LBL-047 Prioritized for Clinical Development in Sjögren's Disease, Systemic Lupus Erythematosus, and Dermatomyositis

About this update from Dianthus Therapeutics, Inc.

NANJING, China, May 05, 2026 (GLOBE NEWSWIRE) -- Nanjing Leads Biolabs Co., Ltd. ("Leads Biolabs"; Stock Code: 9887.HK) today announced that its partner, Dianthus Therapeutics, Inc. (“Dianthus”; NASDAQ: DNTH), has selected Sjögren's disease (SjD), systemic lupus erythematosus (SLE), and dermatomyositis (DM) as the first three priority indications for clinical development of LBL-047 (known as DNTH212 outside Greater China). Strategic Priority: Advancing Clinical Development of LBL-047 LBL-047 is a potential first- and best-in-disease bifunctional fusion protein targeting plasmacytoid dendritic cell (pDC) BDCA2 to reduce Type 1 interferon production, while simultaneously inhibiting BAFF/APRIL to suppress B cell function. By targeting both the innate and adaptive immune systems, this complementary and differentiated approach has the potential to address multiple autoimmune indications with improved outcomes. As a core pipeline asset and strategic priority, Dianthus is advancing the clinical development of LBL-047 in SjD, SLE, and DM — three indications with high unmet medical need. In March 2026, Dianthus completed an upsized underwritten public offering, raising approximately $719 million in gross proceeds, providing a strong capital foundation to support the global development of LBL-047. Phase 1 Data Anticipated in 2H’26 A two-part Phase 1 study in China in healthy volunteers (Part A) and patients with SLE (Part B) was initiated in December 2025, with top-line results in healthy volunteers expected in 2H’26. Upon completion of the Phase 1 study, Dianthus plans to provide an update on next steps for advancing its prioritized indications in clinical development. About LBL-047LBL-047 is a bifunctional fusion protein composed of a humanized anti-blood dendritic cell antigen 2 (BDCA2) antibody and an engineered transmembrane activator and CAML interactor (TACI) ectodomain. It is designed to selectively deplete pDCs to reduce type 1 interferon production, while simultaneously inhibiting B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) signaling pathways to suppress B-cell activation, differentiation, and antibody production. By targeting two key drivers of autoimmune disease pathogenesis, this differentiated approach has the potential to address multiple autoimmune indications. Additionally, LBL-047 has been optimized wi...

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