Good morning, and thank you for coming to the twenty twenty Virtual UBS Global Healthcare Conference. My name is Brandon, and I'm happy to be your host for this session. Our next presenter will be George Lynn, Executive Vice President and Chief Financial Officer of Hua Medicine. A Q and A session will follow immediately after the presentation. To submit a question anonymously to be answered at the end of the session, please type your question in the Q and A prompt on the presentation screen.
We now turn it over to George. Thank you.
Great. Thanks, Brendan, and, thanks everyone for the interest in biomedicine. I will give a short company presentation, which you should have access to. I will go through the I won't go through the disclaimer. The disclaimer you can see is right there, and I'll start on page four.
Hua Medicine is a publicly listed company in the Hong Kong Stock Exchange under the ticker 2552. It is a China based company focused on diabetes. It was founded about ten years ago by two principal gentlemen. As you can see on page four, Doctor. Li Chen, was at that time the Chief Scientific Officer of Roche in China, and Bob Nelson, who's our Chairman and largest shareholder who founded and funded the company along with three other substantial shareholders in that a round about ten years ago, which was Venrock out of Palo Alto with Brian Roberts leading that effort.
The two Fidelity arms, one based in Boston, f prime, and one based in Hong Kong now called Kate Rhodes. And then the last being WuXi Pharmatec with the chairman of that company, doctor Li Ge, personally investing along with his mentor, from Merck, Jack Baldwin. Sale, Chinese VC fund was also, part of that as well. And what we have currently is global rights to, dorzagliotin, is a fourth generation GKA for type two diabetes. We do own global rights to that.
We do owe Roche high single digit royalties, but that is pretty much it. This compound has met its primary efficacy endpoint for approval in our phase three trial, which was the top line results were released last November. This is a first in class and actually an only in class drug to significantly and sustainably reduce HbA1c. It is a first novel concept drug for type two diabetes. I will keep on talking about this throughout the presentation.
But instead of just simply lowering blood sugar, it actually addresses the underlying cause of type two diabetes, which is addressing and trying to restore impaired glucose homeostasis in type two diabetes patients. We have announced results that indicate that the drug is viable in combination with the top selling oral anti diabetic drugs, metformin, DPP-four, and SGLT2. We've also demonstrated that this drug works very well across the entire spectrum of chronic kidney disease patients that also have type two diabetes, a very large market. And as everybody knows, the market opportunity for addressing the underlying cause of type two diabetes is massive with over four fifty million patients globally, one hundred and twenty million plus alone in China. We have a very strong balance sheet with 1,100,000,000.0 of cash renminbi as of the end of twenty nineteen.
Flipping to page five, let's very quickly talk about our mission and what it is that we're going to try to achieve and our strategy for doing so. Our mission is to position dorzagliotin, our compound, as the cornerstone therapy for the treatment of diabetes by restoring glucose homeostasis in type two diabetes patients. We aim to become a global diabetes care company, and we're going to launch dorzaglietin commercially first in China and then globally thereafter. The compound will be used as monotherapy or in combination with other approved anti diabetes drugs, both oral and injectables. We plan to use the approach that was advanced by Roche, which is personalized treatment for diabetes, and augment that and power it with new technology and AI so that we can treat the entire population of type two diabetes in a personalized and tailored way.
We're leveraging our internal team who have a lot of experience at Big Pharma like Doctor. Chen, some of whom actually came over from Roche with him. And we will continue to use our partnership network and outsourcers to continue advancing our current pipeline. In terms of sales, especially for primary care in such a large market, we do plan to partner with both China based as well as international pharmaceutical companies to make the drug available to patients as quickly as possible in China and also outside of China. Flipping to page seven, a quick overview of the current state of the type two diabetes landscape.
Massive market, as you can see, with over $80,000,000,000 of pharmaceutical sales globally. So you might ask, well, why do we need another drug? Well, the key is there is no drug that addresses the unmet medical need of type two diabetes. Nothing actually treats the underlying cause of type two diabetes, which is actually the loss of glucose sensitivity and impairment of glucose homeostasis. It's been very well established with over fifty years of literature that restoring the function of impaired glucokinase, the enzyme that senses glucose level change in the beta cells of the pancreas, is the only scientifically validated means to restore glucose sensitivity in homeostasis.
