Go`od afternoon, everyone. The clock has now ticked past midday, we'll get started with today's quarterly investor briefing with Syntara CEO, Gary Phillips, who also has some updates from the FDA. My name is Alfred. I am part of Syntara Investor Relations team, will assist with running the call. Just a quick run through of formalities. After the briefing, Gary will be taking questions from attendees. If you do have any questions for Gary, there is a button at the bottom of your screen which says Q&A with a little speech bubble. Just pop them in there and we'll read them out. It's obviously a very busy day on Alfred. I am part of Syntara Investor Relations Alfred. I am part of Syntara Investor Relations Alfred. I am part of Syntara Investor Relations being the last day of the month, there's plenty of information for investors to dissect, including these new FDA developments with Syntara. Gary, I won't take up any more of your time. Let me hand over to you.
Thanks, Alfred, good afternoon, everybody. Yeah, I've, I've presented at a couple of investor meetings in the last, last few weeks. Today is a good chance to pull some of the threads that have been going on together and draw some conclusions about where we are as a company right now. Because obviously we've, we've, released quite a lot of data in the last couple of months. I'm just gonna go through the, the highlights of what we've announced, and then, as Alfred says, I'm, I'm very happy to, to take questions at that point. Just let me get my screen up a minute so I can... Yeah, so I think the things in this quarterly update are that I wanted to sort of draw attention to, were first of all, that, you know, as a company, we've been leading the way in fibrosis and, and particularly lysyl oxidase chemistry and biology for a number of years now. I don't think I'm going too far when I lay claim to being global leaders in this space. In the last few months, we've got now clinical proof of concept. We've proved in the clinic, in patients, that inhibiting lysyl oxidase or LOX, does reduce fibrosis, and we've done that in two different diseases. Now, this is a really huge leap forward, for both the field of lysyl oxidase biology, fibrosis, and also for Syntara.
I think that's directly related then, to the FDA's view on, on where we're at as well. They've supported us to carry on development in myelofibrosis. After reviewing that data from this first-in-class LOX inhibitor that we have. We are the only company with a pan, you know, an inhibitor that blocks all of the lysyl oxidase family of enzymes in the clinic. Very recently, they've just cleared the protocol for us to go into the next stage of clinical development with PXS-5505, in myelofibrosis, where we'll be using in combination with the leading JAK inhibitor, ruxolitinib. Some really important steps forward, I just want to unpack that now as we, as we go forward.
This first point is the, you know, what does, what does blocking lysyl oxidase do? It's all around blocking the last stage of fibrosis. I know many of you will have heard me say this before, but it just bears repeating, that what we're doing with with blocking lysyl oxidase, is stopping the very, very last stage of fibrosis. The bit where the collagen that's released from the fibroblasts that are activated in cells in the bone marrow, the skin. They can be in organs like the liver, the lung, the kidney, the heart. That last stage of fibrosis, where those collagen fibers are cross-linked, they're cross-linked by this enzyme called lysyl oxidase, and that's what we block. The, the very final stage of fibrosis, and by blocking that, we stop the scarring, continuing.
In doing so, we reduce the amount of stiffness that's in the tissue. Then that blocks the feedback loop to the fibroblast, which normally leads to more collagen and more LOX. That was the theory, that was the biology that we, we put out, and that's been published in several preclinical journals in some prestigious, prestigious publications. We've now demonstrated it in, in patients as well. The two drugs that we're talking about here are PXS-5505, which is an oral pan-LOX inhibitor, which was patented only in 2018. PXS-6302, which is another pan-LOX inhibitor, but this time topical, to put on the skin, and that was patent filed in 2019.
We're talking about two drugs with a lot of patent life ahead of them, wholly owned by Pharmaxis. No royalties or licenses to pay for anybody else, and which, which gives us a, a great position to, to go forward to into the clinic. That data from the PXS-5505 myelofibrosis study. This, if you remember, was- we were using it in patients who had basically failed all the other treatments available for them in myelofibrosis, the JAK inhibitors. These were patients that were, had finished that stage. They were more or less, at that point, having about 12 months or less to live. They're kind of end of life patients. Some of them in a very serious condition, some of them with life-threatening thrombocytopenia or low platelet counts, coming into the study, actually.
