ArticleJournal of inflammation research2025
Characterization of a Long-Acting Anti-Human MASP-2 Antibody for the Treatment of Complement-Related Diseases.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: The complement system is an important component of the innate immune system, which is essential for orchestrating host defense and regulating inflammation. However, overactivation of the complement system plays a pathogenic role in the onset and progression of various inflammatory diseases and rare diseases. Central to the lectin pathway (LP) among three complement activation routes, dysregulation of mannan-binding lectin-associated serine protease-2 (MASP-2) is associated with conditions ranging from IgA nephropathy (IgAN) to hematopoietic stem cell transplantation-associated thrombotic microangiopathy (HSCT-TMA). Thus, we tend to develop an anti-MASP-2 antibody to treat relevant diseases. Methods: Herein, we developed SHR-2010, a novel fully humanized monoclonal antibody targeting MASP-2. SHR-2010 was generated through mouse immunization with recombinant human MASP-2 protein. The binding affinities of SHR-2010 were determined using surface plasmon resonance (SPR). Then, a mouse surrogate antibody ER011-11165 was developed and subsequently evaluated in the lipopolysaccharide (LPS)-induced acute kidney injury murine model. Additionally, the pharmacokinetic (PK), pharmacodynamics (PD) and safety profiles of SHR-2010 were conducted in monkeys. Results: SHR-2010 exhibited strong inhibition of lectin pathway activation in human and rhesus serum. Administration of ER011-11165 significantly mitigated LPS-induced nephrotoxicity in acute kidney injury mouse model. PK profiling in non-human primates (NHPs) revealed high subcutaneous bioavailability and long half-life of SHR-2010, supporting a potential subcutaneous administration route and long dosing interval in clinic. Notably, PD markers demonstrated sustained LP inhibition, with 65.8-80.1% inhibitory effect on serum LP persisting for 408 hours following a single intravenous dose of 5 mg/kg SHR-2010. The nonclinical toxicology evaluation demonstrated that SHR-2010 exhibits a proper safety profile. Conclusion: Preclinical studies demonstrated that SHR-2010 exhibited superior pharmacokinetics and sustained lectin pathway inhibition compared to OMS721. When coupled with optimized trial design strategies, SHR-2010 could be a promising therapeutic candidate for lectin pathway-driven diseases, including IgAN.
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