All right, welcome everyone to the 42nd annual J.P. Morgan Healthcare Conference. My name's Anupam Rama. I'm one of the senior biotech analysts here at J.P. Morgan. I'm joined by my squad, Malcolm Kuno , Priyanka Grover, Lorea Hall . Our next presenting company is Rallybio, and presenting on behalf of the company, we have CEO Steve Uden. Steve?
Thanks, Anupam. Well, thank you, everybody. Thanks for coming to learn all about Rallybio or get updated as where we are. I'm also, as you can see, joined by our CFO, Jonathan I. Lieber, here, so he'll be here to help out with some of the Q&A. So let's get started. Obviously, the usual forward-looking statements. A little bit about who we are and how we got here. We are based in New Haven. We are a portfolio company. In other words, we put together a team of individuals who have a long track record of doing everything in the whole drug discovery, target identification, development, approval, and commercialization process. And around that team, we were able to acquire financing, and with the financing, we've built the portfolio about which I'm going to talk later, just right now.
Just to quickly put things in perspective, our area, we are in rare disease, and we're really looking for therapeutics that will be completely transformative rather than incremental. And I think you'll see, you know, where the approach that we're taking in each of our therapeutic areas. We're at the moment relatively agnostic to therapeutic areas. We're looking at maternal fetal health, complement biology, hematological conditions, and some metabolic problems. This is the pipeline we've built. We have a sort of international reach with our business development. Interestingly, every one of these projects have been acquired outside the United States. As you can see, we have two clinical programs, both of which are now poised to go into phase 2.
We have a preclinical matriptase-2 antibody, which is undergoing sort of workup to prepare it to go to file an IND and go into the clinic. Then we have two research collaborations. We use this sort of portfolio approach also for research. We have a small molecule approach to inhibit ENPP1, to treat hypophosphatasia, sometimes known as soft bone disease. Then we have a multi-target collaboration with the Canadian company, AbCellera, looking at the use of monoclonals in rare disease. But I'm going to spend most of the time focused on our clinical candidates, and I'm going to start with RLYB-212, which is a preventative treatment for something called fetal and neonatal alloimmune thrombocytopenia. So firstly, what is RLYB-212? It's a fully human monoclonal antibody.
It was actually derived from a plasma cell, and its activity is to bind to and enable them and enable the rapid clearance of platelets that have the HPA-1a antigen on the surface of the platelets, human platelet antigen 1a. To set the scene, and you'll understand why this is important, 98% of us have this particular antigen on our platelets, but 2% do not, and those are the 2% who we'll be treating, mothers who are HPA-1a negative. I'll explain why we need to clear those those platelets very quickly. It's a very small volume, subcutaneous therapeutic. The kinetics are excellent. It will only need to be used during pregnancy.
This is a preventative treatment for during pregnancy, but the mother will only need to be dosed once a month, so it can coincide with her clinic visits. Though we will look into the utility of an auto-injector, should people want to treat themselves at home. The PK are excellent, very limited peak to trough variation, which is going to be so essential as we make sure that we get exactly the right, safe, yet effective dose in mothers who are otherwise well and pregnant with an at-risk baby. The market opportunity we estimate is over $1 billion, with a very conservative model based on the fact that there would be, every year, 22,000 mothers who would need to be treated with this during pregnancy, with RLYB-212 during pregnancy, to prevent them from getting FNAIT.
As you'd expect for a rare disease, we have orphan drug and rare pediatric disease designations, and the composition of matter, the simple composition of matter goes out to 2035. Quick reminder, or primer for, on fetal and neonatal alloimmune thrombocytopenia. It is a rare, bleeding disorder that occurs to the fetus while it's inside the mother's womb. This is due to the fact that the fetus is carrying the normal HPA-1a antigen, but the mother is one of the 2% who've got the mutation. She's known as HPA-1a negative. She has the protein, but there's a subtle change in the amino acid sequence, and she also has, the HLA type DRB3*01:01. So she has to have both. She has to be one of the 2% who are HPA-1a negative and also have HLA DRB3*01:01.
That's her HLA type. Now, at the moment, if this occurs, if this mismatch occurs, so the mom's got is negative for the antigen and the baby is positive. If at any time during the pregnancy, fetal platelets get into her circulation, they'll be recognized as foreign. The mother makes IgG antibodies. They get into the baby, they destroy the fetal platelets. And even though the little baby's wrapped up inside the mother's womb, the smallest bleed will bleed and bleed and bleed, and you end up with intracranial hemorrhage, long-term neurological disorders, miscarriage, and then, of course, during the birthing process, bleeding into every orifice and widespread bruising that will require neonatal intensive care unit. And because this is an immune problem, all future pregnancies will continue to be at risk. Now, one last thing about this.
