Replimune Group, Inc. (REPL) Earnings Call Transcript & Summary

Welcome, everyone, to the 40th Annual JPMorgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior biotech analysts here at JPMorgan. I'm joined by Priyanka Grover, [ Malcolm Kuno and Kalam Smith ] from the team. Our first presenting company kicking off the conference is Replimune. And presenting on behalf of the company, we have CEO, Philip Astley-Sparke. As a reminder, I want to remind all the attendees about the Ask A Question feature in the portal. Please feel free to put all your questions in the portal, and I'm happy to ask on your behalf. With that, Philip, take it away.

Thanks, Anupam. It's a pleasure to be first up at the '22 Life Science JPMorgan Conference. I only wish it could be in person at the St. Francis. Safe harbor. Replimune. So Replimune is developing an oncolytic immunotherapy platform to maximally activate a systemic immune response against a patient's cancer. And it is our ambition to establish our products as a second cornerstone of immuno-oncology. RP1, our lead asset, we plan to establish a major skin cancer franchise. We have 2 registration studies ongoing in PD-1 naive cutaneous squamous cell carcinoma and PD-1 failed melanoma, having generated compelling data sets in prior studies in these 2 settings. Our [indiscernible] CERPASS study in cutaneous squamous cell carcinoma is accruing well. We're on track to have last patient in the middle of the year and the trigger for the primary analysis late in the year and data disclosures shortly thereafter. Our registration-directed study in PD-1 failed melanoma, we also plan to disclose directional data late in the year. RP2, RP3, targeting less immune-sensitive tumor types. With RP2 over the last 15 months, we've disclosed very compelling Phase I data, both as a single agent and in combination with Opdivo in patients that have failed prior checkpoint blockade therapy. All of these patients are immune insensitive and heavily pretreated. We plan to announce initial data from Phase I with RP3 later in the quarter. Already with RP2, RP3, we're expanding our Phase I studies to focus down on patients of most interest to us in mid-stage development. Those include more prevalent tumor types and patients who have metastasized to the liver. Our exact Phase II program in terms of indications we plan to pursue and in terms of line of therapy, we will disclose later in the quarter. We're preparing for potential launch first up in skin cancers. We have a commercial scale manufacturing facility fully operational. Commercial planning activities are well underway, and we have a strong balance sheet funding us into the second half of '24 and well through our 2 pivotal data points. So a reminder on what oncolytic immunotherapy is. It's the use of viruses that select to replicate in and kill tumor cells but do not replicate in healthy tissue. On injection into a tumor, that tumor is either partially or completely destroyed, the virus rips open the tumor cells and the cancer antigens within are exposed to the immune system in an optimal environment and necrotic cell death. It attracts immune-pleasing or antigen-presenting cells to the injection site. They internalize as escape cancer antigens, drains the lymph nodes and prime T cells to destroy uninjected deposits throughout the [ body ]. So you have a direct local killing of the tumor and ultimately the tumor microenvironment followed by the release of tumor antigens igniting a strong systemic antitumor immune response. We believe that it's best, this is the most practical and effective way to make sure a tumor is recognized as foreign in the first instance. Practical, and it's a simple off-the-shelf products, relatively cheap to manufacture, and the modality is well tolerated. In terms of efficacy, effectively, it's a pan universal neoantigen vaccine, not just concentrating on 1 or 2 episodes using the right viral species in treating the both innate and adaptive immunity and using the right viral species you can package in other immune stimulating proteins into the virus that uses a vector to carry those proteins into the tumor microenvironment and further amplify the immune response. Our platform is based on the herpes virus. We believe that it's best, the herpes virus is an ideal oncolytic species. It being highly lytic and inflammatory and having high carrying capacity. Our own construct is based on [indiscernible] that is selected after comparing multiple strains over a variety of gene cell lines to pick out the most aggressively lytic one possible. And from all of our products and part of our platform the expression of virus at glycoprotein, which increases the lytic and image [indiscernible] construct 10 to 100-fold. And this is essentially RP1, where we plan to establish a maybe skin cancer franchise, not just in cutaneous squamous cell carcinoma and PD-1 failed melanoma, but beyond that into less common tumor types as well, including angiosarcoma, merkel and basal. And we have seen very compelling base to date with clear signs of systemic activity and very assurable responses. RP2, over and above RP1, additionally expresses an [ anti-CTLA ] antibody, and RP3 of the [indiscernible] of CD40 and 4-1BB. RP2 and RP3, we're targeting less immunologically responsive tumor types due to more prevalent tumor types. And those cancers that metastasis the liver, where we've seen [ X ] signal that we plan to follow. So back to RP1. As I said, with RP1, we plan to establish a major skin cancer franchise. And it starts with cutaneous squamous cell carcinoma, where we plan to be the first treatment in combination or alone to offer benefit to all CSCC patients. Our [indiscernible] study is the CERPASS study in first-line CSCC, but we also have studies ongoing in second-line PD-1 failed CSCC in patients who have developed the disease after being immunosuppressed for organ transplant, where we're giving RP1 as a single agent. PD-1 is contraindicated in this setting. In these last 2 settings, PD-1 failed CSCC and organ transplant. We plan to present initial data at the end of the quarter. And we're also designing a neoadjuvant study. This is our lead indication and a reminder about cutaneous squamous cell carcinoma, which is the second most common skin cancer. 