JAK Inhibitors vs TNF Inhibitors: Effects on Administration, Efficacy, and Safety

Author(s):

Panelists discuss how JAK inhibitors and TNF inhibitors differ in administration, efficacy, and safety due to their unique characteristics and mechanisms of action, with further variations in binding activities within the TNFi class impacting clinical outcomes.

EP: 1.Intro and Welcomes

EP: 2.Evolving Goals in Rheumatoid Arthritis Treatment: Defining and Achieving Clinical Remission

EP: 3.Prevalence and Management of Poorly Controlled Rheumatoid Arthritis in Clinical Practice

EP: 4.Complications and Prognostic Factors in Uncontrolled Rheumatoid Arthritis

EP: 5.Evaluating and Adjusting Rheumatoid Arthritis Treatment: Adhering to ACR Guidelines for csDMARDs and Advanced Therapies

EP: 6.Exploring the Discrepancy Between Patient Perception and Disease Activity Assessments

EP: 7.Achieving Low Disease Activity and Remission: Managing Patient Expectations

EP: 8.Guidance on Transitioning from TNFi to Non-TNF Targeted Therapies

EP: 9.Advanced Treatment Options for RA: Exploring the Data

EP: 10.Guiding Treatment Decisions: The Role of Remission Data and Head-to-Head Comparisons

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EP: 11.JAK Inhibitors vs TNF Inhibitors: Effects on Administration, Efficacy, and Safety

EP: 12.JAK Inhibitor Selectivity and Dose-Related Toxicity

EP: 13.Outcomes of Class Switching vs Cycling TNF Inhibitors

EP: 14.Cycling Within TNF Inhibitors: Complications and Factors Influencing Treatment Choices

EP: 15.Safety and Efficacy of Janus Kinase Inhibitors

EP: 16.Closing Remarks

Video content above is prompted by the following:

Tumor necrosis factor inhibitors (TNFis) and Janus kinase inhibitors (JAKis) present with differing characteristics and mechanisms of action (MOA), both between the 2 classes and within each class.

Multiple characteristics distinguish JAKis from TNFis. For example, JAKis are stable small molecule proteins with a short half-life whereas TNFis are heat-sensitive monoclonal antibodies with a long half-life. How do their differences affect administration, efficacy, and safety outcomes?
The MOA within the TNFi class also varies. Etanercept binds both TNF-a and TNF-b with high affinity whereas infliximab, adalimumab, golimumab, and certolizumab-pegol bind to TNF-a with high affinity but not TNF-b. What implications are associated with these different binding activities