One of the unusual things, there's lots of things about this rare disease that are unusual, but one of them is that the awareness among obstetricians is virtually 100%. We have not yet spoken to a physician, an obstetrician, should I say, who's never heard of this syndrome and would love to be able to do something about it... Now, some of the audience may sort of been able to draw the connection between this syndrome, the platelet mismatch, and the red blood cell mismatch that used to be catastrophic back in the sixties and seventies, Rhesus disease of the newborn. You may have never heard of it. You may have never heard of it because it's now prevented in the same way that we're going to prevent FNAIT.
But this study is one of the studies modeled on the study that they did to demonstrate that RhoGAM would prevent hemolytic disease of the newborn. So this is a study to show that our drug should prevent fetal and neonatal alloimmune thrombocytopenia. We took male volunteers who have the same platelet mutation as the mothers. They're HPA-1a negative. We have to sort of really beat the bushes to find these individuals, working with the German Red Cross to find these blood donors who were prepared to take part in a phase 1. They came into the clinical phase 1 unit and were given a very small dose of our therapeutic, and I'll talk about the doses in a moment, or placebo, and then sent home. These men are simulating the mom going to the clinic, she gets her shot, and then goes home.
A week later, they came back to the clinic, and we infused into them HPA-1a positive platelets. Remember, the gentlemen are HPA-1a negative. We put in normal HPA-1a positive platelets, simulating the baby bleeding into the mother. So, you know, the mom's had the shot, and then a week later, she trips on the rug, and the baby bleeds, and the baby then bleeds into the mother. And we then followed what happened to those platelets. Now, two of the gentlemen, two of the male volunteers, received placebo, and you can see with the black line that the platelet... So, sorry, what we're plotting here is percent change in platelet counts against time out to one week.
Of course, everybody starts at 100%, and the two individuals who received placebo, the platelets remained in circulation for about a week, with an elimination half-life of about 72 hours, three days. That's normal. If we were all to be injected with platelets at the end of this talk, we'd all have them swilling around until this time next week. Now, now let's talk about the individuals who had been treated a week earlier with 212. Four individuals had received a dose of 0.09 mg, total dose of 212 a week earlier. And you can see that the elimination half-life dropped from 72 hours to six hours. The primary endpoint was speeding up clearance tenfold. This was a very low dose.
We knew that we would have a big safety margin in mom, so we pushed the dose up to 0.29 mg total dose the week earlier. And you can see the elimination half-life dropped to less than 2 hours, with all the platelets disappearing within 6 hours. Now, data like this were done with red blood cells back in the 1960s, and RhoGAM went on to be the drug that it is. We are now very confident that this drug should work, and we're going to go into a phase 2 study, and let me talk about this. The preparation for the phase 2 study is underway.
As I speak, the European protocol assessment process is going on, and we're waiting for the first round of questions that are due towards the end of this month in order to enable us to start this study in the second half of this year. So this phase 2 study will be carried out in pregnant women at high risk of FNAIT. In other words, they are HPA-1a negative, they are HLA-DRB3*01:01 positive, and through fetal DNA testing, we know that the baby is HPA-1a positive. They will be. When they turn up for screening, when they turn up for their regular clinic visit, they'll be tested to see if they are potential patients, and should they agree to join the study, they will then, from week 16, start to receive a monthly subcutaneous dose of two-one-two.
And then we will wait till the mother delivers, doing intensive PK, PK measurement. And the reason we're doing a phase two rather than jumping straight to phase three, is the one piece of this jigsaw that is missing is how the PK, how do pharmacokinetics change in pregnant women as their blood volume changes and heart rate and metabolism changes? So we will be doing intensive PK monitoring, waiting till the baby is delivered, obviously confirming that the baby is healthy, the mother hasn't seroconverted, and we'll have to wait till week 10 to confirm that she hasn't seroconverted, because obviously, we don't want to be measuring our own antibody, thinking that's the antibody that's causing the problem.
