Participants are in a listen-only mode. There will be a presentation provided by management, which will last for approximately 20 minutes, followed by Q&A based on questions that have been submitted either via email or live during the session. If you have a question you'd like to submit, please do so using the Q&A function within Zoom. On the webinar from Syntara today, we have CEO Gary Phillips, and I'll hand it over to Gary to go through the presentation.
Good morning. Thanks very much all for joining, and thanks for the introduction, Matt. I'll just, as Matt said, I'll walk through the data, and then I'm very happy to take your questions at the end. Just to remind you, this is an interim data set. There are still patients ongoing in this study. We expect the last three patients to complete in the next quarter, and we'll be reporting once they've all finished. Just before I dive into the data, just a reminder on myelofibrosis, that it is a type of bone marrow cancer that disrupts the body's production of blood cells. Many of these patients get cytopenias, low red cells, white cells, and platelets. The symptoms they get are driven not only by those cytopenias, but they get very enlarged spleens as well. This is a disease which is an orphan disease.
Patients have about five years' life expectancy from onset. Many of them go on to get leukemia. Their symptoms really drive their lives for the time from they're diagnosed through their life on the primary standard of care, which, as I've mentioned before, is a JAK inhibitor. JAK inhibitors are a class of drugs. There are four of them. They're used in the management mainly of the enlarged spleens that these patients get and some of the other constitutional symptoms that they get. This is what drives the endpoints that we use in clinical trials for myelofibrosis, which are of interest to the FDA, the primary one being the total symptom score. This is measured on a scale of 0-70.
In order to see a responder in this rate, you have to have a 50% reduction in symptom score in order to say that you have a patient which has responded to the drug. The other one is the spleen volume reduction, which is, again, working on this enlarged spleen, which in these patients, as you'll see from our study, a normal patient's spleen is around 300 ml. These patients can get up to over 3 or 4 liters in terms of spleen size. In order to see a responder in this area, you have to see a 35% reduction in the spleen volume. In the patient group that we're looking at, in patients with a suboptimally controlled—so patients on a JAK inhibitor but not well controlled—we think the precedent is there for a 25% reduction in spleen volume being notified as a responder.
These JAK inhibitors are widely used. The primary one, the one that is most used, is ruxolitinib. It's the one that we're using in our study that we're adding on to. They have significant limitations that they do have a lot of side effects and dose-limiting tolerability issues, which include cytopenias or reducing blood cell counts in these patients and an increased risk of infections. Much so that most patients discontinue these drugs within a five-year time frame. Once they come off the drug, they've only got about a year to live. There's a huge unmet need in this area. Patients really need another drug which will help control their symptoms and spleen sizes, but also do something about the underlying disease here.
We think our lead drug, SNT-5505, is very well positioned in this because it's got a very different mode of action to the JAK inhibitors and the other drugs which are in development. It's showing a very much improved tolerability profile, which we think is part of how it differentiates itself. This study is all about looking at to see, okay, as well as that improved safety profile compared with the competition, what does it do to symptoms and to the spleen sizes as well? What happens when you put it on top? This is an attractive area. The JAK inhibitors themselves are selling almost $2 billion worth of drugs for these patients. We think the area that we're in, in terms of the suboptimally controlled patients, is the market opportunity is over a billion.
That's probably driven the very large asset acquisitions in the myelofibrosis drugs, which have several of them in the last few years, all of them been north of $1.7 billion. If we look at our drug and what it does, this chart just shows what happens in myelofibrosis patients, what's driven by the enzyme Lysyl oxidase. On the left-hand side there, you can see the thing that we've talked about a lot is the structural effects of LOX. When LOX is upregulated, collagen fibers become cross-linked within the bone marrow, and that causes a stiffened environment in the bone marrow, which exerts mechanical stress and fosters the abnormal cell development that we see in myelofibrosis patients. The other side of this is also the impact of LOX on the bone marrow cells themselves.