And our compound is the only in class TKA that has actually been able to advance and actually meet positively, successfully the phase three pivotal primary efficacy endpoint which was announced last November. This has been tried by many, many pharmaceutical companies both currently in the diabetes space as well as those that are not. And as I had mentioned previously, this is the fourth try from Roche which we licensed from Roche when Doctor. Chen founded the company about ten years ago. It was in preclinical at that time.
A common question people ask is why did Roche give it up? If you recall about ten, eleven years ago, Roche consolidated its ownership position in Genentech and decided with the pro form a pipeline they have in specialist care, autoimmune and oncology that they were basically going to stop advancing any early stage primary care in cardiovascular and diabetes and torsagliotin was one of those in that portfolio that we were able to get licensed. On page eight, let's get into the mechanics and the science of how do we stop type two diabetes. The goal in treating type two diabetes is actually to maintain blood glucose level within a healthy range, achieving glucose homeostasis. Ninety five percent of the population in the world, ninety five percent, actually do not have type two diabetes because their body can autonomously achieve glucose homeostasis without any other help.
The key problem with type two diabetic patients is they have actually lost that glucose sensitivity function. All the current drugs actually just lower the blood glucose level. Lowering the blood glucose level alone, there are plenty of drugs that do that, but that will not stop the progressive degenerative nature of diabetes, which then leads to additional complications. It weakens all your organs, compromises your various systems. We're seeing it now with COVID-nineteen where diabetes is actually the number two comorbidity.
Once you get infected with the virus, your chances of actually suffering severe complications with COVID-nineteen is much greater if you have diabetes, and this all ties into part of that. On page nine, let's talk specifically and review the progressive degenerative nature of type two diabetes. The chart on the left is super important. This is a chart that measures A1C levels. If you recall, four to six is the healthy range of glucose homeostasis.
Above seven, you're diabetic, so you have high blood sugar. Below three, you're hypoglycemic, which is a very nasty side effect. On the horizontal axis is time over years. Now this is a very well established study, which say basically patients on monotherapy, it doesn't matter what drug, your A1C level is going to go up. And that is the principal reason for that is if you're type two diabetic, instead of 100% beta cell function where your insulin is produced, where your glucokinase resides, the sensor for glucose level changes.
Instead of 100% beta cell function, you actually have 30% as a type two diabetic. 30% of those beta cells will have to do the work of 100% at each meal. And as a result of that, on the right here you can see that those remaining functional beta cells are going to have to work much harder. As a result, they're going to suffer stress, and they're going to accelerate in their death and degeneration so that by the next year, nothing has happened to the drug. You might be taking whatever drug monotherapy, but actually the body has weakened maybe to 25% beta cell function, and you might have to double the dose.
And by the third year, you might have to switch to a more powerful drug. And by the fifth or sixth year, you may just have to forgo all drugs except for insulin and start injecting yourself with insulin. This is the progressive degenerative, current status of type two diabetes, which no current drug can stop or halt, and why insulin market continues to grow despite the fact that there's new classes of drugs. So the key thing with our drug is we're gonna try to make a dent or reverse this slide. Now page 10, a lot of different compounds and classes of drugs have claimed that they could actually improve beta cell function.
You can pull up this document by yourself. In 2019 it was published that the most likely logical scientifically valid potential drugs that could improve beta cell function alone or in combination, you can see here on the right, they actually cannot do it when patients are given those drugs, those drug regimens for one year, and then the drug is halted for three months. There's no improvement in their beta cell. So from that perspective, no current drug right now is able to demonstratively actually indicate that they can improve beta cell function. Page 11 goes into glucose homeostasis.
Glucose is super important as a molecule that powers our cells, provides energy, but very important in our endocrine system. It is a hormone that actually provides a signal to the body that when it's high levels, then it's going to get our endocrine system to behave and react in a certain way. And when it's low, our endocrine system will synchronize and work in another way. So in this sense, you actually need a very important enzyme called glucokinase, which serves as a sensor for glucose level change so that when glucose levels are high, your beta cells are activated by the gluco kinase enzyme, and insulin is released. In the reverse fashion, when glucose levels are low, the alpha cells are activated by the gluco kinase that resides there, and glucagon is released, which then signals the liver to release glycogen to be broken down into glucose when you're sleeping, for example.
