Sareum Holdings (LSE:SAR) — Half Year Results

0:01 Good afternoon, and welcome to the SAREUM HOLDINGS PLC interim results investor presentation. Throughout this recorded presentation, investors will be in listen only mode. Questions are encouraged, and they can be submitted at any time using the q and a tab situated on the right hand corner of your screen. Simply type in your questions and press send. 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.

0:32 And I would now like to hand you over to executive chairman, doctor Steven Parker. Good afternoon to you. Good afternoon, and good afternoon, everybody. Thank you for joining this call. I'm joined today by doctor John Reeder, our CSO, and doctor 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 usual disclaimer with those with all of these presentations, we will be talking about future look forward looking events within this presentation and in the discussion, so please be aware of the disclaimer that goes with it.

1:21 So a quick overview of where we are. You know about the company as being a clinical stage for a molecule drug company with deep expertise in kinase inhibitors, most notably, of course, in the TIC two JAK one field where we will spend most of the time today. But, happily, we're now back involved in the check one side having regained control of SRA seven three seven shortly after the period we're discussing ended. We are well funded now. We closed in the period with cash of 4,100,000 with a further 1,070,000 raised in early March. So the pipeline now looks like this. This, of course, is different from from recent years in that check one is included within our pipeline for the first time in my living memory.

2:22 And on. So highlights for the period. Most of those, of we completed and and announced the completion of the phase one study for SDC 18 o one. John will discuss that, of course, in in in a little more detail. We've been able because of the funds raised during this last year to start looking more actively at eighteen o two again. And, of course, with the return of of seven three seven, we now have a a cancer drug which has already been in the clinic for phase one two studies both as a single agent and in combination.

3:08 And during the period when it was last sublicensed, an IND was opened in The US. So there is now, for the first time, the ability to to conduct trials in in The States. The the financials I've just summarized, although it's it's worth noting that in addition to the post period end placing, we also had an r and d tax credit. So total income during this first quarter has been 1,300,000 approximately into into the company. So move moving on from there, and we'll start looking at the proprietary program.

3:54 I'll I'll be interested in. So very briefly, in summary, the the data the phase one data have demonstrated that we do have a highly selective molecule in 18 o one, 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 could see that there is potential for this in in many autoimmune disorders. We've spoken previously about psoriasis, but that's one of several molecules in the autoimmune in the autoimmune field where we believe that a g n o one could well be applicable.

4:47 And the and and the the positive results from phase one has led us to believe that we we have a very strong story, and we are undertaking this extended tox study to provide, hopefully, a licensee with a ready for phase two compound. With that, I'm gonna pass over to John who will go into more detail through the program. Thank you, Steven. Yeah. So SDC eighteen o one is a, as you know, clinical stage dual TYK2 JAK1 inhibitor. The phase one, trial dosing of the volunteers in Australia completed in June 24.

5:33 We received the unblinded data in q three of twenty four, and the results were very positive. High blood exposure was achieved, and there were no serious adverse events due to SDC eighteen o one. 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, I've seen dose dependent efficacy in models of psoriasis and rheumatoid arthritis.

6:26 We demonstrated that SDC1801 potently blocks TYK2 and JAK1 signaling in human whole blood assays with no measurable inhibition of JAK two. 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 one trial.

6:59 This is a cartoon just to show you why we think dual TIC two JAK one 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 to the interferon receptor, for example, interferon gamma binds to the interferon gamma receptor. It uses JAK one and JAK two to transmit the signal downstream. Now some of blocking some of these JAKs is beneficial because it blocks cytokines that are associated with autoimmune and inflammatory diseases.

7:46 Blocking certain JAKs such as JAK two, you'll see on the left of this molecule, has negative effects because JAK two is very much involved in, ethropoietin and thrombopoietin signaling, and inhibiting JAK two can lead to a number of hematology toxic side effects. So we very much want to avoid JAK two. We see that in contrast to the selective TYK two inhibitors, so TYK2 and TYK2 seven nine, by also inhibiting JAK1, another range of cytokines are inhibited, which could have positive effects in diseases.

