Good afternoon and good morning, everyone. I'm Marty Duvall, CEO of Oncopeptides. Welcome to the Oncopeptides post IMW webcast. Yesterday at the IMW meeting h ere in Vienna, Dr. Fredrik Schjesvold presented a late-breaking abstract on the OCEAN dataset representing the first introduction of trial details in a peer-reviewed public setting. Over the past 24 hours, we've been pleased to hear the feedback on this excellent presentation, as well as the strong interest in the OCEAN data results. Today, you will have the opportunity to hear directly from Dr. Schjesvold and participate in a Q&A on the data and perspectives. To present your question, there's a form in the webcast where you can type that in and we'll have the opportunity to talk about it. If you could flip the slide forward. Importantly, we will be making some forward-looking statements today, so please refer to all of our submissions for appropriate balance on representations and warranties of the data as we describe it. Next slide, please. The format today will be that presentation of the OCEAN data, and Dr. Fredrik Schjesvold will include a couple of additional slides. Most importantly, we will have a question and answer session with Dr. Fredrik Schjesvold and Dr. Klaas Bakker. Klaas Bakker, our CMO, will provide a view on the OCEAN data, the opportunity and regulatory update. We'll also hear about our PORT trial and those phase II data results were presented at the IMW meeting in a poster format and represent an important future expansion of mode of delivery of PEPAXTO from a commercial perspective. I'll provide some closing remarks. We'll move into the program with Dr. Klaas Bakker introducing Dr. Fredrik Schjesvold. Klaas, thank you. Thank you, Marty. Before I hand the baton to Dr. Fredrik Schjesvold, I would like to just make some statements beforehand on the fact that the FDA has approved PEPAXTO in patients who are triple-class refractory and have received four prior lines of treatment. This was under accelerated approval. In the OCEAN study, the superior PFS meeting the primary endpoint was there. However, overall survival was in favor of pomalidomide with a hazard ratio of 1.1. Based on this, the FDA has issued a partial clinical hold. As a follow-up of that, there will be an Oncologic Drugs Advisory Committee meeting, in short ODAC, on the 28th of October 2021. We are, as we speak, cooperating with the FDA on the OCEAN data. Next slide, please. Now it's a pleasure to introduce Dr. Fredrik Schjesvold, head of the Myeloma Center at Oslo University Hospital. Importantly, Dr. Schjesvold enrolled most patients in the OCEAN trial and has a vast clinical experience with melflufen. He is here now to provide you with an extended version of the OCEAN presentation. Dr. Schjesvold, the floor is yours. Thank you. Thanks for the introduction and thanks for giving me the opportunity to show this data again, as you said, a little bit expanded. The OCEAN study, a phase III study randomized, and it's a head-to-head study between melflufen dex and pomalidomide dex. This is not so common in myeloma. There are some studies, of course, but most randomized studies are add-on studies where you have a standard of care versus the same treatment plus something else. These studies had just between two drugs and the additional dexamethasone in both, of course. That gives often a bit more interesting results, and we will look at that here. Next slide, please. Next slide. List my disclosures. Next slide. Melflufen is a very new type of drug. It's what we call a peptide-drug conjugate. That means it's a drug conjugated or bound to a peptide. This conjugate makes the drug lipophilic. It means that it can rapidly into cells, but it can also rapidly diffuse out of cells again. What happens to prevent that is that melflufen is hydrolyzed by aminopeptidases that are enzymes in the cells. After it's been hydrolyzed, it releases alkylating agents, like an alkylating drug. That drug is not lipophilic, so that doesn't diffuse out of the cell as rapidly. What we see with this drug is that in cells that have much of this enzyme, these aminopeptidase enzymes, a larger amount of this alkylating drug is trapped in the cells. It means that the sort of chemotoxicity from this drug is mainly seen in cells that have a large amount of aminopeptidases. The reason this mechanism is chosen is that myeloma cells and also some other cancer cells do have a large expression of aminopeptidases. That means that in contrast to a normal alkylator you give orally or intravenously, which works in the same way in all cells. This drug is captured in cancer cells and does its main effect there. That's the reason why this drug is, if you look in pre-clinical data from the lab, this drug is much more potent than other alkylators and also more potent than the alkylating entity that is released here. If you want to discuss this more, we can do that in the end, but that's a sort of introduction to why this drug is a novelty when it comes to the mechanism. We can move on to the next slide. The study, very standard randomized trial in the study design. Patients with relapsed refractory myeloma, they had to have used at least two-four prior lines and a maximum of four prior lines. This is the typical setting for using pomalidomide today. They needed to be refractory to lenalidomide, and they needed also to have tried the proteasome inhibitor, which are the two most standard drugs in the first lines of treatment. They were randomized one to one with equal number of patients in each group. The control arm, pomalidomide dex you see in red here, was given in a standard fashion in the way we use this drug in routine practice. It's a tablet you get days one to 21 in every cycle, which lasts for 28 days. Dexamethasone weekly, which is the same in the intervention arm. In the intervention with melflufen was given on day one, that is just one day each cycle, the first day of each cycle of four weeks. Both drugs were given until the patients were not able to tolerate it anymore or they progressed and had a relapse from their myeloma or of course in some very few events, withdrew from the study. The primary endpoint of the study was like in most studies, the PFS, meaning progression free survival, which is the point that the patient either dies or have a progression of the disease. This progression free survival was assessed by an independent committee not participating in the study in other ways. Of course, there was secondary endpoints, like in most these kinds of studies. We looked at both safety and overall survival and also the overall response rate. Next slide, please. The baseline characteristics of the patients were well-balanced, meaning that the groups looked very similar. You can see on the top that the median age of patients was about 68, ranging from about 60 to 72. Previous lines of therapy was a median of three. That means that the largest fraction of the patients had three previous lines of treatment. Looking at the characteristics in other terms, it was quite what you expect from a patient population between two and four previous lines. If you look at the box on the bottom, you see that 50% of the patients had received a previous transplant, and this is an important number to take note of. Otherwise, patients were refractory to alkylators, about 30% of them. With lenalidomide almost all or in practice all patients were refractory to lenalidomide, which is not so strange since this was an inclusion criterion. Two-thirds were refractory to a proteasome inhibitor and about 20% to anti-CD38 monoclonal antibodies. There was a slightly higher degree of triple-class refractoriness. That means that the patients are refractory to both IMiDs and proteasome inhibitors and anti-CD38 monoclonal antibodies, with 16% in the melphalan arm versus 12% in the pomalidomide arm. Next slide. Next slide. There we are. Thank you. Overall response rate is the number of patients or the fraction of the patients who has a response that we can measure with at least 50% reduction of the tumor load measured by monoclonal components and free light chains. This overall response rate was 33% in the melphalan arm versus 27% in the pomalidomide arm. Slightly higher. If you look at clinical benefit rate, which is all patients that had at least a 25% reduction in their tumor loads. This was also higher in the