60,000 or 70,000 patients are at high risk, that makes the new regimen opportunity very compelling indeed and why we're pursuing it. But in the meantime, the minimum [indiscernible] population creates the number of deaths which is roughly equivalent to melanoma. We also observed with this disease that its locoregional progression leads to 80% mortality, principally being as lesions of the head and neck where it invades vital structures. In terms of the standard of care, it's currently checkpoint blockade drugs anti-PD-1 with both cemiplimab and [ pembrolizumab ] are approved, and give response rates in the 35% to 50% range and complete response rates in the 5% to 15% range. Our CERPASS study is a randomized study comparing RP1 plus Regeneron's cemiplimab against cemiplimab alone with dual primary independent end points of complete response and overall response. The biggest differentiation we've seen to date in our prior study combining single-arm study with Opdivo is in complete response rate. The way the study is powered is if we see a complete response rate in the [indiscernible] arm, of say, 10% in the middle of the range I just described, then we would meet our end point if we get somewhere in the region of 25% to 27% complete response rate. At the moment, in the sister study that I described, we're running at a 1 in 2 complete response rate or almost 1 in 2 complete response rate of 50%. These responses have been very durable in nature, and what we found is that most responses end up becoming complete responses over time. So 7 and perhaps an 8th to be confirmed out of 9 of our responses are complete responses. And they have been in patients with both metastatic disease and local regional disease. This is a patient that we have presented on in previous conferences, for this patient continues to be a complete response now 2 years out from starting therapy. The injected a lesion in the neck region versus the mono and then [indiscernible] in the checkpoint blockade drugs for cycles 3 weeks later, about 8 cycles in combination. And by 16 weeks, incredibly [indiscernible] disease in the neck was completely resolved, as had a node in the retroperitoneal area. And by 1 year, extensive bone mets have also been cleared. And just an example of a locoregional response, also a very nasty ulcerated foot mass that [indiscernible] this patient had [indiscernible] nodes which were injected and was completely resolved away again, leading to a further complete response. Subcutaneous skin cell carcinoma, our lead indication. We also wanted to test whether we could have efficacy in PD-1 failed disease given checkpoint blockade drugs the use. We've been [indiscernible] to treat skin cancers, and we chose melanoma as the setting. The reality is that most patients get either primary or acquired resistance to checkpoint blockade drugs, so it still remains a real unmet need. The idea here is to reprime the immune system or prime in the first instance, the immune system with RP1. And then once the tumor is [indiscernible] to the immune system, give a second course of the checkpoint blockade drugs make sure the immune response is not inappropriately shut down. If you just gave a second course alone, then the response rates of second course of anti-PD-1, if patients are truly progressed, is really very low and very remote and mid-single digit at best. So we're running a 125-patient cohort with registrational intent with response rate as the primary endpoint. We believe if we get somewhere in the 20% to 30% range in a real-world population of both early and late-stage melanoma patients, we'll be well set to have a conversation with the FDA around accelerated approval, particularly in the light of positive surpass data, if that comes to pass. In our sister study with Opdivo, which led into the 125-patient study, we had a 31% response rate, which could still go higher. There are still patients on study that could respond. And pictures tell a thousand words. This is a spider plot with a change of tumor [indiscernible] diameter on the y-axis and time on the X, and the red lines are PD-1 refraction melanoma and the green PD-1 naive. They don't really correlate, which shows that the signal in the refractory setting is almost as strong as it is in the naive setting. And what you also see is those responses getting deeper over time, being very durable in nature, up 600 days. So these are very profound responses. I give one such example here of a patient who failed anti-PD-1 and anti-CTLA-4, clearly progressing on coming on to study with multiple [indiscernible] lesions in the liver and the spleen and also in the lung. So we injected the lung lesion in the red circle. And you can see by 8 months, the extensive disease in the liver and the spleen has resolved, and you can see disease resolving in the lung. That lung tumor is no longer PET avid. It's not actually clear this patient has any disease over 18 months after coming on to therapy with widespread [indiscernible] metastases having failed multiple checkpoint blockade drugs. This theme of being able to inject liver lesion and clear out liver metastases [indiscernible] beyond the liver, I'm going to come back to you as we move to RP2 and RP3. So RP2, a reminder is RP1, it expresses an [indiscernible] antibody to stop the negative feedback loop of the APC T cell interface. Late in '20, we disclosed compelling single-agent activity, which we updated to durability late last year. We currently have ongoing responses or single-agent RP2 in [indiscernible] esophageal cancer up bearing at 21 months. Again, no longer clear by PET this patient actually has any active disease and ongoing complete response in a totally immune insensitive salivary gland cancer. We also have uveal melanoma response, which is a very intractable disease that lasted out to 15 months. And again, going back to that theme of being able to treat the liver metastases of 2 of these patients we have actually injected liver lesions and see scope and effects. The left-hand patient here is an esophageal cancer