LEADS BIOLABS-B signs a global exclusive licensing agreement with DIANTHUS for LBL-047

According to the announcement from LEADS BIOLABS-B (09887), on October 16, 2025, the company signed a global exclusive licensing agreement with Dianthus Therapeutics, Inc. (Dianthus, NASDAQ code: DNTH), establishing a global exclusive partnership to jointly advance the preclinical asset and the novel anti-BDCA2-TACI bispecific fusion protein LBL-047, which has received Investigational New Drug (IND) approval in the United States and IND acceptance in mainland China. Under the global exclusive licensing agreement, Dianthus will obtain global exclusive rights to research, develop, manufacture, and commercialize LBL-047 outside the Greater China region (including mainland China, Hong Kong Special Administrative Region, Macau Special Administrative Region, and Taiwan). According to the global exclusive licensing agreement, the company will receive an upfront payment of up to $38 million, potential near-term milestone payments, and up to $1 billion in potential clinical development, regulatory, and commercialization milestone payments. The company will be entitled to receive tiered royalties on net sales outside the Greater China region, with rates ranging from single digits to low double digits. The company will take this opportunity to collaborate with Dianthus, which has a recognized leadership position and deep expertise in developing transformative therapies for severe autoimmune diseases. The company believes that signing the global exclusive licensing agreement will strengthen its commitment to advancing innovative drug candidates into clinical stages to address autoimmune diseases and align with the overall best interests of the company and its shareholders. It is reported that B cells and plasmacytoid dendritic cells (pDC) play a crucial synergistic role in the pathogenesis of various autoimmune diseases. BAFF (B cell activating factor) and APRIL (a proliferation-inducing ligand) are key cytokines that promote the survival, maturation, and function of B cells and plasma cells. The TACI domain can bind to BAFF and APRIL, inhibiting their downstream signaling. pDC can secrete large amounts of type I interferon (IFN-I, including IFN-α and IFN-β) and activate T cells and B cells, participating in the pathogenesis of autoimmune diseases. BDCA2 is specifically expressed on the surface of pDC and can effectively inhibit the release and subsequent effects of IFN-I upon activation. LBL-047 targets BAFF/APRIL and BDCA2, aiming to simultaneously inhibit the activity of pDC and the differentiation and activation of B cells and plasma cells. Through glycosylation modification, LBL-047 can more effectively and broadly suppress various abnormal immune responses, showing strong therapeutic potential for autoimmune diseases (including systemic lupus erythematosus (SLE), dermatomyositis, IgA nephropathy (IgAN), and Sjögren's syndrome) that play a key role in B cells and/or pDC. LBL-047 extends the half-life through Fc region modification, which can reduce dosing frequency and improve patient compliance