melphalan arm with 50 versus 41%. If you look at the different types of response, the complete response is that you don't see any more of the monoclonal component and you have low number of cancer cells in the bone marrow at 3% versus 1%. Also for VGPR, which is 90% reduction, partial response which is 50% reduction and minimal response which is 25% reduction. In all these categories, there were a higher number for melphalan dex versus pomalidomide dex. Next slide please. This is the primary endpoint. This is what most studies define if a study is a success or not. The progression-free survival of patients on melflufen and dex was 6.8 months versus in pomalidomide dex, this was 4.9 months. This is a hazard ratio of 0.79, meaning that there's a 21% lower risk of getting progression on melflufen dex versus pomalidomide dex. You can see the P value is 0.03, which means that this is a statistically significant result, and a result that means that it takes a longer time to either progress or die with melphalan than with pomalidomide dex. This was assessed by the independent response committee and not by the study team or the study investigators themselves. Next slide, please. Looking at subgroups, you can see that if you look at the dotted line, vertical line at the place of the one number, you see that if you are on the left of this, that means that this subgroup was by melflufen dex treatment. This is for PFS. Usually, subgroups are in line with the ITT population, that is the total population result where we saw that there was a PFS benefit of melflufen. In a head-to-head study, this can be a little bit different than in an add-on study. We can find some interesting results here. I would like you to look at first the age category in the top, where you see that the oldest patients benefited the most from melflufen dex, and the youngest didn't benefit at all. You see the dot is right on the dotted line. This is probably, we think, connected to what you see in the lower box, where you see that patients with a previous transplant, and that is patients that are younger, they did not benefit from melflufen dex. The result was the same in both groups. If you look at patients who did not receive a previous transplant, they benefited significantly from treatment with melflufen dex. I think probably these age groups and the previous transplant are the same thing since elderly patients do not get, in most cases, a transplant. For the other results, it's not so much to comment. If you look at the only dot that's really on the right side, you see that the confidence interval is really huge. That's because there were very few patients in this group, so I wouldn't put too much emphasis on that. Next slide, please. This is maybe one of the more interesting slides here because here you see that these graphs are PFS. It's the same as the previous one, but now we have divided both the melflufen dex group and the pomalidomide dex group into those who had received a prior transplant and those who hadn't received a prior transplant. As you recall, transplants were given to about half the population, so these four groups are more or less similar in size. Here you can see that the two red graphs, pomalidomide dex with and without the prior transplant, perform more or less equally. They also perform more or less equally with melphalan dex with a prior transplant. The group that really separates from the others are melphalan dex that have not received a prior transplant. Just to mention that, I didn't mention that before, a transplant is also an alkylating agent. A transplant sometimes puts some long-term stress on the bone marrow, and that might be an explanation for this. What you see here is that the group that has no prior transplant and receives melphalan dex is definitely the group in this study that benefited the most. It's this group that drives the PFS benefit that was seen in the total population group of melphalan dex. You can also see that in the median PFS, the difference is larger here than it was in the total population with 9.3 versus 4.6. You can see the hazard ratio is smaller at 0.59, meaning that there's a 41% reduction in risk of progression or death. You also see that the P value is highly statistically significant. Next slide, please. When I looked to this into more detail, on the top you see the patients with a prior transplant. On the bottom, you see those with not the prior transplant. Those two were in the previous forest plot with all the other subgroups. If you would divide the prior transplant into patients who had received prior transplant very recently, within two and a half years, those who have received a prior transplant before more than five years ago, and in between those between two and a half and five years, you see the trend all the way that the longer time that has passed since you had the transplant, the more you benefit from melflufen dex. This is only significant for the ones without the prior transplant, but also for the ones with more than five and 2.5 to 5, the PFS benefit trends toward melphalan. Next slide. This is overall survival, and this is what has led to the partial clinical hold of FDA, which Klaas discussed in the beginning here. What you see is that you can see on the right that this is not a statistically significant finding. You also see that the hazard ratio is 1.1 and that pomalidomide in the red is the group that numerically has a higher survival. This is the reason that that clinical hold was started, and FDA are looking more into this data together with Oncopeptides. I will show you some of the data they are looking into. Next slide. Here we have the subgroup analysis of overall survival. If you look at age first, you see the same as for PFS, that the patients who are the oldest benefit significantly from getting melphalan, and those who are the youngest benefit from pomalidomide, with those in between not benefiting more from one or the other. For the rest of the subgroups here, there's not so much interesting findings. Actually, they are all groups very close to one. If you go to the next slide. Here you can look at especially the previous transplants which we have discussed for PFS. If you look at that, it's the third from the top. You can see that those who have experienced a previous transplant do benefit from pomalidomide, while the patients who had not received a previous transplant benefit from melphalan dex. This finding is not statistically significant, it's at least not the other way around. You can also see for the alkylator refractory in the next line trends towards having a benefit of melflufen dex, which is important since this also has an alkylating mechanism. That means that being refractory to alkylators is in itself not one reason to not use melflufen dex, almost the opposite. On the bottom, you can see overall survival when it comes to renal failure, but those data are a bit confusing because some of the groups are very small. It trends towards less renal failure or normal kidney function benefiting pomalidomide and the other renal failure benefiting melflufen dex to a higher degree. The last group is so small that it's difficult to discuss that point in particular. Next slide, please. These are the overall survival Kaplan-Meier curves. We have already looked at the subgroups and so the hazard ratios and p-values was already there, but here you can see it more visually. If you see on the right, if the patient has received a prior transplant, pomalidomide dex is definitely better for survival. If you look on the left, if the patient has not received a prior transplant, melflufen dex is trending towards a better survival, and this trend is stronger than the trend for pomalidomide dex in the total population which led to the partial clinical hold. You can also see if you look at patients who had not received a prior transplant, and you see below there you can see that the median OS is 21.6 versus 16.5 months. With a 22% reduction in risk of death. The opposite is true for patients with a prior transplant. Next slide, please. These are the same groups that we looked at for PFS. Now it is for OS. You see on the bottom, you see patients with no prior transplant. On the top, those with a prior transplant. You see that as what we have mentioned already that if you have not had a prior transplant, OS is favored by using melflufen