Simon Pimstone
Analyst · Jefferies. Your line is now open. Please go ahead.
Thanks very much. Hugo, that’s an excellent questions. Let me start with the first one. The Phase 2 will likely be a – clearly a multicenter study and we have goals of conducting that in Canada. Beyond the Phase 2 proof-of-concept, as we move into larger development studies which would be Phase 2b effectively, for those range of finding we would likely go beyond Canada. But the first Phase 1, 2 trial for which the protocol is approved is set to be conducted in Canada. We already are setting sites up for the Phase 2. This is a study in terms of numbers of patients that is eminently recruitable in Canada. In fact, Dermira ramdir [ph] ACC inhibitor program for acne in Canada is solely in Canada as well in the initial Phase 2. So, we’re quite confident that the study conducted in Canada will be conducted well. In terms of your next question how transferable is success in one neuropathic pain indication to another for a Nav blocker, I think it’s an outstanding question. And I think the answer at end of the day is we really just don’t know. What I can say, of course, is we do test the molecule in multiple forms of neuropathic pain, in vivo, we’ve looked at a variety of different industry recognized forms of neuropathic pain. We do see efficacy across those models. So, that is certainly our experience in preclinical in vivo models. I think if one goes broadly to pharmacological validation in humans today, not obviously without compound, but in general what we would call dirty our sodium channel blockers, I think it’s tough to say that a given drug is reproducible across all forms of neuropathic pain. We don’t know that’s specifically to be the case, Hugo. But, if we look at a molecule like carbamazepine, for example, it really would be used as a first line treatment, for example, in trigeminal neuralgia. It may not be used as a first line treatment, because of dose limiting AEs in another neuropathic indication like diabetic neuropathic pain. So, I think, it’s going to depend on the molecule. And I think we can make a blanket statement. And obviously, the work we’re doing, the work that others are doing, is this a competitive area – as you know, I think, we’ll certainly start to lucubrate which indications are best suited to this mechanism within the neuropathic timeframe work. So, normal neuropathic pain is equal, we know that. Some have mostly shifted elements. We need to obviously study this drug and others will study their drugs across different indications to identify the best indication. But coming back to our preclinical work, we are encouraged by the breadth of activity we see in our preclinical assays across a broad array of neuropathic models.