Welcome everyone to the 40th annual JP Morgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior biotech analysts here at JP Morgan. I'm joined by Priyanka Grover, Malcolm Kuno, and Caleb Smith from the team. Our first presenting company kicking off the conference is Replimune, and presenting on behalf of the company, we have Chief Executive Officer Philip Astley-Sparke. As a reminder, 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 Rama, and it's a pleasure to be first up at the 2022 Life Science JP Morgan conference. I only wish it could be in person at the Westin St. Francis in San Francisco. Replimune. Replimune is developing an oncolytic immunotherapy platform to maximally activate a systemic immune response against a patient's cancer. 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 two 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 two settings. Our CERPASS study in cutaneous squamous cell carcinoma is accruing well.
We're on track to have last patient in in the middle of the year and the trigger for the primary analysis late in the year and data disclosure 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 were immune sensitive and heavily pre-treated. 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 this phase 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 2024 and well through our two pivotal data points. A reminder on what oncolytic immunotherapy is. It's the use of viruses that selectively 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 of necrotic cell death. It attracts immune policing or antigen-presenting cells to the injection site. They internalize those escaped cancer antigens, drain to the lymph nodes and prime T cells to destroy uninjected deposits throughout the body. You have a direct local killing of the tumor, an altering of the tumor microenvironment, followed by the release of tumor antigens igniting a strong systemic anti-tumor immune response. We believe at its best, this is the most practical and effective way to make sure a tumor is recognized as foreign in the first instance. Practical, it is a simple off-the-shelf product, relatively cheap to manufacture, and the modality is well-tolerated. In terms of efficacy, effectively, it's a pan universal neoantigen vaccine, not just concentrated on one or two epitopes.
Using the right viral species, you're triggering both innate and adaptive immunity. Using the right viral species, you can package in other immune-stimulating proteins into the virus to use as 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 at its 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 a new clinical isolate selected after comparing multiple strains over a variety of tumor cell lines to pick out the most aggressively lytic one possible. From all of our products and part of our platform, we express in the virus a glycoprotein which increases the lytic and immunogenic potential of the construct 10 to 100 fold.
This is essentially RP1, where we plan to establish a major 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. We have seen very compelling data to date and clear signs of systemic activity and very curable responses. RP2 over and above RP1, additionally expresses an anti-CTLA-4 antibody and RP3 the ligands for CD40 and 4-1BB. RP2 and RP3, we're targeting less immunologically responsive tumor types, including more prevalent tumor types and those, cancers that metastasize the liver where we've seen a signal that we plan to follow. 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 banner study is the CERPASS study in first-line CSCC, but we also have studies ongoing in second-line PD-1 failed CSCC. In patients that have developed 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 two settings, PD-1 failed CSCC and organ transplant, we plan to present initial data at the end of the quarter. We're also designing a neoadjuvant study. This is our lead indication and a reminder about cutaneous squamous cell carcinoma. It is the second most common skin cancer. 60,000 or 70,000 patients are at high risk.
That makes the neoadjuvant opportunity very compelling indeed and why we're pursuing it. In the meantime, the minimum adjustable population equates to the number of deaths, which is roughly equivalent to melanoma. We also observed with this disease that it is locoregional progression that leads to 80% mortality, it principally being disease of the head and neck where it invades vital structures. In terms of standard care, it's currently checkpoint blockade drugs, anti-PD-1, with both Cemiplimab and Pembrolizumab approved. They give response rates in the 35%-50% range and complete response rates in the 5%-15% range. Our CERPASS study is a randomized study comparing RP1 plus Regeneron Cemiplimab against Cemiplimab alone, with dual primary independent endpoints 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 Cemiplimab arm of, say, 10% in the middle of the range I just described, then we would meet our endpoint if we get somewhere in the region of 25%-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. Seven, perhaps eight have been confirmed out of nine of our responses are complete responses.