8:28 And just to demonstrate that, we've got some data here from, clinical studies using, a dual TYK2 JAK1 inhibitor, breplucitanib, versus single TYK2 or dual JAK one two inhibition in clinical studies. Slight caveat. You know, 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. Different protocols are used in the clinic, for example. But I think this data does show quite nicely that brepacitinib gave the best readout in a psoriasis trial. We're looking at PASI 75 at 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 of baricitinib.

9:30 So looking at the human pharmacokinetic profile of eighteen o one, we saw a half life of around seventeen to twenty 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 eighteen o one was equivalent to brepacitinib at a hundred mgs. So I'll come on to why that might be important later on. Just going back to our data, the exposure of eighteen o one exceeded the human whole blood interferon alpha and I l 12 I c fifties throughout the entire dosing period.

10:16 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 ten days of dosing. Now in contrast, brepacitinib, that's the molecule I just described on the previous slide giving the best results in the psoriasis trial. Brepacitinib at a hundred mgs caused increased serum creatinine and reductions in reticulocytes and neutrophils. Reticulocytes are in mature red blood cells, and neutrophils are an important part of a white blood cell system. So you don't really want to be reducing those those components of the, of the blood cells.

11:06 So the data I showed you on the previous slide with brepacitinib, that was using Brepo at thirty milligrams. Going higher leads to these side effects, and I think that's why, brepacitinib is limited to typical use of thirty to forty five milligrams in the clinic. So switching back to 18 o one, we've got a very strong set of biomarker data. I p 10 interferon gamma induced protein 10, which is a marker of JAK one and interferon gamma signaling. We've seen dose dependent reductions in I p 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-six signaling, we saw dose dependent reductions in CRP levels in the MAT cohorts.

12:03 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 STAT three and phospho STAT five cells. So when interferon alpha binds to its receptor, it uses TIC two and JAK one to phosphorylate STAT three and STAT five. That's what the p on phospho STAT three phospho STAT five means. So this is direct evidence that we have target engagement with our molecule on the targets that we wanted to hit.

12:50 And we observed that effect in two different cell types of the immune system, T cells and monocytes. So our differentiation versus prepacitinib, and this leads on to our theories around best in class potential for this molecule. Prepacitinib is the most advanced dual TYK2JAK1 inhibitor in the clinic. It's, currently undergoing phase three trials. As I mentioned earlier, it's typically used in the clinic at thirty to forty five mgs once daily, QDs once daily. Going above thirty milligrams in the phase one trial, they observed increased serum creatinine levels, and that was due to the inhibition of October 2. It's a renal transporter, kidney transporter.

13:41 Brepacitinib inhibits OCT two. Eighteen o one has much greater selectivity versus OCT two, so we don't see any effects on serum creatinine levels. When we dose with eighteen o one, giving exposures equivalent to a hundred mgs of brepacitinib, so greater than threefold the clinical dose of brepacitinib, we're not seeing this effect. Likewise, at greater than thirty milligrams of brepacitinib, reductions in neutrophils, those white blood cells, reticulocytes, the immature red blood cells, are observed with brefacitinib. We saw no effect on neutrophils or reticulocytes at doses equivalent to one hundred milligrams of brefacitinib. Our molecule has a greater half life in humans, approximately seventeen to twenty hours versus brefacitinib six to eight hours, and we saw an ideal PK profile for JAK inhibition.

14:36 So average concentration is important for JAK inhibitors rather than the maximum and the minimum concentrations. These are the peak to trough ratios. We see excellent sustained average concentrations with 18 o one. It's driven by the long half life, and we see that as a distinct advantage.

15:00 So as Stevens mentioned, what we're doing at the moment is preparing the molecule for phase two 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 one study. This is advantageous relative to many phase one studies which use solution solutions of the molecule to dose their subjects. We were using capsules straight away in the phase one, but there's some work needed to be done to improve those formulation, to improve the absorption of a molecule, and also to prepare capsule sizes consistent with the expected phase two doses.

15:50 So our sixteen weeks 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. Couple of reasons for that. We were planning to use the GMP material that we had left over from the phase one trial. And then when we did a risk assessment, we saw that 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.

16:47 So we make a decision to prepare a fresh batch of material to take forward into these tox studies.

