | 431 adults with primary IgA nephropathy at risk of progression, randomized 1:1 to atacicept 150 mg once-weekly subcutaneous or placebo on background standard-of-care. | UPCR reduced 46% from baseline and 42% versus placebo at week 36 (p<0.0001); Gd-IgA1 reduced ~68%; hematuria resolved in ~81% of those with baseline hematuria; serious adverse events 0.5% (atacicept) vs 5% (placebo), no deaths. Basis for FDA accelerated approval (Trutakna) on July 7, 2026. | Source | | Phase 2b dose-finding portion of the ORIGIN program in IgA nephropathy (placebo-controlled). | Adults with IgA nephropathy across multiple atacicept dose levels versus placebo. | Met its primary endpoint with statistically significant, clinically meaningful reductions in proteinuria, supporting selection of the 150 mg once-weekly dose advanced into Phase 3 ORIGIN 3. | Source | | Phase 2 randomized, placebo-controlled trial ATAMS in relapsing-remitting multiple sclerosis - The Lancet Neurology (2014). | Adults with relapsing MS randomized to atacicept (various doses) or placebo. | Atacicept UNEXPECTEDLY INCREASED the annualized relapse rate versus placebo; the trial was stopped early. A key cautionary result showing BAFF/APRIL blockade can worsen some autoimmune diseases even as it helps others. | Source | | Earlier Phase 2/3 development in systemic lupus erythematosus (APRIL-SLE and ADDRESS II programs). | Adults with SLE randomized to atacicept doses versus placebo on background therapy. | A high-dose (150 mg) arm was halted after serious and fatal infections, while signals of reduced severe flares and B-cell/immunoglobulin lowering were seen - shaping later dose selection and infection-monitoring practice. | Source | ## Commonly Discussed Benefits renal: https://peptrackerpro.com/benefits/renal autoimmune: https://peptrackerpro.com/benefits/autoimmune Disease Modification: https://peptrackerpro.com/benefits/disease-modification B-cell-modulation: https://peptrackerpro.com/benefits/B-cell-modulation Researching Atacicept? Track it, set reminders, and keep notes in the free app. Track in App (https://app.peptrackerpro.com/?add=atacicept) ## Safety & Cautions - Atacicept (Trutakna) received FDA ACCELERATED approval on July 7, 2026 based on proteinuria - a surrogate endpoint - not yet on proven long-term kidney survival; continued approval may depend on confirmatory two-year eGFR data from ORIGIN 3 (an earlier analysis is expected in Q3 2026). It is a prescription biologic used under specialist supervision, NOT a supplement, nootropic or research chemical, and any 'atacicept', 'Trutakna' or 'TACI-Ig' sold by a vendor outside a pharmacy or clinical trial is unverified and should not be used. - Because atacicept blocks BAFF and APRIL - two signals B cells and plasma cells need to survive and make antibodies - it lowers immunoglobulin levels (IgG, IgA and IgM) and can increase the risk of infections; immunizations should be optimized before starting and live vaccines generally avoided during treatment. - Atacicept has a documented history of WORSENING at least one autoimmune disease: in the Phase 2 ATAMS multiple sclerosis trial it UNEXPECTEDLY INCREASED relapse rate versus placebo, and MS development was stopped. This underscores that BAFF/APRIL blockade is disease-context-dependent and should not be assumed beneficial outside its studied, approved indication (IgA nephropathy). - In earlier lupus (SLE) development, a high-dose (150 mg twice-weekly loading) arm of the APRIL-SLE program was halted after serious and fatal infections, which informed later dose selection; infection surveillance remains important throughout treatment. - Use in pregnancy, breastfeeding, active or chronic infection, or malignancy is not established for atacicept; treatment should be managed by a nephrologist or immunology specialist with monitoring of infections and immunoglobulin levels. It is a targeted immunologic therapy for kidney disease, not a component of a peptide 'stack'. ## Comparisons See how Atacicept compares to related peptides: Atacicept vs Efgartigimod: https://peptrackerpro.com/compare/atacicept-vs-efgartigimod Atacicept vs Rozanolixizumab: https://peptrackerpro.com/compare/atacicept-vs-rozanolixizumab Atacicept vs Povetacicept: https://peptrackerpro.com/compare/atacicept-vs-povetacicept Atacicept vs Sibeprenlimab: https://peptrackerpro.com/compare/atacicept-vs-sibeprenlimab Atacicept vs Felzartamab: https://peptrackerpro.com/compare/atacicept-vs-felzartamab Atacicept vs Frexalimab: https://peptrackerpro.com/compare/atacicept-vs-frexalimab ## Calculator Tools Use our research tools to explore dosing and reconstitution data: Reconstitution Calculator: https://peptrackerpro.com/calculators ## Citations 1. [1] Atacicept in Patients with IgA Nephropathy (ORIGIN 3) - New England Journal of Medicine (2025) PubMed (https://www.nejm.org/doi/full/10.1056/NEJMoa2510198) 2. [2] Vera Therapeutics Announces Positive ORIGIN Phase 3 Data for Atacicept in IgA Nephropathy Presented at ASN Kidney Week 2025 and Published in the New England Journal of Medicine PubMed (https://ir.veratx.com/news-releases/news-release-details/vera-therapeutics-announces-positive-origin-phase-3-data) 3. [3] FDA Approves Atacicept (Trutakna) for IgA Nephropathy - HCPLive (2026) PubMed (https://www.hcplive.com/view/fda-approves-atacicept-trutakna-for-iga-nephropathy) 4. [4] The FDA Grants Accelerated Approval to Atacicept for Adults with IgAN - NephCure (2026) PubMed (https://nephcure.org/fda-grants-accelerated-approval-to-atacicept-for-adults-with-igan/) 5. [5] Vera Therapeutics Announces Alignment with U.S. FDA on Earlier ORIGIN Phase 3 Analysis to Support Potential Full Approval for Atacicept PubMed (https://ir.veratx.com/news-releases/news-release-details/vera-therapeutics-announces-alignment-us-fda-earlier-origin) 6. [6] A Study of Atacicept in Subjects With IgA Nephropathy (ORIGIN) - ClinicalTrials.gov NCT04716231 PubMed (https://clinicaltrials.gov/study/NCT04716231) 7. [7] Atacicept in multiple sclerosis (ATAMS): a randomised, placebo-controlled, double-blind, phase 2 trial - The Lancet Neurology (2014) PubMed (https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(14)70028-6/abstract) 8. [8] Merck (KGaA) Announces Out-Licensing Agreement for Investigational Atacicept with Vera Therapeutics (2020) PubMed (https://www.emdgroup.com/en/news/atacicept-outlicensing-09-11-2020.html) ### Keep researching in the app - Log Atacicept to your private tracker - Set a dosing reminder - Compare it side-by-side with your stack Open PepTracker Pro Free: https://app.peptrackerpro.com/?add=atacicept Browse more peptides: https://peptrackerpro.com/peptides ## Related Peptides ### Efgartigimod High Evidence Efgartigimod (efgartigimod alfa, brand names Vyvgart intravenous and Vyvgart Hytrulo subcutaneous) is a first-in-class antagonist of the neonatal Fc receptor (FcRn) developed by argenx as ARGX-113. It is not a small synthetic peptide but an engineered fragment of the human immunoglobulin G1 (IgG1) antibody - specifically the Fc portion that normally binds FcRn - modified with argenx's ABDEG technology to bind FcRn with much higher affinity than natural IgG at both neutral and acidic pH. FcRn is the salvage receptor that rescues circulating IgG from lysosomal degradation and recycles it back into the blood, giving antibodies their long half-life. By outcompeting endogenous IgG for FcRn, efgartigimod blocks that recycling and drives rapid clearance of IgG - including the pathogenic autoantibodies that cause many autoimmune diseases - typically lowering total IgG by roughly 60-70% within weeks, without reducing IgM, IgA, or albumin. It was the first FcRn blocker ever approved: FDA-approved in December 2021 (Vyvgart IV) for acetylcholine-receptor-antibody-positive generalized myasthenia gravis (gMG) on the strength of the Phase 3 ADAPT trial, followed by a subcutaneous co-formulation with recombinant hyaluronidase (Vyvgart Hytrulo) for gMG in 2023 and for chronic inflammatory demyelinating polyneuropathy (CIDP) in 2024. In May 2026 the FDA expanded the gMG label to all serotypes - including AChR-antibody-negative (seronegative) patients - based on the Phase 3 ADAPT SERON trial, making efgartigimod the first and only therapy approved across every gMG antibody subtype. It is being studied in a broad set of other IgG-driven autoimmune diseases, including primary immune thrombocytopenia, myositis, Sjogren's disease, bullous pemphigoid, and lupus nephritis. Immune Modulation: https://peptrackerpro.com/benefits/immune-modulation Neuromuscular Function: https://peptrackerpro.com/benefits/neuromuscular-function Rare Disease Treatment: https://peptrackerpro.com/benefits/rare-disease-treatment Disease Modification: https://peptrackerpro.com/benefits/disease-modification View Details: https://peptrackerpro.com/peptides/efgartigimod \+ Compare: https://peptrackerpro.com/compare?select=efgartigimod Track in App: https://app.peptrackerpro.com/?add=efgartigimod ### Rozanolixizumab High Evidence Rozanolixizumab (brand name Rystiggo, development code UCB7665) is a humanized IgG4 monoclonal antibody that blocks the neonatal Fc receptor (FcRn), developed by UCB. Like efgartigimod and nipocalimab it lowers circulating immunoglobulin G (IgG) - including the pathogenic autoantibodies that drive many autoimmune diseases - by binding FcRn and preventing it from recycling IgG back into the blood, so unrescued IgG is routed to the lysosome and degraded, typically cutting total IgG by roughly 70-80% while sparing IgM, IgA, complement, and albumin. Unlike efgartigimod's engineered Fc fragment, rozanolixizumab is a full-length humanized antibody, and unlike nipocalimab's intravenous infusion it is given as a rapid subcutaneous infusion (including via an on-body delivery device), typically in weekly cycles that are repeated based on clinical response rather than continuously. The FDA approved Rystiggo on June 27, 2023 for generalized myasthenia gravis (gMG) in adults who are anti-acetylcholine-receptor (AChR) antibody-positive or anti-muscle-specific-tyrosine-kinase (MuSK) antibody-positive - making it the first therapy ever approved to treat both of those gMG subtypes - on the strength of the Phase 3 MycarinG trial. It has since been studied across other IgG-mediated diseases, including chronic inflammatory demyelinating polyneuropathy (CIDP), where it did not show meaningful benefit and was not advanced to Phase 3, and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), primary immune thrombocytopenia (ITP), and other autoantibody conditions where development continues. The European Medicines Agency approved rozanolixizumab in January 2024 and the UK MHRA in March 2024. View Details: https://peptrackerpro.com/peptides/rozanolixizumab \+ Compare: https://peptrackerpro.com/compare?select=rozanolixizumab Track in App: https://app.peptrackerpro.com/?add=rozanolixizumab ### Povetacicept High Evidence Povetacicept (development code ALPN-303) is an investigational, once-monthly, subcutaneously injected recombinant fusion protein that simultaneously blocks two B-cell survival signals - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). It is built from an engineered ('variant') form of the natural TACI receptor's extracellular domain fused to an antibody (IgG) Fc region, so it acts as a high-affinity decoy that soaks up both BAFF and APRIL before they can reach their receptors on B cells and plasma cells. Because BAFF and APRIL drive the maturation and antibody production of the immune cells behind many autoantibody- and immune-complex-mediated diseases, povetacicept is being developed for B-cell-driven autoimmune conditions - most prominently IgA nephropathy (IgAN), where APRIL fuels the production of the galactose-deficient IgA1 that damages the kidney. Originated by Alpine Immune Sciences (acquired by Vertex Pharmaceuticals in 2024), povetacicept has received FDA Breakthrough Therapy Designation for IgAN; in March 2026 the Phase 3 RAINIER trial reported a positive prespecified Week 36 interim analysis (a ~52% reduction in urine protein-to-creatinine ratio from baseline and a ~50% reduction versus placebo), and in June 2026 the FDA accepted