This study was an open-label, and it studied these patients for six months. We've enrolled 21 out of the 24 patients, we just released the data from a further 10, who've completed six months or 24 weeks of treatment. From a safety perspective, the drug continues to be extremely well-tolerated, with no serious drug-related adverse events. The majority of the adverse events noted were mild, and the majority of those were not related to the drug either. We've had 10 patients drop out the study, that is to be expected with this particular group of patients, because as I mentioned before, they are still very much towards the end of their life, and the disease does progress, sometimes quite rapidly at this point for these patients.
The, the, the doctors have no other option but to take them out of the trial and start treating them with other forms, which are more suitable for that stage of the disease. In looking at the efficacy, we were, we were really, really pleased this time around. I mean, we had 9 of the 10 patients were evaluable for bone marrow fibrosis. 1 of the 10 had a didn't have enough tissue collected in the first bone marrow biopsy, so we couldn't, we couldn't assess what level of fibrosis they had, so we couldn't evaluate them. For the other, other 9, more than half of them, 5 of them, had improved bone marrow fibrosis scores. This is graded from 0, 1, 2, and 3.
These patients all had either grade 2 or grade 3 fibrosis coming into the study, and they've all dropped by at least 1 grade. That, that's a really stunning finding and unprecedented in this field. Of those 5, 3 of them also reported symptomatic improvement as well. It's a really good sign that we're having an effect both on the underlying disease and on also the, the effects of the disease as well. 4 overall had an improvement in symptom score, 7 had improved or stable hemoglobin counts, which is an indicator of red cells, and 8 had either stable or improved platelet counts. As I said before, 3 of those 8 came into the study with life-threatening thrombocytopenia or low platelet count. That's a really big step forward.
We, we haven't seen changes in the spleen, yet. Now, these patients often have increased spleen sizes because as the bone marrow stops functioning as a producer of the red cells and white cells and platelets, the spleen tends to compensate and gets bigger and tries to produce red cells on its own, which causes it to enlarge. Now, the JAK inhibitors act directly on that and cause an immediate reduction in spleen volume, but we expect our drug to have a longer effect on that. Once the bone marrow becomes functioning and starts to produce more red cells and platelets, then that reduces the pressure on the, on the spleen. It, it, it's something we would see later on down the track. You know, we've gone to the opinion leaders, Dr.
Masarova is Assistant Professor at the MD Anderson Cancer Center, the largest cancer center in the world, in, in Texas. She's an investigator on the study, we've shown her all the data. You know, she's got available to see all the granularity of each individual patient and what they came into the study and out of the study on. She, again, noted the safety profile. I think from her perspective, you know, the next stage is obviously to combine this drug with a JAK inhibitor. You've got something that controls symptoms, as well as something, something that's giving a disease-modifying effect on top of it. She knows that these patients on JAK inhibitors suffer with the tolerability of those drugs.
Often they get cytopenias themselves, and many of them drop off because they can't tolerate the drugs. Any add-on drug into this area must be well tolerated, and our drug stands out amongst all the drugs in clinical development at the moment as being something that has got a really, really clean safety profile. Having said that, she was also impressed with the... Or encouraged to see the number of patients who had improvements in symptoms and stable or improved blood, improved blood counts. Again, I, I think, you know, what we're hearing back from the physicians in the study is that they're, they're very comfortable with the profile of the drug as it stands.
It's certainly worthy to go forward in, and the lack of overlapping hematological toxicity or the cytopenias, the reduction in, in, in blood cells and platelets, it, it makes PXS-5505 an ideal add-on candidate. With that, as, as a background, you know, we've gone to the FDA, and I'm, I'm really pleased to, to update you on the progress we've made there. I think we've previously announced that we've had a Type C meeting, and that the FDA had encouraged us to submit a protocol for a combination study of our drug plus ruxolitinib. That protocol has now been accepted by the FDA and cleared for us to go forward into the study. This is an open-label study.
It uses the existing trial sites that we have open, so we have 20 trial sites already open for the monotherapy study, which is coming to a close. That allows us to do a really fast start-up. The thing that really slows trials down at the beginning is often signing up those sites and getting the contracts in place. That can take a year to even 18 months at times, particularly with sites in the US with orphan studies at the moment. To be able to use existing sites is a huge bonus. We can go straight into the study, gives us minimal in the site initiation costs. The FDA also accepted that we didn't have to do a dose escalation.