We have several different pathways ongoing here that lead to that cell proliferation and activation of immune cells, one of them being the JAK-STAT pathway, where the JAK inhibitors work. The other one is the PDGFR route. Upregulation of Lysyl oxidase enzyme in these patients drives that PDGF pathway, which also leads to proliferation of fibroblasts and activation of the immune cells. If you think of it in this way, the JAK inhibitors solve some of the problem in the bone marrow cells, but this PDGF route kind of bypasses what's happening with the JAK-STAT route. If you can do something about not only the extracellular matrix over on the left-hand side, but also this PDGF route, that explains what's happening when we dose with our drug.
When we see this happening, the Lysyl oxidase activity boosts this growth factor, induces cell division, stimulates fibroblasts, and that together with the stiffened bone marrow leads to increases in inflammation. The extracellular matrix gets stiffer, and you get more abnormal cells produced, which obviously drives one of the effects of that is driving spleen size. Blood cell production drops, and then that then drives an increase in symptoms and spleen volume. That is the whole thing. That is what LOX and the enzyme is having on these fibrosis patients. Obviously, 5505 comes in, and it is blocking not only the LOX impact on the cross-links and the stiffened matrix, but also on the bone marrow cells themselves. Diminishing that bypass mass mechanism of the JAK inhibitors. The study that we are engaged in tries to make use of that mechanism and the add-on impact on top of RUX.
The study is an open-label study looking at adding our drug on top of ruxolitinib, the leading JAK inhibitor, in patients who are suboptimally controlled, so patients who still are symptomatic and most of them have larger spleens as well. The endpoints we were looking for here was primarily safety, but of course, we're starting to look at some of the efficacy, which we're reporting on today. Just a word on the patient group that we've recruited. This is very much similar to the data that we presented at the American Society of Hematology back in December. These patients had more than three years' experience on ruxolitinib before coming into the study. That's an important parameter because it indicates that actually what we see here is an indication of a very high disease burden in these patients.
Their spleen sizes, their blood counts, their symptom scores, the time they've been on RUX are all indicative of a group of patients who are well down the path in their journey of myelofibrosis and are pretty sick when they came into the study. That probably compares with other studies that have been run in suboptimal patients, which have seen the length of patients, the length of time on ruxolitinib being between 18-24 months. Our study stands out in that sense that we've ended up with a patient group which has been a bit sicker than we've seen in other studies that have gone there. We've obviously had dropouts in the study as well. That's really in line with what we've seen in other studies.
In fact, at six months, you've got sort of about a third of the patients who have dropped out, which is very much in line with other studies that have been run in these suboptimal patients. We've lost another three patients beyond that point. Eight patients have dropped out altogether out of the 16. None of those have been due to drug-related side effects. We still, from a safety perspective, have a drug which is extremely well tolerated. All the SAEs, none of them have been related to our drug. We're now starting to see a considerable amount of exposure of these patients on our drug. Still really comfortable with the safety profile of the drug. It still is a key point of differentiation from other drugs that are either on the market or in development.
The fact that this drug, because of its mechanism, is not driving any hematological toxicity in these patients is a real bonus and one of the things that the clinicians in this area are very much attracted to. When we go and look at the results coming out that we will be presenting in a poster tomorrow, this poster is available on the European Hematology Association portal. It will be behind the paywall as of today. From a hematological point of view, what we are seeing is stability, which in this particular patient group is a good outcome. These patients, as I said, more than three years on ruxolitinib, really going down and down and down. The fact that we have got stable patients and even some signs of a hematological response in some of these patients.
We didn't go out there and try to recruit patients who were transfusion dependent. We only ended up with two patients actually that were transfusion dependent out of the whole group. Despite that, we're seeing stability and some signs of a hematological response. Stability out to now nine months and 12 months for some of these patients is a really positive outcome. When we get to symptom score, I think when we presented at the American Society of Hematology back in December, what we saw was an improving symptom score over time. When we got out to nine months in particular, we were seeing the majority of patients were seeing some kind of symptom response. I'm very pleased to report that what we've seen when we get out now to more patients reaching that nine months. All the patients have now reached six months.
