Good morning, and welcome to Rallybio's conference call. At this time, all participants are in a listen-only mode. This call is being webcast live on the investor section of Rallybio's website at www.rallybio.com. Please be advised that today's conference call is being recorded. I'd now like to turn the call over to Jonathan Lieber, Chief Financial Officer at Rallybio. Please go ahead. Thank you, Michelle. This morning, we issued a press release announcing preliminary clinical data from our Phase 1 multiple ascending dose study of RLYB116, as well as next steps for the RLYB116 clinical program. The release is available on the investor section of our website at www.rallybio.com. We will begin the call with prepared remarks from Dr. Steve Uden, our Co-founder and Chief Executive Officer, and Dr. Eric Watsky, who leads the RLYB116 program. Eric will be referencing a series of slides which have been posted on the investor section of our website. If you have not downloaded them already, I encourage you to do so now. Following Eric's remarks, we will open up the call for questions. On today's call, we are also joined by Dr. Martin Mackay, our Executive Chairman, and Dr. Steve Ryde r, our Chief Medical Officer. Before we begin, I would like to remind everyone that we will be making forward-looking statements on this conference call, and these statements involve certain risks and uncertainties that could cause our actual results to differ materially. Please take a look at the risk factors discussed in our SEC filings for additional detail. These forward-looking statements apply only as of today, and we undertake no duty to update any of the statements after the call, except as required by law. I would now like to turn the call over to Steve. Steve? Thank you, John. Good morning, everyone, and thank you for joining us. We founded Rallybio with a singular goal: to change the narrative for patients with rare diseases. We aim to develop new medicines that possess a clear mechanism of action and effectively address the underlying disease biology across a wide range of unmet needs. We've employed this strategy to build a broad and sustainable portfolio, both in-house and through partnerships and collaborations, spanning multiple therapeutic areas, including maternal-fetal health, immunoinflammation, hematology, ophthalmology, and metabolic disorders. A key pillar of our pipeline is our complement program. Prior to the formation of Rallybio, many of us were involved in the design, development, and approval of complement factor five inhibitors to treat severe and rare diseases. We have long believed in the value of C5 as a therapeutic target. The complement system is known to play a central role in innate immunity, as well as in shaping adaptive immune responses. Dysregulation of this pathway has been linked to more than 50 diseases across multiple therapeutic areas. While antibody and polypeptide-based inhibitors of C5 have been successfully developed to treat a handful of diseases, existing treatment options create challenges for patients, leaving ample opportunity for new, safe, effective, patient-friendly, and accessible approaches to disrupt the market. This is where RLYB116 comes into play. RLYB116 is a novel fusion protein comprised of two components. The first is an Affibody molecule with high affinity for C5, designed to inhibit terminal complement activation. The second is based on the Albumod technology, which is designed to bind to serum albumin to potentially extend the half-life and enable broad tissue distribution. RLYB116 is quite small, approximately 12 kilodaltons in size or 8% of the size of an antibody. We believe that together, these attributes may enable RLYB116 to fill a unique position in the market for complement inhibition. A product that can be rapidly self-administered subcutaneously, once per week with an auto-injector. Our market research is consistent with our belief that this profile will be sought, sought after by a meaningful number of patients, because it offers them a significantly improved alternative. A significantly improved alternative relative to existing C5 inhibitors, which are administered daily by a prefilled syringe or less frequently and intravenously, but in the clinic. As Eric will detail shortly, the initial data released this morning from our phase 1 multiple ascending dose study demonstrates a substantial reduction in free C5 to concentrations that have utility in treating complement-driven disease. Specifically, we are pleased to observe a generally well-tolerated profile with a mean reduction in C5 of greater than 99% at 24 hours and greater than 93% sustained at day 29 pre-dose, with a 100 milligrams low volume, once-a-week dose. We're very excited about these results and believe they support further development of RLYB116 because they address a significant unmet need for patients with generalized myasthenia gravis. Our market research, conducted with both patients and physicians, confirms a once-a-week, small volume therapeutic that can be rapidly self-administered, would be highly attractive and address a continued unmet need for more patient-friendly treatment options in gMG. The results generated to date for RLYB116 are compelling. We see a significant opportunity in gMG and are determined to find a way forward to fund a phase 2 study without impacting the clinical development of our FNAIT program, as well as our existing cash runway. In the interim, we believe that with some additional manufacturing work, we may be able to make further improvements to RLYB116 to enable further reductions in free C5, thereby enabling the treatment of a broader range of C5 diseases. Specifically, our work, which