We'll study three cohorts, a sentinel dose, another cohort of about 3-4 months, and another 3-4 months after that, and then we'll be good to go for phase 3, fully understanding the pharmacokinetics in pregnant women. Now, we're not wasting our time, because this will take a while, this phase 2 study. So we're already starting to sort of, if you like, run the first half of our phase 3 program by running a natural history study that will be the historical control. So we're working with many sites in North America and Europe, physicians who are highly motivated around FNAIT. What they are doing is when they find mothers who are HPA-1a negative, and the baby's positive, and they're HLA-DRB3*01:01, they're just simply following the pregnancy and looking for the outcomes.
Interestingly, we're already finding among those mothers, mothers who have already seroconverted, sadly. So this is a real problem. Obviously, if we'd screened all these moms and none of them had ever, who'd had babies and never seroconverted, you'd be asking yourself, "Is this a real problem?" It is. Sadly, many of the moms can't take part in the natural history study because they've already seroconverted. The good news, of course, is the obstetrician is now alerted and can look after the mom carefully during pregnancy. Just to remind everybody, how will we find these moms? The good news is, when women get pregnant, by and large, they go to the doctor. By and large, at the first visit, they have a lot of blood taken. There are guidelines that tell doctors what tests to do, and at...
What we will be doing is getting testing for HPA-1a added to the testing guidelines, such that, you know, when moms turn up, they'll be screened, and if they're at risk, offered this therapy. So finding the patients should not be so difficult. But in order to make sure that happens, we have our little commercial team are very busy out there talking to players, talking to prescribers, building cost effectiveness analyses, looking at the natural history data, talking to people who work on the obstetrics guidelines throughout North America and Europe, and getting publications out there. We think this is a really exciting program. It's the opportunity not to treat a disease, but to basically confine it to the history books. I'm now gonna go on and talk about our complement program. Now we're sort of in a space that's much better understood.
We have two programs, in the complement space, RLYB-116 for systemic complement disorders, ready to go into phase 2, and we have some preclinical work going on with RLYB-114 for ophthalmological complement-driven diseases, and I'll talk a little bit about that in a minute. But let's focus on the systemic therapeutic first. I'm not going to patronize you by reminding you about the complement or going through the complement pathway. I just want to remind everybody, this is a C5 inhibitor. In other words, it turns the complement system off at the point where it transforms from being an enzymatic cascade to releasing the inflammatory mediators, building the membrane attack complex, mobilizing leukocytes, et cetera, et cetera. We're gonna turn the whole system off at the point of C5, in the same way that Soliris did.
Now, the question is, well, if Soliris is out there or Ultomiris, why do we need this therapeutic? Two reasons. Number one, there is still. These are most of these complement-driven diseases are lifelong problems, and yet patients either have to go to the clinic every two to eight weeks. Even Ultomiris often requires more frequent dosing than eight weekly. Or they have to use complicated at-home subcutaneous infusion systems rather than a shot, and I'm gonna explain in a moment why this will be a simple shot, or they have to dose themselves daily. So let's just talk about the technology. It's built on the Affibody platform. An Affibody is a 60 amino acid protein.
Compare that to sort of 1,300 amino acids in a monoclonal, yet the antigen binding surface shown in red is equivalent to a monoclonal. We stop it from dropping out in the urine by attaching a small albumin binding domain. So the Affibody is now attached to albumin, and it circulates, attached to albumin, and has a half-life similar to a monoclonal. It's such a small molecule, it can be subcutaneous. The albumin should keep it in circulation long enough to make it one weekly therapeutic. It's got deep tissue penetration. You will not get immune complexes as you take a patient off a monoclonal onto our drug because it's monovalent.
Very low cost of goods, which will give us a lot of pricing flexibility to address the other unmet need for complement, which is there are a vast number of complement-driven diseases, and yet only 4 approved indications. We want to see this drug being used in all these other indications in due course. Where are we? We're ready for phase 2, and the reason we're ready for phase 2 is we've just wrapped up the multiple ascending dose study in phase 1. This is the design. It was an adaptive design. We pre-agreed with both the regulators and the IRBs the parameters within which we could adjust the dose, and as each cohort completed, we analyzed the data and adjusted the dose.
On the left, sorry, as you look at it, on the right-hand side are the various pre-agreed cohorts, but on the left-hand chart side, under study cohorts, are the actual doses that we explored, and we looked at single, one, one, once-a-week dosing, we looked at loading dosing, we looked at pushing the dose higher and higher. Where we ended up as the dose that we want to take forward immediately to phase 2, we have plans to for, for a little bit more work that we could do with the therapeutic, is 100 mg, once-a-week, subcutaneous therapeutic. With a very simple formulation, this is a 1 mL, once-a-week, subcutaneous therapeutic, more than suitable for an auto-injector.
