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Suspected side effects can be reported through the MHRA Yellow Card scheme

such binding promotes osteoclast differentiation and osteolytic function in vitro Osteoclast differentiation is dependent on the citrullination of proteins by protein-arginine deiminases Both Fc-dependent and Fc-independent mechanisms are involved in ACPA-mediated osteoclast activation Binding of ACPAs to osteoclasts induces the production of the chemokine IL-8 Infusion of ACPAs into mice causes IL-8-dependent bone loss and IL-8-mediated pain behaviour The unique role of citrullination in osteoclast differentiation and ACPA-induced osteoclast activation might explain important features of the gradual development of rheumatoid arthritis, including why the joints are targeted Abstract A key unanswered question in the pathophysiology of rheumatoid arthritis (RA) is how systemic autoimmunity progresses to joint-specific inflammation

We have already touched on, Amgens MariTide, which is currently in multiple Phase 3 trials, Roche CT388 entering Phase 3, Pfizer continues the promising GLP-1 pipeline it acquired through Metsera in Q425 amongst others (see Table 3)

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