Sareum Holdings plc (SAR) Earnings Call Transcript & Summary

Good afternoon, and welcome to the Sareum Holdings plc interim results investor presentation. [Operator Instructions] The company may not be in a position to answer every question received during the meeting itself. However, the company can review all questions submitted today and publish responses, which is appropriate to do so. Before we begin, I would like to submit the following poll. And I would now like to hand you over to Executive Chairman, Dr. Stephen Parker. Good afternoon to you.

Good afternoon and good afternoon, everybody. Thank you for joining this call. I'm joined today by Dr. John Reader, our CSO; and Dr. Tim Mitchell, our COO. We will each of us be taking part in the presentation and in answering your questions after that's finished. Just moving forwards. Usual disclaimer that goes with all of these presentations. We will be talking about future forward-looking events within this presentation and in the discussion. So please be aware of the disclaimer that goes with it. So a quick overview of where we are. You know about the company as being a clinical-stage small molecule drug company with deep expertise in kinase inhibitors, most notably, of course, in the TYK2/JAK1 field, where we will spend most of the time today. But happily, we're now back involved in the Chk1 side, having regained control of SRA737 shortly after the period we're discussing ended. We are well funded now. We closed in the period with cash of GBP 4.1 million with a further GBP 1.07 million raised in early March. So the pipeline now looks like this. This, of course, is different from recent years in that Chk1 is included within our pipeline for the first time in certainly my living memory. And on, please, Tim. So highlights from the period. Most notably, of course, we completed and announced the completion of the Phase I study for SDC-1801. John will discuss that, of course, in a little more detail. We've been able, because of the funds raised during this last year, to start looking more actively at 1802 again. And of course, with the return of 737, we now have a cancer drug, which has already been in the clinic for Phase I/II studies, both as a single agent and in combination. And during the period when it was last sublicensed, an IND was opened in the U.S. So there is now, for the first time, the ability to conduct trials in the states. The financials, I've just summarized, although it's worth noting that in addition to the post period end placing, we also had an R&D tax credit. So the total income during this first quarter has been GBP 1.3 million approximately into the company. So moving on from there, and we'll start looking at the proprietary program. And again, please, Tim. So very briefly in summary, the data -- the Phase I data have demonstrated that we do have a highly selective molecule in 1801, which is a differentiator against our competitors and one thing which leads us to believe that we do indeed have potential for a best-in-class molecule. The -- we can see that there is potential for this in many autoimmune disorders. We've spoken previously about psoriasis, but that's one of several molecules in the autoimmune -- conditions in the autoimmune field where we believe that 1801 could well be applicable. And the positive results from Phase I has led us to believe that we have a very strong story, and we are undertaking this extended tox study to provide hopefully a licensee with a ready for Phase II compound. And with that, I'm going to pass over to John, who will go into more detail through the program.