For those of you following us, you'll notice that at the beginning of the monotherapy study, we started with three different doses, and we gradually escalated that dose until we were happy with the safety and efficacy we were seeing. The FDA, having reviewed it, said, "You don't need to do that again." Which often they would do when you're starting a study in a new clinical setting. In combination, they would ask you to do an escalation again. We've been allowed to go straight in again. We've selected the highest dose, the one that was used in the monotherapy study, for studying those patients for six months because we've seen no safety issues with it. At the same time, we've seen more than 90% inhibition of the target enzyme that we're going after.
With that, we, we know that that drug is an effective antifibrotic and is safe, so we can go straight into the study with, with no escalation steps. That gives us the fastest route to meaningful data. We'll be recruiting 15 patients who have already received ruxolitinib, and we'll be studying this, them this time for longer. Having seen the data coming out of the 6-month study and noting the trends, we believe it's worth tracking these patients for longer to see what happens. We still believe we'll see that clear antifibrotic effect, obviously, before the end of the 12 months, and we'll have data available at 3 months and 6 months and 12 months as we go through the study. Which we're we're expecting to recruit later this year.
Really, really pleased to let you all know that we're, that we're moving fast on this, and we'll be quickly into the clinic now with that combination study. The combination study is the one that unlocks the commercial value in the product, given that 90% of myelofibrosis patients are receiving a JAK inhibitor, and most of them are on ruxolitinib, which is the market leader in this field. You know, with that, we will have clear data which transposes to the, to the most of the clinical population that's out there, which, as I said, unlocks both clinical value for the drug and also commercial value as well. The other thing we announced this, this last quarter was our results in the skin scarring drug.
You know, I've talked about the effect of blocking lysyl oxidase in patients who have myelofibrosis. You know, there are patients out there with scars where fibrosis forms, not in the bone marrow, as we talked about before, but this is fibrosis in the skin. The skin is an organ in itself, and when we put our cream on the skin, we've already demonstrated that we produce, again, a very, very significant block in lysyl oxidase, the enzymes. This study was designed, it was a placebo-controlled study run by Professor Fiona Wood in Perth at UWA. She looked at patients, all of them with an established scar. Had to be more than 1 year of age and more than 10 square centimeters in size.
50% of them on active, 50% on placebo. Patients were dosed, dosed 3 times a week. They put the cream on their skin. Again, we saw a good safety and tolerability profile here. We had no serious adverse events that were reported. We did have a couple of patients who developed a rash, having put the cream on their skin, but that was reversible. As soon as they stopped, then the rash goes away. Then 3 things. The first was, as I said before, you know, we showed inhibition of lysyl oxidase in the skin. We took skin biopsies at the beginning of the study and after 3 months when they finished. We compared the baseline to what we got at the end, and the active versus placebo.
We saw a 66% reduction in the enzyme activity in the skin, in the active arm, compared to baseline, relative to the placebo group, with a really highly statistically significant result. This, this was taken 2 days after the final dose was given. You know, for the majority of the study, when they're taking the cream, we're expecting, you know, 66% or more inhibition. This was very much a, a trough measurement, we think that's enough to have an effect on scarring. The next result confirmed that, in, in that, we measured the amount of collagen in the, in the scar tissue in these patients. We saw a 30% reduction in collagen in the scars of the patients on active versus those on placebo.
That's a fundamental change in the structure of the scar. Now, we didn't show a change in the appearance of the scars. So obviously, we, we-- this was something that we discussed with Professor Wood, at some length as to the link between the structure of the scar and the appearance of the scar. And she pointed out that, you know, that, you know, this is clearly, the study has greatly enhanced our understanding of the process of scarring and the role of the LOX enzymes. She called the amount of change in the scar composition unprecedented. She, she, she pointed us towards the fact that, you know, patients that have hypertrophic scarring after burn surgery, which she, you know, she obviously focuses on, relative to patients with normal skin.
She felt that what we'd done was reduce more than 50% of the excess collagen that forms between those, that, the patient with the scar and the patient with normal skin. you know, in her mind, that, she labeled it as unprecedented. She hasn't seen that with any other form of treatment. and that gives her confidence that if we studied these patients with established scars for longer, then we would see a change in scar appearance. she pointed just to the fact that, you know, they, they currently use laser therapy a lot for changing scar appearance. and this change in the scar actually doesn't happen immediately after the laser either. It takes a while for the scar to remodel.