patient with our 6 lines of prior therapy, including PD-L1, actually had more than 1 liver lesion. The lesion in red was injected and the abdominal node in yellow started to get smaller and is no longer PET avid. And as I said, it's no longer clear this patient has an active disease. And on the right, uveal melanoma, very intractable disease. Injection into the red lesion and clearance of the liver mets in immune insensitive tumor type with clearance of the uninjected liver mets. We followed the single agent with a 30-patient combination cohort, which we updated dated on late last year. Again, pictures tell a thousand words, that spider plot on the right with tumor diameter on the Y axis. And days on the X shows a picture of patients -- multiple patients going to response, and other patients have a long-term stable disease in a true basket Phase I population that has no other options. But we also show no correlation at PD-L1 status so that we are truly treating cold tumors and immune insensitive tumor types like uveal melanoma and head and neck cancer. So, so far, out of the 30 patients still an ongoing study, and this may tick up. We have 7 response out of 30, all in PD-1 failed disease. And again, shown to be very durable in nature, which is the theme of our modality with up to 425 days, 6 out of those 7 responses are still ongoing. Just to highlight uveal melanoma because it is such an intractable disease, and we are targeting RP2/3 to immune insensitive tumor types, I think for the first of 9 patients in uveal melanoma, we already have 3 responses which is a growing signal. Here is a patient where we injected an abdominal node in short responded in both injected and uninjected abdominal nodes. This patient had failed in [indiscernible] in this disease in any case. I think uveal melanoma is the test bed for us having efficacy in immune insensitive tumor types. It's not the largest indication, but we're also going to follow it. There's also a test bed in terms of being able to treat patients that have liver metastases. 90% of patients with uveal melanoma metastasize to the liver, which given the data I've generate -- just presented is a real area of interest for us to pursue. So beyond uveal melanoma, obviously, we plan to also tackle more prevalent tumor types for liver metastases. It's a very large unmet need, for example, colon cancer in the U.S. It's roughly 37,000 patients incidents with liver metastases. And in terms of the unmet nature of treating these patients, once the patients metastasize to the liver their survival chances plummet as do their response rate to checkpoint blockade drugs. And it's not just because you have a tumor in a vital organ. It may also be because with liver resident macrophages eliminate tumor antigen-specific T cells from the systemic circulation, which produces systemic tumor control. So the hypothesis we're testing here given the data we generated to date is whether RPx can reverse that phenomenon. Destroyed it in the first place, the tumor in the liver, but also, at the same time, activate innate and adaptive immunity to restore or increase systemic tumor control. And that is one hypothesis we're now testing an expansion of our RP2 and RP3 Phase I studies. We're concentrating down on more prevalent tumor types and tumor types that commonly metastases to the liver ahead of launching our Phase II program. The exact detail of our Phase II program with RP2, RP3, we will disclose later in the quarter, both in terms of the exact indications we plan to pursue, in terms of the line of therapy we plan to pursue and in terms of what drugs, if any, we plan to combine with. I do want to touch on manufacturing, again, which is very important, particularly as we have aspirations to potentially launch a drug in the near future. We do have our own facility at 20 miles west of Boston in Framingham, that is producing vials. We plan to release product from this facility later in the quarter using the back end of our studies, having completed extensive comparability work with contract material over the last 6 to 9 months. So my final slide is a summary of the RPx platform and then the milestones to expect throughout the course of this year. With RP1, we have generated very compelling data in spleen cancers, which include complete response in patients and are still tracking towards complete responses, including metabolic complete response and shown a very strong signal in PD-1 failed disease. Our [indiscernible] study, it all starts with CERPASS randomized study is nearing [indiscernible] towards the end of the year. It's accruing well, and we expect the trigger for the primary analysis late in the year. RP2, we've generated very compelling data in hard-to-treat traditionally cold tumor types, including in PD-1 failed disease, including in indications like uveal melanoma and head and neck cancer in patients with liver metastases, and RP3 gives an opportunity to further enhance immune activation to address immunologically cold tumors. In terms of our milestones, as I've said throughout the presentation, by the end of the course, we plan to have 2 data -- supporting data sets to surpass in cutaneous squamous cell carcinoma to present initial data from, including in the PD-1 failed setting and in the transplant setting, initial data with RP3 Phase I. And then we're going to give quite some detail on our RP1 commercialization strategy towards the end of the quarter and our overall RP2/3 development strategy. And I'm very excited as we moved towards the end of the year, the primary analysis trigger for the CERPASS randomized study with the data disclosure shortly thereafter. Directional data from our IGNYTE PD-1 failed melanoma study with registrational intent. But hopefully, first data in lung cancer. And also as we move towards the end of the year, we should have collated data with RP2, RP3 Phase I expansion in more prevalent tumor types in tumor patients that are metastasized to the liver. We're very well capitalized through the second half of '24, a good 18 months past the data points on which we will have registrational data to discuss. And the final slide is just to thank you.