All of the patients have reached nine months. We have still got some patients still in the study that have yet to reach 12 months' worth of treatment. What we are seeing is at week 24, which is the standard length for a myelofibrosis study that has been run in the past, we have got four out of those 11 patients that have reached the TSS 50. When we look at week 24 or beyond, that increases to 73%, so eight out of the 11 patients. At ASH, we had, I think, something like 62% of patients with that patient group at that data cut had reached the TSS 50. We are seeing a gradually still improving situation. It is a very, I think, reassuring picture that we are seeing. Patients that stay on drug continue to see an improvement in their symptom score.
The majority of them are reaching that threshold of the 50% improvement in symptom score. When we look at this and we look at the impact on patients and we listen to clinicians, they're seeing these patients that have been on ruxolitinib on average for three years have had a deteriorating situation, increasing symptom scores in many cases, cytopenias, large spleens. You see that kind of patient have a 50% or more reduction in symptom score after being on a drug and maintaining that beyond six months is a really big differentiating feature for our drug versus those on the market or even those in development as well. This impact of not only just reaching that threshold, but maintaining it and seeing it further improve as time goes on is a key point of differentiation for the product.
It is a very reassuring thing to see based on the mechanism that we have. That safety profile backed up with this is really good. I think maybe that symptom score was more of the same. It was what we saw at ASH, the ASH data set that we presented back in December. Reassuring to see it continued. What was really pleasing to see in this data set was that hint that we had in December that patients were starting to see their spleen volumes improve. The data we had then is once we have seen those patients get to nine months, we have really started to see the spleen volume start to come down. 44% or four out of the nine patients that were in that study beyond the six-month mark getting the SVR 25.
A third of them, three out of the nine, getting an SVR 35 is a really positive reinforcement that what we're seeing in the symptom score is a real effect. The symptom score is a patient-reported outcome. The spleen volumes are measured with an MRI to the nearest mill. This picture we're seeing now is really reassuring to see, I think, points to a real effect that the drug is having. Given that this is likely to be the other endpoint on top of TSS 50 that the FDA would like to see in a pivotal study, the fact that we're starting to see both of them emerge and spleen volume reduction now quite convincingly at this point is really, really positive. Really pleased with this part of the outcome of the study.
Just to reflect on the competitive landscape, I apologize for the busyness of this slide, but it is trying to capture quite a lot of data. What we are seeing is in other studies in drugs which are in development, which are added on top of ruxolitinib in suboptimal patients. This is data on this slide from phase II open-label studies that those companies have run. Pelabresib, navtemadlin, and navitoclax have all run studies in suboptimal patients in phase II open-label. In general, what we are seeing is TSS 50 responder rates in the sort of 30%-40% range. Again, seeing ours now up above 70% beyond six months, as I pointed out, is something which differentiates the drug and gives it a profile which we think will attract attention both from the regulators, from clinicians, and also from patients as well.
Now starting to see the spleen volume reduction. Some of these results here on spleen volumes are SVR 35. The fact that we're seeing SVR 35 at week 38, we're up to about 38% now, which is very much competitive with what we've seen from other drugs in this field. We feel very comfortable now that we've got a competitive drug profile, particularly when we add on the impact on TSS 50 and spleen volume with the much better safety profile that we believe our drug possesses. A reminder that the attractiveness in this space, and we've added another column into this chart from another drug deal that was done relatively recently, December last year, was a drug that was in phase II in MDS and myelofibrosis, both disease indications, which we think 5505 has an application in.
Obviously, we've got data in myelofibrosis, the MDS studies that we are funded to run start in the next month or two. That rounds out. The Takeda deal buying the Keros, that was $200 million upfront for a drug in phase II with a deal value worth over $1 billion. It shows, I think, what's possible with earlier stage drug deals, as well as obviously on this chart, the price for staying on and running the course and running a phase III study and getting positive data at phase III obviously drives very much larger acquisitions. The one non-JAK inhibitor on here is pelabresib, which sold for $2.9 billion. Now, of all those products and the ones on the previous chart, we've started to see drugs actually, pelabresib in particular, run into a safety issue. Navitoclax did not reach TSS 50 in its phase III study.