dex and pom dex for those who have used a prior transplant. You also see here that the longer time that has passed since the transplant, the more you benefit from melphalan. Those who have more than five years of time since their transplant also get on the melflufen side here of the line. Next slide, please. Yes. This is efficacy. I mentioned this briefly. This is efficacy in non-transplant alkylator refractory patients because there's a discussion whether melflufen is just another alkylator or if it has something extra that other alkylators don't have. This is important because there are other alkylators on the market that are available and, of course, cheaper since they're generic drugs, and also used to some degree in myeloma treatment. What you see actually here is that if you look at only the non-transplanted, because we've already seen that that is a group that melflufen is benefiting the most. If you look at that group on the right here, those who are also alkylator refractory, that means that they have used an alkylator before, that is melphalan or bendamustine or cyclophosphamide, and have progressed on treatment with that alkylator. You can see that on the right top here that if they received melflufen dex in this study versus pomalidomide dex, the difference in PFS was 8.3 versus 3.8. That's actually a larger difference than in the total population. The median overall survival is increased from 13.1 with pomalidomide dex to 24.3 with melflufen dex. A very strong signal that it's the transplant that is a problem for melflufen patients not to be refractory to other alkylators. It also suggests that this drug actually is a different thing than the other alkylators that are on the market since patients relapsing on these other alkylators are getting this large benefit from melflufen. Next slide, please. Looking here at when the patients died, if you look at the top orange box, the number of deaths in the total safety population, that is between all patients that has tried the treatment, that received the treatment in the study, is 46% versus 43%, a little bit higher for melflufen but not much. You see that death before 30 days after last dose, that is what we define as on treatment, it's a little bit higher for pom dex at 13% versus 10%. After more than 30 days after last dose is higher for melflufen, 36% versus 30%. It means that the excess deaths of melflufen, at least some of that comes after the treatment has ended, while for pomalidomide maybe a little bit more while on treatment. I can also show you something that is a bit complicating, is that if you look on the top here, you see that 246 patients were randomized to melflufen dex, but only 228 received the treatment. That difference is much smaller from the pom dex arm and we don't have the total explanation for that. Those are patients who didn't receive the treatment, but they are still counted overall survival group. Next slide, please. When it comes to adverse events in this treatment, it was definitely mostly hematological. You can see there's more thrombocytopenia in the melflufen group, but not much bleeding. We only saw 1% of a severe bleeding in these patients in the melflufen group. Neutropenia was higher in the melflufen arm, but infections were higher in the pomalidomide arm. It doesn't seem that this neutropenia leads to infection or this higher degree of neutropenia doesn't lead to a higher degree of infections. Pomalidomide had more infections in all way we counted. Infections in total, grade three and four infections, infected pneumonia and grade three and four pneumonia and also with concomitant neutropenia. Anemia was more common in melflufen arm, but anemia is not something we have a particular problem with managing on the clinical side. It was not many unequal numbers of new malignancies during the study. Next slide, please. If you look at adverse events that were not hematological and not infections, they were not very common, at least not in grade three and four. I'm not going through this, but it's very small numbers. What you can see on the bottom is that those delays and reductions were more frequent in the melflufen arm. This is, I think, part of managing this drug is that you need to sometimes dose delay and sometimes reduce the dose to be able to have the patients on treatment. You need that with all drugs, but as you see here, a little bit more in melflufen than with pomalidomide dex. Next slide, please. Concluding, this was a head-to-head study of melflufen dex versus pomalidomide dex, which is not very common in myeloma. Melflufen dex was still superior to pomalidomide dex for the primary endpoint of PFS. OS trended in favor of melflufen plus dex in patients without the prior transplant and favored pomalidomide dex in patients with the prior transplant. Quite a dichotomy in these two groups that both was half of the population in the study. The safety was as has been reported before on this drug with mostly hematological adverse events that are manageable. It's not a drug that has many other symptoms for the patients. The result, in my opinion, shows that in this group with two to four prior line of treatment who are refractory to lenalidomide. melflufen dex is a better drug for patients who have not received a transplant, while pomalidomide dex is a better drug for those who have received a transplant, especially if it's recently. I think that was all. Is there maybe an acknowledgment slide on the end here? No. Thank you. I'm open to take questions and comments. Thank you very much, Dr. Fredrik Schjesvold, for this very comprehensive overview of the OCEAN data. I see that a lot of questions have already come in, and we'll try to answer them all. Some of these will be answered during the Q&A on the end when it is clear about the regulatory strategy, et cetera. I would encourage everyone on the line to submit questions that are relevant from a clinical perspective, now that we have Dr. Fredrik Schjesvold with us, so that he can share his expertise with you on some questions. When I start with one of the questions, it is from Patrik Ling regarding overall survival. Do you have any data on what subsequent treatments the patients got, and were there any differences between patients receiving PEPAXTO and pomalidomide? Could that then maybe explain some of the difference in OS outcome? Dr. Schjesvold, what's your view there? There were an imbalance in subsequent treatment. There were more patients receiving CD38 antibodies in the pomalidomide group, and there were more patients receiving pomalidomide in the melflufen group. There's definitely an imbalance there. We also have data showing that the patients who received daratumumab as the next treatment were doing the best of the patients that were treated afterwards. There is data suggesting that there's a bias there that can drive the overall survival the wrong way. We also know that it's only about 20% of the patients were refractory and probably not more exposed to CD38 antibodies before. It's a bias there. Personally, I think it's always very complicated to start discussing that because if you had a patient who received melflufen in routine practice and you had a patient who received melflufen in a study, when they are out of the study or getting a new treatment in routine practice, the same sort of decisions are being made. If you were going to use that as an argument, you would have to say that you should, after melflufen, get daratumumab instead of pomalidomide. That's a difficult case to advocate when you want the drug approved and reimbursed. Personally, I think it explains quite a lot, but it's very difficult to move on with that argument, I would say. I think it's much more important to focus on the large subgroup that really benefited from melflufen, disregarding subsequent therapies. That is the question of transplants. Thank you, Dr. Fredrik Schjesvold. We have a question from Peter Welford from Jefferies as to what would be a possible explanation. What would be a mechanistic or biological rationale for why a prior stem cell transplant drives this delta? A transplant is not good for the bone marrow. We know that it can take time for the bone marrow to recover fully and to become a normally functioning bone marrow again. I think that is the time issue. I think that if a number of years have passed, I think that the bone marrow