Okay. Philip, thanks so much for that. If you want to introduce the broader team on the line for the breakout session, we can kind of get started.

Yes, we have the full team with me here today, including our President, Chief of R&D, Robert Coffin; our Chief Commercial Officer, Sushil Patel; our Chief Business Officer, Pamela Esposito; and our Chief Financial Officer, Jean Franchi.

And I just want to remind all the attendees to use the Ask A question feature in the portal, and I'm happy to ask on your behalf.

I'll maybe kick off the breakout session with a question on CERPASS. The slide that you had up showed us a little bit about the powering assumptions, and we know that it's focused on ORR and CR. So given the low CR that you see with cemiplimab alone, when you talk to physicians and do your market research, is CR potentially the more important endpoint relative to ORR in your physician discussions?

Is that a question for Sush then?

Yes, I'm be happy to take that, Philip. Yes. Certainly, CR is an important endpoint for physicians. Ultimately, we will have overall survival, but that will come much later. I think particularly for a tumor like this, which is sort of aggressive and externally growing, I think patients and physicians really value the idea of seeing a response, a complete response and also the time to that complete response. So those are things that we have found compelling in addition to just the overall CR rate.

And it remains the fact that this modality that patients go into complete response, they tend to meet the medical definition of cure of 5 years. So it's obviously very profound, correlates with survival. If you look at things like melanoma, complete response correlates very well with survival, partial response not so much. So I think the answer to your question, Anupam, is yes. And it's a very profound endpoint and the patient benefit is obvious.

And then maybe thinking a little bit about the PD-1 failed melanoma IGNYTE cohort here. Is the late '22 update going to be solely on ORR? Or will be -- will there -- will we be able to get a DOR read as well?

Yes. That update will be really a snapshot of the ongoing data at that point in patients that have had a reasonable length of follow-up such that there is time for them to achieve a response in that period. So it will be a response in those initial patients and also a durability component in relation to those as well. So what we hope is it will provide a useful directional information as to whether both response and the durability component are heading in the right direction.

