Good afternoon and welcome to the Sareum Holdings PLC final 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&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 when it 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 Senior Associate Partner at ICR Consilium, Jessica Hodgson. Good afternoon to you.
Good afternoon, everyone. Thanks very much for joining. This is Sareum's final results for the year ended June 30th, 2024. We have today presenting Dr. Stephen Parker, Sareum's Executive Chairman, Dr. Tim Mitchell, Chief Operating Officer and Co-founder, and Dr. John Reader, Chief Scientific Officer and Co-founder. I'll now hand the call over to Dr. Stephen Parker.
Thank you, Jessica, and good afternoon, everybody. Thank you for joining the call for the final results for the year to June 2024. Before we begin, because it is my first opportunity to talk to you as Executive Chairman, I'd just like to reflect on a couple of issues, one of which, of course, is the fact of that change and that Tim Mitchell has stepped sideways to take up the newly formed role of Chief Operating Officer as a part-time role. Tim's contribution to this company, of course, doesn't need me to go into detail about.
It's very, I'm sure, very obvious to all of you, but I would like to take the opportunity to reflect both my admiration for his achievements thus far and my gratitude that he's staying with us in this new role to work as we move to bring Sareum further into as a clinical stage company and indeed to look to get a partnering or an end stage in terms of the company's future. A couple of words on the drug. Obviously, TYK2 has developed very rapidly now, even in the time that we were going through the Phase 1 trial in Australia, to have become recognized not only as a viable and genuine target, but a very attractive and valuable one as well, and there have been one or two deals already in the space to underline that.
But I do think it also means that the general view when we're out talking to companies around the circuit, that the working assumption is that although there have not been any efficacy trials as such yet, those trials will be successful, and therefore the safety, as ever with any drug, is the key question. As John will go into detail in a few moments, the data coming out of the Phase 1 study were fulfilled all of our hopes and aspirations for the drug. And as a result, we've taken the view not to carry out the very small-scale 1b study, which was still a safety study but carried out in a small number of patients, but to prepare the drug to move forward as rapidly as we can to Phase 2 trials. And we will obviously be discussing that further on as we go into the Slides.
Finally, a word on my philosophy in this sector. To me, it's all about risk management and weighing up the various likelihoods and decisions in front of any stage of both the drug and indeed the company's progress, looking at what the options are in front of us and having a plan depending on the outcome of any particular decision node and point, and as a result, several of the things that you've read about in recent weeks have fallen into place as we prepare 1801, as I say, for Phase 2 studies. With that, I'd like to move into the Slides, so Next Slide, thank you. This, of course, is the usual disclaimer, so please do take note of it. We are discussing forward-looking statements at various stages, and you should treat those with the caution that always goes with them. Next Slide, please.
So moving on then to the overview. You know all of this pretty well, but we are a clinical stage company now. We have a portfolio which is based upon the JAK cell signaling family, principally TYK2, JAK1, although the expertise that we have in JAK2s and 3s has helped John in particular to avoid the pitfalls that some of our competitors have found themselves in. 1801 has completed the Phase 1 clinical trial in Australia, very successfully. And on the back of that, we recently went out and carried out a subscription to raise further funds. And we now, if you then include the tax credit coming back from Australia, we've recently raised GBP 4.4 million to move forward with our plans for getting the drug ready for Phase 2. Next Slide, please. So this is what the company's pipeline is looking like at the moment.
Obviously, the bulk of our efforts have been focused on 1801 for some time now with the benefit that you've all read about. 1802, targeting the cancer immunotherapy, we're now in a position to start to move that forward into preclinical and hopefully prepare for clinical studies. The partner drug, SRA737, is sitting with the new partner that Cancer Research UK concluded a deal with almost a year ago now. We're waiting to hear what the progress they have made is, and obviously, there are milestones which are approaching which, once the partner company has informed CRUK, we will be in position to share with you and with the market. Next Slide, please. So from the year, obviously, the most exciting result of all was the completion of the Phase 1 study. Tremendous set of data coming back from Australia.
No deaths or serious adverse events associated with the drug, which obviously is the first thing you look for. And all the reported adverse events, which were all either mild or moderate, were pretty much spread between the drug groups and the placebo groups. So we do believe that we're in as strong a position as possible to move forward towards Phase 2. As I said just now, the recent funding for 1802 that we received will allow us to move 1802 forward, and we'll look to see an acceleration activity very rapidly there. I already mentioned the 737 program. The deal that was done is worth $290 million with an as-yet unnamed U.S. biopharma company. We are waiting to, as I said, to get permission to reveal names and indeed progress once it's been reported back to the CRUK organizations. In terms of the financials, very brief snapshot here.