Thank you, Stephen. Yes. So SDC-1801 is a, as you know, clinical-stage dual TYK2/JAK1 inhibitor. The Phase I trial dosing of volunteers in Australia completed in June '24. We received the unblinded data in Q3 of '24, and the results were very positive. High blood exposure was achieved, and there were no serious adverse events due to SDC-1801. In fact, the adverse event profile was very similar between treated and placebo groups. All adverse events that were noted were mild or moderate. There were no clinically significant effects on blood components or serum creatinine, and I'll come later to why we see that as being very significant. We also saw a significant dose-dependent reduction in biomarkers of TYK2 and JAK1. So in our preclinical models, we had demonstrated the mechanistic proof of concept, seen dose-dependent efficacy in models of psoriasis and rheumatoid arthritis. We demonstrated that SDC-1801 potently blocks TYK2 and JAK1 signaling in human whole blood assays with no measurable inhibition of JAK2. And the good safety pharmacology and toxicology that we observed in the preclinical studies translated into the clinic. And we found that the human pharmacokinetics were suitable for once-daily oral dosing. So we really were very positive from the results that arose from that Phase I trial. This is a cartoon just to show you why we think dual TYK2/JAK1 inhibition is optimal for the suppression of a number of cytokines linked to several autoimmune diseases. If you look at the cartoon, it's really demonstrating the cytokine receptors when a molecule binds to the cytokine receptor, so the interferon receptor, for example, interferon gamma binds to the interferon-gamma receptor, it uses JAK1 and JAK2 to transmit the signal downstream. Now some -- blocking some of these JAKs is beneficial because it blocks cytokines that are associated with autoimmune and inflammatory diseases. Blocking certain JAKs such as JAK2, you'll see on the left of this molecule, has negative effects because JAK2 is very much involved in erythropoietin and thrombopoietin signaling and inhibiting JAK2 can lead to a number of hematology toxic side effects. So we very much want to avoid JAK2. We see that in contrast to the selective TYK2 inhibitors, Sotyktu and TAK-279 by also inhibiting JAK1, another range of cytokines are inhibited, which could have positive effects in diseases. And just to demonstrate that, we've got some data here from clinical studies using a dual TYK2/JAK1 inhibitor, brepocitinib versus single TYK2 or dual JAK1/2 inhibition in clinical studies. Slight caveat. It's always somewhat, well, not dangerous, but you just need to be aware when you're comparing between clinical studies that these are different groups of patients and different protocols are used in the clinic, for example. But I think this data does show quite nicely that brepocitinib gave the best readout in a psoriasis trial. We're looking at PASI-75 that psoriasis area and severity index. So we're looking at reductions in psoriasis symptoms in patients and the dual TYK2/JAK1 inhibitor appears to be more effective than the selective TYK2 inhibitors or the dual JAK1/JAK2 inhibitor, baricitinib. So looking at the human pharmacokinetic profile of 1801. We saw a half-life of around 17 to 20 hours. That confirms the suitability of a molecule for once-daily oral dosing. In MAD Cohort D, so this is the highest dose group in the MAD experiment, we saw that plasma exposure of 1801 was equivalent to brepocitinib at 100 mg. So I'll come on to why that might be important later on. Just going back to our data, the exposure of 1801 exceeded the human whole blood interferon alpha and IL-12 IC50s throughout the entire dosing period. So that means that we are achieving a concentration of drug in the blood that reduces interferon alpha and IL-12 signaling by at least 50% for the entire dosing period. We didn't see any changes in hematology or serum creatinine after 10 days of dosing. Now in contrast, brepocitinib, that's the molecule I just described on the previous slide giving the best results in the psoriasis trial. Brepocitinib at 100 mg caused increased serum creatinine and reductions in reticulocytes and neutrophils. Reticulocytes are immature red blood cells and neutrophils are an important part of the white blood cell system. So you don't really want to be reducing those components of the blood cells. So the data I showed you on the previous slide with brepocitinib, that was using brepo at 30 milligrams. Going higher leads to these side effects, and I think that's why brepocitinib is limited to typical use of 30 to 45 milligrams in the clinic. So switching back to 1801, we've got a very strong set of biomarker data. IP-10 interferon-gamma-induced protein 10, which is a marker of JAK1 and interferon gamma signaling. We've seen dose-dependent reductions in IP-10 levels in the MAD cohorts. CRP, C-reactive protein, a general marker of inflammation and again, downstream of JAK1 and in this case, IL-6 signaling, we saw dose-dependent reductions in CRP levels in the MAD cohorts. And then in an ex vivo challenge, so this is where we're sampling blood from the volunteers in the clinical trial. We're taking that blood and treating it with interferon alpha, challenging it with interferon alpha. And bear in mind that these subjects have taken our molecule. We saw dose-dependent reductions of phospho-STAT3 and phospho-STAT5 cells. So when interferon alpha binds to its receptor, it uses TYK2 and JAK1 to phosphorylate STAT3 and STAT5. That's what the p on phospho-STAT3 and phospho-STAT5 means. So this is direct evidence that we have target engagement with our molecule on the targets that we wanted to hit. And we observed that effect in 2 different cell types of the immune system, T cells and monocytes. So our differentiation versus brepocitinib, and this leads on to our theories around best-in-class potential for this molecule. Brepocitinib is the most advanced dual TYK2/JAK1 inhibitor in the clinic. It's currently undergoing Phase III trials. As I mentioned earlier, it's typically used in the clinic at 30 to 45 mgs once daily, QD is once daily. Going above 30 milligrams in the Phase I trial, they observed increased serum creatinine levels, and that was due to the inhibition of OCT2, it's a renal transporter, kidney transporter. Brepocitinib inhibits OCT2. 