is already underway, is focused on an innovative addition to the existing manufacturing process specific to the Affibody technology. We believe this change will allow us to improve the tolerability of RLYB116 at higher doses, while maintaining the current attributes, including low injection volume and infrequent subcutaneous administration. If successful, we expect to see even greater C5 reductions that would support the treatment of a broader range of complement-mediated diseases, such as paroxysmal nocturnal hemoglobinuria, or PNH, and antiphospholipid syndrome, or APS. So what is our indication strategy? In RLYB116, we're looking for a once-a-week, low volume, rapid administration via a subcutaneous injection in a patient-friendly format. With the profile we have at the moment, we are confident that it is suitable for a clinical study in gMG. Beyond this and PNH, we are particularly interested in antiphospholipid syndrome, in part due to its connection to maternal health. In short, in the near term, gMG would be our first focus, followed by PNH and APS. To be clear, the results generated to date demonstrate C5 knockdown sufficient for the treatment of gMG. In the spirit of managing our cash runway, we've decided to focus our investments on the manufacturing process instead of immediately proceeding to a phase 2 study in patients with gMG. Today marks an exciting day for Rallybio. We're pleased with the results and the potential of RLYB116. We are confident with the additional manufacturing effort, we're confident that is a sound investment, given our desire to manage our cash runway, and that we can deliver RLYB116 as a patient-friendly option for the treatment of a broad range of complement-mediated disease. With decades of collective experience in the clinical development of complement inhibitors, we feel that our team is uniquely positioned to maximize the value of RLYB116 and ultimately deliver the promise of complement inhibition to many more patients in need. I'll now turn the call over to Eric to review the phase 1 data and why the data supports our next steps in greater detail. Eric? Thank you, Steve. As John mentioned during his opening remarks, I will now go through a slide deck we posted this morning, which can be found on our website. I will refer to the slide number as I go through each slide, so you're able to follow along. Slide 3 highlights what we believe are the key potential differentiators for RLYB116. Low volume subcutaneous injection, suitable for an auto-injector with rapid delivery, differentiates RLYB116 from what is currently on the market. We find that some of the additional highlights and differentiation may include compatibility with at-home use, with less frequent administration and more convenient dosing. This could include weekly instead of daily administration, or a low volume compatible with an auto-injector, versus a volume greater than 2 ml and requiring administration in a clinic. Convenient storage requirements may also be feasible. Currently approved complement blocking treatments for patients with gMG involve in-clinic intravenous infusion every 2-8 weeks, or daily subcutaneous administration with a syringe. FcRN inhibitors are available for weekly subcutaneous injection but involve volumes greater than 2 ml and require administration in a clinic setting. Slide 5 is the study design for the single ascending dose study of RLYB116, which was completed in 2022, with initial results that I will show on the next slide and were preliminarily disclosed in November 2022. A more complete disclosure of the data was presented recently at the International Complement Workshop in Newcastle, U.K., in September 2023. As a reminder, this was a dose escalation study design with 5 sequential cohorts evaluating safety, PK, and pharmacodynamics in healthy participants. The doses selected for the study were based on the exposures observed with the top dose in our toxicology studies, which was also the dose that was the no observed adverse effect level, as well as based on modeling and simulation of the expected exposures. Slide 6 may be familiar to many of you. This shows the initial 100 milligram data we reported in November last year, with single-dose administration and the potential for rapid and complete inhibition of C5. The table on the right indicates that the 100 milligram data demonstrated a reduction in free C5 of greater than 99% within 24 hours of dosing. The terminal elimination half-life for the 100 milligram dose for RLYB-116 was estimated to be greater than 300 hours. There was a low degree of inter-subject variability, with a coefficient of variance estimated at less than 20%. This has been encouraging to us as it points to reliable, consistent, and predictable exposure with subcutaneous administration, important features for a potential future therapeutic. On Slide 7, we show the PK data for all 5 cohorts from single-dose administration... As I mentioned, this was part of a poster this past September at the International Complement Workshop, which summarized the single ascending dose data from the phase I study. This slide highlights the increase in concentrations of RLYB116 with increasing dose, relatively low inter-subject variability, and a mean elimination half-life greater than 300 hours with subcutaneous administration of RLYB116. On Slide 8, we summarize the most common adverse events with single-dose administration. RLYB116 was observed to be generally well-tolerated at the 100 mg dose, with mild to moderate adverse events and no drug-related serious adverse events reported. We observed a higher rate of gastrointestinal adverse events with the 300 milligram dose. The onset of these