That is how glucose homeostasis actually works in healthy people. In type two diabetics, though your glucokinase is impaired, and so the insulin is not released at the proper time. Page 12 shows very simply that if we can fix the sensor, then we have a chance of controlling the diabetes. So glucokinase as the central processing unit, if you will, for your endocrine system as being the sensor controls a whole host of different organs that are instrumental in being synchronized to actually maintain your blood sugar level in a homeostatic state. A lot of these other drugs, like a very good and beneficial new drug, an oral drug, SGLT2 on the right here, that focuses on stopping the absorption of glucose in your kidneys and so you urinate out.
There is no way such a drug will actually address the underlying cause of type two diabetes or boost the performance of beta cells as it only really works on the kidney. However, it does have some very beneficial effects such as reducing the chances of heart failure as we're seeing now with recently reduced data. And also works very well in slowing the progress of more advanced late stage kidney disease. So our drug in combination with SGLT2 could actually be a very good potent drug for that group of type two diabetes. Same thing with a lot of these other drugs.
None of these drugs, as we mentioned, actually focus on the beta cell, and as a result, there's no chance that they can actually cure or stop the progressive degenerative nature of type two diabetes, but they also have different benefits like GLP-one or DPP-four, and in combination with our drug it could be a very viable and potent treatment regimen. Page 13 is the final page on glucose homeostasis. The key on glucose homeostasis, just so people can understand it clearly, is it behaves very simple, very similarly to how the room temperature in your room is actually controlled by two things. One is a thermostat, which is like the glucokinase for monitoring glucose level change. And the other is the air conditioner, which is basically insulin, your beta cells, etcetera.
All current drugs that are approved effectively are operators. They're behaving like air conditioner. They just lower the temperature down when temperature is high. The only thing that actually senses temperature change or glucose change in our analogy is actually the glucokinase which functions as the thermostat. And on page 14, this analogy was discovered and published by Doctor.
Frans Mucinski, our senior consultant, who just earlier this year was awarded by the Nobel Committee at the Karolinska Institute in Stockholm, Sweden, the most prestigious award, the Rolf Lofth Award, for basically publishing on and discovering glucokinase. And it was after fifty years that finally there's a compound, r dorzogliotin, that actually validates that you can restore this glucose sensing function. He did publish in 02/2003, that's when all the other big pharmas started their own GKA program. But because fixing a sensor is much more difficult than just turning on insulin release, it's taken a real long time for him to really But I think all the big pharmas and Roche and ourselves believe that this is going to be the next generation therapy for type two diabetes. Going to the next few slides, page 16.
We show through our various trials that we've done, both clinical and preclinical, of our drug being able to improve beta cell function and repair the glucokinase glucose sensor. If you look on the top left of page 16, this is in our animal studies. You can see a diabetic rat has very low number of insulin producing cells. And as a result of that, you can see versus the control in a healthy rat, the beta cells effectively is much lower than the diabetes rat. The two bars to the right of it is the rats, the diabetic rats being fed for twenty eight days, low dose and high dose of our drug.
And after twenty eight days, we sacrifice them and look at their pancreas. And you can see the increase in the number of insulin producing cells in these two bars. On the top right and the bottom left, these show that we're able to improve the early stage insulin release, which is a clear defect in type two diabetes. If you think about it, if your sensor is broken, then you're not going to release insulin when you need it. In fact, it's going to be delayed.
And so if you look at the top right, you can see the green is before the patient takes the drug. And that green shows that insulin is releasing really about an hour later is when it peaks. After the patient has taken our drug for seven days, you can see there's a push to the left of the insulin release, allowing insulin to be released earlier, which is a very huge part of restoring glucose homeostasis, is to make sure that your spike in glucose when you actually feed, it matches the spike in insulin release as well. That's shown on the bottom left as well over thirty two days, an increase in early insulinogenic index. On the bottom right, this is in our phase two data in China, we published this result in LAMSET in May of twenty eighteen.
It was a twelve week trial where patients were on the drug, on our drug, for twelve weeks twice a day. Then the drug was stopped and a week later we measured them for beta cell function improvement a week after it was drawn to see if there's any lasting effect in improvement of beta cells and as measured by the disposition index. And as you can see here, there was a lasting effect of improvement in beta cell even though these type two diabetes patients were not taking the drug for seven days and not taking any other drug as well. So that's the data on page 16. Page 17 is our phase three top line results that was announced in November.