Cash at the end of June was £1.5 million, which was up from £1.0 million a year before. The loss has not surprisingly gone up slightly to £3.4 million from £3.2 million. Clinical trials are always expensive, and we've refilled the coffers to allow us to move the drug forward and the drugs forward as rapidly as possible with a total of £4.4 million. Next Slide, please, and with that, I'd like to pass the baton over to Dr. John Reader to take us through the inhibitor programs, particularly the results from 1801.
Hi there, Dr. Tim. Please go. I'm just going to unmute you. Dr. Tim, please go ahead.
Hi there, guys.
Dr. Tim, can you hear us okay there? If not, you can refresh your connection. Bear with me one second. Please bear with us, ladies and gentlemen, just while we connect Dr. Tim.
Shall I carry on in the meantime?
Give me one second, Dr. Stephen. Let me just see if I can bring Dr. Tim through now. You just request control there. That's great. Thank you. Dr. Tim, we have got you back on. Thank you very much. Indeed, if you could just turn the other laptop audio up, that'd be great. Thank you.
Okay. Can you hear me?
Yes, we can hear you.
Tim, your speaker's off. We need your speaker's on.
We can hear you, sir.
Hi there. Can you hear me now?
Yes, we can, sir. Please go ahead.
Thank you. Sorry about that. We've had a bit of a technical issue, but hopefully, we can just crack straight on. So thanks for the introductory Slides, Steve. I'm going to talk a little bit more about the clinical trial that we conducted on SDC-1801, dual TYK2, JAK1 inhibitor for autoimmune disorders. As you've heard, the Phase 1 clinical trial completed in June 2024, and we received the unblinded data early in Q3. We were very pleased to see that high blood exposures of the compound were achieved. There were no serious adverse events due to SDC-1801 observed. And indeed, with the unblinded data in hand, we could see that the adverse event profile was very similar in the treatment and placebo groups.
All adverse events were either mild or moderate, and we saw a similar frequency, similar types of adverse events between the subjects receiving SDC-1801 and those receiving placebo. There were no clinically significant effects on blood components, which is a side effect commonly seen with some of the first-generation JAK inhibitors, and we didn't see any effects on serum creatinine, and I'll come on to that in a little more detail later on, and gratifyingly, we saw significant dose-dependent reductions in biomarkers of TYK2 and JAK1 inhibition, so in our preclinical studies previously, we'd seen mechanistic proof of concept, dose-dependent efficacy in models of psoriasis and rheumatoid arthritis. We know that SDC-1801 potently blocks TYK2 and JAK1 signaling in human whole blood assays, and we have not been able to measure any JAK2 inhibition.
The good safety pharmacology and toxicology that we saw in the preclinical studies translated to the clinic, so we've seen no effects on heartbeat, heart rhythm, blood pressure, breathing, any of these safety pharmacology issues, and the toxicology profile we saw didn't differ at all from anything we saw in our toxicology studies. Just a bit of a comment on that. In order to support the Phase 1A and the planned Phase 1B trial, which was to run for 28 days dosing in psoriasis patients, we had a 28-day toxicology experiment to support that, so to dose humans for 28 days, you need to have 28 days of toxicology data in two preclinical species. We had that.
Now that we're preparing for longer-term Phase 2 studies, which may be anything from three to four months, we will need preclinical toxicology in two species to support that for three to four months. So that's what we're really talking about in our objectives for getting the molecule Phase 2 ready. The pharmacokinetics that we saw in Phase 1 were very good, suitable for once-daily oral dosing, and we think there may be a significant advantage in the pharmacokinetic profile that we observed. I'll, again, talk a little more about that in a later Slide. Next Slide, please. So we've talked about SDC-1801 being a dual inhibitor of TYK2, JAK1. We believe that such a profile is optimal for the suppression of cytokines linked to many different autoimmune diseases. So we have potential for broad coverage and increased efficacy across several key autoimmune targets.