If we have reduced, which we've demonstrated, the collagen content of the scar by, you know, about a third, then that will lead to remodeling the scar over a longer time. We also pointed here towards the fact that the patients in the study had an average age of scar of about 12 or 13 years. That is really a very old, scar. We, we may have, we may have, more luck in looking at appearance over a short period of time, because these patients were only treated for three months, if we looked at different kinds of scars. In the future, we are in discussion with Professor Wood and her team, looking to extend that collaboration that we've had with them that's already gone for a number of years.
The, the result we've got opens up a very wide, you know, universe of different scars that we could now approach on the skin. Those include younger scars, where the scar turnover by the body is a lot quicker, and therefore, we might see a faster response to that change in structure. We might look at scar prevention post-surgery, and we are looking specifically here at a patient group that's had burns, and then gone in for surgery to correct that, and then using a LOX inhibitor after the surgery in order to prevent these bad scars forming. There's nothing for these patients at the moment, so that's something we're looking at specifically. We're also looking at different kinds of scars.
Keloid is a scar that forms in Asian and African skin types, populations. It's a disfiguring scar in some patients, and it leads to a lot of loss of function and obviously appearance problems. We're looking very closely to see what the structure of those scars are and whether the kind of results we've seen in the established scar that we've had can be transferred into that area, and whether we deal with keloids as a treatment of the keloid itself, or we deal with perhaps preventing keloids in patients who are prone to them whenever they have surgery or injury.
Now, Dupuytren's is a, is a disease where there's a fibrotic nodule on the tendon in the hand, which causes your, your fingers to flex upwards, and you can't, you can't extend them. It's very, very common. Almost no treatments at the moment other than surgery, to try and release the tension in the tendon. We-we're talking to the world's leading experts in this area to see whether the change in fibrosis that we can form may give us an angle to, to go into that one as well. Surgical adhesions, they're very often, in, say, abdominal surgery, the tissues bind together afterwards internally, because of fibrosis. That's something maybe we can, we can, we can also treat.
There's many different angles we can go forward in here, and as I said, we are in discussion with Professor Wood and other opinion leaders worldwide, and we will give an update on our plans for that skin scarring development line later in the year. Just to wrap up, you know, we have ongoing studies. Obviously, in the myelofibrosis, that's the key one. Combination due to start soon. Huge commercial opportunity. That market's worth $1 billion. The companies that have exited with phase IIb data in this area in the last one year, two years, have gone for over $1 billion each. There's a real, real prize to be had here to showing combination data with our drug in myelofibrosis.
We're also obviously looking forward to, to recommencing further studies with Professor Wood and her team and other dermatologists and surgeons globally in the skin scarring area. We have a drug in looking at Parkinson's disease, which is about to recruit its first patient. Newsflow later in the year that you can expect is that the, the announcement of starting the patient's recruitment on that, that combination study with a JAK inhibitor in myelofibrosis. Starting a, a study in scar treatment, post-surgery and burns, again, for a pan-LOX inhibitor. Then the study starting in, in, in, in Parkinson's disease as well. Some, some real things to look forward to.
We'll be publishing more of this data that we've announced on myelofibrosis at ASH, the American Society of Hematology, later in the year, in December, which will be a, a high point for us, and discussion with also potential partners at that point as well. Looking forward to the rest of the year now on the basis of a really strong first six months, and with that, just wrap up with a, a look at our register, which is still dominated by institutions which are, are specialist healthcare investors, BVF, Carspeed Platinum, all specialist healthcare investors. All see the opportunity to, to, with Syntara now, to really leap forward in valuation. And just to say that we finished the half with a, a pro forma cash of $14 million.
With that, Alfred, I'll, I'll hand it back to you, and I'm, I'm happy to take any questions at this point.
Excellent. Thank you very much, Gary, for that informative presentation, and congratulations on the exciting FDA developments. We've had a few questions come through, which we'll be answering in a moment. If anyone does have any others for Gary, please type them into your Q&A box, at the bottom of your screen. Gary, the first question comes from Alan: Has there been any new industry interest in PXS-5505 since reporting the final interim data earlier in the month? Is the data enough to attract potential funding partners?