And a clarification question that we actually have in the portal is that it says the study requires an observed ORR of 22% to a discount of the true response rate less than 15% and observed response rate of 28% and a true response rate of 20 -- of less than 20%. So I mean, I guess, maybe you can walk us through that statement as well as how we think about the competitive benchmarks or the literature benchmarks for OR and DOR in this setting?

So statistically, those are the lower bounds of the 95% confidence interval. So one can discount at 95% certainty that the true response rate is less than the numbers indicated if we see those observed response rates. I think what physicians and everybody will really focus on is the actual number seen rather than the lower bound and 95% confidence interval. But we do think to demonstrate useful activity to the FDA we have to count it in statistical terms, and those are statistical terms in which it is and has been counted, for example, at the Type B meeting. We certainly see that anything over or discussion with physicians is that anything over 20% with good durability is thought to be clinically meaningful and worth taking note of. But we're certainly hoping for somewhere over 30% in the final data.

We have another question in the portal. What prior examples are you learning from best practices to commercialize this modality?

That's definitely Sush.

Yes. Hi. So in terms of best practices, I mean, if you think of different modalities like cell therapies, I think Philip told you earlier that we do believe this is a more practical approach. And so we don't think it's going to be as complex as that. Certainly, we have an approved oncolytic virus on the market T-VEC. And so there are certainly lessons we've learned that many of this team is very experienced with around commercializing an oncolytic virus. And since they and we believe we've got a more potent platform here and be able to sort of build on that experience. So those are some of the lessons we're learning right now.

Certainly, we're not hearing any reason why intratumoral treatment shouldn't be possible. There's many analogies to thinking of this similar to reverse biopsy. Clearly, there will be required some change in behavior and close collaboration with radiologists and oncologists as we think about injecting deeper tumors. But nothing so far that's been a deal killer from that perspective.

Got it. Maybe a question from me then on both CERPASS and IGNYTE. I guess these are both registrational -- potential registrational studies. So what keeps you up at night about these studies? And what could be the biggest risk we should be thinking about?

I think, obviously, it all starts with CERPASS as our [indiscernible] randomized study. So I think we're feeling pretty good about it because we now have that insurance policy of CR, and we're seeing across the board a tendency for our responses to track towards CR. So given the fact that we have that insurance policy, I think we're sleeping pretty well.

Got it. And then -- so the initial -- some non-melanoma skin cohort data and transplant data also expected in 1Q, right? What are going to be the size and scope of those updates? What's kind of a win scenario in your mind here for RP1?

Rob?

So in both of those settings, PD-1 failed non-melanoma skin cancer and in organ transplant recipients with CSCC. There really is no therapy which could be given to those patients at that point sensibly. So any level of activity would be clinically meaningful. But if I go back to my answer in relation to PD-1 failed melanoma, I think we really need to be seeing response rates above 20% to be with good durability to be thought of as clinically meaningful. And as I said, worth taking note of by physicians as a potential therapy for those patients. With regard to scope, as we have reported before, in the organ transplant study, there have certainly been headwinds to enrollment, particularly in relation to COVID, where such patients do their best very sensibly to avoid hospital settings where they might catch COVID. And as a result, that data set will be relatively modest, but we do think will be sufficient to give, again, a directional idea as to whether we're heading past that target threshold of roughly 20%. In PD-1 failed CSCC, there are increasing numbers of patients out there with PD-1 failed CSCC, both cemiplimab and pembrolizumab being in -- having been in the market for a little while now in CSCC and other PD-1 -- PD-L1s being available for other non-melanoma skin cancers. So that group has been recruiting relatively well. Bearing in mind, we only opened it relatively recently. So again, it will be a relatively small number of patients. But still, we think directionally appropriate to see if we're headed in the right direction and whether we're getting to or may get to a target response rate, which is clinically worth taking note of and potentially could lead to either a label expansion or potentially [indiscernible] listing, depending on how we go about it.

We have another question in the portal, which is you have a bunch of 1Q updates. Are these going to be individual updates? Or are you planning on hosting an R&D Day or event?

We haven't made an official announcement, but it will be most likely, it would be all at one event later in the quarter.

Okay. Then a question from me, just thinking about RP2. You've had monotherapy and sort of combination data at ASCO and SITC. The ORR seems to be in a similar range, but maybe there's some differentiation in durability here. How do you think about the updates and even dating back to ASCO, some of the pushback has been on is a combination truly additive?

For RP2?

Yes, for RP2.

Rob?