is more normalized, at least on average, also depending on further treatment, of course. If you have performed a recent transplant, I think the tolerance for an alkylating drug like melflufen is lower. I think that's the main mechanism. I think it's difficult for a bone marrow that has received a transplant in the recent couple of years to tolerate melflufen. I think that's why we see more deaths of melflufen in the melflufen group after they have stopped therapy with melflufen. I think that when you have the combination of a transplant and then melflufen, your bone marrow will have struggles to tolerate treatment afterwards. I think the treatment afterwards will be probably less tolerated, more dose-reduced, and more stopped. I have to say that this is a speculation. It can also be a clonal selection from the transplant, which is more important the closer it is to this clonal selection. That's also a possibility because I do think that the transplant, which is a very high dose of an alkylating agent, and melflufen, which is locally in the cells, a very high concentration of an alkylating agent. They are probably selecting some of the same cells. I do believe more in the first that it's difficult to tolerate subsequent treatment if you first have a transplant and then within not so much time, melflufen. I also think it goes back to the point with the subsequent treatment, because we know that pomalidomide plus dexamethasone, which is a more bone marrow suppressive treatment than daratumumab, and pomalidomide was more common in the melflufen arm than in the pomalidomide arm, which got more daratumumab afterwards. It can also be a factor there. Main answer from me is the bone marrow tolerance is too low for melflufen with a certain time of recent transplants. Thank you. Thank you very much. We have several questions on one topic, which I think is important to highlight. Also from Adam Karlsson is, what proportion of multiple myeloma patients in the real world actually undergo a stem cell transplant? What would be potential trends there? The proportion today is, I would say, about 40% or something like that. The median age of myeloma diagnosis is around 70, and not many centers perform transplant over the age of 70. That means that 50% just disappears there, even though there are some exceptions who do give transplant to elderly, but that's not enough to see in the statistics. Also under the age of 70, there are a fraction of the patients, maybe 10, 15%, that are not eligible for transplants. There are two trends. One that is not even a trend anymore, it's much more established now than some years ago, is that 10 years ago it was quite common to give a transplant at relapse. We gave a transplant in first line, and then you gave a transplant in second line, because we didn't have that many drugs available. That has been becoming much less common. Not many countries do that in many patients now. That means that for the average patient, the time to the last transplant will be longer in a certain treatment. The other trend is that we have done studies to eliminate transplant for a long time. So far, the studies have not succeeded. I think the closest was the largest and most recent, the IFM 2009, which showed that even though there was a PFS difference when they treated with VRd induction and transplant and maintenance versus only VRd and then maintenance. There was a PFS difference, but not an overall survival difference. I have to say that in that study, many patients got transplant at relapse, so it is mostly being used as argument for it is possible to delay relapse. What has happened the last couple of years is that bispecifics and CAR-Ts have shown response rates and PFS results in late line of treatment that is totally unprecedented. It's extremely effective drugs. Now very many studies are being set up in 1st line that includes these drugs, one or more of these drugs, and eliminate transplant. Some are randomizing against transplant, and some are just doing studies with these drugs without transplant and planning to just show that the results are better than the transplant. There's also been several papers the last couple of years that has showed that transplant is inducing a lot of mutations that leads to secondary malignancies later. Now we see that the life years, so the overall total survival of myeloma patients has moved up from about three, four years to maybe 10, 15 now in the best centers. That means that to get a second malignancy from the transplant treatment is much worse now than before when your life expectancy was lower. The general trend is to move away from transplant, definitely. The studies first have to succeed in doing that, and so far they haven't. I think it's a quite general impression that when we see data from bispecifics and/or CAR-Ts in first line, they will prevail over transplant treatment. Transplant might be, at that point, actually not so relevant anymore. In the elderly, the best treatments now in first line are without alkylators. That's dara, REVLIMID. The best treatments in relapse are without alkylators. Today in the patients who do not receive transplants, if they are treated as guidelines suggest, they are mainly treatment totally without alkylators for several lines of treatment. Hope that answered the question. Thanks, Dr. Schjesvold. I have some questions from Patrik Ling from DNB Markets, but I think one important one to touch on now, and we'll come to the other questions of you, Patrik, later, is about the cross-resistance between lenalidomide and pomalidomide. We've talked about that before, and how did that play out in the OCEAN trial? Did the resistance profile materialize as you had expected? I think sort of. We know that pomalidomide is a better drug than lenalidomide. We know that it's more efficacious, and we also know it's better tolerated. We also know that the response rate is not far away from where it's in this study in those populations from earlier studies. I think a response rate of 27% in a lenalidomide-refractory patient is more or less what we would have expected, I would say, and also for the PFS of about four months. I wasn't very surprised by that. It is a better drug. In many patients it doesn't work in lenalidomide-refractory patients, but it does work in a significant fraction of the patients, and that's why pomalidomide is a standard in this population that are lenalidomide refractory. I've seen, of course, many patients in this situation, and I see patients who just doesn't respond at all, and I see patients who have a tremendous response to pomalidomide after being refractory to lenalidomide. The cross-resistance is there. If you give pomalidomide to patients who are not refractory to REVLIMID, the response and PFS are better. I don't think the pom dex data here were very surprising. Yep. Thank you. I would like to take another two questions here, because we're also mindful of your time, Dr. Schjesvold. I have a question here that I think we could either fairly quickly about could you comment on whether we saw any differences in secondary malignancies between the melflufen and the pomalidomide arm? There's no differences and very few events in both groups. Yes. Very good. Also I have a question is that could it be a possibility that daratumumab is particularly given in an higher extent to younger patients resulting in the advantage for the overall survival for pomalidomide? Could that be the reason from your perspective? It's possible. I think you would have to look at the data for this in which countries this was happening and in what age groups the patients got daratumumab. If you have countries where daratumumab, for instance, is an expensive drug, and pomalidomide is equally expensive, I would think that most doctors would give daratumumab if they had the availability. Could also be that the availability of daratumumab, pomalidomide, wasn't the same in all centers. It could be that if you make a choice after melflufen, you have a choice in addition to the others. You have pom, you have dara. Doctors' decision will always be based on many things. It was always clear that more patients in melflufen arm would get pomalidomide in any case. I think it's very difficult to answer that. You would have to look at if the patients who received daratumumab was younger. It might be. I don't know. I think a study