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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
BAFF (B cell activating factor) and APRIL (a proliferation-inducing ligand) are tumor necrosis factor (TNF) family cytokines that drive the pathogenesis of autoimmune disease via their roles in the activation, differentiation, and survival of B cells and other immune cells. BAFF binds BAFF-R (BAFF receptor), TACI (transmembrane activator and calcium modulating ligand interactor), and BCMA (B cell maturation antigen), while APRIL binds TACI and BCMA. BAFF and APRIL are dysregulated in autoimmune diseases including IgA nephropathy (IgAN) and primary membranous nephropathy (pMN). Povetacicept is an Fc fusion protein of an engineered human TACI domain (with 3 amino acid [AA] substitutions in the 2nd cysteine-rich domain/CRD2) designed to inhibit both BAFF and APRIL with high affinity and potency superior to wild-type (WT) TACI-Fc molecules (i.e., atacicept and telitacicept). However, improved affinity alone may not account for the enhanced efficacy of povetacicept in preclinical disease models, suggesting clinically relevant differences in pharmacokinetics and/or biodistribution.
In a study designed to evaluate tissue biodistribution, povetacicept (12 mg/kg) or molar-matched dose levels of Fc control or telitacicept were administered IV to C57BL/6 mice, and serum and tissues were collected 18 hours post-injection and evaluated by quantitative immunohistochemistry for human Fc+ immunolabeling. Povetacicept demonstrated increased serum exposure and distribution vs. telitacicept to nearly all tissues evaluated. Povetacicept’s enhanced tissue biodistribution may be attributable to its biophysical characteristics, including a lower molecular weight, greater target affinity, and/or a more acidic isoelectric point (pI) compared to WT TACI-Fc. A 2nd study was conducted to address which biophysical attributes of povetacicept contribute to its broader tissue penetrance by testing various analogs of TACI-Fc, including atacicept, telitacicept, and an altered full-length WT TACI-Fc containing WT CRD1 and the 3 AA substitutions in CRD2 from povetacicept (‘alt-TACI’).
Both povetacicept and alt-TACI demonstrated enhanced tissue distribution +(including in kidney, lymph node, heart, and salivary gland) vs. WT TACI-Fc, confirming that the increased affinity of povetacicept for BAFF and APRIL conferred by the 3 AA substitutions in CRD2, and/or its reduced pI, is driving deeper tissue penetration than its WT counterparts.
Based on these and other data, povetacicept has the potential to mediate potent B cell control in antibody-associated diseases like IgAN and pMN.