The primary efficacy endpoint was to achieve 0.4 over the placebo group, which we were able to do. We were able to do it in a very statistically significant way with p value less than 0.0001, as you can see here. Forty five percent of the patients during this twenty four weeks achieve a target HbA1c level of below seven. Very importantly, if you look at the bottom here, less than one percent incidence of hypoglycemia. As you all know, antidiabetic drugs drop blood sugar level, but you don't want it to drop below three when then you suffer hypoglycemia.
Given that our drug is fixing the sensor, if it's doing that properly and restoring the sensor to the healthy state, when it senses that glucose level is too low, it should lose efficacy. This is one of the reasons why we have such a low incidence rate of hypoglycemia. It had a very good and clean good safety profile after twenty four weeks. And very importantly, it was very tolerable. So no GI issues like you're seeing with GLP-one.
No nausea, no vomiting, etcetera. Our remaining phase three trial for this phase three trial in China 301 is actually a 28 open label safety trial. And that last patient out was achieved on 03/02/2020 without incident despite the coronavirus outbreak in China. On page 18, this gives you a sense of our trial design so you can see what additional data will be coming. At the top here you can see, as I mentioned, our fifty two week was completed 03/02/2020, four sixty three patients.
We look forward to announcing that data early third quarter, so in a couple of months or so as we're going through database lock, data cleaning, etcetera. We have another phase three trial which is even larger, seven sixty six patients in China. This twenty four week was also completed in the midst of the outbreak without incident. That last patient out for twenty four week was 02/16/2020, and they should finish their fifty two week at the August. So the twenty four week double blinded placebo control, that data is likely also to be coming out in the next two to three months.
And the fifty two week for this last phase three data will come out towards the end of this year. So two big data events that are about to come out. Page 19, you can see here that we demonstrated that our drug actually works in late stage chronic kidney disease patients, so stages three to five of chronic kidney disease, which at the bottom here you can see that comprises about twenty one point nine percent of type two diabetes patients. Now if our drug does have the ability to slow down or halt or reverse the progressive degeneration of type two diabetes, you're gonna logically want to prescribe this drug early, if not first stage, if not first line. And the reason for why this trial is so important is, as you probably know, is that metformin and sitagliptin and some other TPP-4s actually require dose adjustment for this category of chronic kidney disease patients.
So they cannot be used unless there's dose adjustment, which really defeats the purpose. In SGLT2 inhibitors, the fastest growing oral drugs right now, those are actually contraindicated. So you can see with our positioning and our drug being safe in this category that that first line and early prescription of dorzagliotin is going to be really powerful for this group of patients who can't take these oral antidiabetic drugs. Page 20 shows the results for our drug drug interaction trial with sitagliptin, the largest oral antidiabetic drug in the world. It's the number two drug for Merck after their PD L1.
You can see that there's no drug drug interaction, so combination is fine. The synergies, the two together, those two drugs together, can boost the drug, the glucose lowering effect much more than either one of them alone. So this will be able to sit on this massive population of DPP-four Januvia users, and our drug can be used as combination for them. This trial was done in The US. On page 21, a very similar trial for SGLT2.
We did the same thing. We announced these results last month with drug interaction with empagliflozin. This is the top selling SGLT2 class sold by Eli Lilly and Barrigold Englein. And you can see the synergies here is even more compelling here in combination. So proving ourself that the viability for combination is very, very strong.
Page 22, this really summarizes the profile of dorzagliotin in a very, very large type two diabetes pharmaceutical. But it also reminds people why all the big pharma tried this approach. They just couldn't get it done because it was so difficult. But the main reason is right, its ability to restore glucose homeostasis to optimize the time that you're in that healthy range, the potential to protect beta cells and to restore beta cell function and improve beta cell function. These two top attributes are the only, GKA is the only chemical compound that actually can address these.
Whereas all the other drugs, all these commercials you see on TV in The United States, all focus on HbA1c reduction, which is the symptom. And then limited side effects like hypoglycemia. Some even push weight loss, given that insulin induces weight gain. And then there's a whole bunch of side effect issues such as GI, which we don't have. So you can see the priority attributes.
This is why our compound could be so compelling. The secondary attributes, we've got a ton of very positive things such as the use in patients with chronic kidney disease, as I mentioned earlier, long term sustained efficacy by focusing on the beta cell. And then a lot of different opportunities, such as the potential, even for prediabetes patients and impaired glucose tolerance patients. And also we do own fixed dose combination patents out to 2030 line. So a very long patent for this drug.