Those are now looking more questionable in terms of their futures. And navtemadlin is the other one still in phase III, started phase III earlier this year. We believe that we're well differentiated from that drug in terms of safety and potentially efficacy as well. That gives us great optimism for the future and the kind of commercial value that the drug program will have. I'll finish up at this point and open up for questions in just a second. Just to remind you that Syntara is not a one-shot on goal. SNT-5505 is where the company, the bulk of the company's investment is going. Clearly, that trial in myelofibrosis is now starting to wind down. We do have $18 million in the bank as at the end of March.
We are burning around $1 million a month, and that's declining as this study runs down. We have cash through until the second half of next year. That covers all of the trials on this list here. The myelofibrosis phase II, two myelodysplastic syndrome studies, another blood-related hematological cancer that we expect to get phase one C efficacy and safety data by the middle of next year. There is a scarring program running in both hypertrophic and keloid scars. The hypertrophic scar, we expect to see data by the middle of next year. It is a study which is due to start next month. Finally, the Parkinson's disease study, which is well underway, we expect to see fully recruited by the end of the year and data in the first half of the next year.
The MDS study and the Parkinson's disease study are both funded, if you remember, by non-dilutive cash from grant money that's coming in. As I said at the outset, the company's main investment is in the myelofibrosis study. We've got cash there to take us through news flow, which looks really quite strong for the next few months and well into next year. The next milestone is really our discussion with the FDA on the data that we're seeing today for the first time that we're presenting at the European Hematology Association meeting. The discussion with the FDA is around what's the design of the next study that we would need to run, what's the pivotal study design that we would need to get an approval. We expect to get an engagement and a discussion and an answer from the FDA in quarter three.
That will be the next milestone coming up. Following on from that will be data from those other studies that I've just talked about. With that, I'll finish my presentation, Matt, and I'm very happy to take any questions.
Thanks, Gary. As you mentioned, we'll move on to the Q&A. Again, these questions are based on those sent through earlier via email and live during this session. If you still have a question, please type it in using the Q&A function within Zoom. Gary, the first question, and it comes back to what you were just talking on at the end there, can you just go into a bit more detail around those next steps, what you'll be looking for out of meeting with the FDA, and maybe what sort of questions you'd be likely to ask as part of that?
Sure.
Those of you that have been following us know that we had fast-track designation granted to us by the FDA last week, which was really, really pleasing to see. That does give us certain opportunities for more frequent and rapid interaction with the FDA. Based on the data we have, this is the interaction we're about to have, it's not an end of phase II meeting. That will only happen once we've got all the data set completed in quarter three and then probably a meeting with them later on in the year. This next interaction with them gives us the opportunity to get confirmation from them that, first of all, the safety data set that we have with the studies that we've run both in monotherapy and now in combination with ruxolitinib is sufficient for us to go and progress into a pivotal phase III study.
Secondly, we're seeking to get confirmation from them that a single phase III study with our drug will be sufficient for an approval. Thirdly, to engage them with the proposed design for that phase III study. There are two sides to that. One is how large does the study need to be? That's likely to be driven by the number of patient exposure the FDA would like to see on our drug before it's comfortable with the overall safety profile to give an approval. We believe that a phase III study of around 300-350 patients is probably what would be enough to satisfy that tick. We're seeking guidance on that from the FDA in terms of just confirming what we think.
There will be the study design clearly on top of a JAK inhibitor, ruxolitinib being the obvious one, but there are other JAK inhibitors as well. It'd be an interesting point of discussion with them as to what they think about other JAK inhibitors and what kind of label we could get in a phase III and what kind of design that might need to look like. We'll also be asking clearly about endpoints. Our expectation based on previous discussions with the FDA is that TSS 50 is most likely to be the primary endpoint. We know that the discussion over secondary endpoints is broader. There's more flexibility there.
Given what we're now seeing in spleen volume, we'll be likely looking to see whether the FDA is comfortable with what would look like a fairly standard design of phase III study in myelofibrosis, which is a primary endpoint of TSS 50 and spleen volume reduction of 25% for the secondary. It is an interaction where we're seeking to put forward what we think based on precedent and the profile our drug has, what we think a phase III trial would look like, and to get their early comments on whether they think that would be acceptable. Clearly, the next step beyond that is then a much more detailed study design based on this.
