And every antiseizure medicine that’s being developed that has activity and is active in the CNS has CNS-related adverse events, and we see that with all of these drugs that the drugs that are very active have dose-dependent adverse events in the CNS, things like dizziness, somnolence, fatigue, and headache. So, that’s fully expected. And then when we specifically look at the KV mechanism when we look at drugs like flupirtine, ezogabine in 1101, we see dose dependence and dizziness. And as you push these drugs higher and see significant activity in the CNS, you see the adverse events associated with that. So, those are some of the things that we would be looking for as we’re evaluating competitive molecules and then obviously, the efficacy data when we think about the patient population that we’ve treated, we believe that we potentially have best-in-category efficacy for this molecule.
And obviously, nobody else has generated efficacy data to-date.
Chris Kenney: This is Chris. Just to quickly add to that. I mean one thing we’re definitely confident with XEN1101 is that it’s penetrating the central nervous system. There’s no doubt about that, right? Preclinical experiments, we have clinical data. We know for sure, there’s penetration of the CNS.
Ian Mortimer: Thanks Chris.
Unidentified Analyst: Great. Thank you.
Operator: Our next question comes from the line of Andrew Tsai from Jefferies. Please proceed.
Andrew Tsai: Thanks. Good afternoon. Thanks. Congrats on the progress. So, I wanted to ask more on the MDD program because you have data in Q3. We generally have a good understanding of what we want to see on the primary endpoint. You shared some details about it earlier. But I did want to ask about how you’re thinking about kinetics in terms of the efficacy curve over time. I mean my question is, do you think 1101 could show a rapid-acting effect within weeks one or two, for instance, similar to what the drug has shown in epilepsy. I don’t believe ezogabine has shown it in depression or epilepsy, but you’ve seen in epilepsy. So, I thought I’d ask for compression. Thanks.
Ian Mortimer: Thanks Andrew. Yes, I’m happy to start and then Chris Kenny please add in. So, yes, I mean, what we — I think you actually — you did a really nice job, Andrew, kind of summarizing what we know. We know that 1101 has early onset to efficacy and stat sig in epilepsy in terms of seizure reduction at week one. So, we do know that we are getting enough drug into the CNS and to target to have an impact on seizures very early in treatment with no titration in an epilepsy population. Obviously, we don’t have that information yet in depression. When we look at the clinical data – the placebo-controlled clinical data generated to-date with ezogabine and this is from the cost publication and the Mount Sinai Group is they did start to see separation early on.
So, there’s definite separation in the curves between active and placebo as we look at MADRS and obviously, those separated more over time. We will be looking at that. So, it’s a week six endpoint, but we will look at all of — we do have weekly — we will have MADRS data throughout all of the weeks up to week six. So, we’ll be able to at least see those curves, Andrew, when we unblind data and be able to answer your question more directly when the data are available. Chris, any additional comments?