events was relatively rapid and did not appear to be fully consistent with the pharmacokinetics of RLYB116. The events began prior to the maximum concentrations being reached, and most resolved within hours, even as concentrations of RLYB116 were still increasing. Moving on to the multiple ascending dose data. On Slide 10, you will see the multiple ascending dose study design. As we stated previously, this was an adaptive study design that included multiple cohort design options to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of RLYB116 in healthy participants following multiple dose administration. Our goals for the study also included understanding the potential for a low-volume, subcutaneous, weekly administered dose of RLYB116. Based on the adaptive study design on Slide 11, you'll see the four cohorts we ultimately studied. We found that the results with the 100 mg dose demonstrated consistent pharmacology and low within, as well as inter-subject variability, and are confident that the 100 mg dose merits further clinical investigation in gMG. We are also interested in testing higher exposure, but observed dose-limiting adverse events with a 150 mg dose with the current drug product that we expect can be addressed with manufacturing changes. In the subsequent slide, I will discuss PK and PD data from each of these cohorts, as well as summarize the adverse events, the most common of which included injection site reactions and headache. Slide 12 shows the PK data for all four cohorts in a single graph. The PK data here shows sustained concentrations were achieved with subcutaneous administration of RLYB116, with low inter-subject variability, and that were consistent with the long half-life of subcutaneously administered RLYB116. Interestingly, the single ascending dose data with a 100 milligram dose anticipated our findings with a multiple dose administration, both in terms of pharmacology as well as the adverse event profile. Across cohorts, we were able to achieve up to a nearly 3 micromolar mean concentration of RLYB-116 at steady state during the FIH, when measured pre-dose at day 29. In Cohort One, in which weekly 100 milligram subcutaneous was administered, RLYB-116 mean concentrations at steady state were in excess of 1.5 micromolar. The concentrations of RLYB-116 in that first cohort were sufficient to reduce free C5 by greater than 99% at 24 hours and greater than 93% sustained with measurement pre-dose at day 29. Beginning on slide 13, we show the data for the 100 milligram weekly cohort, which was primarily highlighted in the press release. As a reminder, this is the dose where this is the cohort where the dose resulted in greater than 99% reduction at 24 hours and greater than 93% sustained decrease in free C5 concentrations at measured pre-dose at day 29. Next on Slide 14 is Cohort Two, which included administration of a 100 milligram dose 3 times in the first week for induction dosing and then administered weekly. Induction dosing was introduced to assess whether reaching an earlier steady-state concentration would result in a more rapid effect on free C5 concentrations. The results here were higher concentrations of RLYB116, but similar sustained effects as Cohort One on free C5. Here, we expected to rapidly reach steady state with induction dosing and potentially produce a larger free C5 reduction. Although we saw a more immediate effect on free C5, the concentrations by day 29 pre-dose were marginally higher than the prior cohort, with a greater than 94% reduction at day 29, and this convinced us to evaluate a higher dose. On Slide 15, we have Cohort Three, which was initially planned with a 150 mg dose, but where adjustments were made to the dosing level based on the emergent adverse event, event data in the cohort, starting at 150 mg weekly and then adjusting to a 125 mg weekly. We observed liver function test elevations with a 150 mg dose in one participant with a history of hepatitis A infection. We discontinued this participant from the study and completed this cohort with the 125 mg dose. The liver function test elevation onset was within 24 hours of study drug administration and started to improve within 1 day of onset. It did not appear to be fully consistent with the pharmacokinetics of RLYB116. Reductions in free C5 concentrations at day 29 pre-dose were greater than 93% and similar to 100 milligrams weekly. Finally, on Slide 16, we have the last cohort, Cohort 4. As a reminder, dosing was 75 milligrams 2 times for the first week and then 100 milligrams twice per week. In this cohort, we found that a near doubling of the concentrations of RLYB116 resulted in more than halving of the sustained concentration of free C5 compared to the prior cohorts. We were successful here in pushing the concentrations higher, where the higher exposure demonstrated a larger effect on free C5, with a greater than 97% reduction at day 29 pre-dose. The further reduction in free C5 with higher exposure gives us confidence that RLYB116 has the potential to achieve its target profile of a low-volume, rapid delivery, subcutaneous dose suitable for an auto-injector with a higher dose. Next, I will provide a summary of the most common adverse events in the multiple ascending dose study of RLYB116 on slide 17. RLYB116 was observed to be generally well-tolerated with a 100 mg once-a-week dose. The most common adverse event was injection site reaction, which occurred in 60% of the participants in this cohort, with all events being mild in severity. The majority of ISRs were due to erythema. The ISR rate across the 4 cohorts of the MAD was 59.2%, and again, all were mild in severity. Additionally, all adverse events during