needs to show its results as they are, and if you speculate too much on what comes afterwards, it becomes very difficult to argue for a drug. You would have to argue that melflufen would only give a benefit if you give daratumumab afterwards, which is a sort of strange path to take, I would say. I think it's good to look at all this data. I don't have the data you're asking for there, the age of the daratumumab patient. It's possible. Daratumumab monotherapy, if I were to choose between daratumumab monotherapy and pomalidomide dexamethasone, it's not that clear that daratumumab is necessarily better because daratumumab's efficacy is mostly seen in earlier lines with combination treatment. As a monotherapy, its efficacy is not that much better than pom. Yeah. Now I'm just babbling here because I don't have the real question to the answer, but I'm not sure that's the explanation. Let's put it like that. Right. Yeah. I've been able to quickly look at some of the data. To answer the question directly there, it doesn't seem to me to be too much differences between age and the frequency of daratumumab being given. It's more the age as such that drives or is more likely to be connected with the transplant than the use of daratumumab according to age groups. I'd like to highlight one final question for you, Dr. Schjesvold, and I know we're over time, but from Christopher Eude from SEB. Dr. Schjesvold, in your view, is the proposed mechanism of PEPAXTO beyond dispute given the human PK profile and given the secondary malignancies being broadly similar to pomalidomide? If the mechanism action is beyond dispute, if you look at secondary malignancies. Can you repeat the question once more? Yeah. I think I'm try to clarify. Given what we see that there were no differences between pomalidomide and melflufen in terms of the rate of secondary malignancies and given the pre-clinical data that is out there, is there any reason to believe that it is really a different drug? It is beyond every doubt that this is another drug when compared to other alkylators? I think that when you're talking about secondary malignancies, I think you have a follow-up of 15 months, and you have two drugs that both give secondary malignancies. We know that both IMiDs and alkylators do that. To have a difference between those two in a period of 15 and a half months is impossible. What you see in secondary malignancies, usually they come after several years. I don't think that a low and equal rate of secondary malignancies would impact on the belief in the mechanism. I think the most important part that makes me believe in the mechanism is actually from this study, and it's that the benefit is so large in the alkylator-refractory patients, those who are refractory to melflufen, those who are refractory to cyclophosphamide and bendamustine. I think that's the most important data to answer this question since this question popped up several years ago when melflufen first started doing studies. It's been asked, how is this better than other alkylators or different from the other alkylators? I think the most important data are actually in this study that the benefit is so large in the alkylator-refractory population, both for PFS and for OS versus pomalidomide. I believe in that more now after this study than I did before this study when we didn't have such data to look at. We know the mechanism works like this from preclinical studies. What we don't know is how that translates into clinical findings. I think the efficacy you see here in alkylator-refractory patients are sort of confirming that, I would say. Are you talking, Klaas? I can't hear you. Sorry, I wasn't on mute. Thank you, Dr. Schjesvold. I think we still have a lot of questions pending that we will be happy to take. We'll also address some of the questions in the follow-up part of this webcast. For now, I would like just to thank you for your time to not only present the data yesterday during the weekend, but also here with us today during this webcast. That's much appreciated. I just wondered if you had any final thoughts you would like to share. No, I think we touched upon the most important parts, I would say. Okay. Thank you very much, Dr. Schjesvold. Hope to speak to you soon. I can say that I've been asked several times the last couple of days, what will the FDA say? I cannot answer what the FDA would say. It's always difficult to know those sorts of things. What I think they should say, I think they should say that this drug is beneficial for non-transplanted patients, and let's move on with them. Like they did with venetoclax and BELLINI. They said this drug is very beneficial for the 11, 14 patients. Let's move on with that, both with studies and with approval. I think that will be what I think they should say based on this data. Thank you very much. We'll speak again soon. I think we can move on with the rest of the webcast. Thank you very much, and have a nice evening, Dr. Fredrik Schjesvold. Yes. Thank you. Bye-bye. Okay. Thank you all for listening in. We have some other slides that we would like to share, and I know there are still a significant number of questions pending, and I will try to touch upon them as we go along, and otherwise, we'll take them during the Q&A in the end. If we go to the next slide, please. We have mentioned the ODAC meeting earlier, and we have also sent out a press release on that. The purpose of the ODAC planned for the 28th of October is an update basically on OCEAN, where we showed a hazard ratio of 1.1 in favor of the control arm, pomalidomide. There will be a general discussion on what would be the appropriate next steps for the product. You've just heard Dr. Schjesvold's view and whether the indication should remain on the market while additional trials are conducted. That's really the purpose of the ODAC on the 28th of October. Next slide, please. If we then zoom in a little bit deeper about what actually is an ODAC meeting? Well, it is a committee of 13 voting members, including the chair, where data concerning the efficacy and safety of drugs, whether they are on or not yet on the markets, are discussed, and where the panel will then make appropriate recommendations to the FDA. The committee generally consists out of experts in the field of general oncology, pediatric oncology, hematologic oncology, and also some very technical experts. The vote is very informative, often the FDA follows the direction of the ODAC committee, but please note that the vote is non-binding. This committee is really to give guidance to the FDA. Next slide, please. What would be potential outcomes of the FDA review, including the ODAC? I've seen a couple of questions coming by where I will try to touch up upon. The answer right now is, of course, that we don't know the outcome. What we do know is that the FDA has signaled a level of concern around the overall survival data. We believe based on communication with the FDA, which has been quite extensive over the last couple of months as you may appreciate, that we still believe there is a possibility to end up with a label that includes third- and fourth-line use of the drug. With a restriction, for example, for non-transplanted patients or better set for stem cell transplanted patients so that it would include the non-transplant patients in third and fourth line. A second scenario is where they say, "Well, this is a very interesting hypothesis, and it warrants further study in your development program." In that case, it could be that we would have to verify the benefit in another study. It could also be that that would lead to a potential, another accelerated approval based on the OCEAN data, which then needs to be confirmed. That is also a possibility. We have a worst-case outcome, and we mentioned that specifically because it is mentioned in the ODAC briefing message that should PEPAXTO stay on the U.S. market, we see this as a very unlikely scenario, but we mention it, and that is withdrawal of PEPAXTO from the U.S. market. Of course, during all these communications with the FDA, it is not unlikely that during the coming months, the current HORIZON label will have a safety update based on the data from OCEAN. To what extent and how, that is currently impossible to comment on. I think it is in general very important to note that the HORIZON population was a very late population. Even