ProfG is at the European Neurology Meeting in Amsterdam.
Today, there is a SANOFI GENZYME Satellite Symposium: From clinical data to real world experience – similar results, similar benefits for multiple sclerosis patients?
I guess MS CARE extension data will be presented. The message will be alemtuzumab is a very good drug.
The bad news will be that the proportion of people with secondary autoimmunities from the trials, about 20% will have dramatically increased to about 50%.
Here is the programme
Rogier Q. Hintzen, Rotterdam,
Welcome and Introduction. Rogier Q. Hintzen, Rotterdam, The Netherlands
Mechanism of Action:New Insights into Immunomodulation
Luisa Klotz, , Germany
From Phase 3 controlled trials to extension trials: What do the data
tell us? Celia Oreja-Guevara, Madrid, Spain
Daily practice: How does real world evidence reflect clinical data? Tjalf
Ziemssen, Dresden, Germany (lead author of ECTRIMS abstract-2013 on binding and neutralizing antibody responses).
Q & A:Rogier Q. Hintzen, Rotterdam, The Netherlands
We can see there is a Q & A session which is great.
If you are there scratching you head seeking a question, maybe you can ask a few questions.
I wonder what are the new insights? Weren’t they publish last week:-)? http://jamanetwork.com/journals/jamaneurology/article-abstract/2630681
What is the mechanism?
Wonder if memory B cells will get a mention? Give us a tweet.
If they don’t here’s a few questions for the Q&A.
Q. Why do you think MS is a CD4 Th17 T cell mediated disease given that treatments targeting CD4 T cells have typically failed in MS?
Q. Why do you think there is an increase in Treg T cells when their absolute numbers are decreased by over 80%?
Q. Why are you not associating Tregs influences as a major influence on B cell autoimmunities?
Q. Do you think memory B cells are involved in the action of alemtuzumab?
I will guess. Most people don’t get a third course, few got 3 or fewer get 4 courses of drug. This indeed impressive.
I guess this is not mentioned that most people develop binding and neutralizing antibodies, which they must do given the levels at cycles one and two (about 80%).
Q. How many people develop binding and neutralizing antibodies on cycle 3 and cycle 4?
Q. At 12 months after last infusion how many people have persistent anti-drug antibodies and do they affect depletion.
Q. What is the proportion of people who stop depleting or what is the proportion of people who only partially deplete? We already known at the population level there is depletion (Kousin-Ezewu et al. 2014) but at the individual level, are there people who neutralise the alemtuzumab response.Q. If there are, what is the titre of neutralizing antibodies associated with lack of efficacy.
Q. Are their any non-depleters.
Q. Is there any difference in anaphylaxis/anaphylactoid reactions after third or forth infusion given that most people make binding antibodies and over 70% of people have persistent anti-drug antibodies. Does this relate to pre-existing titres of alemtuzumab binding antibodies?
I suspect if you ask these questions there may be some blank looks .
COI None relevant