This year UCL our UCLP partner hosted the 5th Barts Research Day.They chose the venue, the format and the speakers
In contrast to what had been done previously the Research Day 2014, was in my opinion not really so much about research.
The topics had a feel that were more general, although with a healthy smattering of our clinical research.
The Lab based science was split into two themes QMUL research and UCL lab-based research.
Its a difficult one to balance giving new data that is light years from the clinic.
Professor David Baker
A lot or most of the people that on MS drugs already, if you add in another drug, do you have to look at the safety right from the start again because you have a combination now of 2 drugs, for example?
We don’t have to go all the way round the board again. When you are doing testing you may do it on top of the drugs, so you will get that safety information. Because drugs do interact with each other, it is a part of development process to make sure that the drugs are safe. If you think about it, as in many other diseases, at the early stages it’s like a straight disease modifying drug and maybe few symptomatics, but as time goes by the drugs will be layered on top of each other, I think.
Do you have any thoughts on statins and blood lipid levels, bad vs good cholesterol?
The question with statins is knowing exactly how the drug works. We did some work with statins ourselves and thought that maybe the action has nothing to do with cholesterol synthesis; it’s just that one of the precursors that creates cholesterol was involved in the process of getting cells into the brain, and if you interfere with that process, cells cannot get into the brain. I think with the progressive trial there is another mechanism as well. If you look for example at Alzheimer’s disease genetics, there is a link perhaps with cholesterol synthesis, immune function and few other things. I think we have to learn a lot more about what statins are and what are they doing. ‘I do not know’ is the answer.
If a lot of your research is trying to get through the fat layer, brain barrier, why can’t you then go straight into the brain?
It is a bit drastic. Baclofen is a good example, you pump it into the spinal cord, but it’s a very expensive procedure and we cannot just keep injecting into the spine. The point that I am trying to get across is that we can use these properties in order to make drugs have a better side effect profile. By just getting the drugs in and then seeing how they work, and once we see they do work, we can try to make them better.
What is the chance of the whole drug development thing being quicker than 10-15 years, in the future? Is there any hope for that, because it’s quite a long time?
How would I speed it up? I would get the regulators to make it less of a tedious process. For example, why do we need to have 3 trials for some drugs? If we can make do with one trial for progressive MS for example, this will make it quicker and cheaper. This is one way, and then in terms of how we do the first bit? Well obviously we need to use science to speed this process up, and it can be done. Some of the companies, once they have an idea, they push these things along really quickly, as they can do them at the same time. When we did it we had to do one step, then wait to get some money, go to the next step and wait again to get some more money. With pharmaceutical companies, time is very important, so they do all of the steps simultaneously. It also depends on what the target is. So for our symptomatic drug we have planned our trial to get done within a month, when it is for neuroprotective drugs we don’t really know how long trials need to be, maybe a year or if we are to do a proper trial it can be 3-4 years, we don’t know.
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Presentation 2 Professor Kenneth Smith, UCL
Results too top secret to talk about?
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