LEADS BIOLABS-B(09887) has signed a global exclusive licensing agreement with DIANTHUS for LBL-047.

LEADS BIOLABS-B (09887) announced on October 16, 2025, that the company has entered into a global exclusive licensing agreement with Dianthus Therapeutics, Inc. (Dianthus, Nasdaq code: DNTH). The company has formed a global exclusive partnership with Dianthus to jointly advance pre-clinical assets and a novel anti-BDCA2-TACI bispecific fusion protein LBL-047. LBL-047 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 receive exclusive rights to develop, manufacture, and commercialize LBL-047 outside of Greater China (including mainland China, Hong Kong, Macao, and Taiwan). Under the global exclusive licensing agreement, the company will receive an upfront payment of up to $38 million and potential near-term milestone payments, as well as up to $1 billion in potential clinical development, regulatory, and commercialization milestone payments. The company will also be entitled to tiered royalty payments on net sales outside of Greater China, ranging from single digits to low double digits. Through this collaboration, the company will partner with Dianthus, a recognized leader in the field of developing transformative therapies for severe autoimmune diseases. The company believes that the global exclusive licensing agreement will strengthen its commitment to advancing innovative drug candidates into clinical stages for addressing autoimmune diseases, in the best interests of the company and its shareholders. It is known that B cells and plasmacytoid dendritic cells (pDCs) 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 the survival, maturation, and function of B cells and plasma cells. The TACI domain can bind to BAFF and APRIL, inhibiting their downstream signaling. pDCs can secrete large amounts of type I interferon (IFN-I, including IFN- and IFN-) and activate T cells and B cells, contributing to the pathogenesis of autoimmune diseases. BDCA2 is specifically expressed on the surface of pDCs and can effectively inhibit the release and subsequent actions of IFN-I after activation. LBL-047 targets BAFF/APRIL and BDCA2, aiming to simultaneously inhibit the activity of pDCs 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 in which B cells and/or pDCs play key roles, such as systemic lupus erythematosus (SLE), dermatomyositis, IgA nephropathy (IgAN), and Sjgren's syndrome. By prolonging half-life through Fc region modification, LBL-047 can reduce dosing frequency and improve patient compliance.