By combining or having the dual inhibition, we can get greater coverage than the single inhibitors of TYK2 and JAK1. We've reduced toxicity. This is primarily by not targeting JAK2, which has the main effect on blood components. Because SDC-1801 is a small molecule drug, it's convenient for oral administration by contrast to the cytokine-targeting antibodies. If you see in the schematic at the bottom of the Slide here, we're really showing on the left-hand side of the Slide in red the first-generation JAK inhibitors that have effects on JAK2. JAK2 is very much involved in erythropoietin and thrombopoietin signaling, and that's where the side effects that affect blood components are arising. If we look at the JAK1 inhibitors, so this is primarily, I suppose, the main exemplar of this is Rinvoq from AbbVie.
You can see that it affects a number of signaling downstream of a number of cytokine receptors. I won't go through all of those, but you can see them on the list there. And then the TYK2 single inhibitors, again, I guess the best well-known exemplar is Sotyktu, now marketed by BMS, primarily affecting the type I interferons, interferon alpha and beta, and the IL-12 and IL-23 signaling pathways. So by combining TYK2 and JAK1 dual inhibition, you can see that we have coverage over all of these cytokine receptors responsible or implicated in many different autoimmune disorders. Next Slide, please. So there is clinical evidence to support the assertion that dual TYK2, JAK1 inhibition is more effective than single inhibition of either target. And I'm just showing here a Slide that has some clinical data in Phase 2 psoriasis trials. Just a quick explanation of this.
What we're looking at is a thing called a PASI 75 reduction. PASI is a score, stands for Psoriasis Area and Severity Index, and it's really a score of how severe a patient's psoriasis is. The 75 refers to a 75% reduction in PASI score. So if you look, really, it's the light blue columns that are of interest here. These are the placebo-adjusted totals. And if you look at, for example, deucravacitinib, you can see a placebo-adjusted percent of patients achieving PASI 75 at 12 weeks is somewhere around the 38% region. For TAK-279, these are both allosteric selective TYK2 inhibitors. TAK-279, giving a placebo-adjusted PASI score of around about 60%. And if you look at the right-hand side, this is brepacitinib, the most advanced clinically developed TYK2, JAK1 inhibitor. That's giving a placebo-adjusted score of around about 70%.
So a word of caution, it shouldn't really compare across clinical trials because they're different patient sets, different readouts sometimes. But this is a good set of evidence to show that dual inhibition of TYK2 and JAK1 can have a greater efficacy than single compounds alone. It's not just been seen in psoriasis either. There's evidence from psoriatic arthritis, alopecia, and ulcerative colitis trials that also show a similar effect here. So we think there's very strong evidence for showing that the dual inhibition is more effective than the single inhibition. Next Slide, please. A bit more detail about the pharmacokinetic profile that we observed then. A half-life of 17-20 hours confirms the suitability for once-daily oral dosing.
Drilling down a little into MAD cohort D, so this is the multiple ascending dose, the final cohort for highest exposure, we were getting plasma exposure very similar to that observed in the Brepacitinib Phase 1 trial, their MAD with 100 mg once daily QD, means once daily. The plasma exposure that we were observing in cohort D exceeds the human whole blood interferon alpha and IL-12 IC50s throughout the dosing period, so we are inhibiting by more than 50% both of those cytokines throughout the entire dosing period. We're not seeing any hematology or serum creatinine changes after 10 days of dosing SDC1801. In contrast, Brepacitinib at 100 mg caused increased serum creatinine and reductions in reticulocytes. These are immature red blood cells that go on to form mature red blood cells.
Also, neutrophils are a component of the white blood cells in their Phase 1 MAD study after 10 days dosing. So what I should have said on the previous Slide is that that clinical data that showed Brepacitinib performing so well in a psoriasis trial, that was dosed at 30 mg once daily. And we think that's around the maximum dose that Brepacitinib can be dosed at before these side effects start to have a major effect. So we're very pleased that we're seeing plasma exposure around the Brepacitinib 100 mg mark. We would expect that if we're able to achieve this in longer-term studies, that we would have better efficacy than that demonstrated by Brepacitinib at 30 mg. Next Slide, please. So to back up what I've just said, we had some compelling biomarker data. We looked at three biomarkers called IP-10, HS-CRP, interferon alpha.