Page 24 is our personalized medicine approach. As I mentioned, Doctor. Chen coming from Roche really likes personalized medicine. He doesn't feel why personalized medicine should not be used in type two diabetes. It's used in all these other disease categories, in type two diabetes people follow a very regimented, despite the fact that the American diabetic may be very different from the Chinese diabetic, by phenotype and should be treated differently.
We're going to use personalized medicine approach. We have actually validated this in one trial that was done for the type two diabetic A type for the monotherapy. And we were able to show that the response rate can be doubled in this group of patients. And that was published in Diabetes, Obesity, and Metabolism in '28 as well. On page 25, this is our portfolio.
Dorsagliotin is the main cornerstone. We will be producing an extended version that in the future could allow for once daily. An injectable version that could be used in combo with other injectable antidiabetic drugs. And as you can see, a lot of combination for all the different types of type two diabetics. We've already proven that the top three, metformin, SGLT2, and DPP four are already viable in trials we've done in The United States.
The score on the bottom we will be doing in the next twelve to twenty four months. Page 26 is our pipeline. What's indicated in blue is what is active. What is in gray is what we have planned. You can look at this at your leisure, but clearly a lot of full robust pipeline for development with very low risk and huge markets in each one of them in expanding that label.
And page 27 is our results coming in the next twelve months. A lot of data that's coming, but the most important are two, three, and four, which all involve the phase three. We expect to announce two and three, and I've guided investors that we will announce these in the third quarter of twenty twenty. And hopefully with these done, we would then select our partner for commercialization in China. The last part is just the company and our advisors.
Page twenty nine is our team. This team is mostly big pharma oriented with the exception of me. I came from the investment banking field. I was an investment banker for eighteen years starting at DLJ in Los Angeles, then Credit Suisse in Los Angeles moving to San Francisco focused on biotech, and then ran the investment banking for Asia for consumer retail and healthcare for both Credit Suisse and Bank of America Merrill Lynch and then joined Hua Medicine in the end of twenty seventeen. Doctor.
Fuxing Tang on the right here just joined us. He was formerly at the FDA, the US FDA, and also with Allergan and Forest. Then another important recent hire was Wenjie Shu. She joined us right before IPO a year and a half ago. She was responsible for the most successful anti diabetes launch with Farxiga when she was at AstraZeneca where she led the business unit for diabetes there before joining us.
And page 30, this is super important, is on the right here is our Chinese KOLs. Doctor. Yang Wenying was the former president of the Chinese Diabetes Society. She's the one that put Akerbose as the number one drug for Bayer in China, and she is leading our combination with metformin phase three trial. Doctor Zhu Da Long, right under her, is the current president of the Chinese Diabetes Society.
He's leading our other phase three trial, which announced results last year in November. And Doctor. Li Xiaoying is also participant in our trials. He's the vice president of the Chinese Diabetes Society. On the left, Franz Muczynski, I already talked about him.
Ralph Dufranso is the number one KOL in The US. He launched metformin and invented SGLT2. He'll be working with us as we expand our trials in The US. 31 are photos and pictures of our president of the Chinese Diabetes Society presenting his data, his top line phase three data. And page 32 is our board members.
The top is the interested directors and the bottom is our independent directors with a very blue chip, board that will leave you to look, on your own. And then page 33 is the list of our CROs. We have over 160 employees by tackling a big problem with big trials over 1,300 patients, etcetera. So we do rely on these top quality partners in order to advance that. So I will conclude here and see if there's any questions from the audience.
All right. We will now move to the Q and A portion of the presentation. As a reminder, if you'd like to anonymously submit a question, please type your question in the Q and A prompt on the presentation screen. All right. Our first question for George is, could you provide a bit of color on the expected timing of dorzagliotin commercialization?
Has COVID-nineteen affected the prior guidance of a 2021 launch?
Very good question. I guess this is probably the best way to put it is for us to submit our NDA, we need the fifty two week trial from the fifty two week data from both trials. And so as I mentioned, we probably won't announce the second phase three fifty two week until the end of the year, which means then we would submit the NDA towards the end of the year or first quarter of next year. And in China for a first in class drug, the response is anywhere from one hundred and thirty days to up to six months. So really, you're looking at a launch in that sort of year end or fourth quarter of twenty twenty one, at the earliest.
