Drs Nehad Soloman, Joy Schechtman, and Robert Levine share their thoughts on how MSRC test results impact the treatment selection for patients with RA.
Nehad Soloman, MD: Are you actively using this molecular signature testing in your practice? Tell us how you’re using it; when are you ordering this test, and how is it impacting your decision?
Joy Schechtman, DO: I also was a part of the AIMS [Accelerate Information of Molecular Signatures] study, and I think where this test should be used is very early on. If you have a patient on methotrexate and you know in your heart that that patient probably is going to go on to a biologic, I would get that test as early as possible. Then I would have that in my data bank, and then if that patient fails methotrexate, or their initial DMARD [disease-modifying antirheumatic drug], then I would look at, let’s look at your testing and your data, and let’s make this decision together as to what the next level should be by the mechanism of action according to what we’re seeing on the MSRC [Molecular Signature Response Classifier] test.
Nehad Soloman, MD: Let‘s say if they are a predictor to nonresponse to TNF [tumor necrosis factor], Bob, what would you choose and why would you choose it? Clearly, if they’re a predictor of nonresponse, you may stay away from TNFs, but where would you go next?
Robert Levine, MD: If they have a strong signal of nonresponse and the higher the number is the stronger the prediction is that they won’t respond, you’re looking at an ACR 50 of 24 weeks of about 5%-10%. I think none of us would say that that’s a good result and we think we can do a lot better. I think the key in those patients who have that signal of nonresponse, try to get an alternative MOA [mechanism of action]. It really doesn’t distinguish between the other MOAs at this point, and I know there’s research going on to look at other MOAs to try to give us a predictor of those, and I’m excited to see that data. The bottom line is to use something else. I think that we have a much better chance and it enhances the chance of getting that patient down to lose disease activity and remission on the first shot. We’re stuck due to insurance formularies. We’re restricted in our access to alternative MOAs as first-line or even second-line therapies. By the way, you don’t need to just use this in a methotrexate or traditional DMARD incomplete responder. You can use this in a biologic DMARD or even a targeted synthetic DMARD incomplete responder as a piece of data that helps you maybe pick the next therapy, whether that’s TNF or non-TNF at this point. It’s incredibly helpful ,and we’re all trying to get our patients to low disease activity and remission as directly and as efficiently and as quickly as possible to improve quality of life, improve outcomes, and improve risk of comorbidities and joint damage. This makes a whole lot of sense to me to go to something else, and we should be discussing those something else’s, and I don’t give up. Oftentimes even when there is a formulary, I look to try to appeal to the insurance company, to write letters and do a peer-to-peer with their medical director, if possible. Occasionally I’ve gotten that approved using this test to help me get the patient what I think is a better choice for them based on the science.
Nehad Soloman, MD: So, you talk about insurance companies being the villain here, and now we finally have a tool, if you will, and some data to help us be in the driver’s seat.
Transcript edited for clarity