And I expect that those results will be available late this year, early next. And the goal there is, gosh, if we see what we saw in Phase II for VX-548 acute pain, that would be a home run. So the diabetic peripheral neuropathy program, this is a multiple-dose-ranging proof-of-concept study where we also have a gabapentin arm for context. So what you should be looking for there is improvement in the pain score from baseline to the 12-week time point when we have the pain endpoint and you’ll be able to make assessments versus the gabapentin arm that’s in their fourth context. That study is fully enrolled and should also be available in terms of results late this year, early next.
Operator: The next question is from Evan Seigerman with BMO Capital Markets.
Evan Seigerman: Kind of a follow-up to Mohit’s question on the Vanza Triple, Talk about what the added benefit of the vanza triple needs to be versus TRIKAFTA to get patients to switch. You also mentioned getting patients to levels of carrier levels of sweat chloride. Could you ever get to a wild-type level of sweat chloride?
Reshma Kewalramani: Yes. Let me take the second half of your question, Evan and then I’ll turn it over to Stuart to talk through how we’re seeing the commercial opportunity for the vanza triple. So when you look at parents, so carriers of the CF mutation, for those who don’t have disease. When you are at those carrier levels of sweat chloride, you have virtually no manifestation of disease. That’s why we’re targeting carrier levels of sweat chloride. You’re fundamentally — just like you and me, I don’t — I’m not a carrier and I’m not a patient with CF. But if you are a carrier of CF, you are fundamentally unaffected. That’s why that’s the highest bar to achieve. And that’s why that’s the bar we continue to chase. The TRIKAFTA triple gets some patients there, the vanzacaftor triple will get more patients there.
But our research continues and we’ve already identified additional potentiators and correctors that will get us to that ultimate goal of carrier levels of sweat chloride. Stuart?
Stuart Arbuckle: Yes. So — and in terms of the sort of uptake and what’s attractive of the profile, we know from speaking with CF clinicians if vanzacaftor has the sort of profile that Reshma described earlier, where it’s delivering increased levels of benefit in terms of CFTR function as measured through sweat chloride that, that in and of itself will be an attractive proposition because as Reshma said, the link between increases in CFTR function and improvements in outcomes has been demonstrated through our own work. In addition, you were talking about patients potentially transitioning. I do think there’s an important group we should also consider which is — there have been a number of patients who over the years have discontinued their CFTR modulators.
It’s probably somewhere north of 6,000 patients who we know want to be on a CFTR modulator but have had to discontinue over the years. And I do think that’s another population who will welcome an additional treatment option being available.
Operator: The next question is from Colin Bristow with UBS.
Colin Bristow: Congrats on the quarter. Maybe one of the CRISPR-based DMD program. Are you still on track to file the IND in the second half? And then assuming all goes to plan, would it be reasonable to expect some clinical data in 2024? And then maybe if I could just have a quick follow-on to the vanzacaftor triple question. Just what do you think you need to see for this to be a launch that is as a major component of switches versus just a new patient acquisition launch?