1801 has much greater selectivity versus OCT2. So we don't see any effects on serum creatinine levels when we dose with 1801, giving exposures equivalent to 100 mgs of brepocitinib. So greater than threefold the clinical dose of brepocitinib, we're not seeing this effect. Likewise, at greater than 30 milligrams of brepocitinib, reductions in neutrophils, those white blood cells and reticulocytes, the immature red blood cells are observed with brepocitinib. We saw no effect on neutrophils or reticulocytes at doses equivalent to 100 milligrams of brepocitinib. Our molecule has a greater half-life in humans, approximately 17 to 20 hours versus brepocitinib, 6 to 8 hours. And we saw an ideal PK profile for JAK inhibition. So average concentration is important for JAK inhibitors rather than the maximum and the minimum concentrations. These are peak-to-trough ratios. And we see excellent sustained average concentrations with 1801. It's driven by the long half-life, and we see that as a distinct advantage. So as Stephen has mentioned, what we're doing at the moment is preparing the molecule for Phase II studies. And this has necessitated a resynthesis of the drug substance. And this has had some knock-on effects on our toxicology studies, which I'll explain in a little moment. We're also working on optimizing the formulation. So we used capsules in the Phase I study. This is advantageous relative to many Phase I studies, which use solutions of the molecule to dose their subjects. We were using capsules straight away in the Phase I. But there's some work needed to be done to improve those formulation to improve the absorption of the molecule and also to prepare capsule sizes consistent with the expected Phase II doses. So our 16-week toxicology studies are scheduled to commence in May 2025, and we'd expect them to complete in the fourth quarter of this year. This is a delay relative to what we told you at the IMC meeting in December. And this has really been driven by a need to resynthesize the drug. A couple of reasons for that. We were planning to use the GMP material that we had left over from the Phase I trial. And then when we did a risk assessment, we saw that potentially that's a very clean batch of drug, and we could run into difficulties if any subsequent batches of drug have a, let's say, a dirtier side effect profile. So if they had impurities in subsequent batches that were not present in our tox batch, that would mean that our toxicology studies were of no use, they would be defunct. So we made the decision to prepare a fresh batch of material to take forward into these tox studies. Batches of drug used in tox studies tend to be dirtier than those that you're going to take forward into human trials. We've also decided that we're going to increase the doses used in the tox studies because we're not seeing particularly large effects in the tox studies. And sometimes the regulators really want to see some maximum toxicity. So we're going to increase the levels of exposure that we get in the toxicology studies. Okay. If I move on to the next slide. So that concludes 1801. I'll just talk briefly on 1802. As Stephen said, we have begun to ramp up the translational and the preclinical studies around 1802 using the funds from the recent share subscriptions. The development of 1801 has given us some experience that will certainly feed through to aid the development of 1802. And we've got a strong patent position around 1802, covering not only cancer, but also some immune disorders as well. So we're confident about 1802. We're going to push forward very strongly now with accelerated studies. So I'm going to talk now about Chk1, SRA737, a selective Chk1 kinase inhibitor suitable for once-daily oral administration, which has completed a couple of Phase I/II trials already. Just to say with the given change in control, we now control the program and have an increased slice of the economic benefits up to 63.5%. So it has gone up to 63.5%. The molecule was originally developed by ourselves in collaboration with several Cancer Research U.K.-funded organizations, successfully completed 2 Phase I/II trials with the original license partner, Sierra Oncology. It was subsequently licensed to a private U.S. biopharma company and the license was returned to CPF, a cancer pioneer fund, in Q1 of '25. We've now negotiated with CPF to take over the program, pushed our economic interest up to 63.5% from 27.5%, and we're currently reviewing the licensing and development options to take the program forward. Some very compelling clinical development paths supported by preclinical models with synergistic antitumor activity and a strong mechanistic rationale. What I'm showing you here is a model in mice. It's called a syngeneic model. So these are mice with a functional immune system. And they have a small-cell lung cancer, that's the SCLC, a mouse small-cell lung cancer. So what we're demonstrating here is that combining an anti-PD-L1, this is the immunotherapy that has revolutionized cancer treatment over the last 10 years or so. Combining anti-PD-L1 antibodies with SRA737 and low-dose gemcitabine has a pronounced effect on the volume of the tumors. In fact, 80% of the mice in this study have sustained complete responses. The tumors have entirely disappeared. You'll see if you -- I won't go through it all, but the lines above the triple combination basically show you the effects of 737 by itself, low-dose gem by itself, the antibody by itself and then various combinations. But you can see it's only when you bring the 3 things together that you get these really profound reductions in tumor volumes. Also, we saw the effects on the innate immune signaling. So things like STING and interferon are drastically altered by this triple combination. Also important to say we saw similar effects in a colorectal cancer model. And then moving on to a model in combination with PARP inhibitor. So PARP inhibitors have also found a large market in particularly treatment of ovarian cancer, starting to show some effects in prostate cancer as well. But PARP inhibitor resistance is an emerging unmet clinical need. And we have some data that we're showing here that shows that combination of 737 with a PARP inhibitor is well tolerated, but also has pronounced antitumor activity in a model of high-grade serous ovarian cancer in this case, which has developed resistance to a PARP inhibitor by itself. So again, you can see combination of 737 with a PARP inhibitor led to 4 out of 9 complete responses in this mouse model. So big clinical opportunity there, a potential for Phase Ib/IIa clinical trial of 737 with a PARP inhibitor in PARP inhibitor resistant or refractory patients. So just to summarize 737, it's a clinical-stage development candidate, has a defined Chk1 inhibitor mechanism and a clear development plan. Demonstrates promising clinical activity. It's well tolerated as a single agent and in combination with chemotherapy. The strong clinical validation for its mechanism as ATR/Chk1 axis; SRA-737 is competitively positioned within this DDR class. It's a very good molecule. It's got excellent drug-like properties, low drug-drug interaction potential. So we think it's very eminently suited for combination with other clinical agents. And the data supports potentially rapid clinical development paths in anogenital cancers and additional clinical potential when combined with, for example, PD-L1 or anti-PD-1 antibodies or PARP inhibition, I showed you some data supporting that. Also WEE1 inhibition, there's some data that we put out on X recently or on LinkedIn that shows some potential for combining with WEE1 inhibitors. So lots of potential opportunities for taking this molecule forward in the future. I'm going to hand over there to Tim to take you through the unaudited financial results for the period.