You can see the key below, and if you want to find out more about these, but essentially, IP-10 is a marker of JAK1 and interferon gamma signaling. We saw dose-dependent reductions in IP-10 levels in the MAD cohorts. HS-CRP, a marker of JAK1 and IL-6 signaling, again, dose-dependent reductions in the levels in the MAD cohorts. And we did an interferon alpha ex vivo challenge. So this is taking blood from the subjects on the trial. Remember, these are healthy subjects, rather. And take that blood and challenge it with interferon alpha. And then we look downstream of interferon alpha at these molecules that are called the STATs. And we look at how these STAT populations change.
We saw dose-dependent reductions in the phosphorylation of STAT3 and STAT5, and in the numbers of STAT3 and STAT5 positive cells as a percentage of parent in the 1801 treated groups relative to placebo. We observed this in two different immune cell types, T cells and monocytes. Good data there supports our optimism that we'll see good efficacy when we get this molecule into patients. Next Slide, please. I just want to talk a little more about the differentiation versus Brepacitinib. As I've said previously, Brepacitinib, a molecule discovered originally by Pfizer, is really the most clinically advanced dual inhibitor of TYK2 and JAK1. Used in the clinic generally at 30 mgs once daily QD, once daily. They have done some trials where they've used short induction periods, typically 45 mgs to 60 mgs. But they generally use this at 30 mgs in the clinic.
We think this is because at higher than well, actually, even at 30 mg, you do see some effects on increased serum creatinine. Pfizer have said why this is. It's due to a kidney transporter called OCT2, which their molecule inhibits. We have greater selectivity versus OCT2. And at doses equivalent to 100 mg of Brepacitinib of SDC-1801, we see no effect on serum creatinine levels. Also, at doses of Brepacitinib greater than 30 mg once daily, there are clear clinically significant reductions in neutrophils and reticulocytes. In contrast, we've seen no effect on neutrophils or reticulocytes at doses equivalent to 100 mg of Brepacitinib. And then SDC-1801 has a greater human half-life. So we're seeing between 17 to 20 hours in contrast to Brepacitinib, 6 to 8 hours.
We think we have an ideal PK profile for JAK inhibition, where a sustained average concentration is much more important than a high peak and a low trough. We see a lower maximum concentration of SDC-1801 compared to Brepacitinib. We see this as a positive because it shows high concentrations of drug where side effects can start to kick in. We're not seeing that with our profile. We're getting good sustained (this is because of the human half-life) good sustained average concentrations of SDC-1801. Next Slide, please. Okay, just moving briefly on to SDC-1802. This is our cancer immunotherapy development candidate. We have previously demonstrated good efficacy in several preclinical models of cancer. I think it's fair to say that SDC-1802 has been on the back burner during the past period while we've been concentrating so much of our effort on SDC-1801.
But with the new funds from the recent share subscriptions, we'll be accelerating the translational and preclinical studies on 1802, aiming to get this into development. The experience with 1801 will help with the development of 1802, and this is particularly in the chemistry space where the molecules are quite closely related. And then just a reminder here, I mean, this was pre-period, but in June 2023, U.S. Patent Office gave us a patent that gives SDC-1802 use in autoimmune diseases. So there is some scope for this molecule beyond immuno-oncology, and we're going to be doing some experiments to have a look at its potential in a specific aspect of autoimmune disease, which hopefully we'll have some data to share at a later meeting. Next Slide, please. Okay, I'm going to hand back to Stephen now just to talk through the JAK1 co-development program. So that's it from me.
Thank you. Thank you, John. Could I have the Next Slide, please? This is pretty much a retreading of what's already been said, but it's probably just worth reminding you of some of the details of this. This is a program which was originally developed by Sareum in collaboration with several arms of Cancer Research UK. The co-development ownership lies currently with CRT and the fund that was generated by CRT, the Cancer Pioneer Fund, CPF. The drug was licensed to Sierra Oncology, where Sierra completed two Phase 1 clinical trials successfully. Sierra was then acquired by GSK specifically for the late-stage drug, momelotinib, which was with the FDA and all other programs that Sierra had. There were, I think, three others that were all handed back to their original licensors. Subsequently, CPF have relicensed the drug to a U.S. biopharma company.
That was in December of last year for a relatively small upfront signature fee, but with another payment due within 12 months or on the licensee completing a funding milestone. We, like you, are waiting with bated breath to see the outcome of the 12 months or the funding. We are not, and I've said this many times before, but it's worth repeating, we are not a party to this license deal. Our economic benefit comes from a separate deal we have with CPF, the Cancer Pioneer Fund, which grants us 27.5% of the financial benefits and also, I should say, burdens from this program. So we do not have contact directly with the licensee. We are reliant on the licensee telling CPF what progress it's making and that being reported back to us. So when we know, you will know 24 hours later. So moving on, please.
