We are going to oxidase chemistry and other technologies to develop novel medicines for blood cancer and conditions linked to inflammation and fibrosis. Once again, a reminder on questions, if you have one you'd like to submit, do it using the Q&A panel within Zoom, and we will take some questions at the end. To start with, I'll hand it over to Gary to deliver the presentation.
Thanks very much, Matt, and welcome to all of you who've joined the conference today. I've got a presentation I'll run through, but I'm very happy to take some questions at the end. There's quite a lot of news flow coming out of Syntara, and we announced some news yesterday as well, so I'm happy to dive into some of the details as you want to. Syntara, you know, I find with talking to investors that there's a need at the beginning to sort of position the company in terms of who we are, what we've done, and why we're sort of differentiated from quite a few ASX biotech companies. You know, we are a clinical stage biotech, as Matt has said, but one that has its own in-house drug development group, which is relatively unusual, and that's allowed us to develop a pipeline of drugs.
The group has actually been extremely productive and put, you know, five drugs through phase one and some of them already in phase II. That puts us in a strong position for the future. It's often sometimes a funding challenge as well, and you'll see we've been very successful at getting non-dilutive cash to fund some of that pipeline, where the money that we've raised as a company has been targeted and focused on the haematological cancers that we're going to talk about in a little bit. The team is a very experienced one. We've taken drugs through to FDA and EMA approval. We've also done commercial deals and pulled in more than $100 million in the lifetime of the company as well. We're backed by a register, which is also different from a lot of biotechs in that we are more than 50% institutionally held.
I'll just dig into that in a little bit more detail. This is the current market cap of the company. You know, we're approaching AUD 130 million market cap. The stock has some momentum behind it because of the news flow that we've had since December of last year around our lead asset and now secondary programs and anticipation of further milestones to come. Just over AUD 20 million in the bank at the end of December, which gives the company a strong position from a cash perspective. It takes us out to the middle of 2026 and past a lot of the milestones that we're going to talk about and see. That register I talked about, more than 50% institutional, many of them specialist healthcare investors.
When we get a bit later and we talk about the commercial value of the lead indication we're in, I'll point to a couple of the companies there that have exited after phase III data, and we've got shareholders in common. We do have institutions on our register who hold a major position, who have made money by investing previously in companies that were developing drugs in the same indication we are. You know, they understand the market, they understand what we're doing, they understand the trials that we have to run, and they think and have come in and backed us through the last couple of raises in the capital markets. Also nice to see the volumes picking up as well.
From a liquidity point of view, we are generating a lot more liquidity day by day, again, coinciding with that news flow since December last year. The board is chaired by Kathleen Metters, ex-head of basic research at Merck, Simon Green, ex-head of plasma research at CSL, and a strong commercial background as well. Myself, background in big pharma and then more than 20 years in biotech in the last 10 years as the CEO of Syntara, Pharmaxis before that. Also on our board, Hashan De Silva, who is an investor. Hashan has invested in the last two rounds where the company has raised capital. You have a board member who is very familiar with the investor market in Australia with ASX companies, and has also put his money from his fund. I think the first investment he made from his fund was actually in Syntara.
The science behind the company is the lead assets is in fibrosis. Fibrosis is the part where, you know, if we have injuries on our body, and that can be injuries also to our organs, there's an inflammatory process followed by a scarring process where we form scar tissue or fibrotic tissue. That's a normal process. We need that in order to fully heal when we have damage. That damage can come from injuries. You know, you fall over and scrape your knee. It can also come from metabolism, from your genes, defects, chemicals, metabolic injuries that can occur to our lungs, our liver, our heart, our kidneys, but also to our bone marrow, which we'll talk about. In the case where you get these injuries that cause that need scarring in order to heal, the body has cells called fibroblasts. They become activated.