though patients were included that had stem cell transplant, these patients were often beyond the five-year window. That makes that you cannot compare or translate the OCEAN outcomes to the HORIZON label. For that reason, I also not dare to speculate about an impact there since this is truly a different patient population, and we strongly believe there is a good likelihood that we will be able to continue to commercialize in the fourth-line plus setting there. Next slide, please. A timeline, and we have compressed it due to the numerous of events over the last couple of months. A lot has happened since the top-line results, the initial top-line results were disclosed on the May 25th. We have seen the issuance of a partial clinical hold, the safety alert, and now we are at the stage where we have just presented the data to a broad scientific audience. The interpretation of the data is quite homogeneous, where we see responses not only from Dr. Fredrik Schjesvold but also from other key opinion leaders, where they think it is plausible what we see because there is a biological rationale, and there is an important place for melflufen in a non-transplant setting. That is especially because of the high unmet need, and I will talk about that in one minute. We have the clinical response letter that is pending. We aim to submit that in the coming weeks. We have an ODAC meeting on the 28th of October. One of the questions touched upon the fact whether there would be a response to the clinical response letter before the ODAC meeting, given that the FDA needs to issue a response within 30 days. We can only speculate about that, since the response letter can also hold information that they want to await the ODAC meeting, and that could be their response. That would be pure speculation to say if we would get kind of more information before the ODAC. What I can say is that we have submitted five abstracts with further deep dives on data on OCEAN, and we very much look forward to present these at ASH in December. In December, we also anticipate the publication of OCEAN results, this is of course pending review and acceptance by the medical journal. Next slide, please. If we look to the profiles of these non-transplanted and transplanted patients, I think this is a key slide to remember, if we look at the real-world treatment landscape, we see that non-transplanted patients are generally older. That's also what we saw in the forest plots where we see a clear signal of melflufen being more efficacious in older patients, even significantly more efficacious. That is because they are non-transplanted patients. But that means that these non-transplanted patients are generally older. If you look at the fact that the average relapsed refractory multiple myeloma patient is a 70-year-old patient and then starts its treatment in the RRMM setting. You can almost deduct that is the majority of the patient population. The performance status, because they are elderly and more frail, is somewhat lower. We see that they have had the same previous exposure as in OCEAN, other than that they have received regular dose alkylators and not the high-dose melflufen used for the transplant, which is, of course, one of the story for the transplanted patients who are in general much younger. That's also the reason why you see that the patients who benefited from pomalidomide were in the majority below 65 years of age, which is the population that is generally being transplanted. These patients generally are in a somewhat better condition. If we go to the next slide, and this is a very recent study, published this year. On the left hand, you see the survival probability on the y-axis, while on the x-axis, you see the second-line overall survival. Why did we take it from the second-line treatment? Because the transplant in itself is considered a treatment that is different from another. You start to actually measure from the fact when the transplant has worked out in the first line versus people who have had their initial treatment but were not transplanted. You see, if you look at the median PFS, that is 46 versus 28 months. That speaks to the green curve, the non-transplanted patients, where there is so much to win and so much to gain. What we see there with the 9.3 versus 4.8 months PFS, which also translated in an overall survival benefit with the same magnitude, five months delta. That is very important to take into account when looking at these OCEAN data and what it means for the real-world practice. These are patients that are older and have a high unmet medical need. Next slide, please. Again, to reemphasize this, we see here the differences as pointed out by Dr. Fredrik Schjesvold earlier, where you really see no difference between pomalidomide and melflufen in the transplanted patients. Whereas in the non-transplant patients, you see clearly the benefit of melflufen with a 9.3 versus 4.4 month or 4.6 month for pomalidomide. This is just to reemphasize that, and as Dr. Fredrik Schjesvold had mentioned before, melflufen flufenamide in alkylator refractory patient is 8.3 months versus 3.8 months for pomalidomide. Very clearly speaking to the differentiated profile of melflufen dex there. Next slide, please. This is something that Marty may also touch on in his closing remarks and where Dr. Fredrik Schjesvold talked about extensively, that is what is currently the treatment landscape when we look at the non-transplant versus transplant setting. Well, the basic message is that if we look at the non-transplant setting in the U.S., it's about 50/50. In the EU, it's about 60/40, that in the next five to 10 years, we anticipate that medical need population in the non-transplanted setting only to grow, and as such, very relevant for melflufen. Next slide, please. To shift gears a little bit, and I will come back to some of the questions on OCEAN. Don't worry, we'll first finish this part of the presentation. We also presented data from PORT at IMW, and that was very important because so far, melflufen had been administered via central catheter. For patient convenience, it would be worth to see whether it would also be possible to give it via peripheral catheter, so without having a permanent access. We go to the next slide. PORT is a very elegant phase II study, I would say. It has a solid design, and if we look to the upper right-hand study design, you see that these are all patients with relapsed refractory multiple myeloma, have had at least two prior lines of therapy, and were then randomized to get either melflufen flufenamide via peripheral catheter versus a central line. What happened then is that the same patient in the next cycle would get it via the other mechanism. A patient who have got melflufen first via peripheral catheter, then got it via central catheter, and vice versa. This means you have the in-patient control, I would say, which gives you the most reliable data, especially when it comes to pharmacokinetics, because we also wanted to know, given the high lipophilicity of melflufen, whether there's any differences between administration centrally or peripherally. This is the study design, 20 patients, as said, focused on the PK, but also on local adverse events. Since melflufen can be considered a local irritating cytotoxic, it's important to also exclude that you will have negative consequences from peripheral administration. Next slide, please. A very complicated story told very short in this slide. That's only because you need to look at the right graph where you have the PK AUC curve, basically between PVC, so peripheral, and CVC, central. As you can see, this is in 19 patients, but even with this relatively small sample size, you can already see that the lines are almost overlapping. That means that we are confident to state that there is no difference between the profile of the drug, whether you administer it peripherally or centrally, which is of course very important. Next slide, please. Other conclusions beyond the same pharmacokinetics is that there were no, that means zero, local reactions after peripheral administration of melflufen. Not one single grade one adverse event. It makes us very comfortable to also, from our perspective, consider peripheral administration safe. This is of course, and this speaks to 1 of the questions that I saw coming through off-label because in the label