This next interaction should give us a very clear idea about whether we are in a good position to jump straight now into that pivotal study with a study design that we can be confident about delivering on.
Thank you. The next question I've got is, there appears to be a mild correlation between responses, both SVR and TSS, and time on prior RUX. Can you elaborate on what this may mean for designing inclusion/exclusion criteria for a registrational trial?
Yeah, that's quite a complicated topic in that we are looking for whether we can get a reaction from these patients within a length of time. Do we run the study for six months? Do we run the study for nine months? Because it looks like the response rate gets better the longer they stay on the drug.
Our trial this time round was in patients who seem to be at the more severe end of the spectrum of myelofibrosis patients. I think I caution to look too deeply into the data because of the small data set, but it does appear as though patients who are on perhaps a slightly higher dose of ruxolitinib and are not so far down the journey in terms of their time from diagnosis of myelofibrosis and time on ruxolitinib, those patients with perhaps a little bit less time on RUX and still able to tolerate higher doses of RUX appear to get a bigger response to our drug as well. Maybe going back to that mechanism that I talked about earlier as being something that comes into play here.
In any case, I think the phase III study is likely to have a patient population which will still include patients who have relatively severe myelofibrosis, but we'll be looking to expand the patient pool with patients who are not as severe but still have enlarged spleens and significant symptoms, but perhaps have been on RUX for less time than the average length of time on this study. This study really pushed the edges in terms of the severity of the patients coming in, which on the one side has been sometimes difficult because these patients are sick and they do progress. I can't undersell how sick some of these patients are coming in.
That in turn has led to being quite a convincing small data set because we are making a difference to these patients, but it might not be that patient population you want to take into a broader phase III. You need to look at a broader set of that suboptimal group.
Thank you. The next question and understanding is only so much you can say on this front, but has Syntara been approached or had commercial discussions with regards to partnership?
Yeah, given the commercial attractiveness of this area and the deals that have already gone, you would imagine that any drug that comes through that starts to see positive data in phase II does attract attention. As a company, Syntara has a lot of experience in doing partnering deals in the past. We have been making sure we do our bit.
We have been approaching and been approached by potential commercial partners for over a year now as we have gone through the monotherapy data and now into the combination data. I will be seeing some companies when we are at the European Hematology meeting. I met some of them at ASH in December. There is a BIO, the major partnering event of the year, coming on next week as well. Yes, we are exposing potential partners to the data sets we have got and trying to gauge what their interest is. At the same time, we are talking to investors as well about what we would need to do for the phase III study to carry on ourselves.
On a related note, someone else has asked, what impact may a revised US Reimbursement Scheme have on a potential commercial deal?
Again, difficult to predict.
It's difficult to predict much at the moment, isn't it? One of the things that's going to change in the climate of myelofibrosis is that the lead drug in this area, ruxolitinib, which is sold by a company called Incyte in the U.S. and elsewhere in the world, Novartis, that drug comes off patent in 2028. We believe that the environment for us will be actually improved by the time we get there because payers will not have to fund the current amounts, which is anything between $150,000 and $250,000 a year per patient. That number will drop very, very significantly and makes room for a treatment to come in which can add on to that drug and really improve the lives of these patients. We think from a payer's perspective, the situation is we're helped by that.
It's not as though we're coming in and we're going to be adding on an equally priced drug on top of an already expensive drug and doubling the burden on payers and the co-pays on patients. We'll wait and see. I think that there's cause for some optimism there in terms of the environment that we're heading into and the way that this thing will develop as time goes on.
Okay, the next question is, thanks and congratulations on the update. Regarding discontinuations, half of patients stopped by 36 weeks. Can you elaborate more on why this was and why you would typically expect this from inpatients?
As I said, this patient group, they've all been on ruxolitinib for an average of three years. The life expectancy of these patients is five years.