Yes and yes. I, I was at BIO, which took place in Boston this year. It's the world's largest sort of pharma biotech acquiring thing. You know, I, I had a, a long list of companies that wanted to talk to us about our data. It's a little bit early, that we, we couldn't really talk too much about the data that we, we've just released. Obviously, we could talk freely about the data that we had at the end of last year, that we, we published at ASH. There's certainly strong interest in our data as it stands at the moment as a monotherapy.
As I mentioned earlier in my commentary, the data with combination with a JAK inhibitor releases a whole new level of commercial opportunity. I think whilst there is interest at this stage, the value of the asset in de-risking it and showing the effect it has in combination with a JAK inhibitor is, is almost exponential. There's certainly a strong driver for the company to explore those discussions with potential partners. Then also to, to keep on sharing more data as it comes through.
The advantage of the study we're about to start is, again, it's open-label, so even by the middle of next year, we will have some data which starts to give us an indicator of what happens when you add five five oh five to a JAK inhibitor in a myelofibrosis patient. That's, that's a really exciting time point to be around, I think, as we go. I mean, but it's, the data from when we start that first patient to when we get, you know, through the first three to six months of that study will be, will be fascinating to look at and, and really valuable for the company.
A question from Dennis: With the JAK combo study, will patients be dosed with 5505 for 12 months or 6 months?
They'll be dosed for 12 months. We'll obviously get data at 6 months. We'll, we'll get data right the way through, but the, you know, the, the sort of defined time points when we'll be taking, for example, looking at fibrosis scores, will be after 3 months and 6 months, and then 12 months. We expect to see results which are indicative of what the drug does in combination at 6 months, but we feel the opportunity to see what happens if you leave them on longer. See the, the, the further effect of the improvement in the bone marrow fibrotic environment, was something that we, it would be very good to learn, and also potentially valuable for both patients, regulators, and potential partners.
Thanks, David, Gary. Question from Kai in regards to 6302. What are the next steps? Are you in any near-term discussions with potential partners for it?
Yeah, that's an interesting point. I think, you know, the data that we have, I think as Fiona would say, you know, unprecedented. The level of change in structure of the scar. Nothing else been able to demonstrate that. That clearly attracts people who would like to talk to us and see what we're planning to do, and whether there's an opportunity for them at this point. There's a lot of companies out there who specialize in dermatology. There are no drugs in the clinic in development for scarring. Scarring itself is a market which is worth $19 billion a year worldwide, and even if you look at the subsegment of hypertrophic and keloid scarring, that's, that's worth $3.5 billion.
Current therapies are basically, I guess, would fall into the category of devices in the sort of laser or cryotherapy to try and improve the scarring. There is some pharmacology in terms of injections, of steroids and things like that into the scarring, but they tend to have short-lived effects and have quite a lot of side effects as well, and don't produce really much in the way of a change in the structure of the scar. Or you're looking at physical things like silicone sheeting and pressure bandages to try and improve. I think we've got something which is absolutely unique. I think we've got something which is potentially extremely valuable. I think the study we've done gives us clinical proof of concept and real confidence to go into the next stage.
I think the value of the asset will be a lot higher when we show also a change in the appearance of these scars going forward as well, on top of the change in structure. We are certainly engaged in discussions with potential partners about this, but at the same time, very much planning to plow our own path to the next studies, which we aim to you know, to start some of them in the next 6 months. I said, we're in discussion with Professor Wood and her team at the moment. We've got a study which we're expecting to start recruiting, which will be in patients that have burns, who are post-surgical.
To look at the, the effect of our drug in a, in a, a scar prevention phase, as well as a scar im- sort of improvement, a amelioration of an existing scar phase. A couple of other opportunities as well. I think it's a really exciting time for us to be there, and we've got data which is attracting people. I'm not sure I'm ready to, to partner it just yet. I think there's a, there's a, there's a really valuable opportunity here for the company if we get the next study right.
Thanks, Gary. Jawahar, that answers your question also about the timeline for the trials. Another question from Jawahar is, "Can you talk to the more clearly defined batches of patients that you might be enrolling in the next set of extensive human trials?
Yes. Well, the one which is absolutely clear now is to look at scar prevention post-surgery. In doing that, we've, you know, because of our collaboration with Professor Wood, who obviously has a very large burns clinic in Perth, in Western Australia. She looks at a very large number of patients from all over Western Australia every year. We're looking at that particular group and the burns where they might have, say, you know, more extensive burns, may more than 5% of their body area, to see whether by using LOX inhibition, we can prevent the scar, a bad scar forming. All, nearly all these patients end up with scarring after surgery.