16:56 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 wanna see some maximum toxicity. So we're gonna increase the levels of exposure that we get in the toxicology studies.

17:27 Okay. If I move on to the next slide. So that concludes eighteen o one. I'll just talk briefly on eighteen o two. As Steven said, we have begun to ramp up the translational and the preclinical studies around eighteen o two using the funds from a recent share subscriptions. The development of eighteen o one has given us some experience that will certainly feed through to aid the development of eighteen o two. And we've got a strong patent position around eighteen o two covering not only cancer, but also some immune disorders as well. So we're confident about eighteen o two. We're gonna push forward very strongly now with accelerated studies.

18:15 So I'm gonna talk now about selective Check one kinase inhibitor suitable for once daily oral administration, which has completed a couple of phase one two, 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 UK funded organizations, successfully completed two phase one two trials, with the original licensed partner, Sierra Oncology.

19:00 It was subsequently licensed to a private US biopharma company, and the license was returned to CPF, a cancer pioneer fund, in q one of twenty five. We've now negotiated with CPF to take over the program, pushed our economic interest up to 63 and a half percent from 27 and a half percent, and we're currently reviewing the licensing and development options to take the program forward.

19:33 There's 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.

20:06 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 ten years or so, combining anti PD L1 antibodies with SRA seven thirty seven and low dose gemcitabine has a pronounced effect on the volume of the tumors. In fact, eighty percent 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

20:41 triple combination basically show you the effects of seven three seven by itself, low dose GEM by itself, the antibody by itself, and then various combinations. You can see it's only when you bring the three things together that you get these really profound reductions in tumor volumes. Also,

20:59 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.

21:16 And then moving on to 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 seven thirty seven with a PARP inhibitor is well tolerated, but also has pronounced antitumor activity in a model of

21:53 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 seven thirty seven with the PARP inhibitor led to four out of nine complete responses in this mouse model.

22:09 So big clinical opportunity there, potential for phase one b two a clinical trial of seven thirty seven with a PARP inhibitor in PARP inhibitor resistant or refractory patients. So just to summarize seven thirty seven, it's a clinical stage development candidate, has a defined CHEC-one inhibitor mechanism and a clear development plan, demonstrates promising, clinical activity, It's well tolerated as a single agent and in combination with chemotherapy.

22:44 A strong clinical validation for its mechanism is ATR check one access access. SRA seven three seven 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 with other clinical agents.

23:11 And the data supports potentially rapid clinical development paths in anogenital cancers and additional clinical potential when combined with, for example, p d l one or anti p d one antibodies, PARP inhibition. I showed you some data supporting that. Also, we want inhibition. There's some data that we put out on x recently or on LinkedIn that shows some potential for combining with we one inhibitors. So lots of potential opportunities for taking this molecule forward in the future.

23:48 I'm gonna 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 six months results to the period ending 12/31/2024.

24:14 So comparing with the same period last year, actually, I'll I'll I'll first note that the the the results for the six months to December 2023 have been restated. This was was because there was a finance charge on the income statement for for the 2023 figures, which has since been settled by shares. So so that that charge has gone away. That is 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 so this is mainly because of the reduced clinical trial costs. So there have been some trial costs that that carried on into the the the end of last year. So so the the the follow-up of the biomarker studies, for instance, was that that that was that was concluded during the last part of the year.

25:16 And and then it all feeds through the yeah. The so the tax credit is less because we we've had less clinical costs. It ended up in a in results in in a loss after tax of of just over 1,000,000 compared to 1,750,000 for the corresponding period last year. Then if we look at the the balance sheet, the the investment in associate is is essentially the cash left in the the the SARE seven three seven check one partnership with the CRT pioneer fund. That that that money, less some expenses partly due to the handover, will will come back to us at some stage.

26:02 But I think the the 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 1,000,000 or so from this year plus a little bit of a tax credit. But the the the cash position as of the end of December is is is just over £4,000,000. So we're well financed for our our current activities going forward. And I think with that, I will hand back to Steven to talk about what's coming up for this year. Yes. Thank you, Tim. Well, thank you, John. So during during the year, let's just break it down into three main programs for eighteen o one.

