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    Home > Active Ingredient News > Immunology News > Lilly and Rigel have authorized a $960 million partnership to develop RIPK1 inhibitors to treat autoimmune and inflammatory diseases!

    Lilly and Rigel have authorized a $960 million partnership to develop RIPK1 inhibitors to treat autoimmune and inflammatory diseases!

    • Last Update: 2021-02-23
    • Source: Internet
    • Author: User
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    19, 2021 // -- Eli Lilly and Rigel Pharmaceuticals have jointly announced that they have reached a global exclusive license agreement and strategic partnership to jointly develop and commercialize R552 for all adaptations, including autoimmune and inflammatory diseases.
    R552 is a inhibitor of the subject interaction serine/suline protein kinase 1 (RIPK1).
    cooperation agreement, Lilly will also lead the clinical development of brain-penetrating RIPK1 inhibitors in all central nervous system (CNS) diseases.
    R552, Rigel's lead RIPK1 inhibitor, has completed Phase I clinical trials and will launch Phase II clinical trials in 2021 as part of the partnership.
    Rigel is also conducting preclinical research activities on its pilot CNS penetration RIPK1 inhibitors.
    under the terms of the agreement, Lilly will pay Rigel $125 million in cash advances.
    Rigel is eligible for potential development, regulatory and commercial milestone payments of up to $835 million, as well as tiered royalties from the median to the high single digits, which will vary depending on Rigel's clinical development investments.
    and Rigel will jointly develop the R552 at the specified contribution level.
    Lilly will be responsible for all costs of the global commercialization of R552 and Rigel will have the right to commercialize R552 jointly in the United States.
    Lilly will be fully responsible for all clinical development and commercialization of brain-penetrating RIPK1 inhibitors in CNS adaptations.
    RIPK1 is a key signaling protein involved in a range of key inflammatory cellular processes, including programmed cell necrosis (necroptosis, a regulated cell death) and cytokine production.
    in programmed cell necrossion, cell rupture causes cell content to disperse, triggering an immune response and enhancing inflammation.
    inhibition of RIPK1 may be a new treatment for a variety of autoimmune, inflammatory and neurodegenerative diseases.
    in preclinical studies, R552 was shown to prevent joint and skin inflammation in mice with RIPK1-mediated inflammation and tissue damage. "At Lilly, our immunology strategy focuses on finding new targets that have the potential to develop best-in-class drugs to treat autoimmune diseases," said Dr. Ajay Nirula,
    Lilly's vice president of immunology.
    RIPK1 inhibitors is a promising method, and R552 is an exciting addition to our immunology pipeline.
    look forward to working with Rigel to advance its clinical development.
    , President and CEO of Rigel, said, "We are excited to have this strategic partnership with Lilly.
    this collaboration will provide important resources and expertise to support our extensive investigation of multiple disease adaptations by RIPK1 inhibitors.
    Lilly has extensive knowledge of immune and central nervous system diseases and is our ideal partner to ensure the clinical and commercial success of our RIPK1 inhibitor program.
    ": Lilly and Rigel Enter Strategic Collaboration to Develop RIPK1 Restors for The Potential Treatment of Immunological and Neurodegenerative Diseases
    This article is an English version of an article which is originally in the Chinese language on and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.
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