They've been in patients with both metastatic disease and locoregional disease. This is a patient that we have presented on in previous conferences, but this patient continues to be a complete response now two years out from start of therapy. We injected a lesion in the neck region versus the node and then layered in the checkpoint blockade drugs cycles three weeks later for eight cycles in combination. By 16 weeks, the incredibly bulky disease in the neck had completely resolved, as had a node in the retroperitoneal area. By one year, extensive bone metastases have also been cleared. Just an example of a locoregional response also, a very nasty ulcerated foot mass. Actually, also this patient had inguinal nodes which were injected and was completely resolved away. Again, leading to a further complete response.
That's cutaneous squamous cell carcinoma, our lead indication. We also wanted to test whether we could have efficacy in PD-1 failed disease with the checkpoint blockade drugs used ubiquitously to treat skin cancers. We chose melanoma as the setting. The reality is that most patients get either primary or acquired resistance to checkpoint blockade drugs. It still remains a real unmet need. The idea here is to re-prime the immune system or prime in the first instance the immune system with RP1, and then once the tumor is outed to the immune system, give a second course of checkpoint blockade drugs to 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 have truly progressed, is really very low and very remote and mid-single digit at best. 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%-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 CERPASS 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's still patients on study that could respond.
Pictures tell a thousand words. This is a spider plot with change of tumor diameter on the Y-axis and time on the x-axis. The red lines are PD-1 refractory melanoma and the green PD-1 naïve. They don't really correlate, which shows that the signal in the refractory setting is almost as strong as it is in the naïve setting. What you also see is those responses getting deeper over time and being very durable in nature at about 600 days. These are very profound responses. I give one such example here of a patient that had failed anti-PD-1 and anti-CTLA-4, clearly progressing when coming onto study, with multiple visceral lesions in the liver and the spleen and also in the lung.
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 onto therapy with widespread visceral metastases, having failed multiple checkpoint blockade drugs. This theme of being able to inject a liver lesion and clear out liver metastases and see abscopal effects beyond the liver, I'm gonna come back to as we move to RP2 and RP3. RP2, a reminder, is RP1 that expresses an anti-T cell antibody to stop the negative feedback loop of the APC T-cell interface. Late in 2020, we disclosed compelling single-agent activity, which we updated for durability late last year.
We currently have ongoing responses for single-agent RP2 in hard-to-treat esophageal cancer out there at 21 months. Again, no longer clear by PET this patient actually has any active disease, and an ongoing complete response in a totally immune-insensitive salivary gland cancer. We also had a uveal melanoma response to the very intractable disease that lasted out to 15 months. Again, going back to that theme of being able to treat liver metastases, two of these patients we have actually injected liver lesions and seen abscopal effects. The left-hand patient here is an esophageal cancer patient who failed six lines of prior therapy, including PD-L1, actually had more than one liver lesion.
The lesion in red was injected and the abdominal node in yellow started to get smaller, but is no longer PET-avid, and as I said, it's no longer clear this patient has any active disease. On the right, uveal melanoma, very intractable disease, injection into the red lesion and clearance of the liver metastases in immune-sensitive tumor type, the clearance of the uninjected liver metastases. We followed the single agent with a 30-patient combination cohort, which we updated data on late last year. Again, pictures tell a thousand words. That spider plot on the right with the tumor diameter on the y-axis and days on the x shows a picture of patients, multiple patients going into response and other patients having long-term stable disease in a true basket phase I population that has no other option.
What we also show is no correlation to PD-L1 status so that we're truly treating cold tumors and immune-insensitive tumor types like uveal melanoma and head and neck cancer. So far, out of the 30 patients, still an ongoing study, and this may tick up, we have seven responses out of 30, all in PD-1 failed disease, and again, showing to be very durable in nature, which is the theme of our modality, with up to 425 days, six out of those seven responses are still ongoing. Just to highlight uveal melanoma, 'cause it is such an intractable disease, and we're targeting RP2 immune-insensitive tumor types. I think for the first nine patients in uveal melanoma, we already have three responses, which is a growing signal.