In a lot of them, it's disfiguring and disabling as well, and requires a lot of treatment afterwards with laser therapy, surgical correction very frequently. There's, there's nothing for these patients, and it's a real goldmine. That's really high on our list of things to do. I haven't also, you know, we, we, we certainly haven't given up on the other aspect, which is improvement of existing scars. I think, you know, keloids is something we see a really big commercial opportunity in, and where there's a really unmet medical need. Really, again, nothing for these patients. And, if we can find a way of studying that, you know... We, we're looking at our data, and we're sharing that data with opinion leaders who focus on keloid scarring globally.
Trying to understand which of the particular, particular groups of keloid patients we think could be recruited into a study, and which ones, and what the design of that study has to be in order to, to really get us a, a result which not only satisfies the clinicians and the patients, but one that would also stand up in front of a regulator like the FDA when they look at it. That's, I think, one of the unknowns in the scarring clinical development, is there really aren't any defined endpoints which the regulators currently accept for scarring. We need to work with them, and with the clinicians, and with the patients to understand getting the right design.
Which is why we're just taking a chance just to pause here and, and make sure we, we can, we can go through those discussions before we, we kick off for the next study. Because the next study is potentially the one which is, which is, you know, really unlocks the, the value in the drug and the company.
Thanks, Gary. We are starting to run tight on time, so I might just ask two more questions her
One more from Kai: "Can you please talk to why the share price is where it's at, and whether you think this fairly values Pharmaxis?
Yeah, I mean, our, our enterprise value, the sort of difference between cash and, and the value of the company is, is only about AUD 20 million. I think that's extremely low for a company with our stage of drug in, with phase II, phase II clinical trial data there. It, it may be a, a, you know, an artifact of the, the history of the company. You know, we've been listed for, more than 20 years, and I think there's a, maybe an element there we need to, to demonstrate more. I think the, the reaction to the last set of data was, was positive. We're looking forward now to, to demonstrating, you know, I think we're, we're, we're showing what we can do. We're on time with what we're doing.
The next myelofibrosis study, the combination arm, is one, you know, Well, probably, you know, we've talked about the, it starting quickly, using existing sites. We've got 20 sites open. We need to recruit 15 patients. They now come from the broadly, the broad group of myelofibrosis patients that are already treated on JAK inhibitors. We expect fast recruitment, fast results from that, with a study that's gonna cost less than half of what the monotherapy study did. You know, I think, yeah, I'm not happy with where the valuation sits at the moment. I have, you know, I accept it, it's the market.
I think the way we'll correct that is with further data. I think the data we've got coming is going to be, you're not gonna be able to ignore it.
Thanks, Gary. Just one last question, another one from Alan. Where is it? There it is. The ASH conference coming up, who is the target audience there, and what sort of data or information might you be able to present there that hasn't already been released by the ASX?
It will be, probably, a more detailed... The, the, the audience at ASH is, is hematologists primarily. You know, globally, I mean, it's the world's largest hematology conference. People come from all over the world. I think last year there were in the order of 20,000 people there. It's obviously taken advantage of by every pharmaceutical company as well, that's, that's interested in the field. They come to present their own data. They also come to look at other people's data. There's plenary sessions and discussions which go on, which really, you know, people are allowed to dig in and, and talk about the data that's there. The data that we'll present will be a more detailed analysis of the data that we've already put up to the ASX.
The ASX has the, you know, the headline data of the results of these trials and the patients. The ASH poster that goes up in December tends to give more information on the individual patients, the demographics, so that the hematologist can understand the context of the results that they're seeing, and draw more comparisons with, with the development of other things which they're seeing in the clinic. We'll obviously wrap up with any further fresh data we have at that point from the monotherapy study, but it's unlikely that we'll be showing combination data at ASH in December.
Excellent. Thank you very much, Gary. I will wrap up the questions there, as we are out of time. If anyone does have any further questions, please feel free to email them through. Gary and David's contact details are at the end of the slide presentations and the bottom of the ASX announcements. A recording of this webcast will also be made available on the Syntara website. Gary, on behalf of the investors in attendance, thank you very much for your time today.
Thank you.