I arrived in Stockholm this morning on one of the first flights out of Heathrow. Terminal 2 was chaos. I assume everyone who was meant to be on one of the BA flights that was cancelled, transferred onto a competitor airline in Terminal 2. My flight was full and I am sure I was allocated the last seat on the plane. A small half-sized seat at the far left of the plane. The seat was up against the toilets and didn’t tilt. It was very uncomfortable. Fortunately my discomfort was short-lived and temporary, not like having MS.
I have given my first talk this afternoon around a case study of the ‘real MS’; smouldering MS in someone who is relapse and MRI activity free on fingolimod, but is getting markedly worse. Do you tell them they have SPMS and stop their fingolimod? Or do you escalate their treatment and hope for the best?
The problem with labelling someone as having SPMS is unhelpful without another treatment option or strategy in place for them. Telling someone with MS you now have SPMS is like telling them they have a terminal disease, i.e. it is now all downhill from here. At least having a potential new treatment for SPMS will allow us to offer some hope. The problem that I have is I have no evidence that switching someone who is NEDA2 with worsening MS onto another DMT will make any difference to them. This is an evidence vacuum that needs filling.
I am involved in another meeting tomorrow afternoon run by the MS in the 21st Century initiative to tackle this thorny issue about when and how to tell someone they have progressive MS. In reality, I think this is an academic exercise in that there is now ample evidence from a biological perspective that everyone has both relapsing and progressive MS together and the latter is there from the start. What we are trying to do with our treat early and effectively message is to protect brain reserve so that clinically apparent worsening stage of MS occurs much much later in life, Do you agree or not?
At the afternoon and evening meetings I attended, I was asked if there would be anything new being presented at the ECTRIMS. To be honest with you I don’t think so. Sure there will the positive ponisemod and ofatumumab studies, but these are really old news. Both these drugs are ‘Me Toos’; ponisemod being the 4th in-class S1P modulator and ofatumumab a 3rd generation anti-CD20 monoclonal antibody. There is really nothing new here. Me toos are very low hanging fruit for Pharma with much less risk associated with their development. Believe me, there is nothing transformational that is going to happen on Friday when we get new sets of data; only old news. What we will be arguing over is the percentage differences in relative efficacies between DMTs. We won’t be saying wow what an interesting finding; this is teaching us something new about MS.
What the MS field needs is some novelty, something new in terms of a mode of action, a new class of therapy, a new insight, a new paradigm, etc. That is what I will be looking out for and not the same old, same old.