With that, we get to the financial results, and I'll ask Tim if he will pick it up and just walk you through these briefly. Next Slide, please.
Thank you, Stephen, and good afternoon, everybody. Thanks from me for joining this presentation. Yes, so we published our year-end financial results today. I'll just go through the highlights of those, so starting with the income statement, we see the administrative expenses. So this also includes our R&D expenses are up a little bit from the previous period. This mainly reflects the extra cost of clinical trial running. There's a couple of lines on share of loss of associates and other operating income. This is associated with the SRA737 deal. So it reflects the running costs and then our share of that small upfront payment less the direct costs involved with that deal.
So it gives us an operating loss of GBP 4.6 million. The taxation line there, you'll see that as a positive number, but that reflects the tax credits that we receive. In the statement this morning, we already announced that we've received GBP one million in tax credit from Australia. The Australian authorities are actually very good at turning around their tax credit claims. So we get that one nice and quickly. The rest of that we'll receive from the U.K. tax authorities. That generally arrives in December or January, depending on how quick they are. So overall loss of the year, GBP 3.4 million, I'd say, up a little bit from the previous period, reflecting the more clinical focus we've had during the last period. Can we have the Next Slide, please?
On the balance sheet, so investment in associates is basically our share of the cash that's in the project bank account. The trade and other receivables, most of that is the tax credit that I talked about on the previous Slide. And we've received GBP 1 million of that, as I've already said. Then cash and cash equivalents. That's the end of June figure. So, of course, we've got the GBP 4.4 million that we've received in share subscriptions and tax credit to add on to that, to have in the pot for the forthcoming period and beyond. And then the rest is just standard stuff, trade and other payables. It's just normal trade payables, leaving us with net assets of just over GBP 2 million. So with that, I will hand back to Stephen, I believe. Right.
Now, looking forward here with the anticipated milestones in the next period, obviously, we've completed the Q3 milestones successfully, and we're looking forward to the clinical study report. It's worth having a word just on this because, obviously, we are a science-driven company, and we are looking to do deals with science-driven companies. The importance of data being presented and published in peer-reviewed journals cannot be overestimated, and therefore, the detailed clinical trial results will be published in that form. We will obviously issue an RNS to inform the market that that publication has published when it happens, but that will be the first place that the detailed data tables and such like do appear, then, moving on from there into 2025, we are very much hoping there will be a positive update on 737. There will certainly be an update because of the 12-month target.
There will be more information on the 1801 drug product and tox studies going forward. We very much hope that there will be an increasing amount of data flowing from the 1802 work that we'll be picking up. Next Slide, please. Just very briefly in summary, because you've heard all this probably at least three times before, but this has been an extremely successful year for the company. The outcome of the trial for 1801 really could not have been very much better, if at all. We think we do have an ideal pK profile, which is looking towards once-a-day dosing. We genuinely believe that when looking at data of drugs that are a bit in front of us, we have the potential to be best in class.
We do think that this gives us a very positive platform to take out to discuss future partnering deals. We're very excited about the year for 1801. Next Slide, please. With that, I'll just hand you back to IMC briefly.
Perfect. Dr. Stephen, John, Tim, thank you very much indeed for your presentation. Ladies and gentlemen, please do continue to submit your questions using the Q&A tab situated on the top right corner of your screen. While the company takes a few moments to review those questions submitted today, I would like to remind you that a recording of this presentation, along with a copy of the Slides and the published Q&A, can be accessed via our Investor dashboard. As you can see, we have received a number of questions throughout today's presentation.
And Jessica, if I may now hand back to you to chair the Q&A and ask you to read out the questions where appropriate to do so, and I'll pick up from you at the end. Thank you.
Thank you. So just as a reminder, I will now run through submitted questions. If there isn't sufficient time to address all the questions that have come in via the platform, responses will be posted in due course. So I'll now start with the first question, which I think is probably a question for Stephen. Apologies, but a question for Dr. John Reader. Can you provide more detail on the proposed 1801 toxicology studies? For example, will they be in humans, animals, or utilize AI? Will the trials remain in Australia, and what timescale is required?