They release two things: protein fibers called collagen and an enzyme called Lysyl oxidase. The lysyl oxidase causes those collagen strands to organize themselves into layers, and it cross-links them. That gives us the tough, thick scar tissue that we would see on our skin if we injure ourselves, but also scar tissue which forms in the organs that we do not see: the liver and the lung and heart. You have heard about people having liver fibrosis, for example. That is what that is. It is scar tissue in the liver. That scar tissue is non-functional. It does not work as normal tissue. If you have a fibrotic liver, your liver function drops over time. If you have scar tissue on your skin, that scar tissue does not contain hair follicles or sweat glands. It is non-functional. We have a drug which fully inhibits those lysyl oxidase enzymes.
It stops the cross-linking of the collagen fibers. It's the very last stage of fibrosis. When you do that, we see in all the models we've run and now in two groups of patients, both in patients with fibrotic bone marrows and also fibrosis on their skin, we show we reduce fibrosis in those tissues. This is an antifibrotic that works and is also proven to be very safe as well. We've published our data in a large number of scientific journals. The company is really well validated from both an investor perspective with the smart money coming from specialist healthcare investors and also the peer-reviewed publications in Nature and Nature Communications, which we've seen in the last couple of years from the collaborators that we've worked with. I'm going to show you the data that we presented in December at the American Society of Haematology.
It's interim data from our study in myelofibrosis. Myelofibrosis is the fibrosis of the bone marrow. It occurs in patients normally after the age of 50. Their bone marrow has become fibrotic. The bone marrow is your body's blood production unit. It produces red cells, white cells, and platelets. When that happens, these patients get a lot of adverse effects, lots of symptoms: bone pain, night sweats. Their spleens get much bigger, sometimes 10 times the size of a normal patient. They get very tired. These patients have a life expectancy of about five years. The current standard of care are called JAK inhibitors. JAK inhibitors are good at relieving the symptoms of the disease, but very limited in terms of what they do to the underlying disease mechanism and in particular the bone marrow itself. They're also not very well tolerated drugs.
A lot of patients discontinue at 75% discontinuation at five years. That is driven because these drugs also cause cytopenia, so drops in red cells and platelets in particular. The very thing that the disease is causing, those drops in red cells and platelets and white cells, is exacerbated by JAK inhibitors in controlling the symptoms. The way that the clinicians at the moment control them is to just down-titrate. The normal patient would be on 20 milligrams of a JAK inhibitor twice a day, and that gets reduced over time. You will see patients in our studies often have doses less than 10 milligrams twice a day.
There is a great opportunity here for a drug that will work on top of a JAK inhibitor that will improve the symptoms and control of the disease of these patients, but also do something about the underlying disease and be a disease-modifying agent. The study we are running at the moment is a second study in myelofibrosis. The first one was in patients who had failed on a JAK inhibitor, were end of life, had one year left to live. We reported that in 2023 at the American Society of Haematology. In those patients, we showed the drug was safe, and it produced some benefit in symptoms and spleen volumes and bloods. Encouraging signs of efficacy, but really it was the safety mechanism, the safety that really stood out in that study.
We took that back to the FDA, and they gave approval for us to start a study in patients who were already on a JAK inhibitor. These are patients on a JAK inhibitor but are suboptimally controlled. They still have symptoms. They're still symptomatic. They still have relatively large spleens and often low blood counts as well. This is the group of patients that we're studying. It's a 12-month study, open label. In December, we presented interim data, which was from the first group of patients that had reached both six months and nine months' worth of therapy. Interestingly, if we look at the demographics of the patients, which this slide does, there's a couple of things just to point out. I'm sorry, it's a busy slide. The average length of treatment on RUX for these patients, the JAK inhibitor for these patients, is over three years.
This was a really experienced group of patients. They're well down the journey of having myelofibrosis and being on a JAK inhibitor. You know, if they've been on for over three years, life expectancy five years, we're moving to the later stages of the disease. That was borne out by their symptom scores. Symptom scores are measured on a patient-reported outcome scale between 0 and 70. 70 is very bad. 0 is very good. Any patient over 20 is considered to be very symptomatic, and we had an average symptom score of 23. That suggests that these patients are both struggling on their JAK inhibitors. Their average dosage was 20, so half of the recommended dose, and a symptom score over 20. From a safety perspective, we were really pleased already. This is the same as the monotherapy study, which we've already reported.