Now, we still need to go and speak with the Chinese regulatory authorities and, anything could change. We currently do enjoy what would be termed in The US sort of as a fast track, the ability to go and speak to them and have access to them. So really we won't know that with definitive timeframe whether we can go faster or whether it will be according to the timeline that I talked about until actually we go and speak to them after our data is completed from this third quarter. So in this third quarter we're going to announce the twenty four week. And then the first fifty two weeks with that we would have another meeting with them.
The COVID-nineteen for us, thank goodness, has actually not impacted any of our trials. We don't have one patient with COVID-nineteen even though ten percent of our sites and patients were in the Hubei province. It did slow us down in being able to have database lock because getting access to those sites, are in the hospitals, was actually very, very tight until the March, early April. So that did impact our ability to kind of release earlier. We were hoping to release probably in June previously, in in time for The US ADA.
But this year, it's gonna look more like, you know, sometime in July or August before for that release and that database lock and the data cleaning. That was delayed. But our trial cannot be delayed based on the protocol, obviously.
All right. Thank you. And our next question is, can you provide a little bit of color on the anticipated fifty two week data readout? Could you give an idea on how it will be differentiated from the twenty eight week top line results?
Well, okay. So sorry. If I heard it right, those two should be the same. So the trial is fifty two week, right? But it's two stages.
The first part is twenty four week, and that actually is double blinded placebo controlled. But after you finish the and that is measuring the primary efficacy endpoint of being superior over placebo. After that first phase of 24 double blinded placebo control is finished, everybody continues on on the drug. So the placebo was switched on the active drug, and they would have the drug for twenty eight week out of the fifty two weeks. The other active one, the people that were on the drug in the first twenty four weeks double blinded, they would continue for twenty eight weeks.
They would have fifty two weeks. So both groups would actually become on the drug for fifty two weeks. And The US authorities and the Chinese authorities, what they're looking for there is safety. Okay? Because you've already achieved primary efficacy endpoint.
They don't really care what your efficacy endpoint is. Why? Because they know that that patient's beta cell function has actually deteriorated. Right? The first day you started a trial, your beta cell function's gonna be a lot better than the last day, three sixty four.
Right? So they know that. So at twenty four week, they stop looking at efficacy, and they look to 52. So right now for the twenty eight week, we actually have seen that. So looking at safety, basically people are not going to expect that much of a change.
There shouldn't be. But the one thing that'll be interesting is if we are really doing something positive on the beta cells, then will you be able to sustain efficacy? All current drugs look like a swish logo from Nike. So at first, you drop the blood sugar, but at 16 or 18 or 24, you're gonna lose efficacy. Right?
And then you'll probably have to double the dose or switch to some other drug. That's that chart. If you're helping the beta cell and that's your MOA, then is it possible you look less like a Nike logo and you look more like an L, which would again authenticate and validate the fact that you're doing something positive in the beta cell. So we'll look at what our curve looks like in the third quarter, but that would be something that would be very differentiated.
Got it. And I guess we have time for one more quick question. Can you give us a picture of how the company expects to leverage its cash position in the coming months?
Yeah. So we actually, because we're so focused on one compound with such a huge amount of, different opportunities that have high probability of success, we don't have to spend that much, and we can actually see very early whether those phase three will come out positive enough. So a lot of these phase ones we've done in The US have indicated synergies, better, you know, better glucose lowering and also, no drug drug interaction so that we can then go to a phase three. Those phase threes will be much more expensive. So we're not gonna start the phase three until we actually raise more funds on the back of positive data from our 2452 week.
And also finding a partner, especially one that is in China that will actually help us sell the drug, which would then involve an infusion of capital as well with from payment for the right to help sell our drug. So this year, you know, really sequentially, it's about launching our two phase three data in high quality and ideally, knock on wood, fingers crossed, they're positive. And then finding a partner and then, getting a upfront payment from that. And with those two combined positive catalysts, the stock will continue moving upwards and then we would raise some capital, based on where the stock price is.
Great. Well, we'd like to thank George from Hua Medicine for presenting today, and thank you all for attending the twenty twenty Virtual UBS Global Healthcare Conference. You're now free to disconnect from the conference line. Thank you.
Thank you.