Thank you, John. Good morning, everybody. It's Tim Mitchell here. So I'll just take you through the results, which you may have seen were announced today. So these are the 6 months results to the period ending 31st of December 2024. So comparing with the same period last year, actually, I'll first note that the results for the 6 months to December 2023 have been restated. This was because there was a finance charge on the income statement for the 2023 figures, which has since been settled by shares. So that charge has gone away. That's essentially a contingency charge and that's gone. So that's the reason for restating the results. So you'll see that the operating expenses for the period to December 2024 are considerably lower than they were for the corresponding period to 2023. So this is mainly because of the reduced clinical trial costs. So there have been some trial costs that carried on into the end of last year. So the follow-up of the biomarker studies, for instance, was -- that was concluded during the last part of the year. And then it all feeds through, so the tax credit is less because we've had less clinical costs. It ended up in results -- in a loss after tax of just over GBP 1 million compared to GBP 1.75 million for the corresponding period last year. Then if we look at the balance sheet, the investment in associate is essentially the cash left in the SRA737 Chk1 partnership with the CRT Pioneer Fund. That money, less some expenses partly due to the handover will come back to us at some stage. But I think the big difference compared to last year is our cash position. So as a result of the share subscriptions we undertook during last year and, of course, topped up by a further GBP 1 million or so from this year plus a little bit of a tax credit. But the cash position as of the end of December is just over GBP 4 million. So we're well financed for our current activities going forward. And I think with that, I will hand back to Stephen to talk about what's coming up for this year.