These are the data why we think this is gonna be a therapeutic that will certainly work in Myasthenia Gravis, probably not quite yet ready at this dose for things like PNH. What we're looking at here is a concentration of 3 different proteins, shown with a molar scale, shown on the y-axis, and time out to a week, on the x-axis, x and y-axis. The yellow solid line at the top are the concentrations of 116. Couple of things to notice: we sustain levels of 1 micromolar or higher. Look at the incredibly small inter-subject variation. Now, I know this is a log scale, but these aren't standard errors, these are standard deviations. So in other words, we will be able to get good control of the pharmacokinetics.
Just below that, in the dotted line, are the levels of total C5. This is a monovalent binding protein, but it's quite obvious that there's more than enough 116 to bind all of the complement that's circulating. And if you look, this is a log scale, but if you look carefully, the level of complement does increase during the four weeks, which always happens with Soliris, Ultomiris, et cetera, et cetera, and yet we maintain a good clearance in molar concentration between our drug and total C5. But what really counts is how much of that C5 is active.
That's the free C5 shown at the bottom, and you can see that we're getting at least 99% inhibition in the first day or two after dosing, and even at the end of each week, we're still getting 93% inhibition. More than enough, in our experience, many of us worked at Alexion, by the way, to treat myasthenia gravis. This is the totality of the data, looking at loading dosing, doses up to 150 mg. Clearly, what you're seeing here is, again, good inter-subject variability, and this is now a linear scale, so the error bars are a little bit broader. We're able to always sustain levels above 1 micromole per liter. In fact, we start to approach 3 micromoles per liter....
The reason that we're not taking doses above 100 mg once a week into phase 2 just yet is because as we approach 150 mg, we started to see dose-limiting adverse events. These were mild gastrointestinal symptoms and injection site reactions. The mild intestinal reactions were very similar to some of the problems that were seen with this molecule when it was in the hands of the previous owner, at doses of lower than 10 mg per ml. And our working hypothesis is this is due to process impurities during the drug manufacture. The reason we believe that is because we changed the manufacturing process and have been able to take the doses way up above 100 mg before these side effects start to appear.
Believe me, they are much milder than what's seen with the old manufacturing process. So, we've and by the way, what we've now done, and we so in fact started at the beginning of last year, is we're running another manufacturing run, using and adding a sort of novel, but some straightforward additional steps in the manufacturing process to further remove any process-related impurities from the drug substance, so that we could push the dose higher in future studies. I talked a little bit about myasthenia gravis, and that's where, you know, we are capital constrained, but where we would go first. The reason we believe that this will work in myasthenia gravis is that we've compared this therapeutic, albeit in vitro, with zilucoplan. Zilucoplan, you remember, was developed by Ra Pharma and is now owned by UCB.
They did not do free C5 work, so we can't compare our free C5 data with theirs. That, in our opinion, is the biomarker that counts. But we did look at their hemolytic inhibition assay. What we're plotting here is percent inhibition of hemolysis due to complement against concentration, and you can see that RLYB-116 is at least as good as zilucoplan. I'm not going to claim it's better because this is, you know, the difference is small, but it clearly does everything that zilucoplan does. At the moment, we're focusing, and we'll talk a little bit about this, I believe, with Anupam, on making the next drug batch of drug substance.
Once we have adequate capital, we would then want to take the new drug into the clinic, both in terms of myasthenia gravis and pushing the dose higher, maybe in another phase 1 study. Just quickly touch on the ophthalmological approach. When we acquired these assets, we had a pegylated version of the antibody, which we did some preclinical work that showed it should do everything that Eylea did. But we're also in a research collaboration with EyePoint to see whether their Durasert technology could have a therapeutic that could be given once every six months or even less frequently, which is what patients really need. Everyone's holding their breath and crossing their fingers. We're waiting to hear back from EyePoint to see whether or not this antibody is compatible with their Durasert technology.