a Biologics License Application for accelerated approval with a target action date of November 30, 2026. Povetacicept is an experimental biologic given only in clinical trials; it is not a supplement, nootropic, or research chemical. View Details: https://peptrackerpro.com/peptides/povetacicept \+ Compare: https://peptrackerpro.com/compare?select=povetacicept Track in App: https://app.peptrackerpro.com/?add=povetacicept ### Sibeprenlimab High Evidence Sibeprenlimab (brand name VOYXACT; nonproprietary name sibeprenlimab-szsi; development code VIS649) is a humanized monoclonal antibody that binds and neutralizes APRIL (a proliferation-inducing ligand), a cytokine that drives the abnormal, antibody-producing B cells behind IgA nephropathy. By soaking up circulating APRIL with very high affinity, it lowers production of galactose-deficient IgA1 (Gd-IgA1) - the mis-glycosylated antibody whose immune complexes deposit in the kidney and cause the proteinuria and progressive damage of IgA nephropathy (IgAN). Given as a fixed 400 mg subcutaneous injection once every 4 weeks from a single-dose prefilled syringe, sibeprenlimab is designed for at-home self-administration. Originated by Visterra (acquired by Otsuka Pharmaceutical in 2018), it advanced through the Phase 2 ENVISION trial and the pivotal Phase 3 VISIONARY trial - the largest Phase 3 study conducted in IgAN - where it produced a roughly 50-54% placebo-adjusted reduction in proteinuria and signs of preserved kidney function (eGFR). On the strength of those data and an FDA Breakthrough Therapy Designation, the U.S. FDA granted VOYXACT accelerated approval in November 2025 to reduce proteinuria in adults with primary IgAN at risk of disease progression, and Otsuka began a rolling supplemental filing in 2026 seeking traditional approval on longer-term kidney-function data. Sibeprenlimab is a prescription biologic administered under medical care; it is not a supplement, nootropic, or research chemical. View Details: https://peptrackerpro.com/peptides/sibeprenlimab \+ Compare: https://peptrackerpro.com/compare?select=sibeprenlimab Track in App: https://app.peptrackerpro.com/?add=sibeprenlimab ### Felzartamab Medium Evidence Felzartamab (development codes MOR202/MOR03087, and TJ202 in Greater China) is an investigational fully human IgG1 monoclonal antibody that targets CD38, a protein carried at high density on the antibody-producing plasma cells and plasmablasts of the immune system. Rather than blocking a single circulating antibody or downstream mediator, felzartamab depletes the very cells that manufacture pathogenic (disease-causing) antibodies, with the logic that shutting down the factory stops the harmful antibodies at their source. CD38 antibodies are an established drug class in cancer (daratumumab and isatuximab are approved for multiple myeloma), and felzartamab is being repurposed to switch off the autoantibody-driven immune attack behind several serious kidney diseases. It is given as an intravenous infusion in defined treatment courses (for example, a roughly five- to nine-dose regimen) rather than indefinitely. Felzartamab has become one of the most closely watched agents in nephrology because it is advancing through three separate Phase 3 programs in rare, antibody-mediated kidney diseases: IgA nephropathy (IgAN), primary membranous nephropathy (PMN), and late antibody-mediated rejection (AMR) of a transplanted kidney. It originated at MorphoSys AG, was licensed to Human Immunology Biosciences (HI-Bio), which Biogen acquired in 2024, and Biogen consolidated the Greater China rights from TJ Biopharma in 2026. It holds FDA Breakthrough Therapy designation in primary membranous nephropathy. Felzartamab is an investigational prescription biologic administered under medical supervision; it is not approved for kidney disease, and it is not a supplement, nootropic or research chemical. View Details: https://peptrackerpro.com/peptides/felzartamab \+ Compare: https://peptrackerpro.com/compare?select=felzartamab Track in App: https://app.peptrackerpro.com/?add=felzartamab ### Frexalimab High Evidence Frexalimab (SAR441344) is an investigational second-generation, fully human monoclonal antibody from Sanofi that blocks CD40 ligand (CD40L, also called CD154), a costimulatory 'second signal' that helps activate B cells, T cells and antigen-presenting cells and drives adaptive autoimmunity. Rather than depleting immune cells, frexalimab interrupts the CD40-CD40L checkpoint upstream - a mechanism related to but distinct from the OX40-OX40L blockade of amlitelimab. Its lead indication is relapsing multiple sclerosis (RMS), with a second program in nonrelapsing secondary progressive MS (nrSPMS). In the Phase 2 relapsing-MS trial (NCT04879628, published in the New England Journal of Medicine in 2024), frexalimab cut the number of new gadolinium-enhancing brain lesions at week 12 by 89% (higher-dose IV arm) and 79% (lower-dose subcutaneous arm) versus placebo, and open-label extensions out to two and three years show that disease control and reductions in neurofilament light have been sustained. Crucially, frexalimab is engineered so its Fc region does not activate platelets, which is designed to avoid the thromboembolic complications that halted first-generation anti-CD40L antibodies decades ago. It is now in the Phase 3 FREXALT (relapsing MS, versus teriflunomide) and FREVIVA (nrSPMS, versus placebo) trials, with additional Phase 2 programs in type 1 diabetes (FABULINUS) and systemic lupus erythematosus; a Sjogren's syndrome study was discontinued in 2024 after it fell short on efficacy. Frexalimab is investigational and not approved by any regulator. Immune Modulation: https://peptrackerpro.com/benefits/immune-modulation Inflammation: https://peptrackerpro.com/benefits/inflammation autoimmune: https://peptrackerpro.com/benefits/autoimmune Disease Modification: https://peptrackerpro.com/benefits/disease-modification View Details: https://peptrackerpro.com/peptides/frexalimab \+ Compare: https://peptrackerpro.com/compare?select=frexalimab Track in App: https://app.peptrackerpro.com/?add=frexalimab ## Structured data ```json [ { "@context": "https://schema.org", "@type": "Organization", "name": "PepTracker Pro", "url": "https://peptrackerpro.com", "logo": "https://peptrackerpro.com/favicon.png", "description": "Evidence-based educational resource dedicated to improving peptide research literacy.", "contactPoint": { "@type": "ContactPoint", "email": "hello@peptrackerpro.com", "contactType": "customer support" }, "sameAs": [] }, { "@context": "https://schema.org", "@type": "MedicalWebPage", "name": "Atacicept", "description": "Atacicept (brand name Trutakna) is a recombinant soluble TACI-Fc fusion protein and the first dual BAFF/APRIL inhibitor approved for IgA nephropathy (IgAN). It fuses the extracellular ligand-binding domain of the TACI receptor to the Fc region of human IgG1, letting it soak up two B-cell survival cytokines at once - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). By starving autoreactive B cells and plasma cells of both signals, atacicept lowers production of galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody that drives immune-complex deposition and kidney injury in IgAN. It is given as a 150 mg once-weekly subcutaneous self-injection with an autoinjector at home. On July 7, 2026 the FDA granted atacicept accelerated approval (as Trutakna) to reduce proteinuria in adults with primary IgAN at risk of progression - the first and only BAFF-and-APRIL inhibitor cleared for the disease - based on the Phase 3 ORIGIN 3 trial (NCT04716231, 431 adults), in which it cut urine protein (UPCR) 46% from baseline and 42% versus placebo at week 36 (p<0.0001), reduced Gd-IgA1 by 68%, resolved hematuria in 81% of those with baseline blood in the urine, and produced serious adverse events in only 0.5% of patients (versus 5% on placebo). Originated at ZymoGenetics and developed by Merck KGaA (Merck Serono) before being out-licensed to Vera Therapeutics, atacicept sits alongside the anti-APRIL antibody sibeprenlimab and the engineered dual BAFF/APRIL