it's considered to be in the instructions of use to be a central line, but it needs to be an updated label. Will we submit an sNDA on the PORT data? Ultimately, this will be part of a sNDA, yes, to get the label updated. Whether physicians want to use it already right now peripherally, that's really up to the prescribing physician, but please note that would be outside the current label. These data are public and people are of course, free to do with the data what they judge is in the best interest for the individual patient. That's basically the story of PORT. Very encouraging. Will be used for an sNDA so that it also allows peripheral administration. Next slide, please. Marty, I think it's up to you now for some concluding remarks and then I think we can pick up the Q&A again afterwards. Happy to hand over to you. Thank you very much, Klaas. Again, thanks to Dr. Schjesvold. Next slide, please. The slide in the top left-hand corner, you've seen that a couple different times and Klaas very nicely suggested on PORT there was one picture that told the story and I think this is the picture on the OCEAN trial. Looking at the primary endpoint of progression-free survival, seeing that absolutely all the PFS differential we see in the non-transplanted patients in the benefit of melflufen dex. Want to reiterate the point that was so nicely brought out by Dr. Schjesvold regarding the alkylator-refractory population and that differential in terms of a five-month delta between the melflufen dex and the pom dex arm in alkylator-refractory patients holds up. Really appreciated Dr. Fredrik Schjesvold's view on how the novel peptide-drug conjugate, PEPAXTO, delivering an alkylating payload is really proven out here in a head-to-head comparative trial very nicely translating what we've seen from preclinical evidence on the differentiated activity of melflufen over the past several years and we're continuing to be committed to that work. I also think it's interesting to point out, and perhaps we will play this out in a slide in the future, thinking about that time to transplant. When we take those patients from time to transplant and play that out, we see a very consistent clinical result playing out over the entire population of the OCEAN trial where secondary endpoints or primary endpoint of PFS and the secondary endpoints of overall response rate, depth of response and overall survival absolutely align and tell a very common story. The conclusions that Dr. Schjesvold mentioned from the stage yesterday and today, phase III head-to-head study, superior outcome on the primary endpoint of PFS across the intent-to-treat population. The overall survival trended in favor of pomalidomide in patients with a prior transplant, but favored melflufen in the non-transplanted patient population. Safety on par for what we've seen relative to melflufen in prior clinical studies. Again, we look to reach conclusion with regulatory authorities, not only in the U.S. but around the world on the role that melflufen or PEPAXTO can play in benefiting patients. Next slide, please. A summary from the webcast here today. The data presented at IMW we would consider to be very encouraging. The OCEAN phase III head-to-head study, the PORT phase II study. I know there's a question in the chat regarding the applicability and when physicians can utilize this method of administration, so we'll touch on that. Our near-term focus is to reach agreement with the FDA. The ODAC meeting, as we've talked about, on October 28th will be important. There are a variety of outcomes and obviously, we would align to Dr. Schjesvold's view regarding how he sees the OCEAN data and his thoughts regarding regulatory action of that. We understand, appreciate the process and we'll work hard to reach that common agreement. In the meantime, commercialization of continues in the U.S. We are very pleased to hear patient stories coming in all the time regarding the drug's ability to help patients, because that's what this is really all about. We haven't mentioned the EMA, but that process is ongoing and thus far proceeding according to plan. We look forward to ASH 2021. As Klaas mentioned, we have five data presentations or five abstract submissions on the OCEAN data, and I believe another five that deal with other aspects of our pipeline or pre-clinical work. Finally, in conclusion, the picture on the right-hand side represents part of the Oncopeptides contingent that was together in Vienna. Given the strange times from a global perspective, it was fantastic for myself to be able to meet such a talented group of individuals who are committed to advancing our product, advancing our pipeline, and advancing patient care, and really happy and pleased with the results of what we accomplished. I'll stop there, and we'll move into the questions. Klaas, I know you've had the opportunity to stay very close in touch with the ones that are pending, so maybe I'll let you sort out the ones that you think are important, and I'll also look through them as well. Very good. I will just start on the top. Some very specific questions, and I may answer them pretty soon. Bertrand Deldicque, have you already started to collect data over more recent data cut to be submitted to the ODAC members, or will the ODAC only review the February cut of data? Thank you. This will only be the February cut of data. If we could provide more numbers on the HORIZON population, such as the percentage of patients with a prior stem cell transplant. Yes, that is about 70% of patients, but as said, most of this was a long time ago. Since we don't see a detriment or even a benefit, I would say, in patients who have been transplanted before, we do not see this as concerning for the HORIZON population. Fredrik Jacobson asked whether it's prudent to send the final response letter so that it forces the FDA to answer before the ODAC and would it not be better to submit the final response in the beginning of October? It's a very interesting question and good question. The only piece is that we are actually bound to respond within three months. We also need to finalize our clinical response before the end of September. That's not an option. Michael Svensson asked a very good and relevant question. With a large benefit on PFS in non-transplanted patients, wouldn't it even be unethical and very tough to recruit a new study where these patients, if unlucky, would be randomized to pomalidomide? Very good question. Very relevant question. That could be considered difficult. I am in full agreement with that, and that also speaks to the discussions we're having with the regulatory bodies if we need to confirm this finding into another study, how would such a study look like, given that the difference is so striking with 9.3 versus 4.8 months, that you might indeed consider another design and not expose these patients to pomalidomide since that would be really harming these patients. Richard McDowell on what the management opinion is about the different ways the FDA can choose, what percentage of each way. I would love to give that. I really don't have percentages, and we haven't got percentages on the table during discussions even. I think it would be, and Marty, chime in if you feel differently here. I think we feel broadly that another study to confirm in each or whatever way this finding is likely. Whether that would be after a new accelerated approval in non-transplanted patients or whether it would be based on a total new study, I really don't dare to speculate. Some kind of confirmatory study is likely in our opinion. I already touched on the ODAC as such that we feel very confident that this drug will stay on the market. I would say that were my two main takeaways, new study likely. In what form, we don't know. ODAC, we are very optimistic there. Yeah, I would agree. There was a regulatory session at IMW as well that we listened to with great interest, both FDA and EMA participating. The idea of the heterogeneity of multiple myeloma came up and the need to focus in on specific patient populations in clinical trials is important. It's becoming a very crowded field. Again, I think we'll stand behind the data and work hard with the regulatory body. We see a very clear view of the data here. Some of the questions that came in asked about the overall survival in the ITT population. There are ways in which