Yeah. Thanks, Jessica.
So the toxicology studies will be performed in two species of animals. The aim is to get the program Phase 2 ready. So depending on the exact disease that we or partner companies choose to take into Phase 2, we would want some flexibility around the dosing period. But it's likely to be, I think, in the presentation, I showed some 12-week data. Most of these diseases, you can get a readout in 12 weeks to 16 weeks. So we'd like to give ourselves the option to be able to dose for up to 16 weeks in patients. And in order to do that, you have to have tox studies in two species for a minimum of 16 weeks. And that's a regulatory requirement, unfortunately, at the moment, as far as I'm aware.
No regulatory authority will accept AI-derived results, for example, in place of animal studies, so we have to do that, and just to clarify on that, so to do a 16-week toxicology study, you need an absolute minimum of six months to do the necessary preparation, but mostly afterwards, where you're looking at the analysis of data or the histopathology and the report writing, etc., at the end of the study, so don't think a 16-week study takes 16 weeks. It actually takes, as I say, a bare minimum of six months, potentially a little longer, but we'll be looking to do them as quickly as we possibly can. Yeah, so I hope that's helped. There's something about trials remaining in Australia.
I think if we're talking about trials in patients, which I think is probably what the question was about, if we're doing a Phase 2 or if a partner company is doing a Phase 2, typically looking at groups of 40, 50, 60 patients, and these are usually multi-center sites done in more than one territory, so the potential with Australia could be one of those territories. It's unlikely that we would do all of any trial in Australia in its entirety, but yeah, I think our experience with Phase 1 was very positive, so we have no qualms about going back to Australia for a portion of the Phase 2 if we do it or if any potential partner company does that. I hope that answers the question.
Great. Thank you very much, John. I think the next question is one for Stephen.
Milestone payments relating to 737 are due at the end of this year, and we've touched on this already. If we receive shares in the U.S. bio company, will you announce who that company is?
Well, as I said before, of course, we are not a party to the agreement. So it will not be for us to decide spontaneously to name a company or not. That will depend on the permission given by the licensee. However, to my mind, it would be extraordinary to receive shares in a company which, by definition, has a name on it, not to be allowed to say who that company is. But that's something for the future.
Great. Thank you, Stephen. Next question. At what point will the company seek a new chief executive officer? I spoke before about risk assessment and decision trees.
There are certain scenarios in which it clearly makes sense to appoint a new CEO. Equally, there are scenarios where it makes no sense at all, and we will take an informed decision as we move forward along those decision trees.
Thank you. Another question, I think, for Stephen. It's been many years now that there's been talk of deals being made. What is the biggest blocker to sealing a deal?
Well, whenever you're going to do a deal, probably of any sort, but specifically with a drug, there are three parts, really. The potential licensee has to be excited by the drug and by the data generated. It has to be excited by the IP, and of course, there have to be terms which are mutually agreed and beneficial.
The evidence so far is that the limited amount of information that we have put into the public domain about the Phase 1 study has caused excitement and certainly interest. Are we going to be able to agree terms at this stage? That's something for the future. But if not, we are moving, as you know, forwards very firmly to prepare the drug for Phase 2, whether it is us or it is a licensee company that is taking it forwards.
Great. Thank you. Next question, I think, is for John. Can you elaborate if there were specific toxicology concerns that emerged during the Phase 1A trial which prompted the decision to extend the toxicology studies? What were the key findings or observations that led to this course of action? Well, there were no toxicity concerns raised from a Phase 1 trial.
So, I mean, I think the decision to look at extended toxicity studies is purely based on the regulatory requirement to conduct a Phase 2 study. And we've had a steer, I suppose, from potential commercialization partners that they didn't see the benefit of a short validating Phase 1 B trial because the targets are clinically validated. They saw some benefits in taking the program straight into Phase 2 trials. So we're going to get the program Phase 2 ready for our own good reasons rather than any negative reasons arising from the Phase 1 trial.
Great. Thank you. Next question, I think, for Stephen. Are you able to confirm if the original investors which were involved in previous fundraisers are still engaged and on board?
As you all know, under U.K. law, if you own less than 3% of a company and you're not a company director, then you have the rights and the privilege of remaining anonymous. And I think we should extend that rights and privilege to all of our investors.