Yes. Thank you, Tim. Thank you, John. So during the year, let's just break it down into the 3 main programs. For 1801, of course, there is the submission of the academic paper to a peer-reviewed journal. That's in progress, but that will hopefully come shortly. What happens after that, of course, just to remind you, is entirely out of our hands in the peer review process can move quickly or it can take some time. Those of us who publish papers in our time will know the full range of time lines on that. Then, of course, we have the completion of synthesis and formulation for the new drug product that John has been talking about and launching the long-term tox trials, which, as we've said, we would expect to have completed in Q4 in this year. On 1802, we're commencing the manufacturing of drug product for formal preclinical trials. That is, again, as John has said, we're expecting to benefit from the process development learnings from 1801 in that. And from that, look to initiate preclinical studies and in parallel, look at target cancers for the clinical testing. But of course, for the cancer drug, it's -- the norm is to go into Phase I/II studies in patients straight away. Lastly, 737, a pleasure to talk about that again. Complete receipt of data, which hasn't quite happened yet. We're expecting that process is going well at the moment and then review future options on the basis of material sent back to us and KOL advice and indeed contacts with third parties who may have an interest in licensing the drug from us. So that concludes the presentation and summary of the results.

I'm very happy to take questions, and we'll do that. Many of you have been kind enough to pre-submit questions. I will read them out and then, as appropriate, either answer or pass to John and Tim for them to answer. I know that some of you have been submitting questions during the slides deck. I do hope that we will get to those as well. As the host of the call said, we will go through all questions submitted and provide a list of written answers at some point in the near future. So first of all, a question about 737. In taking over the license, was it by mutual agreement or did they approach Sareum? Broadly speaking, this was, as you can imagine, stimulated by the return of the license from the private U.S. company, which happened at the end of December last year. CPF is a fund, which is looking to wind down at the moment. And so they were very happy for us to step in and also for us to renegotiate the economics. I know that several of you have asked the related question, which is what do we have to pay for this? And the answer is nothing apart from, of course, the legal costs that always go with these things. But this was a deal which was entirely mutually agreed by all parties. So moving on. Perhaps, John, you could talk a bit about -- in more detail about the paper for 1801 moving that forward.

Yes. So the paper 1801 is in progress. I think it's -- we have to be very, very careful that we've got our patent position fully sorted out before we submit that data because once that's published, we have put the prior art out in the public domain, and it would prevent us from patenting anything related to that data. So we're confident we've got our patent position in good shape and hope to submit that paper for peer review shortly.

Thank you. There have been several questions here about PR and our market-facing activities. Just to say that I do intend that we can ramp up PR activities during the year. And in fact, I am booked to give a presentation at one of the investor meetings in June. I will -- I also intend that according to whichever is the specific topic that one of us will, on a more regular basis, interact with the likes of Edison or indeed IMC in recording interviews and making sure that everybody is aware of progress. So we are looking in this year to be more active on the PR side. There's also been questions about the appointment of Oberon as a new joint broker. The reason for doing that is that I am very conscious that it's very important that we have a broker who is active in the secondary trading position as well as providing a good service for primary issuance. And so I felt it's important that we were balanced between Hybridan and we introduced Oberon into the mix who do have a secondary trading position. And I'm sure that we will see the benefit of that going forwards. So other questions that have come in just recently. There's various questions again about use of advisers for doing deals. We do, of course, have a roster of advisers who are contracted to us, most notably on Nomad. But for specific deals, we're certainly not shy to engage with financial advisers with specialist knowledge or specialist ability in addition to help us to get deals over the line. We didn't -- if you may like to know, we didn't involve external advisers for the 737 transaction, but we may well do if the need arises for 1801 licensing or anything further than that. There's a question about the work done by the private U.S. company in the last year. We are not able to talk about that. We are under very clear confidentiality restrictions. Suffice it to say that anything that they have achieved now forms part of our data pack that we can then exploit going forward. Yes, please, Tim.

I'll just add one thing, actually, one thing we can say from the private U.S. company, they filed the IND, which we mentioned earlier before. And actually, there was a question -- I'm sorry, apologies for not explaining that. An IND is an investigational new drug. So this is the clearance by the regulatory authorities to undertake a clinical trial. So that work was done by the private U.S. company last year.

Thanks, Tim. One or 2 questions around the delay in the launch of the tox study. I don't think we need to go into great detail about this. Of course, John has explained that very well, I would say. But somebody is asking effectively why didn't we build up enough material to start already. And the simple fact is that when you are synthesizing drug, this is done in a batch process. So you have nothing or you have everything. It doesn't come. It's not drip fed.

I think the other thing just to say to that is it's always a balance of risk, isn't it really? So we could have prepared 10 kilograms of material last year and kept 8 kilograms in stock for any subsequent studies. But of course, that costs a lot of money and we could have had a negative result from a clinical trial, which would have rendered all that material useless. So we're always trying to sort of balance the risk of what we do with the time lines versus the expense of doing certain things.

Yes. Thank you. Going back to perhaps some of the pre-submitted questions. There's a question here, is consideration being given to a dual listing on NASDAQ. I think the answer to that is nothing is ever ruled out, but I'm also very conscious that the grass is actually not greener on the other side of the fence. There have been several stories in recent months of U.S. companies, which on paper should have been very successful, failing dismally. So I think we will -- we'll always be aware of it. We'll always look, but we'll also be cautious before we leap in the NASDAQ direction. So now just looking down the list -- sorry, Tim, can you read that one?

