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Abstract: FR-PO659

Updated Interim Results of a Phase 1/2 Study of BION-1301 in Patients With IgA Nephropathy

Session Information

Category: Glomerular Diseases

  • 1303 Glomerular Diseases: Clinical‚ Outcomes‚ and Trials


  • Barratt, Jonathan, University of Leicester, Leicester, Leicestershire, United Kingdom
  • Kooienga, Laura, Colorado Kidney Care, Denver, Colorado, United States
  • Agha, Irfan, Dallas Renal Group, Dallas, Texas, United States
  • Thomas, Hanna, Dallas Renal Group, Dallas, Texas, United States
  • Workeneh, Biruh, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
  • Iyer, Sai Prasad N., Chinook Therapeutics Inc, Seattle, Washington, United States
  • Narayanan, Rangaraj, Chinook Therapeutics Inc, Seattle, Washington, United States
  • Sathaliya, Taher, Chinook Therapeutics Inc, Seattle, Washington, United States
  • Sorensen, Bess, Chinook Therapeutics Inc, Seattle, Washington, United States
  • Schwartz, Brian S., Chinook Therapeutics Inc, Seattle, Washington, United States
  • King, Andrew J., Chinook Therapeutics Inc, Seattle, Washington, United States

BION-1301 is a novel humanized monoclonal antibody that blocks a proliferation-inducing ligand (APRIL), a soluble factor that is elevated in patients with IgAN. APRIL promotes the production of pathogenic galactose-deficient IgA1 (Gd-IgA1), leading to immune complex deposition and kidney injury. Blocking APRIL with BION-1301 is a potential disease-modifying approach to directly target the pathogenesis of IgAN. In a Phase 1/2 study (NCT 03945318) in healthy volunteers and patients with IgAN, BION-1301 was well-tolerated with no SAEs and durably reduced free APRIL, IgA, Gd-IgA1, IgM and to a lesser extent, IgG. Here we present updated interim results in BION-1301-treated patients transitioned from IV to subcutaneous (SC) administration (Cohort 1) as well as novel data from IgAN patients with de novo SC administration (Cohort 2).


For the ongoing phase 1/2 open-label, multicohort trial, eligibility criteria include adults with biopsy-proven IgAN, eGFR ≥30 mL/min per 1.73 m2, baseline urine protein excretion ≥0.5 g/24 hrs or UPCR ≥0.5 g/g, and on stable/optimized RASi (or intolerant). Cohort 1 (n= 10) received 450 mg of BION-1301 administered IV every 2 weeks, transitioning to SC at 600 mg every 2 weeks after at least 24 weeks. Cohort 2 (n= 10) receives 600 mg of BION-1301 SC every 2 weeks.


In patients with IgAN who transitioned from IV to SC (Cohort 1), BION-1301 was generally well-tolerated, with no SAEs or terminations due to AEs as of last observation (May 23, 2022). Durable reductions in serum levels of free APRIL and immunoglobulins were observed. As previously reported, clinically meaningful reductions in proteinuria were seen as early as 12 weeks (30.4% geometric mean UPCR reduction, n=7), were sustained through 52 weeks (70.9% geometric mean UPCR reduction, n=6), and were associated with reduced Gd-IgA1 levels. Preliminary response is consistent in patients transitioning from IV to SC. Updated data from Cohort 1 and novel data from Cohort 2 will be reported at the time of presentation.


BION-1301 offers disease-modifying potential by directly targeting the initiating pathogenesis of IgAN. Interim biomarker and clinical activity responses support advancement of BION-1301 into later-stage development for patients with IgAN.


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