This stands out amongst the treatments that are on market, but also the treatments that are being developed as being a really safe drug. We've had no serious adverse drug events which were related to the drug at all. Really, really encouraging, very promising data that differentiates this drug from the competition. We looked at symptom score, and in this endpoint, we look for the TSS 50. That's a 50% reduction in symptom score. If a patient comes in with a symptom score of 30, we'd have to reduce them to 15 in order to call them a responder. In this first, the 12 weeks of the study, remember, we're running this to 52 weeks. At 12 weeks, these patients had six out of the 13 had reached that TSS 50. That's almost 50% of them had reached that landmark of TSS 50.
As a comparator, JAK inhibitors and the competition in clinical trials now are achieving between 30 to 40% TSS 50 at six months' worth of therapy. To see more than that already at three months was encouraging. We then looked at what happened to those patients as they went longer. This slide shows the patients, all the patients, full length in the study. Some of them have reached nine months, and we can see that as the study has progressed, more and more patients have hit that TSS 50. If we look at this in our group, we've now got 62% of these patients hitting TSS 50. The TSS 50 continues to improve over time. That's a really important and unique finding.
We have not seen that in the JAK inhibitors, which often reach their peak improvement at three months, no further improvement at six months, and often decline after that. This is a really promising result. One, again, with the safety really makes the drug stand out versus the on-the-market drugs and the competition. When we look at the spleen volume, spleen volume is measured by percentage again. We are looking at whether how much these patients improve. We have seen that nine out of the 11 patients had either a stable or reduced spleen volume. We are seeing additional improvements in spleen volume reduction at week 24 and week 38. We are now waiting to see what this data looks like when we move out to week 52. This is the data from just those patients that have reached nine months. It is a really promising picture.
We're very happy with the TSS 50 scores. We think that's very competitive. We think that the SVR reduction is also competitive, what we've seen before, not maybe different from what other drugs have shown, but certainly in the right ballpark. Interim data in December, we've got more data from this study coming in Q2. Why is this important? These are the last three deals that have been done in myelofibrosis. All of these three companies and their associated drugs in myelofibrosis were sold after phase three data, one step beyond where we are now. One of them for $1.7 billion, the one in the middle, CTI. Two of our shareholders were significant. One of them was the major shareholder in CTI before it was sold to Sobi. When I say institutional insiders, that's what I mean.
Another couple also invested in MorphoSys, which sold to Novartis for $2.9 billion in February last year. Interestingly, that Novartis drug has since run into safety problems. We considered it to be a competitor of ours, but more of the patients on the active drug transformed through to acute myeloid leukemia. That is delaying the submission of that drug and may stop the submission of that drug without further trials. We believe that the market is opening up for us. There is space for a new drug to come in and show what it can do on top of a JAK inhibitor. We think our drug is well differentiated and looking good to go. In summary, consistent with the monotherapy data, a safe and well-tolerated drug. We have got a good improvement in symptom score.
We're happy with the improvements we're seeing in symptoms and spleen that continue importantly to improve over time. Looking forward to seeing the data out to 12 months, which we expect to present to the market in Q2. I said at the outset that Syntara was a company with a pipeline. This is the pipeline. SNT 5505 is the drug I've been talking about. It's in two different indications. Both of them are haematological malignancies, so blood cancers. Myelofibrosis, which we've just discussed, interim 12-month data due in Q2 this year. Really big market. It's over $1 billion of sales in drugs, even though it's only symptomatic. Myelodysplastic syndrome, another blood cancer where we've got good preclinical data. Two studies due to start in the middle of the year and interim data by the end of the year.
Both those studies are funded by non-dilutive cash, one from the Australian government and one from the German Cancer Foundation. Really excited to get those studies going. That extra indication will add a lot of commercial value to 5505. 9465 is a drug which we announced yesterday. We've had a long-term collaboration with Professor Fiona Wood in Perth looking at skin scarring. We've presented one study already which shows that a pan-LOX inhibitor applied topically to the skin fundamentally changes the scar structure. We think this is a huge commercial opportunity. We've brought forward a backup compound which we think is better tolerated than the original drug we used in that first study. That's due to go into a phase 1b study in next quarter.
