Jade Biosciences Presents New Data Demonstrating a Favorable Preclinical Safety Profile of JADE101 and a Translational Analysis of APRIL Mediated Biomarker Responses at the American Society of Nephrology Kidney Week 2025

SAN FRANCISCO and VANCOUVER, British Columbia, Nov. 08, 2025 (GLOBE NEWSWIRE) -- Jade Biosciences, Inc. (“the Company” or “Jade”), (Nasdaq: JBIO), a clinical-stage biotechnology company focused on developing best-in-class therapies for autoimmune diseases, today presented two posters for JADE101, its investigational anti-A PRoliferation-Inducing Ligand (APRIL) monoclonal antibody for the treatment of immunoglobulin A nephropathy (IgAN), at the American Society of Nephrology (ASN) Kidney Week 2025.

JADE101 is designed to selectively inhibit APRIL, a key driver of pathogenic IgA production in IgAN, a progressive autoimmune disease that frequently leads to end-stage kidney disease over a patient’s lifetime. Jade has engineered JADE101 with properties intended to capture the full efficacy of APRIL pathway inhibition while enabling patient-friendly subcutaneous dosing, supported by a differentiated pharmacokinetic and pharmacodynamic profile demonstrated in non-human primates (NHPs). JADE101 is currently being evaluated in a Phase 1 healthy volunteer trial, with interim data expected in the first half of 2026 that is anticipated to define the dose and dose interval for future studies in IgAN patients.

“We believe the selective anti-APRIL class will represent the foundational therapeutic approach for treatment of IgAN, and JADE101 has been specifically engineered to deliver the full potential of this mechanism,” said Andrew King, Ph.D., Chief Scientific Officer and Head of R&D at Jade Biosciences. “These new preclinical data in NHPs demonstrate that JADE101 is highly selective, is well tolerated at toxicological doses, and is not broadly immunosuppressive. Additionally, our translational modeling builds further confidence that biomarker responses observed in healthy volunteers are expected to translate into meaningful outcomes for patients with IgAN. Interim biomarker data from our ongoing Phase 1 healthy volunteer study are anticipated to define the dose and dosing interval selection for JADE101, with the goal of supporting rapid advancement into IgAN patient trials with a potentially best-in-class therapy.”

Nonclinical Safety Profile of JADE101 (Poster #SA-PO0255)

New preclinical safety data highlight JADE101’s favorable safety profile and support its potential as a selective, disease-modifying treatment with low risk of toxicity:

• JADE101 was well tolerated in NHPs at all doses tested preclinically, including the highest dose evaluated in GLP toxicology studies, which was established as the no observed adverse effect level (NOAEL). These results provide wide safety margins that support the first-in-human doses being evaluated in the ongoing Phase 1 healthy volunteer trial.
• Across studies, JADE101 showed no off-target binding in a panel of more than 6,000 human proteins, no human tissue cross-reactivity, and no cytokine release in human whole blood assays.
• In NHPs, JADE101 treatment resulted in reversible reductions in serum immunoglobulins consistent with its mechanism of action, including IgA and IgM reductions of approximately 55–68% and 62–75%, respectively, and a more modest IgG reduction of 35–48%, all of which returned toward baseline following JADE101 clearance.
• Despite reductions in circulating immunoglobulins, JADE101-treated NHPs generated antibody responses to a test immunization (KLH) that were comparable to untreated controls, consistent with the preserved vaccination response observed in healthy volunteers following administration of a previous anti-APRIL monoclonal antibody.
• JADE101 administration in NHPs did not impact serum concentrations of BAFF or inflammatory cytokines, resulted in no histological changes in tissues, and had no effect on circulating immune cell populations, including B, T, or NK cells - supporting its potential as a well-tolerated treatment, devoid of broad immune suppression.