inhibitor povetacicept in the fast-moving IgAN pipeline.", "url": "https://peptrackerpro.com/peptides/atacicept", "lastReviewed": "2026-09-29", "reviewedBy": { "@type": "Organization", "name": "PepTracker Pro Research Team", "url": "https://peptrackerpro.com" }, "isPartOf": { "@type": "WebSite", "name": "PepTracker Pro", "url": "https://peptrackerpro.com" } }, { "@context": "https://schema.org", "@type": "BreadcrumbList", "itemListElement": [ { "@type": "ListItem", "position": 1, "name": "Home", "item": "https://peptrackerpro.com" }, { "@type": "ListItem", "position": 2, "name": "Peptides", "item": "https://peptrackerpro.com/peptides" }, { "@type": "ListItem", "position": 3, "name": "Atacicept", "item": "https://peptrackerpro.com/peptides/atacicept" } ] }, { "@context": "https://schema.org", "@type": "FAQPage", "mainEntity": [ { "@type": "Question", "name": "People with IgA nephropathy (or their families) who heard that a new once-weekly, at-home injection was FDA-approved and want to understand what atacicept (Trutakna) is, how it works, and whether it might slow their kidney disease.?", "acceptedAnswer": { "@type": "Answer", "text": "Atacicept is a research peptide studied in preclinical models. Atacicept (brand name Trutakna) is a recombinant soluble TACI-Fc fusion protein and the first dual BAFF/APRIL inhibitor approved for IgA nephropathy (IgAN). It fuses the extracellular ligand-binding domain of the TACI receptor to the Fc region of human IgG1, letting it soak up two B-cell survival cytokines at once - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). By starving autoreactive B cells and plasma cells of both signals, atacicept lowers production of galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody that drives immune-complex deposition and kidney injury in IgAN. It is given as a 150 mg once-weekly subcutaneous self-injection with an autoinjector at home. On July 7, 2026 the FDA granted atacicept accelerated approval (as Trutakna) to reduce proteinuria in adults with primary IgAN at risk of progression - the first and only BAFF-and-APRIL inhibitor cleared for the disease - based on the Phase 3 ORIGIN 3 trial (NCT04716231, 431 adults), in which it cut urine protein (UPCR) 46% from baseline and 42% versus placebo at week 36 (p<0.0001), reduced Gd-IgA1 by 68%, resolved hematuria in 81% of those with baseline blood in the urine, and produced serious adverse events in only 0.5% of patients (versus 5% on placebo). Originated at ZymoGenetics and developed by Merck KGaA (Merck Serono) before being out-licensed to Vera Therapeutics, atacicept sits alongside the anti-APRIL antibody sibeprenlimab and the engineered dual BAFF/APRIL inhibitor povetacicept in the fast-moving IgAN pipeline." } }, { "@type": "Question", "name": "Nephrologists comparing the rapidly expanding IgAN toolkit - atacicept (dual BAFF/APRIL), sibeprenlimab (anti-APRIL), povetacicept (engineered dual BAFF/APRIL), iptacopan (complement factor B) and targeted-release budesonide - and deciding where a dual BAFF/APRIL blocker fits in the treatment sequence.?", "acceptedAnswer": { "@type": "Answer", "text": "Atacicept is a research peptide studied in preclinical models. Atacicept (brand name Trutakna) is a recombinant soluble TACI-Fc fusion protein and the first dual BAFF/APRIL inhibitor approved for IgA nephropathy (IgAN). It fuses the extracellular ligand-binding domain of the TACI receptor to the Fc region of human IgG1, letting it soak up two B-cell survival cytokines at once - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). By starving autoreactive B cells and plasma cells of both signals, atacicept lowers production of galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody that drives immune-complex deposition and kidney injury in IgAN. It is given as a 150 mg once-weekly subcutaneous self-injection with an autoinjector at home. On July 7, 2026 the FDA granted atacicept accelerated approval (as Trutakna) to reduce proteinuria in adults with primary IgAN at risk of progression - the first and only BAFF-and-APRIL inhibitor