LEADS BIOLABS-B (09887) announced on October 16, 2025, that it has entered into a global exclusive licensing agreement with Dianthus Therapeutics, Inc. (Dianthus, Nasdaq: DNTH). This partnership will focus on advancing the preclinical asset and novel anti-BDCA2-TACI bispecific fusion protein LBL-047, which has received IND approval for clinical trials in the U.S. and acceptance of IND in mainland China. Under the terms of the exclusive global license agreement, Dianthus will be granted global exclusive rights to develop, manufacture, and commercialize LBL-047 outside of Greater China (inclusive of mainland China, Hong Kong SAR, Macau SAR, and Taiwan). LEADS BIOLABS is set to receive an upfront payment of up to $38 million, potential near-term milestone payments, and up to $1 billion in potential milestone payments related to clinical development, regulatory, and commercialization. Additionally, the company will be entitled to tiered royalties on net sales outside Greater China, with rates ranging from single digits to low double digits. This collaboration aims to leverage Dianthus's recognized leadership and deep expertise in developing transformative therapies for severe autoimmune diseases. The company believes that executing this global exclusive license agreement will strengthen its commitment to advance innovative drug candidates into clinical stages to address autoimmune diseases, aligning with the best interests of the company and its shareholders. It is noted that B cells and plasmacytoid dendritic cells (pDC) play crucial synergistic roles in the pathogenesis of various autoimmune diseases. BAFF (B-cell activating factor) and APRIL (a proliferation-inducing ligand) are key cytokines that promote B cell and plasma cell survival, maturation, and function. The TACI domain can bind to BAFF and APRIL, inhibiting their downstream signaling. pDC can secrete a large amount of type I interferon (IFN-I, including IFN-α and IFN-β) and activate T cells and B cells, thereby participating in the pathogenesis of autoimmune diseases. BDCA2 is specifically expressed on the surface of pDCs and, upon activation, effectively inhibits the release and subsequent action of IFN-I. LBL-047 targets BAFF/APRIL and BDCA2, aiming to simultaneously inhibit pDC activity as well as the differentiation and activation of B cells and plasma cells. Through glycosylation modifications, LBL-047 can effectively and broadly suppress abnormal immune responses significant to autoimmune diseases involving B cells and/or pDC, including systemic lupus erythematosus (SLE), dermatomyositis, IgA nephropathy (IgAN), and Sjögren's syndrome, showing substantial therapeutic potential. LBL-047 is engineered with Fc region modifications to extend its half-life, reducing dosing frequency and improving patient compliance.