Here is a patient where we injected an abdominal node, and saw response in both injected and uninjected abdominal nodes. This patient had failed ipi- pembro, not that ipi- pembro does an awful lot in this disease in any case. I think uveal melanoma is the testbed for us having efficacy in immune-insensitive tumor types. It's not the largest indication, but we're also gonna follow it. There's also a testbed 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 generate just presented is a real area of interest for us to pursue. Beyond uveal melanoma, obviously we plan to also tackle more prevalent tumor types with liver metastases. It's a very large unmet need.
For example, colon cancer in the U.S., it's roughly 37,000 patients incidence with liver metastases. In terms of the unmet nature of treating these patients, once the patient's metastasized to the liver, their survival chances plummet, as do their response rates to checkpoint blockade drugs. It's not just because you have a tumor in a vital organ. It may also be because the liver-resident macrophages eliminate tumor antigen-specific T-cells from the systemic circulation, which reduces systemic tumor control. The hypothesis we're testing here, given the data we generated to date, is whether RPx can reverse that phenomenon, i.e., destroy 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.
That is one hypothesis we're now testing with expansion of our RP2 and RP3 phase I studies. We're concentrating down on more prevalent tumor types and tumor types that commonly metastasize 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, in terms of what drugs, if any, we plan to combine with. I do wanna touch on manufacturing again, which is very, very important, particularly as we have aspirations to potentially launch a drug in the near future.
We do have our own facility 20 miles west of Boston in Framingham that is producing vials. We plan to release product from this facility later in the quarter to use in the back end of our studies, having completed extensive comparability work with contract material over the last six to nine months. 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 skin cancers, which include complete response in patients that are still tracking towards complete response, including metabolic complete response, and shown a very strong signal in PD-1 failed disease. Our banner study, It All Starts with CERPASS randomized study, is nearing full enrollment 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, head and neck cancer, and patients with liver metastases. 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 year, we plan to have two data supporting datasets for 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 from phase I. We're gonna give quite some detail on our RP1 commercialization strategy towards the end of the quarter and our overall RP2/3 development strategy.
Then very exciting, as you move 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, and hopefully first data in lung cancer. 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, including patients that are metastasized to the liver. We're very well capitalized through to the second half of 2024, a good 18 months past the data points from which we will have registrational data to discuss. The final slide is just a thank you.
Okay. Philip, thanks so much for that. If you wanna introduce the broader team on the line for the breakout session, we can kinda get started.
Yes. We have the full team with me here today, including our President, Chief Research and Development Officer, Robert Coffin, our Chief Commercial Officer, Sushil Patel, our Chief Business Officer, Pamela Esposito, and our Chief Financial Officer, Jean Franchi.
I just wanna remind all the attendees to use the ask the 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. 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 Sushil then?
Yeah, I'm happy to take that, Philip.
Yeah.
Yes, certainly CR is an important endpoint for physicians. You know, ultimately we will have overall survival, but that'll 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 or, you know, a complete response and also the time to that complete response. Those are things that we have found compelling in addition to just the overall CR rate.
It remains the fact with this modality, the patients go into complete response. They tend to meet the medical definition of cure of five years. Something very profound correlates with survival. If you look at things like melanoma, complete response correlates very well with survival. Partial response not so much. I think the answer to your question, Alan, fundamentally is yes, and it's a very profound endpoint, and the patient benefit is obvious.
Maybe thinking a little bit about the PD-1 failed melanoma IGNYTE cohort here. Is the late 2022 update gonna be solely on ORR, or will we be able to get a DOR read as well?
Robert?
Yeah. That update will be really a snapshot of the ongoing data at that point in patients who've had a reasonable length of follow-up such that there is time for them to achieve a response in that period. It will be response in those initial patients and also a durability component in relation to those as well. What we hope is it will provide useful directional information as to whether both response and the durability component are heading in the right direction.
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%, an observed response rate of 28% and a true response rate of less than 20%. I mean, I guess maybe you could walk us through that statement as well as how we think about the competitive benchmarks or the literature benchmarks for ORR and DOR in this setting.
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 numbers seen rather than the lower bound of the 95% confidence interval. We do think to demonstrate useful activity to the FDA, we have to count it in statistical terms, and those are the statistical terms in which it is and has been couched, for example, at the Type B meeting.