subcutaneous administration with a 100 mg weekly dose were mild in severity. Dose-limiting adverse events were reported for doses above 100 mg per week, including an increase in the rate of ISRs, gastrointestinal adverse events, and the previously mentioned occurrence in a participant with a history of hepatitis A, of liver enzyme test elevation that resulted in study treatment discontinuation. There were no serious adverse events reported for participants receiving study treatment. It is noteworthy that the gastrointestinal adverse events observed tended unbalanced to be first dose effects that emerged within minutes to hours of subcutaneous administration and generally did not recur with repeat dosing. Based on what we have observed in the clinic, we think that it is possible that the adverse event profile may be influenced by the presence of residual process-related impurities in the drug product. Support for this comes from the timing of the onset of adverse events relative to RLYB116 administration, as well as not observing a worsening of the adverse event profile in cohort 4, where we nearly doubled steady-state concentrations of RLYB116 relative to prior cohorts. Moving on to slide 18, which summarizes our anti-drug antibody findings in the clinic thus far. As we know here, there appears to be no ADA impact on PK, PD, or the safety data. The ADA data also appears to be consistent with other reported experience with Affibodies. On slide 19, in an effort to better understand how RLYB116 might compare with treatments for gMG, we show data from the conduct of a CH50 hemolytic inhibition assay under conditions reported by Tang et al. this year, in which we included research-grade zilucoplan as a control. We conducted this experiment in part due to the lack of published free C5 data available for zilucoplan, which we view as an informative control for RLYB116. Our data on slide 19 demonstrated that the RLYB116 effect in this assay appears to be comparable to, or in fact, numerically greater than zilucoplan when evaluated under identical conditions. In our view, this provides added support for the potential effectiveness of RLYB116 in gMG. On slide 20, we review our manufacturing activities. At the time a prototype C5 Affibody was first studied in the clinic, prior to the acquisition of RLYB116 by Rallybio, similar transient adverse effect events emerged at a dose of 10 milligrams. At the time of the acquisition, evaluation of the nature and time course of these adverse events led us to believe they could be addressed through improvements in the manufacturing process. Therefore, after we acquired RLYB116, we developed a manufacturing process that included a change in E. coli strain and added purification steps. Our data demonstrate improved tolerability that enabled advancing to higher doses. Based on the similarities of the adverse events to those observed previously and inconsistencies that we have observed between the PK of RLYB116 and many of the adverse events, we suspected the persistence of residual process-related impurities from the current manufacturing process could be having a role in the adverse event profile. We are working with a contract manufacturer to introduce innovative changes to the manufacturing process as part of continuous improvement methodology. We are pleased to have identified new analytical tools that reach beyond standard test methods and enable us to more sensitively measure for the presence of process-related impurities. Additionally, we are introducing a custom step that can be easily implemented into our future manufacturing process that we anticipate will enable further removal of process-related impurities. Before I turn the call over to John for any comments on the company's financials, let me close on slide 21 with a few points to summarize these slides and our next steps. The reduction in free C5 with once-weekly subcutaneous dosing of RLYB116 at a 100 milligram dose, was to a concentration that we believe has the potential to be effective for the treatment of generalized myasthenia gravis, and could afford significant benefits in terms of the potential for weekly rapid delivery auto-injector administration for patients. We believe that adjustments to the manufacturing process may enable high dose administration and further improve the tolerability profile, enable even greater pharmacologic effects. ... on free C5, and we have already progressed with this effort. And with that, I'd like to now turn the call back over to John for any comments regarding the company's financials. Thanks, Eric. As mentioned in our press release this morning, our existing cash and cash equivalents, which as of September 30 was $121.4 million, will now take us into the third quarter of 2025. We expect to provide additional plans on our cash conservation measures sometime in the first quarter of 2024, after the J.P. Morgan conference. This concludes our prepared remarks, and I'd like to turn the call back over to Michelle for Q&A. Thank you. To ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. The first question comes from Laura Chico with Wedbush. Your line is open. Good morning. Excuse me. Thank you very much for taking the question. I guess, one on the, the injection site reactions, and then a second one related to the indication selection here. I just wanted to clarify, is the hypothesis that eliminating these manufacturing impurities will improve the tolerability profile? I was just trying to understand if the frequency of these events dissipates over time. And then secondarily, you know, the, the myasthenia gravis therapeutic space has become a lot more crowded since Soliris was first introduced in this area. So, it