Yes. So there's a question just coming on 1801. So is there a possibility that we go -- we take on the Phase II if our shareholders are supportive? And are we already in discussions with potential partners for SDC-1801? The answer to that is yes for both. So we're pursuing essentially a dual path here. So we're getting the compound ready for a subsequent Phase II trial. And then we'll take a view near the time as to what's the best deal for us and our shareholders as in whether to press ahead into a Phase II trial, if there's support from shareholders to fund that for that? Or is there a good offer from a potential partner for a licensing deal for SDC-1801. So yes, the current strategy we're taking -- of taking essentially most of this year to get the compound Phase II ready allows us to assess options for both licensing and raising money for a Phase II. But I think if there's a good license deal out there, I think that would be our priority.

Absolutely. Yes. Absolutely. There's another question about which country we're looking to test 1801, in Australia or in England and why? So if we were to do a Phase II trial with 1801, and I think if anyone were to do a trial with 1801, it's likely it would be done in multiple territories. So you start to need to look in a much larger group of patients. Phase IIa, probably each group would have something like 48 patients in it. You might want to test a couple of doses and placebo. So you're looking at 120, 130 patients. You're likely to need to go to multiple territories to do that. I certainly would have no issue whatsoever with conducting a trial in Australia again. I wish I could say the same about the U.K. I mean we did have a very negative experience of MHRA. I think they're getting their act together to some extent, but whether we'd want to test that again, I don't know, but likely multiple territories.

Indeed. Indeed. So I think we are -- all right. There's a question here -- thank you. There's a question here as to whether we are likely to take 737 into a clinical trial in the near future. Again, as John just said, I think that's not our current intention. But if the opportunity were to arise and we have been approached by Medex as well as by companies, then there may be an argument for it. But if that were to be the case, then we would certainly be informing you of that at an early stage because it's -- whilst we are currently funded for all the programs that we are currently planning, 737 was an opportunistic acquisition. And therefore, a clinical trial with 737 would fall outside of that, and we would need to come back to shareholders to raise funds to do that. So you will know where that to change, but that's not the current plan.

I've got a related question here about actually conversations -- and this is going back to our dual strategy of exploring funding options for further trials versus license agreements. So have you already had conversations with other pharma about on-licensing SRA-737? How quickly could this happen? So the answer is yes. So while the 737 program was essentially under option to the U.S. biopharma compound last year, we did have a number of inquiries about the program coming in, which we had to -- we had essentially put on hold because the first refusal was with this U.S. biopharma. But as soon as we got the notice from this company that the program was going to come back to us, I've been following up on all those previous inquiries. And we can't really say about the progress of those until something has happened, but there are a number of inquiries which we are following up. And of course, now in the partnering meetings such as the BIO-Europe Spring meeting that I was at last week, we've got that 737 is very much in our shop window. So we're looking to attract new license partners as well as the ones that we've already been talking to.

Thank you. So I think that's probably rather answering specific questions. But as you can imagine, there have been several questions per topic. So I think we have probably covered most things here.

Stephen, if I may just jump in there, and thank you for addressing all those questions from investors today. And of course, as the company has mentioned, we will review all questions submitted today, and we'll publish those responses on the Investor Meet Company platform where appropriate. But Stephen, before we redirect investors to provide you with their feedback, which I know is particularly important to the company, if I may just ask you for a few closing comments.

Yes, of course. Thank you for that. And in closing, I do want to thank you for sticking with us. I'm very, very aware that we're all aware as shareholders/partners officers that this has not been a happy time with regards to the share price. We are looking to improve shareholder value, of course, for everybody's benefit. And we are looking at all options in front of us to do that. So I do hope that we will be able to have a happier story when we next meet in an IMC. In the meantime, we do appreciate your feedback, and I'll be very happy to answer questions directly or generally from shareholders. So thank you all.

Stephen, Tim and John, thank you once again for updating investors today. Could I please ask investors not to close this session as you will now be automatically redirected to provide your feedback in order that the Board can better understand your views and expectations. This will only take a few moments to complete, and I'm sure will be greatly valued by the company. On behalf of the management team of Sareum Holdings plc, we would like to thank you for attending today's presentation, and good afternoon to you all.