Many of our patients have already had four or even five years' worth of exposure to ruxolitinib as well. So what you're trying to tease apart here when you look at the drop, the withdrawal rates in the study is, first of all, what does it look like at six months? And how does that compare with many other studies which have been run in this kind of patient group, all being not quite as sick out to six months? And what we saw there is about a third of the patients dropped out at six months, which is about par for the course for this particular patient group with other trials that have been run. All bet that our study group was probably sicker. So that compares quite well. When patients get out beyond six months, all bets are off, really.
I mean, there haven't been hardly any studies in this suboptimal group to look at how long these patients can stay on drug. What we can see is that there are still some dropouts. None of them are related to side effects that the drug is inducing itself, which is different from the drugs in clinical development in that all of them have a fairly, they have a tolerability profile, which is, we believe, not as good as 5505. Dropouts on other drugs beyond six months are likely to be driven by the side effects of the drug. Now, that's not happening with us. What we're seeing is a natural attrition of this patient group from advancement of the disease. That's why we're not seeing any drug-related serious adverse events.
None of the dropouts have been down to any impact that the drug has, adverse effect that the drug has had. It is something we have to bear in mind for the study design of the phase III as well. You have to take account of the fact that you do see patients advance in these patients because they are sick. Some of them, their disease does progress. Even though we might be slowing it down and we are obviously clearly improving the lot of some patients significantly, those patients who are already quite sick, some of them do unfortunately progress.
Thanks, Gary. Next question I have is, you mentioned that there was no treatment-related hematological events. Can you confirm that the grade 4 thrombocytopenias were not treatment 5505 related?
Yes, that is right. Yeah.
Thank you. Next question is, seems that both TSS 50 and SVR improves as time goes on.
Given how long patients have been exposed to JAK inhibitors, please recap the mechanism you think that SNT-5505 is working by.
Yeah, so I've tried to sort of it's a complicated area with several different pathways that are impacting on both the bone marrow cells and on the microenvironment that surrounds them. We've always thought of a pan-LOX inhibitor as being primarily an antifibrotic. It works right at that final stage of fibrosis where the collagen is cross-linked. There's no downstream of it. It's the very last stage of fibrosis. In the monotherapy study that we ran that we reported on at ASH in 2023, in the bone biopsies that we took, we saw clear evidence that we were improving the bone microenvironment. We were reducing the amount of fibrosis in the bone marrow of those patients. We know that the drug is an antifibrotic.
I think when we looked at the data set we had in December last year in the combination therapy study, we were also seeing quite a fast improvement in symptom score in these patients and also early signs of spleen volume reduction, which is something that we, I guess, looked at and wondered that is a drug that's just working on the bone marrow microenvironment and on that cross-linking going to produce that fast effect. We have started to do more work in this area. We have included some slides within the deck now to fully explore the impact of LOX and its upregulation on that second pathway of PDGFR, which seems to work alongside the JAK-STAT pathway where the JAK inhibitors are working.
The impact on that signaling path within the bone marrow cells, by inhibiting that, we believe we have a direct impact on the proliferation of cells, the abnormal cells that myelofibrosis patients characterize as myelofibrosis and drives that spleen volume size. What we're seeing in those early stages is certainly the impact of that and then hopefully see the impact on fibrosis the longer the patients stay on drug as well. This is very much a drug which is working in two different pathways. It's something that we're still actively exploring within the company.
A follow-on from that question was, does it make you consider a longer trial versus the standard six months?
That will be something that's obviously a discussion point with the FDA. We're clearly seeing a drug which works beyond six months and is improving beyond six months.
We'll look very carefully at the design of the study, probably trying to pick up endpoints both at six months and also beyond that length of time as well. It'll be driven in the end by the numbers and the stats and what we think we can show because clearly there's a swings and roundabouts effect here. It's good to see an impact at six months. If you see an improved impact as time goes on, then your attempt is certainly to run the study for longer. Given the health of these patients and how severe their disease is, you also run the risk of more dropouts the longer you go on and you start losing patient data as well. It needs to be a balance between those two things. That's certainly a key point of discussion with the FDA on study design.
Thank you. And then just a couple that are a bit of a step away from 5505. Someone's asked, with regards to the shareholder register, does the company make efforts to facilitate block trades between known sellers and potential willing buyers?
