LAS VEGAS – Although biologics have transformed treatment of many rheumatologic disorders, their structure and mechanism of action can come with immunogenic baggage. “They’re proteins; consequently, one can expect immunogenicity,” said Daniel Furst, MD, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.
Immunogenicity can increase clearance of drugs; it can also interfere with the function of the drug. Although physicians may be tempted to think that developing an antidrug antibody to a specific drug is the principal cause for lack of efficacy in an individual patient, “in fact, it’s not that simple,” said Dr. Furst. “There are comorbidities, other drugs, which can affect the immunogenicity itself; there’s even the specific epitope that’s being affected by the drug antibody, which may or may not result in neutralization and an effect.”
In the broad class of tumor necrosis factor inhibitors (TNFIs), about 30% of patients taking adalimumab or infliximab will develop autoantibodies. This is higher than the 10% rate of autoantibody development for other TNFIs.
For non-TNFIs, including abatacept, tocilizumab, and rituximab, “the incidence of immunogenicity is significantly lower,” on the order of 1%-5%, said Dr. Furst, who has appointments at the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence, Italy.
Still, “there’s reasonable evidence that antidrug antibodies to TNFIs decrease efficacy and increase toxicity, particularly skin reactions,” he said.
Global Academy for Medical Education and this organization are owned by the same parent company.
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