I'll just quickly and briefly touch on our preclinical programs. As I said, we have a matriptase-2 antibody, 331. That's in preclinical workup. There will, in fact, be animal data that we'll be releasing, all being well, in the first half of this year. We have an ENPP1 inhibitor, which we think will have utility in hypophosphatasia. Please don't get us mixed up with Inozyme. Inozyme are replacing ENPP1. We are inhibiting ENPP1. They are treating brittle bones. We are treating soft bones. We're expecting to have a... It's a partnership with Exscientia, the U.K.-based med chem company with this big sort of artificial intelligence platform. And all being well, we'll have a candidate ready for IND-enabling during this year, and then finally, the AbCellera partnership.
So I'm going to wrap up there. Thank you very much for your time. Hopefully, you realize we're going to have some of the milestones, feedback from the regulators, that we can actually go and start to treat otherwise healthy pregnant mothers. We will have additional data on our matriptase-2 antibody, starting the phase 2 in FNAIT, and wrapping up the manufacture, and in the event that we have adequate capital, moving 116 forward and/or finding a partner for it. So Anupam, thank you very much for the opportunity.
Thanks, Steve. And so many of you have heard this, but there's three ways to ask a question. You can raise your hand, I'll call on you. You can send a question through the portal, and it'll come up on my computer. Or you can just email me, which is cool, too. So, I'll start out the questions. You talked about initiating that phase two study, and you briefly touched on this, in your presentation about some of the key outstanding regulatory sign-offs that you need. Maybe you could just review that?
Absolutely. So this is the FNAIT.
Yes, FNAIT.
Yeah. So, the intention is to run the clinical phase 2 study in Europe. A couple of reasons. The natural history study is also generating very interesting data in ethnically diverse patients. The epidemiology is well understood in Caucasians. We're getting a lot of ethnic diversity data from the U.S. So we're going to run the study in Europe, where there happens to be the center of gravity for FNAIT research. Now, the Europeans, the EMA, have something called the Protocol Assessment Process, and this is a collaborative process where you work with the regulators to agree the design of a phase 2 or phase 3 study. And obviously, you know, it's not usual to go into clinical studies treating pregnant women during pregnancy with potentially healthy babies, but are at risk. The way...
It's a choreographed process. There are certain days when you can submit the package. The package has gone in, they review the package, and a bit like the refusal to file, they'll tell you whether you can go or not. We've had that. They said the package is complete. We are expecting. What happens, you get a series of questions. You're given a window to answer the questions. You respond, they have another window to respond to that, and then there's the... Either they agree with you or there's a face-to-face, or nowadays, a Zoom meeting to finalize the design of the protocol.
So the intent here, Anupam, is to not just sort of throw a phase 2 protocol over the wall, but having pre-discussed it with the regulators so that when we get to filing the CTA, sort of the initial review has been conducted. Does that make sense?
Yep.
Yeah.
And you talked about the phase II being run in Europe. How are you selecting the sites in Europe? Are there any read-throughs from the enrollment dynamics in the natural history study?
Absolutely. I mean, as I said earlier, one of the reasons we're doing the natural history study is to sort of get things ready to go for both phase II and phase III. And, you know, I kind of would say this, wouldn't I, Anupam? But there is huge enthusiasm around this program, both in terms of the investigators and mothers willing to take part in just the natural history study. Now, as you've realized, Anupam, we will be selecting sites that are screening lots of moms and turning up lots of moms who are HPA-1a negative, and HLA-DRB3*01:01 positive. So, you know, where the good news is that we're gonna be able to select sites based on data rather than, you know, the investigator seems like a jolly nice person.
Yep. Questions from the audience? You talked about this a little bit in your presentation. How should we think about the cadence of sort of data disclosure around the Phase II study, given the stepwise enrollment dynamics that you kind of talked about?
No. So... Well, the good news, Anupam, is that it's single arm, and it's open, hence, obviously open label. I think what everybody's gonna be looking for is the pharmacokinetics. So our intention would be to share data as we complete each cohort, so that in full disclosure, the first mother we treat will be a sentinel dose, just one mother. But once we get to the end of that, we will share the PK. We will then complete the second cohort, that's more data, and then the third. And it will also be reporting whether or not the mother is seroconverted. Now, I'll be very honest, the numbers of moms we're studying would not be adequate to get to a 0.05 level of significance.
But if you sort of run the binomial probabilities, if we treat 10 moms at a 1 in 3, 1 in 4 chance of seroconversion and none of them seroconvert, you're getting, you're getting jolly close to the statistical significance. But the primary focus is PK, and we will be sharing those data as they emerge on it within each cohort. Does that help?