Not generally. I mean, we obviously, we maintain close relationships with all of our shareholders and the larger ones we meet regularly. Certainly, if there is a need to do something like that, we would try and facilitate, put them in touch with people that we know. I spend quite a bit of my time on the road talking to potential new investors as well. There's always that you can't sit there on your hands and assume that everybody's going to hold your stock forever.
It would be wrong of me to rest on my laurels and not go out and actively look to expand the shareholder base and look for investors which are right for the stage which the company is at as the drug advances.
The question, how is the U.K. Parkinson's trial progressing?
Yeah. We reported earlier in the year that we'd had some recruitment issues with the U.K. site. There are two sites in this study, one in Sydney and one in Oxford. The U.K. site had been held up because these patients have to have a PET scan. The equipment in the U.K. had a problem, a technical problem, and then it required further work and calibration and validation. That site opened up late. The U.K. site also has a very large pool of iRBD patients, which are the patients being recruited into this study.
The recruitment went well within the Sydney group. I'm pleased to say it's now going well in the U.K. We expect to see that study fully recruited by the end of the year. It's 40 patients in total that we're looking for, and it's a three-month study. If it's fully recruited by the end of the year, we'd have results probably in the back half of the first half of next year, but towards the second quarter. Yeah.
The final one, fairly broad one for you, Gary, but someone's just cited the different programs that the company has and has asked, are there shared mechanistic insights or regulatory pathways being leveraged to accelerate development across your programs and enhance capital efficiency?
I think I said during my chat that the company's been very good at getting in non-dilutive cash from grants and things to support the program. I think one of the key differentiators of Syntara as a company is that we do have our own internal drug development group. That's enabled us to produce a pipeline of drugs rather than just one drug and a company which is just doing one trial, one drug, and it's either going to work or it doesn't work. I'm very pleased to have a pipeline there and multiple shots on goal that generate news flow, reasons to hold the stock, and potential value accretion points for investors to focus on. At the same time, it does place a burden on funding.
Hence the focus that we've had on grant applications and getting in non-dilutive cash and being as efficient as we can. Certainly, the efficiencies come in getting the drug to the clinic. Because of our expertise, particularly in amino oxidase chemistry, we've been very successful at getting a number of drugs through that are based on that chemistry into the clinic. The hit rate that the team has had in a short length of time is startling. I mean, it really is. They've done an outstanding job at generating the number of, there's a huge attrition rate as you go through preclinical to get to the clinic. To have the number of drugs we have in the clinic at the moment is a huge achievement. Once you get there, then that sort of efficiencies drop away and you have to start funding them.
We still have choices to make and decisions to make about what we do, what we focus on as a company. Clearly, we're making our key investments in 5505 and making sure that both the myelofibrosis and now the MDS studies generate good data and ones that generate commercial opportunities. Running behind that, I would say, is the skin scarring program where our knowledge of pan-LOX inhibitors has enabled us to bring forward a compound which we think is going to be first rate and now going straight into the clinic in a study which we hope to demonstrate an endpoint which is improvement in scar appearance and function. Then we'll see what happens with that. That study is an investment of around about $2 million. It will give us a result. It is well within the cash runway of the company.
We'll give us a result by the middle of next year, well within the funding that we have. With that study result, we think it will generate its own ability to fund itself either through partnering or further raises either within the company or even as a spin-out, given the nature of it and the size of the commercial opportunity there. The Parkinson's drug is totally externally funded. That one looks after itself for the moment.
Thanks, Gary. That's all the questions. I'll just throw it back to you to provide a closing comment.
I'd just like to thank everybody for joining this morning. I'm actually currently in Europe, ready to go to Milan. It's about 2:00 A.M. here in the U.K. on my route to Milan in a couple of days' time.
The quality of the data we've had has kept my adrenaline up and being able to stay up late and present to you. I hope that the data we've presented is clear and you've got a good idea now of the potential value in the clinical trial that we've presented and what the next steps of the company are. I look forward to updating you again in the near future. I'd say that next milestone with the FDA, we do expect an outcome from those discussions in quarter three.
Great. Thanks, Gary. Thanks again to everyone in the audience for joining.
Thank you.