We expect data in the first half of next year showing that the drug is safe, that it's better tolerated than the first drug, and showing that patients with a young hypertrophic scar, so a severe scar, can see physical and visual differences in their scar by the end of the study. Data from that in the first half next year. Fiona Wood and her group are going on and doing a study with the first-generation topical drug in keloid scarring, which we think is also an opportunity. We're looking at that as an exploratory study where they're trying to understand the biology of keloid scars and whether pan-LOX inhibition can work in that area. Last but not least, SNT 4728 is a drug which we've got in Parkinson's disease studies. It's currently underway, 25% recruited.
Data by the end of the year, two centers, Sydney and Oxford. We are looking to see whether we can improve sleep quality in these patients and reduce inflammation in their brain, which will be a strong indicator that this drug's got a life in delaying the onset or preventing Parkinson's disease. Again, a big commercial opportunity and a study that is fully funded by Parkinson's U.K. after being audited by many neurologists globally on an opinion leader investment panel. Really excited by the pipeline. That, of course, drives a news flow, which is really strong going from this point forward, going towards the end of the year. Again, as I said, that nine and 12-month data from the myelofibrosis study to be reported in Q2. we will be submitting our proposal for the next clinical study in myelofibrosis to the FDA in Q2.
We expect an outcome from that around the middle of the year, with the FDA coming back and giving us feedback on what study can we do next. A phase two, three study is mooted that would be a pivotal study that gets us an approved drug. Also around the middle of the year, starting those two studies in myelodysplastic syndrome and then reporting on both of those myelodysplastic syndromes and the Parkinson's disease sleep disorder study towards the end of this year. A busy news flow for the company going through the year. Lots for investors to get interested in. As I said, the stock has some momentum at the moment. We hope to support that with a strong news flow between now and the end of the year, with a cash balance that supports that in a strong way.
Matt, I'll finish there, and I'm happy to answer any questions that you've got. Great.
Thanks very much for that, Gary. Once again, as a reminder to the audience, if you do have a question you'd like to submit, just type it in using the option within Zoom. Gary, I know you only presented on it yesterday, and there's a few people in the audience who were on that webinar as well. Can you just recap on yesterday's announcement regarding the skin scarring program, including what happened on Solaria 2 and what comes next?
Yeah. Solaria 2 was the study that we did with Professor Wood's group in Perth. It was placebo-controlled. It was 40 patients that were on our drug, SNT 6302, for a period of three months versus a placebo. At the end of the three-month period, we showed the drug was well tolerated.
We had no serious adverse drug events. We did have two patients on the active arm drop out because of skin reddening. We felt that there was a potential improvement there that could be made to tolerability. Having said that, the drug did work. We saw a 30% reduction in collagen content of the scars of these patients. These patients had scars that were on average 13 years in age. These were old gnarly scars that were very difficult to treat. Nothing else had worked. Fiona Wood at the time described the result as unprecedented, seeing the reduction in collagen. We since backed that up with an announcement about a month ago, which looked at a subgroup of those patients. We looked at a sort of optical imaging system that looks through the skin.
We could show improved vascularization of that scar tissue. Again, starting to normalize the scar tissue and turning it from a phenotype, which is scarred and fibrotic, through to normal skin. With that encouragement, we think we really do have a mechanism which works. The drug development group here in Sydney brought forward a backup really quickly. It is one of the advantages of having an in-house drug discovery group. We brought forward that backup compound really quickly. It is ready to go into a study. We are starting that in the next quarter. We will start off with a single ascending dose, looking at three different doses and checking that the drug, see what the inhibition of the enzyme in the skin is. We are looking at markers of efficacy in that sense.
Having selected a dose, we'll then test those healthy volunteers for a month and check that we're not seeing that reddening of the skin that we saw with the previous drug. We're confident that we won't see that. We go straight into a study with 10 patients open label who have a hypertrophic scar, but importantly, this time, less than two years in age. We're looking at younger scars that we think are easy to remodel, but ones that we can clearly show that there's a change in appearance and physical properties of the scar. Yeah, really excited about that. I think we had a good reaction from the market yesterday as well.