So I mean, these are Phase I patients with different patients enrolled in the 2 parts of the study, and it's very hard to compare 2 different Phase I populations, different types of tumor, different prior therapies, different extents of disease, et cetera. I think we can clearly say that RP2 monotherapy is very much clinically active, and we can certainly separately say that RP2 plus nivolumab is very much clinically active. And in both cases, PD-1 failed patients have responded and achieved very durable responses. I think it is hard to -- from the data we've generated so far show claim that RP2 plus nivolumab is actually better than RP2 alone. But we do believe that the logic of the combination is extremely strong, and we would expect in larger studies in larger numbers of patients, particularly in homogenous populations that one really would see a benefit of adding nivo to RP2 even if it's not clearly evident in the data we presented so far. What I also think is worth noting is that there has been no added safety issues when adding nivo to RP2 across each of RP1 and RP2. Tolerability has been extraordinarily good, which really does indicate that we should be able to combine with all sorts of different modalities, including anti-PD-1. And therefore, there's certainly no reason [indiscernible] not to. I think one aspect of the data one could look at in the combo as compared to the monotherapy is that the patients in the combo who didn't or have not yet achieved response did seem to have a much longer periods of stable disease than the monotherapy patients. If you look at the monotherapy data, all of those who weren't responders went off very quickly for progression, whereas in the 30-patient combo data, many of -- more of those are lasting much longer before, either still an ongoing story or before ultimately progressing. That's certainly very much anecdotal and not in any way something which is conclusive, but certainly looks a little bit interesting. So our conclusion is RP2 alone and RP2 in combo are clearly clinically active and ripe for continued clinical development. And as Philip mentioned, we'll be rolling out what the plans are for Phase II clinical development of RP2 and RP3 at the same probable combined investor event towards the end of the complete quarter.

For RP2 and RP3, is there a chance that both or only one would move in liver mets? I know that's a strategy that's been outlined for both, that indication. How do we think about that?

We are going to have an interest in liver mets for everything we do with RP2 and RP3. I would more call it a sort of enrichment for patients with liver mets than an entire focus on patients with liver mets. We will certainly be treating patients with patients who don't have liver mets and types of tumors which aren't necessarily prevalent in the liver as well. But we -- as I said, we will certainly have a focus on patients with liver mets. We do intend, however, in the RP2/3 development program to keep flexibility built in and not plump too early for one or the other. And therefore, there is definitely likely to be a period of parallel development before we may or may not plump for one or other in different circumstances.

And then maybe a final question from me here. Later in '22, you're planning a non-small cell lung cancer update in P-1 failed patients. How is enrollment going? What's the size and scope of the data? What's kind of -- how do we think about a win here in that update?

So again, this is a PD-1 failed setting, where any evidence of activity whatsoever would be clearly interesting and indicate that the platform has the potential to be developed in that setting. I think tolerability of treating patients with lung cancer is also important. However, as Philip said, the real intention with RP1 is to develop a skin cancer franchise around RP1 and everything which is in skin cancer, the intention is to develop RP2 and/or 3 in those more challenging settings. Therefore, anything we see with RP1 may not lead to further development of RP1 in non-small cell lung cancer, but would actually more likely does further inspire us to be wishing to develop RP2 or RP3. However, to come back to the first part of your question in relation to the size and scope of the data enrollment, enrollment has been rather challenging for us in non-small cell lung cancer as we have, I think, previously indicated. There have been a number of reasons for that, including the protocol initially had rather strict inclusion criteria to focus on patients who maybe have a better chance of doing well and also the protocol was originally rolled out for treating largely skin cancer patients and therefore, had the -- didn't have lung investigators associated. Since then, we have more recently amended the inclusion criteria to make them a lot broader and also brought on board some lung-specific investigators and also broadening the protocol out to additional countries beyond the U.S. So while currently, the number of enrolled patients is pretty modest, as the effects of those changes kick in, we anticipate that by the end of the year, as Philip indicated, we would have a sufficient amount of data to demonstrate hopefully feasibility and also initial evidence of activity, which as I said, would largely be supportive of the RP2/3 program rather than further development of RP1 itself in that setting.

Okay. Well, Philip, Rob, Pamela, and I would like to thank you guys so much for taking the opportunity to kick off the conference for us and having a productive breakout session.

Yes, our pleasure.

Thanks, guys.

Thanks, Anupam.