So those are the time lines we’re looking forward to. With regard to the pain studies and what you could expect there, I don’t really see read-through from acute to chronic neuropathic pain or vice versa. What I do see read through is from the Phase 2 studies to Phase 3. And I also see read-through from the NaV1.8 class. That is to say VX-150, which already showed efficacy in acute neuropathic and musculoskeletal. So as I look forward to the VX-548 pain study results, and the VX-548 dose-ranging Phase 2 neuropathic range neuropathic study results, that’s where I’m looking to for precedents, the Phase 2 program in VX-548 itself in acute pain, and the VX-150 program across the three pain types.
Andrew Tsai: Very clear. Very helpful. Thank you.
Reshma Kewalramani: Sure.
Operator: The next question will come from Will Pickering with Bernstein. Please go ahead.
Will Pickering: Hi, thank you for taking my question. Another one on pain. For the neuropathic pain study, could you talk about reasons to be optimistic that this drug will compare favorably to existing treatment options based on your experience with VX-150? And then very quickly on sickle cell and the CGT access model, how does the time line for that program compared to the expected launch time line for exa-cel? Thank you.
Reshma Kewalramani: Sure. The first question on how do we think about VX-548 in neuropathic pain and what are our expectations. As I shared with you earlier, when we were waiting on the acute pain Phase 2 results, I have high expectations for the VX-548 program in general, and that extends to neuropathic pain. And the reasons for that are multifold, but here are three reasons. One, NaV1.8 as a target has often been called the holy grail in the pain setting because pain signals go through the NaV1.8 channel, and that’s how these signals are propagated. So they are central to the perception of pain. That is for acute and that is the same for neuropathic. Two, VX-150, the predecessor molecule already delivered positive proof of concept in neuropathic pain.
That study had patients, the 150 study had patients with something called small fiber neuropathy, and it also had patients with diabetic neuropathy, that’s the study we’re doing now, diabetic neuropathy. And three, the VX-548 molecule is multifold, more potent and has better drug-like properties, which is why we went on to seek another molecule despite the success with VX-150. You put that all together and that sort of gives you a sense for why we have our high expectations for this. I think you had a second question on TDT. Let me ask Stuart to comment on that.
Stuart Arbuckle: Yes. Well, so on the CGT access model, I would consider this kind of complementary to our ongoing efforts with both government and commercial payers, secure access for exa-cel as close to approval as we possibly can. The model has only just been announced, and so it’s obviously going to take a while for that to be fleshed out and then implemented. We’re certainly not relying on that to be in place for a successful launch of exa-cel. As I said in my prepared remarks, we’ve been having extensive discussions with both government and commercial payers for the last few months, and we’ll continue to up to and post the approval of exa-cel and so we are working with them. We’re not relying on the CDT access model for a successful launch.
What I do think it is a signal of though, is just how important payers consider getting innovative therapies like exa-cel through these traditionally underserved patient population. So to us, it’s a real indicator of a groundswell of opinion that people want to get these transformative medicines to patients that has been poorly treated in the past.
Will Pickering: Thank you.
Operator: The next question will come from Jessica Fye with JPMorgan. Please go ahead.