Yep. Yep. And, I think you've previously guided to some natural history data post this conference.
Mm.
What is the size and scope of that data? What are you gonna be looking for? I think this will probably give you some more ethnic diversity data. Is-
Yes.
How do we think about it?
Yeah. So, let's just sort of set the scene. Now, the goal that we set ourselves last year was to recruit 7,600 mothers. We slightly exceeded that. In fact, we could have done a lot more mothers, but we have to be thoughtful about how we deploy our capital. So we had to sort of put the brakes on a little bit in certain sites that we're recruiting like billy-o. We've now got adequate data, I feel, Anupam, that we could start to draw appropriate inferences about the epidemiology. You know, if you've got something that only occurs in sort of 0.5% of mothers, and you go out with 1,000 screened moms, I mean, you know, whatever you see, it's gonna be wrong.
In fact, whatever we see within the 7,600 will be wrong. But we'll certainly be well north of 7,600 mothers, hopefully approaching 10,000 moms that we could go out with. We would hopefully, by then, be able to identify what's the frequency in ethnic groups outside Caucasians. We'll be able to demonstrate that there are mothers who've already seroconverted, and what proportion of moms today are going into the doctor already at risk of FNAIT, and may have some preliminary data on how many of the high-risk moms have actually seroconverted.
Questions from the audience?
I think the other thing, obviously, I don't know, Anupam, will be also to reassure everybody, investors and physicians and everybody that, you know, mothers are willing to take part in this sort of research. I think it will be important.
Yep. You know, one thing that we struggled with is, you know, the FNAIT market, just because it's such a novel market. Like, what do you think the Street is missing in terms of the market opportunity for FNAIT?
Where do you want me to start? Okay. Right, well, I think the first thing is you've hit the nail right on the thumb, Anupam. This is not a therapeutic space for which there really are any other comps. I talked about earlier about RhoGAM for Rhesus disease of the newborn. That's a drug that was approved 60 years ago. It sort of ages me, when I was at medical school, this was the big breakthrough that occurred. So in terms of pricing, it's, you know, totally genericized and what have you. So there's really no comps for a rare disease therapeutic to prevent to use treating a mother during pregnancy. I think there are sort of appropriate, not concerns, but appropriate questions about will you get on guidelines?
If you think of typical guidelines, like, you know, the guidelines for treatment of SLE, you know, every four or five years, you know, a bunch of guys get together, or gals and say: Hey, let's update the guidelines. And I think people think, "God, does that mean, you know, just gotta wait till people wake up and start to say..." The difference between most therapeutic areas and obstetrics and the management of pregnancy is that nearly all of the major bodies have an update cycle. Because the thing about pregnancy is that so many things are changing. It's not just screening, it's management of preeclampsia, you know, management of breech delivery, et cetera. So there is a... Most of these bodies, ACOG, the Royal College, where I come from, have an update cycle. But I don't think people realize that.
They're like: How are you gonna get on these guidelines? There's an update cycle. There's a process where you submit data. So getting on guidelines, there are no comps. I think there's the very real concern as well, and I think the Street does get, if we're honest, is that phase II will be slower than your average phase II. We are treating healthy mothers with otherwise healthy babies, and we're just having to be, you know, appropriately thoughtful about how we push that forward. You know, the kinetics will be so important before we launch phase III. Having said that, I think once we get to phase III, we will move at quite a clip. So those are things. How are you gonna get on guidelines? Is it cost effective? We're doing a lot of work in that space.
And we can, you know, we have and will share those data. Getting on guidelines, as I said, you know, it will take long to get moving, and just really no familiarity with the space. I'll stop there.
Questions from the audience? Quick strategic question. Would you consider out-licensing fully or part of the 212 FNAIT program? Well, actually, the 116 program, right? To help fund FNAIT.
Absolutely. I mean, you know, let's be realistic. I mean, you know, our stock price is suffering, I think probably because of the question you just asked. Both therapeutics could require adequate capital. 116 is a drug. There are a lot of people wanting to get into myasthenia gravis. So the quick answer to your question, Anupam, is, of course, that's something that we will consider. I mean, but, you know, any biotech that's worth its salt looks at its entire portfolio at any point in time and says: You know, could it be partnered? But I think one of the ways that we're looking at to get value from 116 would be to find a partner.
Okay. Any final questions? Thanks, everyone.
Thanks, Anupam. Thank you, everybody, for coming. I hope you find it helpful. Thanks.