would also seem the efficacy bar is higher, too, as because they're discussing kind of minimal disease now. What do you need to demonstrate on an efficacy basis to remain competitive in gMG? Thank you. Thanks, Laura. Two great questions. I'll probably. It's Steve here, by the way. I'm gonna get Eric to address the toleration profile and the ISRs and what have you, and then I'll sort of jump back onto the indication strategy. So, Eric? Oh, great. Thanks, Steve. Yeah, so with regards to the adverse event profile and manufacturing, yes, we do expect to see improvements, particularly in the gastrointestinal adverse event profile that we showed increased with increasing dose. The injection site reactions rate looks similar to what's been disclosed, published previously by Affibody. So we don't know to what extent the injection site rate itself will be changed. What we do know, though, is that the injection site rates that Affibody have reported appear to diminish over time and tend to be mild in severity, and that's consistent with what we've seen. And the events tend to be more on the order of most common are erythema. So the injection site reactions appear to be reasonably well tolerated and do seem to diminish over time. We only dosed out to one month. What Affibody has reported is, dosing extends out beyond that period. The injection site reaction declines substantially. Does that help, Laura? Yes. Yes, it does. Thank you. Okay, and I'll just jump onto the lead indication, gMG. So the first thing is that we've, is it a crowded space? Well, it is an area that sort of, as you said, Alexion sort of blew open with Soliris. First thing to remember is that patients who respond to complement inhibitors, it's not every patient that responds. Others seem to do much better on FcRN. So really, we are having to compete with other complement inhibitors. As Eric referred to, all of our in-house data show that this therapeutic delivers everything that, everything that at least zilucoplan delivers. So in terms of efficacy, we're not expecting anything less than that. The thing that we were working at in our previous company was this idea of the sort of small volume, 1 ml subcutaneous, once a week therapeutic delivered in an auto-injector, and that hasn't changed. And, you know, we would say this, wouldn't we? But our market research confirms that this is still what patients would prefer over everything else, including all of the orals and all of these other things. This, this is the format that they're looking for. So we think that where we're going to compete here is to give patients what they're looking for. gMG is a lifelong disease, something they can use to treat themselves at home, delivering all of the efficacy that the other therapeutics offer. But instead of it being either once a day or having to go into the clinic every two weeks, and even with things like Ultomiris, it's not always every eight weeks. We've found there are patients who need to go in more frequently than that. So you do not have to spend hours commuting to and from the hospital. It's a sort of 10-second event once a week. I've got our Chief Medical Officer here, who led the charge on gMG in our previous life. Have I missed anything, Steve? No, you've captured it. I think the fact that there are people in the development space speaks to the extant medical need. It still remains quite great. I think the world has told us, the patient world has told us, that once-weekly auto-injector in a very easy-to-use device that can be rapidly administered, is a very preferred method of treatment across therapeutic spaces. I mean, this is proven time and time and time again. This was the goal. I mean, Soliris in a NovoPen, sorry for the use of a proprietary word there, was the goal that we were after, and it still remains an extremely valuable proposition. The market research is unequivocal. It's unequivocal. It actually surprised me, and that's saying something, because I've seen these data in the past. It's unequivocal and highly attractive. Thank you for the question. Thanks, Steve. Back to you, Laura. Thank you very much, guys. I guess maybe I'll sneak in one last one, just around the LFT elevations. I think I heard that subject actually had a concomitant hep A infection or prior infection. Does that influence or change anything in terms of your patient selection criteria for gMG? Thanks very much, guys. Yeah, thanks a lot. Eric, do you mind to respond to that as we think about sort of the design of the study? Thanks, Laura. Yes, we will. Well, first off, if we will be evaluating the impact of the manufacturing changes. As far as moving forward with the current material, yes, we would expect to be excluding patients who have prior history of liver disease, based on this. It's not unusual, actually, in any sort of phase two study, quite frankly. Sorry, Laura. No, thanks very much, guys. Thank you. Please stand by for the next question. The next question comes from John Wolleben with JMP Securities. Your line is open. Hey, thanks for taking the question. I was hoping you could talk a little bit about the interplay between the changes in the manufacturing and then how that could broaden the potential indications. Is this just a function of improved tolerability, or you wanna even bump up the C5 reductions? I just hoping to better understand how the manufacturing will broaden the application. Absolutely. I'll sort of start, and Eric can sort of add more sort of technical color. So just to remind everybody that when we acquired this therapeutic, you couldn't take the dose above 10 milligrams. You know, various forensics have demonstrated that there were impurities from the manufacturing