Roy M. Fleischmann, MD
Clinical Professor of Medicine
University of Texas Southwestern Medical Center at Dallas
Co-Director, Division of Rheumatology
Texas Health Presbyterian Medical Center and Co-Medical Director
Metroplex Clinical Research Center
With respect to ACR treatment guidelines for RA, do you differentiate between conventional synthetic and biologic DMARDs?
When should DMARDs be used as monotherapy in RA patients? What is the optimal patient profile for combination therapy? How do you biomarkers to guide your decisions? And which biologics have been shown to be successful as monotherapy?
What are the side effects of TNF inhibitors and how do you manage risk for infection? And how does this side effect profile compare to that of IL-6 inhibitors?
What clinical trials have been conducted and/or are currently in progress evaluating IL-6 inhibitors for the management of RA? Can you discuss both tocilizumab and sarilumab and the specific trial designs?
What key clinical parameters, biomarkers, symptoms, and patient-reported outcomes do you prioritize when determining the need for escalating therapy in RA?
Can you provide an overview of the mechanism of action of IL-6 inhibitors in RA, rationale for their use, and what we have learned from landmark trials evaluating the safety and efficacy of sarilumab, tocilizumab, and other drugs in this class?
Considering the positive results from the SARIL-RA-TARGET, SARIL-RA-MOBILITY and EXTEND studies, as well as the recently reported MONARCH study, how do you differentiate among the agents and RA patients to identify ideal candidates for ...
The new EULAR guidelines—as well as ACR recommendations for RA management—are relatively agnostic as far as which biologic DMARD should be used to intensify RA therapy after a methotrexate or other synthetic DMARD failure. What factors ...
Can you discuss the critical recommendations for biologic therapy in RA issued by the ACR guidelines and compare these to the recently reported EULAR guidelines for RA? How are they similar? How are they different? Where do IL-6 inhibitors ...
Are there any specific patient profiles in RA or biomarker signatures that would suggest that an individual patient might respond better to one biologic DMARD and MOA — including IL-6 inhibition — versus another?
How do you differentiate among the available biologics with respect to their propensity to produce side effects or other treatment complications?