Excellent. I know you went to JP Morgan and similar events over the last 12 months. Can you talk about the level of interest you saw there with 5505 from potential partners off the back of that interim data?
Yeah, I guess there's two groups of companies we talked to. One is a group which already has a drug in the market for myelofibrosis, so a JAK inhibitor. Our study is showing that if you add our drug on top of a JAK inhibitor, that it brings additional benefit to those patients. Clearly, we have a drug which is of interest to those companies. We talked to all of them at ASH. We've shown them the interim data. They're very interested to follow up and see us again once we've got data, more mature data, 12 months.
Probably importantly, when we've got feedback from the FDA that the FDA are happy with the data we've got, and they are comfortable with the clinical trial design that we're proposing for the next stage. The other group of companies are companies that have an interest in haematology, not necessarily specifically myelofibrosis, but still our drug, given that it works in both myelofibrosis and we hope in myelodysplastic syndrome. It's of interest to companies with a pipeline in haematology that are looking to expand. That makes the universe of companies quite wide. We'll continue to talk to them during this period leading up to the more data and the outcome from the FDA and see what level of interest we attract then. At the same time, we're actively talking to investors that could fund the phase three study beyond this as well.
We'll go in this with all options, and the board is looking to make decisions that will be in the best interest of shareholders at that time.
Excellent. A couple of questions that have come through that I'll link together around the timing of the next 5505 data cut. Has that moved, and can you give some color around that? Following on from that, when do you expect the final data from 5505 to be announced?
The next data cut will come when we've got the last couple of patients that have crossed the nine-month treatment period, so probably later in Q2. We think it's important to have as complete a data set as we can before we update the market. I realize that this is open-label data, but it's a small number of patients. The interpretation of that can swing around.
We think it's important just to announce it when we've got the maximum amount. We don't think we need to wait. The final patient will finish their 12 months in quarter three. We don't think it's necessary to wait for that one patient to come through before we update the market on where we're at. It doesn't change our timeline with the FDA. We'll still be looking to make our application to the FDA for a meeting in Q2, early in Q2. The update on the data will come around the middle of the second half of Q2.
Very good. One final one. Has SNT 9465 gone through animal preclinical or in vitro tests? What's the rationale that it will have reduced inflammatory reactions?
When we looked at that, the intellectual property was generated by Syntara scientists. We have a long experience now in developing LOX inhibitors in particular. We have produced a wide range of them as we have gone through this process that we have tested preclinically. Before we put a drug into the clinic, we characterize it against a wide range of panels, which gives us feedback on the level of activity we can expect, the level of side effects we can get, the level of drug interactions that we might see with the compound.
When we looked again at 6302, the first-generation pan-LOX inhibitor that was applied topically, we could see that there were one or two places in the molecule structure that were potentially reactive that could have been the cause of that reddening and then the skin that we saw in 10% of the patients in that first study. We addressed that. We worked at that.
We produced a few different options. We put them through our panels. We have tissue studies that we can run that look at tolerability, the reactivity, I would say, against tissue types. That has given us the confidence to bring this one forward. Yes, it has gone through extensive preclinical testing to get us to the point where we feel confident that we have a drug which is materially different from 6302. 6302 was dosed three times a week to stay on top of that skin reddening issue. We believe this drug will be well tolerated, and we will be able to dose it daily, which gives us the opportunity to improve not only the tolerability, but maybe the efficacy of the drug as well.
Very good. I should just add as a reminder for anyone in the audience, the replay of the webinar from that session yesterday, which also had Professor Fiona Wood on there, is available via the ASX announcement that went out yesterday morning. Gary, that's all for today. Thanks very much for your time and giving that presentation.
Appreciate it. Thanks very much for your time.
Next up at the NWR Virtual Healthcare Conference, we'll have Paradigm Biopharmaceuticals, and that will be in about 10 minutes from now. I hope you can join us then.