process still there, which as Eric referred to, we've been. You know, we're able to resolve, and we've now got a therapeutic that knocks down C5 at least adequately for gMG, and we can get to 100 milligrams quite easily. You've sort of hit the nail on the head, John. The intention is to. We think that the improvements in manufacturing would then enable us to push the dose higher, because we do think it's these residual impurities that are driving things like the ISR, ISRs. We can get more drug on board, and hence, get more knockdown of free C5. Now, of course, the obvious next question is, well, okay, then you're needing a bigger dose, so the volume. Please be aware that this is the 100 milligram per ml solution is the simplest formulation that we could have possibly come up with. So if we find that we would need higher doses, and actually, we've already started this work, we would be looking at formulation enhancements, which are, you know, sort of common or garden these days. Obviously, we didn't kick those off right away because we weren't quite sure the dose range that we'd be operating in. So in summary, you know, we've taken the dose up from 10 up to 100 milligrams. We've sort of not unusual, but not typically used analytical methods. We think there are still impurities, which should improve the toleration, which will enable us to get more free C5 inhibition. This is all underway, but I'll see if I've forgotten any highlights there, Eric. Well, I'd simply add that we also, in the work we're doing on the manufacturing process, are excited by an innovative approach we're taking regarding an additional step in the process, which we can easily implement, that we expect will enhance the material and, as Steve said, will enable us to push the dose higher, be able to establish even lower concentrations of free C5, with favorable tolerability. Thanks, Eric. And John, John, I forgot to say thank you for joining us. It's my excitement about the program that... Is there anything else that we could help you with? Yeah. One more. You mentioned the manufacturing modifications are ongoing. Any sense how long it would take to, you know, get through that process? And then, you know, can you talk a little bit about next steps? Is it to run another multiple dose study with the, the new formulation? Just, you know, talk a little bit about timelines and then getting to the next potential inflection with 116. Yeah. Well, we've. You'll not be surprised to hear that we've already sort of started the, you know, the preliminary work for the manufacturing process. So that's already in train. And as you know, you've got to sort of set up assays and do dry runs and all that sort of stuff. So that's all in train. We'll be working with our partners to get a firm date for when that would be completed. I think we would do, you know, depending on where our cash runway is and the markets and what have you, I think we would do two things. One would be to, as you imply, see, you know, go into another normal volunteer study, seeing whether we can push the dose higher. But of course, you know, we're good to go in gMG. So if we have the capital, that study would start in parallel with us pushing the dose higher and, you know, using our common sense, we'd use the newly manufactured drug material to dose in that study. And if you look at the timelines to get the new material and the timelines to ramp up a phase two study, they come together quite nicely. Well, in due course, we'll work with our partners once we've got a line of sight on when they actually think they can deliver the drug. Obviously, we're in the queue with a lot of other people, but it would not be rate limiting, certainly in the event that we're able to start a gMG study, financial considerations notwithstanding. I'll pause there. Pass back to you, John. I would only add, Steve. I would only add, Steve, that I would characterize the manufacturing activities as well underway. Yes. We have actually every reason to be hopeful that the target product profile of an auto-injector, very low volume, well-tolerated, easy to administer on a once-weekly basis, where we have every expectation that the manufacturing processes are going to lead in that direction, but I would characterize them as well underway. Thanks, Steve. Yeah. Back to you, John. Thanks for taking the questions. Not at all. Great to hear your voice, sir. Talk soon. Please stand by for the next question.... The next question comes from Anupam Rama with JP Morgan. Your line is open. Hi, guys. This is Priyanka on for Anupam Rama. I just have a quick question from our side. When you say you are committed to fund 116 without impacting cash runway in the FNAIT program, is the focus now on out-licensing the program? Thanks. I'll probably get John to add any comment in case I miss anything. You know, we keep all options open. You know, we're excited by the program. However, we're always cognizant of the financial environment we're in. So, you know, obviously, that will be one of the things that we would consider, and that could take all sorts of different flavors, of course. You know, it could be... With the thing about a complement inhibitor is there's a number of indications. There are a number of different territories. So, you know, partnering it and, you know, even with our FNAIT program, is something we talk about. So it would... I won't say we're committed to it, but it does mean that we will, you know, continue to look at that as a path forward. Either, you know, if for the right, you know, financial, whatever, the whole asset or, you know, it, separate indications or territories and all that sort of stuff. But it's something that's ongoing all