26:49 Of course, there is the submission of the academic paper to a peer reviewed journal that's in progress, but, but that will hopefully come shortly. What happens after that, of course, just to remind you, is entirely out of our hands in that the peer review process can move quickly, or it can take some time. Those of us who publish papers in that time will will know the full range of timelines 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 q four in in this year.

27:40 On eighteen o two, we're commencing the manufacturing of drug products for formal preclinical trials. That is, again, as John has said, we were we're expecting to benefit from the the process development learnings from eighteen o one 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 one two studies in patients straight away. Lastly, seven three seven. Great pleasure to talk about that again. Complete the receipt of data, which hasn't quite happened yet.

28:29 We're expecting but that that process is going well at the moment. And then review future options on the basis of materials sent back to us and KOL advice and indeed contacts with third parties who may have an interest in in licensing the drug from us. So that that concludes the the presentation and summary of the of the results. I'm very happy to take take questions, and we'll we'll do that. Many of you have been kind enough to 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 the slides. I I do hope that we will get to those as well. As the the hosts of the the call said, we will go through all questions submitted and provide a list of written answers at some point in the in the near future.

29:37 So first of all, question about seven forty seven. In taking over the license, was it by mutual agreements, or did they approach SAREUM? Broadly speaking, this was this was, as you can imagine, stimulated by the return of the license from the private US company, which happened at the end of December last year. CPF is is a fund which is looking to wipe down wind down at the moment, and so they were very happy for us to step in and also for us to renegotiate the the economics. I know that several of you have asked the the related question, which is what do we have to pay for this? And the answer is nothing apart from, of course, the the legal costs that that always go with these things. But this was a deal which was entirely mutually agreed by by all parties.

30:41 So moving on, perhaps, John, you could talk a bit about in more detail about the the paper for eighteen o one Moving that forwards. Yes. So the paper '18 o one is in progress. I think it's we had 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 I we're confident we've got our patent position in good shape and hope to submit that paper for peer review shortly.

31:31 Thank you. There's been several questions here about PR and and our market facing activities. Just just to say that I I do intend that we should ramp up PR activities during the year, and I, in fact, 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 the the specific topic that one of us will, on a more regular basis, interact with with the likes of Edison or or indeed IMC in in recording interviews and and and and making sure that everybody is is aware of of progress.

32:27 So we are looking in this year to to be more active on the PR side. There's also been questions about the appointment of Oberon as the as a new joint broker. The 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 as as providing a good service for primary issuance. And so I felt it was important that we were balanced between hybrid and and we introduced overall into the mix who do have a secondary trading position. And I'm I'm sure that we will see the benefit of that going forwards.

33:19 So other other questions that have come in just recently. Various questions again about use of advisers for doing deals. We do, of course, have a roster of advisers who who are contracted to us, most notably our nomad. But for specific deals, we will we're certainly not shy to engage with financial advisers with specialist knowledge or specialist ability in addition to to help us to to to get deals over the line. We didn't if you may like to know, we didn't involve external advisers for the $73.07 transaction, but we may well do if the need arises for eighteen o one licensing or anything further than that.

34:21 There's a question about the work done by the private US 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 they have achieved now forms part of our data pack that we can then exploit going forwards. Yeah. Please, Dan. So I'll just add one thing. Actually, the one thing we can say from the private US company, they filed the the IND, which we mentioned earlier before. And, there was a question of and I'm sorry. Apologies for not explaining that. An IND is an investigational new drug. So this is the the clearance by the regulatory authorities to undertake a clinical trial.

35:09 So so you say that work was done by the private US company last year. Thanks, Jim. One or two questions around the the delay in the launch of the top study. I don't think we need to go into to great detail about this because John's explained that very well, I would say. But somebody is asking effectively why didn't we build up enough material to start already. The simple fact is that when you are synthesizing drug, this is done on a batch process. So you have nothing or you have everything. It doesn't come it's it's not drip fed.

35:56 I think the other thing just to say to that is, you know, it's always a balance of of of risk, isn't it, really? So, you know, we could have we could have prepared 10 kilograms of material last year and kept eight 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. We're always trying to sort of balance the risk of what we do with the with the timelines versus the expense of doing certain things. Yes. Thank you. We're going back to perhaps some of the pre submitted questions. There's a question here. It says considering the 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 is is actually not as not greener on the other side of the fence.