you can credibly explain away differences, subsequent treatment, patients randomized but not treated, and begin to chip away at that 1.104. When you zoom out and take a 30,000-foot view of this study, I think it's pretty clear that we see the benefit of our drug being delivered in patients who have not received a prior transplant. In those patients that have got within 2.5 years, we see a detriment. We certainly would move accordingly, being data-driven, benefit risk-driven, and look for that to be the outcome here. The science and data will rule the day in our mind and can put a probability of success on the outcomes. Yeah. No, very good. Thank you, Marty. I have a question from a private investor on the overall response rate in the non-transplant subgroup. I don't know the exact number by head, but it is in the 40% and higher. Also there, we see this from a secondary endpoint perspective. We see the same trend being more efficacious in the non-transplanted group. A question from Hampus Ekström, who asked whether it's probable that the maturity of the data set will render statistical significance in the OS hazard ratio favoring melflufen plus dex in non-transplanted patients. Yes, given what we are seeing today, this is very well possible. However, of course, further cuts of the data is also something we need to agree with the agency. I just do want to remember everyone that this study met its primary endpoint and, as such, is successful. If you then also look and you see that in the subgroup of transplant or non-transplanted patients, the full PFS benefit is preserved in the overall survival, that is a very substantial finding. Of course, it signals risk in the earlier transplanted patients, but we see a clear benefit in the non-transplanted patients, and that may even render statistical significance. However, I strongly believe that it's not critical for our discussions with the agency because we are speaking about a study that met its primary endpoint and has a very significant benefit in this group of patients. Also, on the ASCT, Michael Svensson asked whether was not a predefined subgroup, as I understand it. It actually is a predefined subgroup. This is not an exploratory subgroup, so to say. This was a predefined subgroup, and as said, half of the patients got a transplant. This is not as in the BELLINI trial. Dr. Fredrik Schjesvold alluded to that. I personally think that this is a completely other study where the BELLINI trial showed a hazard ratio of 2.0, whereas it shows a hazard ratio of 1.1 here with not just a subgroup, but I would say half of the patient population deriving a clear benefit both in PFS and OS. Hey, Klaas, I also liked how Dr. Schjesvold, and I think it was in response to a question, was talking about kind of the future and the trends. In our OCEAN study, we see about a 50/50 mix between the transplant and the non-transplant patients. His view was that less patients would be transplanted in the future based on the CAR-T, the BiTEs coming forward. Our view is having a powerful novel peptide-drug conjugate that is able to deliver, whether we call it a soft transplant or not, is a growing opportunity as we would see it. Of course, it's up to us in our clinical development program to shape that. Certainly, the landscape is set for that to be a possibility. There are questions that kind of ask about transplant and age. Yeah, it was quite remarkable to see the subset analysis by age and the trends for both PFS and OS. This is likely, we see a very high benefit for PEPAXTO in older patients. That really, in our multivariate analysis, is really driven by the question of transplant or non-transplant. In terms of the biologic basis here, it's more consistent, we think, and more sound to be thinking about this differentiation of the patient population and where the benefit is delivered to think about it in the transplant versus non-transplant rather than the age setting. All that being said, certainly a doublet with this kind of concentrated efficacy in non-transplanted patients who are older is, I think, a good place for us to be and a place in which we can deliver a substantial amount of benefit to patients and patient care. Absolutely. Marty, if you are fine, I just have a couple of questions in front of me that I think I can easy relatively fast. That is about GK ask whether comments on risk for need for new clinical trials versus adjustments and use of the already ongoing studies. We also have a question on LIGHTHOUSE and whether the design would be changed. That is all very likely. We have found some remarkable differences here, when we talk about the response letter, that is about how do we want to pursue our current clinical development program, what would that mean. From that perspective, it is very likely to think that indeed, some study designs will have to be amended to this finding of the benefit of melflufen in non-transplanted patients, but more importantly, to exclude patients that have been transplanted early, because that would be particularly putting patients at risk, which is, of course, not what we would do. Another question on the 18 versus three patients who were randomized but not treated from both Patrik Ling, but also from others, whether that shouldn't be excluded. If you look in the safety population, and that is really the patients where the 18 and three are taken out of the consideration, the hazard ratio goes down substantially and moves towards one. That is, of course, one of the arguments that we would or have already put forward to the agency as well, since, of course, it is a particular imbalance that speaks to that. I see Christopher Eude from SEB, a significant PFS benefit in non-transplant patients, but not an OS benefit. The only significant OS benefit is in older patients. I would then come back to the question that this is a significant study. PFS is the primary endpoint, OS is a secondary endpoint, so that is not needed to show an OS statistical significance. However, overall survival is also a safety endpoint. When the FDA speaks about their concerns, and this is purely from a safety perspective, so not from a registrational perspective, they see the transplant population as a risk population, and we concur with that view, and that's also how we present our data. That doesn't mean that if you met your primary endpoint with a subsequent trend in overall survival, that you need now suddenly statistical significance in a predefined subgroup. That is something that we would say is not impacting the chances of success. I would say. Maybe given the time, I'm not sure if anything here jumps out. We're going to have multiple opportunities over the next several months leading into ASH. I think there's some investor conferences and of course one-on-one meetings that we can have to discuss results further. From the OS and PFS subgroup slides, you can see there's a wealth of data. OCEAN will be a story that keeps on giving. I think what you saw yesterday and today is really the high-level view of what we think is the essence of this positive OCEAN trial and where we will continue to work with regulatory bodies in helping to conclude on a label for PEPAXTO moving forward. Perhaps at this point we conclude the call unless anything else has come in. Klaas, that you see that might be interesting to pick off? No, just one piece that I can easily answer. Why some of the data that was presented today was not presented at IMW yesterday. The answer is very simple, time constraints and number of slide constraints. We would have loved to also include these slides at the meeting yesterday, you are only allocated a certain amount of time. We felt it was appropriate to share it today with the analyst and investor community to even give a broader picture beyond what was shared yesterday at IMW. That's the very simple answer to that question. I think Dr. Fredrik Schjesvold had 10 minutes for his presentation yesterday. He had 30 in this particular webcast, so there was substantial more opportunity. Again, on behalf of Oncopeptides and the team, thanks to everyone for joining the webcast. We look forward to our future interactions and appreciate your continued interest in the story and digging into it and helping us move forward as a company. Much appreciated. Thanks. Have a great rest of your Sunday evening, and take care now. Bye. Thank you.