of the time. John, have I missed anything? I think I've hit the highlights there. I think you hit the highlights. The only thing I would add is, as you mentioned in the release earlier, obviously now the bulk of our financial resources and time going forward is going to be directed at RLYB212 for FNAIT. So, that would just be the only thing I would add there. Yeah. Thanks, John. We're in the sort of fortunate position of having two good drugs and, but in a very difficult financial environment at the moment. Gotcha. Thanks, guys. Thanks for the call, question. Send out response to Anupam. Please stand by for the next question. The next question comes from Mitchell Kapoor with HC Wainwright. Your line is open. Hi, everyone. Congrats on the data, and thanks for taking the questions. The first one I wanted to ask about is, could you just talk a little bit about the trend in, in free C5 and the PK data broadly, at about 700, could you just talk about what's driving a more drastic response there? And, how does this trend in PK compare to that of other C5 inhibitors? Great question. I'm gonna hand this one definitely to Eric, because he's been working on this nonstop for the last several months. So, Eric. Right. So what you're seeing on the graph is a measurement of free C5 after the dose, the last dose is given. So the reason you see that bump in effect is because of a spike in concentration of RLYB116 with that last dose. Okay. Is there anything different about that last dose versus the other doses that were administered leading up to them? Nope. No, no, and the measurements that you're seeing prior are trough measurements. And so that's where you're seeing the consistency of exposure, and you're not seeing the fluctuation in C5 concentrations as much because the measurements are trough measurements pre-dose. Whereas at day 29, we did a more meticulous measurement of concentrations both before and after administration of drug. Eric, to orient, you're specifically looking at slide 13, is that correct? I'm looking at, yeah, 13, 14, 50. Just broadly seeing kind of similar trend among the four cohorts. But I think that explains it. Yeah, it's just that we, you know, these full profiles are quite burdensome, even though they are volunteers. So we do a full one on day one and then another one on the last day of dosing. In between, as Eric said, you're just seeing trough levels, and we don't completely repeat the full profile in between those, the beginning and the end of the study. It caught me by surprise the first time I saw it, too, so don't worry, Mitchell. Gotcha. Understood. And then the last thing I had to ask is just on, you know, any potential to avoid black box warnings as seen with other C5 inhibitors. Is there any reason to believe that maybe that could be something that 116 could achieve at some level? Well, the Chief Medical Officer, Steve, is shaking head. No, it's fundamental to the pharmacology of complement factor 5 inhibition. It's something that everybody has, and it's certainly not a risk that we would ever take with patients or volunteers. Steve? I would just add that, yes, it's inherent to the pharmacology. In fact, it comes from patients, people born with C5 deficiencies- Yeah Genetically, have a several thousand-fold risk of Neisseria meningococcal infections. We've spoken with the world's experts, expert, singular, in about this issue, and it's something that's been known, and it, and it is well managed. It's managed through both vaccines, and if you really want to protect yourself, I think one of the preferred methods that we were advised was through pen prophylaxis. But it's a very well-managed side effect, and C5 inhibitors are remarkable for the absence of essentially all other significant AEs, unlike some other products that, for example, can have pancreatic issues or hepatotoxicity. This is, this is not the case. But a several thousand-fold elevation in risk for meningococcal infection is inherent to the pharmacology, but it is well managed. It's been described for now 20 years, and it's very well managed. Thanks, Steve. Hope that helped, Mitchell. Gotcha. Great. Yes, very much. Thank you, and congrats again. Thank you. Great hearing your voice. Please stand by for the next question. The next question comes from Catherine Novack with Jones Trading. Your line is open. ... Hi, good morning, team. Congrats on the data. I was wondering if you can talk a little bit more about you mentioned APS in addition to GMG. So can you talk a little bit about, you know, your thoughts on that indication, the role of C5 inhibitors, you know, and meaningful clinical endpoints that might impact how you prioritize this indication relative to GMG? Thanks. Yeah. Well, so thanks for that. So, you know, why APS? It, the obvious sort of line of sight with maternal health, and as I'm sure you're aware, it's a well-described cause of recurrent miscarriages. There's extensive literature implicating complement overactivity driving it. There's really no therapy other than oral anticoagulants, you know, with all of the inherent risks. Warfarin. Warfarin, which is sort of about as old as it gets as oral anticoagulants. In terms of endpoints, Steve has been giving this a lot of thought. So, I'll pass over to you, Steve, in terms of, you know, how you would see a program playing out. Yeah, thank you for that question. And, APS, antiphospholipid syndrome, has been on our radar screen for some time. There was the hope among us and many others 15 years ago, 10-15 years ago, that the direct-acting oral anticoagulants were really going to provide a substantive improvement. Quite the opposite has happened, and if you follow the literature, you're seeing