36:55 There have been several stories in recent months of US companies, which on paper should have been very successful failing dismally. So think we will we'll we'll always be aware of it. We'll always look, but we'll also be be cautious before we we we we leap into the the Nasdaq direction. So now I'm just looking down the list. Sorry. Sorry, Tim. Can you can you reach that one? Yes.

37:43 So so there's a question just coming on eighteen o one. So is there a possibility that we go we take on the the phase two if our shareholders are supportive, and are we already in discussions with potential partners for SDCA 10 o one? The answer to that is is is yes for both. So we're we're pursuing essentially a dual path here. So we're getting the the compound ready for a a subsequent phase two trial, and then we'll take a view nearer the time as to what's the best deal for us and our shareholders as in whether to press ahead into a into a phase two trial if there if there's support from shareholders to to fund that for that, or is there a good offer from a potential partner for a licensing deal for s t SDCA eighteen o one? So the yeah. The the the current strategy we're taking get of of of taking essentially most of this year to get the compound phase two ready allows us to assess options for both licensing and raising money for a phase two. But I think if there's a good license deal out there, I think that would be our priority.

38:58 Absolutely. Yes. Absolutely. There's another question about which country we're looking to test eighteen o one in, Australia or England and why. So if we were to do a phase two trial of eighteen o one, and I think if anyone were to do a trial with eighteen o one, it's likely it would be done in multiple territories. So you start to need to look in a you know, a much larger group of patients. Phase two a, 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, you know, hundred and hundred and twenty, 130 patients. You're likely to need to go to multiple territories to do that. I'd certainly would have no issue whatsoever with conducting a trial in Australia again.

39:53 Wish I could say the same about The UK. I mean, we did have a very negative experience of FHRA. I think they're getting their act together to some extent, but whether we'd want to test that again, I I I don't know, but likely multiple territories. Indeed. Indeed. So let's just I think we are Yes. There's a question here. Thank you. There's a question here as to whether we are likely to take seven three seven into into a clinical trial, in the near future. Again, as as as John just said, I think that's not our current intention.

40:43 But if the opportunity were to arise and we have been approached by medics as well as by companies, then there may there may be an argument for it. But if that were to be the case, then we would certainly be informing you of that as as an as an early stage because it's whilst we are currently funded for all the all the programs that we are we are currently planning, seven thirty seven was an opportunistic acquisition, and therefore, a clinical trial with seven thirty seven would fall outside of that, and we would need to come back to shareholders to to to raise funds to do that.

41:32 So you will you will know why that's changed, but that's not the current plan. I've I've got a related question here about actually oh, conversations and 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 seven three seven? How quickly could this happen? So the answer is yes. So so while the seven three seven program was essentially under option to a to The US biopharma compound last year, we did have a a number of inquiries about the program coming in, which we had to we had essentially put on hold because the the the the first refusal was with this US biopharma.

42:20 But as soon as we got the the the notice from this company that the program was gonna come back to us, I've been following up on all those previous inquiries, and, well, we we we can't really say about the progress of those until something's happened, but, yeah, there there are a number of inquiries which are we are following up. And, of course, now in the the partnering meetings such as the BioEurope spring meeting that I was at last week, we've that. Seven three seven is is very much in our shop window, so we are we're looking to attract new license partners as well as the ones we've already been talking to. Yes. Thank you. So I think that's probably we'd rather answer in groups from specific questions.

43:10 But as you can imagine, there have been several questions per topic. So I think we have probably covered most things here. Steven, 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, Steven, 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 in closing, I do want to thank you for sticking with us. I'm very, very aware that we're all aware as shareholders, quite often as officers, that this has not been a happy time.

44:02 But 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 all options in front of us to do that. So I do hope that we will we'll be able to to have a a happier story when we next meet in a in an INC. In the meantime, we do appreciate your feedback, and I'll be very happy to answer questions directly or or generally from shareholders. So thank you all. Steven, 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?

44:56 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.