Long-Term Results from an Open-Label Extension Study of Atacicept for the Treatment of IgA Nephropathy

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064165%3A_____%2F25%3A10488703" target="_blank" >RIV/00064165:_____/25:10488703 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11110/25:10488703

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=.1L4IeFZ5x" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=.1L4IeFZ5x</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1681/ASN.0000000541" target="_blank" >10.1681/ASN.0000000541</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Long-Term Results from an Open-Label Extension Study of Atacicept for the Treatment of IgA Nephropathy

Popis výsledku v původním jazyce

Background: B-cell activating factor (BAFF) and A proliferation-inducing ligand (APRIL) play key roles in the pathogenesis of IgA nephropathy. Atacicept is a novel fully humanized fusion protein, self-administered at home by subcutaneous injection, that binds and inhibits BAFF and APRIL. By inhibiting BAFF and APRIL, atacicept targets the underlying B-cell-mediated pathogenesis driving disease progression. This study evaluated the long-term efficacy and safety of atacicept in patients with IgA nephropathy over 96 weeks. Methods: Participants with IgA nephropathy who received atacicept (25, 75, or 150 mg) or placebo in a 36-week phase 2b, randomized, blinded trial were enrolled in an open-label extension study and received atacicept 150 mg for an additional 60 weeks. Key efficacy outcomes were changes in galactose-deficient IgA1 (Gd-IgA1), percentage of participants with hematuria, urine protein-creatinine ratio (UPCR), and eGFR over 96 weeks. Long-term safety data were also evaluated. Results: There were 113 participants (67 [59%] male; 46 [41%] female) who ranged in age from 18 to 67 years who received &gt;=1 atacicept dose. Over 96 weeks, safety data demonstrated that atacicept was generally well tolerated. There were also sustained reductions (mean+-SEM) in Gd-IgA1 (-66%+-2%), percentage of participants with hematuria (-75%; 95% confidence intervals, -87 to -59; in participants with baseline hematuria), and UPCR (-52%+-5%). The mean annualized slope of eGFR was -0.6+-0.5 ml/min per 1.73 m2 through 96 weeks. Conclusions: Atacicept was well tolerated over the duration of the study. Atacicept treatment reduced Gd-IgA1, hematuria, and UPCR with stabilization of eGFR through 96 weeks.

Název v anglickém jazyce

Long-Term Results from an Open-Label Extension Study of Atacicept for the Treatment of IgA Nephropathy

Popis výsledku anglicky

Background: B-cell activating factor (BAFF) and A proliferation-inducing ligand (APRIL) play key roles in the pathogenesis of IgA nephropathy. Atacicept is a novel fully humanized fusion protein, self-administered at home by subcutaneous injection, that binds and inhibits BAFF and APRIL. By inhibiting BAFF and APRIL, atacicept targets the underlying B-cell-mediated pathogenesis driving disease progression. This study evaluated the long-term efficacy and safety of atacicept in patients with IgA nephropathy over 96 weeks. Methods: Participants with IgA nephropathy who received atacicept (25, 75, or 150 mg) or placebo in a 36-week phase 2b, randomized, blinded trial were enrolled in an open-label extension study and received atacicept 150 mg for an additional 60 weeks. Key efficacy outcomes were changes in galactose-deficient IgA1 (Gd-IgA1), percentage of participants with hematuria, urine protein-creatinine ratio (UPCR), and eGFR over 96 weeks. Long-term safety data were also evaluated. Results: There were 113 participants (67 [59%] male; 46 [41%] female) who ranged in age from 18 to 67 years who received &gt;=1 atacicept dose. Over 96 weeks, safety data demonstrated that atacicept was generally well tolerated. There were also sustained reductions (mean+-SEM) in Gd-IgA1 (-66%+-2%), percentage of participants with hematuria (-75%; 95% confidence intervals, -87 to -59; in participants with baseline hematuria), and UPCR (-52%+-5%). The mean annualized slope of eGFR was -0.6+-0.5 ml/min per 1.73 m2 through 96 weeks. Conclusions: Atacicept was well tolerated over the duration of the study. Atacicept treatment reduced Gd-IgA1, hematuria, and UPCR with stabilization of eGFR through 96 weeks.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30217 - Urology and nephrology

Projekt

—

Návaznosti

N - Vyzkumna aktivita podporovana z neverejnych zdroju

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of the American Society of Nephrology

ISSN

1046-6673

e-ISSN

1533-3450

Svazek periodika

36

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

9

Strana od-do

679-687

Kód UT WoS článku

001342121200001

EID výsledku v databázi Scopus

2-s2.0-85207939353