now that there's an unacceptable risk of, especially intracranial events with the direct oral anticoagulants that really hasn't provided the uptick that you've seen in other spaces where Eliquis and other DOACs have really provided significant relief to patients with other thrombotic conditions. This is not so. So we're left with warfarin, which, as you know, is an extraordinarily difficult therapeutic to use because of the panoply of drug interactions. Complement is definitely involved in the process, no question, and there are some literature reports, can provide them to you if you'd like, where there's very dramatic improvement in patients with recurrent thrombosis despite state-of-the-art therapy. We're going to speak to a bunch of KOLs. I think it's premature for me to elucidate a clinical development program in its fulsome nature, but going after the thrombotic component of APS will be our desire. We understand that there may be some intriguing biomarkers that have come into existence. Some calls that we've had with KOLs already say that we can get potentially a higher at-risk patient population. All of this is to come as we get deeper into the development plan, but extremely interesting space and one that is of great medical need. Thanks, Steve. I think I'm correct in saying, Steve, that, you know, the thromboses that occur in this are much more frequent than things such as, you know, myocardial and whatnot. Absolutely. You know, you wouldn't need... You'd need a reasonable-sized study, but not huge. This would be an appropriate size study that. And again, I would offer that some of our initial discussions are that we can identify patients at higher risk. Thanks, Catherine. Anything else? Great question, though. We have, you know, it's something we really would love to get, you know, get into once, once we can finance, what have you. But any other questions before us? Yeah, that's it for me. Thanks. Very much. Thanks again. Great to hear. Yeah, no, thank you. Great to hear your voice. Talk next year. Please stand by for our next question. The next question comes from Yasha Patel with Evercore. Your line is open. Hey, it's Gavin here. I was just wondering if you could provide some more details on the time course of ADA development. When in the dosing did most of these emerge, and was there any difference in ADA rate across the different doses? Oh, thanks. Thanks for the question. And the time course, as we expected with ADA development, really was after extended period following exposure. So we tested ADA out at day 99 after the initiation of dosing. So we had a good long follow-up after the start of the study to be able to evaluate that. And no, we don't see any relationship to dose. And I would offer that, please recall that our elimination half-life is 300 hours with this molecule, so well into the time period where ADA development may impact PK. And we don't see this, so it's joining the long list of ADAs that are really laboratory findings, but without clinical impact. This is, of course, well known in the biological space. Thanks, Steve. Thanks, Uncertain. Does that, Gavin, stick to you? Yeah. No, it's very helpful. Did you say what the rate of neutralizing ADAs was specifically? That's typical for this stage of development. We don't have an assay for neutralizing ADAs at this point. So that's something we would. But as I said, the evidence we have does not point to that because there does not seem to be any. There's no evidence of impact of ADA on concentration or on PD or on adverse events, in relation to adverse events. Yeah, that's very helpful. Thanks for taking the questions. Well, it's all Gavin. Great to hear your voice. Thanks for joining the call. I show no further questions at this time. I would now like to turn the call over to Stephen Uden for final remarks. ...Thank you, Michelle. Before we close the call, let me take a few minutes to address our lead program, RLYB212, for the prevention of fatal and neonatal alloimmune thrombocytopenia. We expect to enter a phase two study for RRLYB212 in the second half of 2024. This will be a dose confirmation study focused on sentinel dosing with sequenced cohorts and the first RLYB212 study in pregnant women. Our FNAIT Natural History study continues to progress well, and we are pleased to have met our goal of screening 7,600 mothers by the end of 2023. We will provide our estimated screening for 2024 in the first quarter after the JP Morgan conference. Finally, we announced in the Q 3 of this year that regulatory interactions had commenced for RLYB212. We expect feedback from the European authorities sometime in the first half of 2024 and intend to provide an update when we're able to do so. As we close out our second full year since our IPO, I'm pleased with the progress the team has made advancing our two clinical programs. RLYB212, entering phase 2 in the second half of 2024, and RLYB116, which is ready to enter phase 2 clinical trials in generalized myasthenia gravis. RLYB212 is our lead program, and that is where we intend to focus the bulk of our efforts and resources. We recognize a laser-like focus on managing our cash runway as required, particularly in the current environment. Hence, we will seek to make selective investments in our portfolio, such as manufacturing work for RLYB116. In addition, we continue to advance our preclinical programs by investing with a staged approach. In parallel, we're also evaluating additional opportunities to move these programs forward through partnering and or other creative options. With that, we thank you for your time, and thank you for joining us for today's call. Have a nice day, and a happy holiday season. Thanks a lot.