Great. Thank you. Next question for Stephen again. Following earlier fundraisers in which private investors were invited to take part, is it possible to invite current private investors to take part this time at the current favorable share price offered? This really arises from the structure of the offering. In the spring, we undertook a conventional placing. And because of that, we were able to use the Winterflood Wrap product to open the product up to all our individual shareholders. And I was delighted and gratified with how many of you took the opportunity of taking part in that.
This last fundraising that was done over the course of the last couple of weeks was a direct subscription from the company. And as such, the wrap vehicle was not available to us going forward. The reason why we decided on the direct subscription was that we were very anxious to minimize the dilution as best we could for existing shareholders. And the typical going rate for placing is much closer to a 50% discount than the 24 or 25 that we ended up having with this last fundraising. So, unfortunately, in this instance, it isn't available and cannot be available with a subscription. Thank you. Next question, I think, is probably for all three of you. If you believe we have possibly a best-in-class product, why are none of you investing more into the company to show confidence to the market?
Is the lack of direct buying down to a lack of faith in the company or due to NDAs being flexible?
Well, why don't I pick this one up on behalf of us all, but Tim and John do chip in if you feel the need. The answer, quite simply, is that all the directors have been fully. We remain excited by the company and its products. We have been buying shares over the course of the last year, both in the placing in the spring and by spending about six months in which we took shares in lieu of part of salary. So I do feel that we are fully committed and remain so. It is very difficult for directors to buy shares with regard to company law, of course.
Not only are there the formal closed periods, but the NOMADs and the broker have to be confident that the directors do not hold inside information, even of an informal nature, in order to allow us to make those purchases, and of the nature of a company like this, those gaps are few and far between, so it is absolutely not anything to do with lack of faith.
Thank you. Next question will be probably initially for Stephen again. In view of the recent updates with regards to the program of research, is it the view that an earlier date is being sought rather than moving on to further trials, which will be at greater risk?
Well, of course, our strategy in the company has always been to look to partner at late preclinical or early clinical.
But as I said before, there are three parts to any deal, one of which is acceptable commercial terms. And so I would say that we are certainly open to a deal on the right terms. But if we do not attract sufficiently attractive commercial terms, we're not afraid of taking it forwards to the next stage ourselves.
Thank you. Next question, I think, is for John. Can you confirm my understanding that the current focus is on preparing the ground for the tox studies and the product synthesis and writing up of the clinical studies report, and that there are no clinical trials being conducted currently?
Yes, that's correct. Well, certainly no clinical trials being conducted currently. But the clinical study report from the Phase 1 trial is being written up as we speak. We're expecting to receive that before the end of the year.
And so the focus is on toxicology studies. And we are doing some new synthesis of drug product as well. Yeah. So correct.
Great. Thank you very much. Probably have time for a couple more questions. Previously, SDC-1801 spent a long time in long-term tox studies. Why the need to repeat these?
I can take that again, Jessica. Yeah. Well, hopefully, the questioners, if they were able to hear the presentation, have got the answer now. So we had conducted a one-month study to support the MAD phase, which was 10 days dosing, and the planned for Phase 1b study, which would have been 28 days dosing in patients. And now we're looking to get the molecule Phase 2 ready. Those studies are likely to be more like 12-16 weeks. And so we want to give ourselves the toxicology data to support 16 weeks dosing in humans.
So that will be up to 16 weeks toxicology studies.
Great. Thank you very much. That does conclude the Q&A session at this point. Thank you very much for submitting your questions. We will endeavor to answer all these via the platform in due time. And I'll now hand back to Investor Meet Company.
Perfect. Thank you very much, Jessica, for sharing the Q&A. And as Jessica mentioned, of course, the company will review all questions submitted today and will publish those responses on the Investor Meet Company platform. But Dr. Stephen, before we redirect investors to provide you with their feedback, which I know is particularly important to the company, could I please ask you for a few closing comments?
Thank you. Yes. Well, thank you again for taking part in this broadcast. I've been most impressed by the numbers I can see on the screen here.
So again, it reflects the commitment that you all show to the company. And we are all very grateful for that. Hopefully, the year to come will also provide many positive talking points and hopefully a significant step forward in the affairs and fortunes of the company. So thank you again. And I'll just hand you back for the closing session to IMC.
Fantastic. Dr. Stephen, John, Tim, 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'd like to thank you for attending today's presentation.
Good afternoon to you all.