cleared for the disease - based on the Phase 3 ORIGIN 3 trial (NCT04716231, 431 adults), in which it cut urine protein (UPCR) 46% from baseline and 42% versus placebo at week 36 (p<0.0001), reduced Gd-IgA1 by 68%, resolved hematuria in 81% of those with baseline blood in the urine, and produced serious adverse events in only 0.5% of patients (versus 5% on placebo). Originated at ZymoGenetics and developed by Merck KGaA (Merck Serono) before being out-licensed to Vera Therapeutics, atacicept sits alongside the anti-APRIL antibody sibeprenlimab and the engineered dual BAFF/APRIL inhibitor povetacicept in the fast-moving IgAN pipeline." } }, { "@type": "Question", "name": "Patients weighing atacicept against sibeprenlimab or povetacicept: dual versus single cytokine blockade, once-weekly versus monthly dosing, and what the proteinuria and Gd-IgA1 numbers actually mean for them.?", "acceptedAnswer": { "@type": "Answer", "text": "Atacicept is a research peptide studied in preclinical models. Atacicept (brand name Trutakna) is a recombinant soluble TACI-Fc fusion protein and the first dual BAFF/APRIL inhibitor approved for IgA nephropathy (IgAN). It fuses the extracellular ligand-binding domain of the TACI receptor to the Fc region of human IgG1, letting it soak up two B-cell survival cytokines at once - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). By starving autoreactive B cells and plasma cells of both signals, atacicept lowers production of galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody that drives immune-complex deposition and kidney injury in IgAN. It is given as a 150 mg once-weekly subcutaneous self-injection with an autoinjector at home. On July 7, 2026 the FDA granted atacicept accelerated approval (as Trutakna) to reduce proteinuria in adults with primary IgAN at risk of progression - the first and only BAFF-and-APRIL inhibitor cleared for the disease - based on the Phase 3 ORIGIN 3 trial (NCT04716231, 431 adults), in which it cut urine protein (UPCR) 46% from baseline and 42% versus placebo at week 36 (p<0.0001), reduced Gd-IgA1 by 68%, resolved hematuria in 81% of those with baseline blood in the urine, and produced serious adverse events in only 0.5% of patients (versus 5% on placebo). Originated at ZymoGenetics and developed by Merck KGaA (Merck Serono) before being out-licensed to Vera Therapeutics, atacicept sits alongside the anti-APRIL antibody sibeprenlimab and the engineered dual BAFF/APRIL inhibitor povetacicept in the fast-moving IgAN pipeline." } }, { "@type": "Question", "name": "Researchers and immunologists interested in the BAFF/APRIL axis, galactose-deficient IgA1 (Gd-IgA1) and the 'four-hit' model of IgA nephropathy, and in TACI-Fc decoy design.?", "acceptedAnswer": { "@type": "Answer", "text": "Atacicept is a research peptide studied in preclinical models. Atacicept (brand name Trutakna) is a recombinant soluble TACI-Fc fusion protein and the first dual BAFF/APRIL inhibitor approved for IgA nephropathy (IgAN). It fuses the extracellular ligand-binding domain of the TACI receptor to the Fc region of human IgG1, letting it soak up two B-cell survival cytokines at once - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). By starving autoreactive B cells and plasma cells of both signals, atacicept lowers production of galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody that drives immune-complex deposition and kidney injury in IgAN. It is given as a 150 mg once-weekly subcutaneous self-injection with an autoinjector at home. On July 7, 2026 the FDA granted atacicept accelerated approval (as Trutakna) to reduce proteinuria in adults with primary IgAN at risk of progression - the first and only BAFF-and-APRIL inhibitor cleared for the disease - based on the Phase 3 ORIGIN 3 trial (NCT04716231, 431 adults), in which it cut urine protein (UPCR) 46% from baseline and 42% versus placebo at week 36 (p<0.0001), reduced Gd-IgA1 by 68%, resolved hematuria in 81% of those with baseline blood in the urine, and produced serious adverse events in only 0.5% of patients (versus 5% on placebo). Originated at ZymoGenetics and developed by Merck KGaA (Merck Serono) before being out-licensed to Vera Therapeutics, atacicept sits alongside the anti-APRIL antibody sibeprenlimab and the engineered dual BAFF/APRIL inhibitor povetacicept in the fast-moving IgAN pipeline." } }, { "@type": "Question", "name": "People who followed atacicept's long, bumpy history in lupus and multiple sclerosis and want to understand why a drug that once increased MS relapses went on to succeed in kidney disease.?", "acceptedAnswer": { "@type": "Answer", "text": "Atacicept is a research peptide studied in preclinical models. Atacicept (brand name Trutakna) is a recombinant soluble TACI-Fc fusion protein and the first dual BAFF/APRIL inhibitor approved for IgA nephropathy (IgAN). It fuses the extracellular ligand-binding domain of the TACI receptor to the Fc region of human IgG1, letting it soak up two B-cell survival cytokines at once - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). By starving autoreactive B cells and plasma cells of both signals, atacicept lowers production of galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody that drives immune-complex deposition and kidney injury in IgAN. It is given as a 150 mg once-weekly subcutaneous self-injection with an autoinjector at home. On July 7, 2026 the FDA granted atacicept accelerated approval (as Trutakna) to reduce proteinuria in adults with primary IgAN at risk of progression - the first and only BAFF-and-APRIL inhibitor cleared for the disease - based on the Phase 3 ORIGIN 3 trial (NCT04716231, 431 adults), in which it cut urine protein (UPCR) 46% from baseline and 42% versus placebo at week 36 (p<0.0001), reduced Gd-IgA1 by 68%, resolved hematuria in 81% of those with baseline blood in the urine, and produced serious adverse events in only 0.5% of patients (versus 5% on placebo). Originated at ZymoGenetics and developed by Merck KGaA (Merck Serono) before being out-licensed to Vera Therapeutics, atacicept sits alongside the anti-APRIL antibody sibeprenlimab and the engineered dual BAFF/APRIL inhibitor povetacicept in the fast-moving IgAN pipeline." } }, { "@type": "Question", "name": "Investors and industry watchers tracking Vera Therapeutics, the July 7, 2026 accelerated approval, the confirmatory eGFR requirement, and the competitive IgAN market against Otsuka's sibeprenlimab and Novartis's iptacopan.?", "acceptedAnswer": { "@type": "Answer", "text": "Atacicept is a research peptide studied in preclinical models. Atacicept (brand name Trutakna) is a recombinant soluble TACI-Fc fusion protein and the first dual BAFF/APRIL inhibitor approved for IgA nephropathy (IgAN). It fuses the extracellular ligand-binding domain of the TACI receptor to the Fc region of human IgG1, letting it soak up two B-cell survival cytokines at once - BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand). By starving autoreactive B cells and plasma cells of both signals, atacicept lowers production of galactose-deficient IgA1 (Gd-IgA1), the abnormal antibody that drives immune-complex deposition and kidney injury in IgAN. It is given as a 150 mg once-weekly subcutaneous self-injection with an autoinjector at home. On July 7, 2026 the FDA granted atacicept accelerated approval (as Trutakna) to reduce proteinuria in adults with primary IgAN at risk of progression - the first and only BAFF-and-APRIL inhibitor cleared for the disease - based on the Phase 3 ORIGIN 3 trial (NCT04716231, 431 adults), in which it cut urine protein (UPCR) 46% from baseline and 42% versus placebo at week 36 (p<0.0001), reduced Gd-IgA1 by 68%, resolved hematuria in 81% of those with baseline blood in the urine, and produced serious adverse events in only 0.5% of patients (versus 5% on placebo). Originated at ZymoGenetics and developed by Merck KGaA (Merck Serono) before being out-licensed to Vera Therapeutics, atacicept sits alongside the anti-APRIL antibody sibeprenlimab and the engineered dual BAFF/APRIL inhibitor povetacicept in the fast-moving IgAN pipeline." } } ] } ] ```