We certainly see that anything over, our discussion with physicians, is that anything over 20% with good durability is thought to be clinically meaningful and worth you know taking note of. 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 on best practices to commercialize this modality?
That's definitely Sushil,
Yeah. Hi. In terms of best practices, I mean, if you think of different modalities like cell therapies, I think Philip told you earlier that, you know, we do believe this is a more practical approach, and so we don't think it's gonna be as complex as that. Certainly, we have an approved oncolytic virus on the market, T-VEC, and so there's certainly lessons we've learned that many of this team is very experienced with around commercializing an oncolytic virus. Since then, like, we believe we've got a more potent platform here and be able to sort of build on that experience. Those are some of the lessons we're learning right now. Certainly, we're not hearing any reason why an intratumoral treatment shouldn't be possible. There's many analogies to thinking of this similar to reverse biopsy.
Clearly, there'll 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 potential registrational studies. You know, what keeps you up at night about these studies and what could be the biggest risk we should be thinking about?
I think that, you know, obviously it all starts with CERPASS, as our randomized study. I think we're feeling pretty good about it 'cause we now have that insurance policy of CR and we're seeing across the board a tendency for our responses to track towards CR. Given the fact that we have that insurance policy, I think we're sleeping pretty well.
Got it. The initial non-melanoma skin cohort data and transplant data also expected in 1Q, right? What are gonna be the size and scope of those updates? What's kind of the win scenario in your mind here for RP1?
Robert?
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. Any level of activity would be clinically meaningful. 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. As a result, that dataset 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 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. That group has been recruiting relatively well, bearing in mind we only opened it relatively recently.
Again, it'll 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 compendial 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 gonna be individual updates, or are you planning on hosting an R&D day, or event?
We haven't made an official announcement, but it'll be most likely all at one event later in the quarter.
Okay. A question from me, just thinking about RP2, you've had monotherapy and sort of combination data at ASCO and SITC. You know, 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 the combination truly additive?
For RP2?
Yes, for RP2.
Robert?
I mean, these are phase I patients with different patients enrolled in the two parts of the study. It's very hard to compare two 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. We can certainly separately say that RP2 plus Nivolumab is very much clinically active. 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 us that claim that RP2 plus Nivolumab is actually better than RP2 alone.
We do believe 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 Nivolumab 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 Nivolumab 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 in inverted commas 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 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 the 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.
Our conclusion is RP2 alone and RP2 in combo are clearly clinically active, and ripe for continued clinical development. As Philip mentioned, we'll be rolling out what the plans are for phase II clinical development of RP2 and RP3, at the same probably combined investor event towards the end of the quarter.
For RP2 and RP3, is there a chance that both or only one would move in liver metastases? I know that's a strategy that's been outlined for both, but that indication, how do we think about that?
We are going to have an interest in liver metastases for everything we do with RP2 and RP3. I would more call it a sort of enrichment for patients with liver metastases than an entire focus on patients with liver metastases . We will certainly be treating patients who don't have liver metastases and types of tumors which aren't necessarily prevalent in the liver as well. We, as I said, will certainly have a focus on patients with liver metastases . We do intend, however, in the RP2/3 development program to keep flexibility built in and not plunk too early for one or the other. Therefore there is definitely likely to be a period of parallel development before we may or may not plunk for one or other in different circumstances.
Maybe a final question for me here. Yeah, later in 2022, you're planning a non-small cell lung cancer update in PD-1 failed patients. How's enrollment going? What's the size and scope of the data? How do we think about a win here in that update?
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 isn't skin cancer, the intention is to develop RP2 and or RP3 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 just 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 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 that the protocol initially had rather strict inclusion criteria to focus on patients who maybe have a better chance of doing well. Also the protocol was originally rolled out for treating largely skin cancer patients, and therefore 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. 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 sufficient amount of data to demonstrate, hopefully, feasibility, and also initial evidence of activity, which, as I said, would largely be support of the RP23 program rather than further development of RP1 itself, in that setting.
Well, Philip, Robert, Pamela, and Sushil 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.
Yeah. Our pleasure.
Yeah.
Yep.
Uh-huh.
Thanks, guys.