Greetings, and welcome to Viridian Therapeutics' third quarter 2022 earnings call. At this time, all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. I would now like to turn the conference over to your host, John Jordan, Vice President of Investor Relations. Please go ahead. Thank you, Brock. Good morning, everyone, and welcome to the Viridian conference call to discuss the positive clinical data reported earlier today for VRDN-001 in patients with thyroid eye disease. Before we begin, I'd like to remind everyone that this conference call and webcast will contain forward-looking statements about the company. These statements are subject to risk and uncertainties that could cause actual results to differ. Please note that these forward-looking statements reflect our opinions only as of today. Except as required by law, we specifically disclaim any obligation to update or revise these forward-looking statements in light of new information or future events. Factors that could cause actual results or outcomes to differ materially from those expressed in or implied by such forward-looking statements are discussed in greater detail in our most recent filings on Form 10-K and 10-Q and other reports on file with the SEC. I'm joined today by Dr. Jonathan Violin, President and CEO, Dr. Barrett Katz, our Chief Medical Officer, and Kristian Humer, our Chief Financial Officer and Chief Business Officer. I would now like to turn the call over to Jonathan. Thanks, John, and good morning, everyone. Thanks for joining us. Over the last quarter, Viridian continued to execute on all pillars of our strategy designed to deliver the most complete portfolio of products for the treatment of thyroid eye disease across the world. TED, as you know, is currently a $2 billion market in just the United States and is expected to grow to over $4 billion globally, with just one product currently approved. We're advancing a portfolio of intravenous and subcutaneous programs towards this opportunity. For our IV VRDN-001 program, we're excited to share positive results from our second proof-of-concept cohort. Data we'll review today for 20 mg/kg confirm the profile we initially presented for 10 mg/kg a few months ago. The data compares favorably to TEPEZZA on each key endpoint, including proptosis response rate, overall response, change in clinical activity score or CAS, proportion of patients achieving a CAS of 0 or 1, and resolution of diplopia. VRDN-001 safety profile continues to look very promising. With all adverse events mild to moderate, no SAEs, no hearing impairment, no drug-related hyperglycemia, and no infusion reactions reported in the 20 mg /k g cohort. I'm pleased to share that the 3 mg/kg cohorts for VRDN-001 is now fully enrolled. In fact, over-enrolled due to patient demand, and we plan to present top-line data in early January 2023. I'm also excited to share that this month we initiated our first phase III trial, the THRIVE trial, in active TED. Sites are now active and are screening patients. In the THRIVE program, we're evaluating two regimens of VRDN-001, the standard eight infusion course and a shorter, patient-friendly 5-dose regimen, which would be 43% shorter than the eight infusion TEPEZZA regimen. Our confidence in the efficacy of the shorter 5-dose regimen is enhanced by new 12-week data from our 10 mg/kg cohort, showing that between week 6 and 12, with no further dosing, VRDN-001 activity is maintained. This supports our assessment that five infusions of VRDN-001 with a 12-week course will deliver the meaningful benefit patients need. In parallel to the VRDN-001 program, we also continue to make progress with our subcutaneous programs, where we aim to deliver a convenient, low-volume auto-injector that patients can self-administer at home, and we aim to be the first to market with this offering globally. Today, we reported the final data for VRDN-002 from our healthy volunteer study, confirming that VRDN-002 PK exceeded our expectations with a half-life of up to 43 days, about 4-fold better than TEPEZZA, VRDN-001, and all other IGF-1R antibodies in development. This is actually longer than the initially estimated 30- to 40-day half-life we reported a few months ago and positions 002 well for its upcoming subcutaneous proof-of-concept trial in TED patients. Both VRDN-002 and our half-life extended version of VRDN-001, called VRDN-003, are on track and advancing quickly. We're poised to bring the first self-administered TED therapy to patients in need of better options. We're very well funded to execute on these plans with cash to advance rapidly through multiple key milestones. We've ended the quarter with over $430 million in cash, providing a runway into the second half of 2025. Let's now discuss the data from the 20 mg/kg cohort in more detail. I'll hand the call over to Barrett Katz, Viridian's Chief Medical Officer. Thank you, John. This cohort, like the 10 mg/kg cohort for which we announced data in August, enrolled eight patients. Six randomized to receive two infusions of VRDN-001 three weeks apart. Two patients randomized to receive placebo. We measured safety, tolerability, and efficacy at baseline and at six weeks. Let's start with the baseline patient characteristics and epidemiology, which have been very similar across drug and placebo groups across our trial and that the TEPEZZA phase II and phase III trials with similar levels of baseline proptosis, CAS scores, and rates of diplopia. As you saw in our press release this morning, we are pleased to announce data from our 20 mg/kg cohort after the last patient's six-week visit, but last week, and the data further validates the efficacy of VRDN-001 and its rapid and clinically meaningful effects. I'd like to start with an overview of the data. We'll review the data from today's 20 mg/kg cohort, as well as the data for all patients treated with VRDN-001 in the 10 mg/kg And 20 mg/kg cohorts. I'm encouraged to see the reproducibility of our findings. VRDN-001 performs at least as well as TEPEZZA at the six-week time point with robust and consistent results on every single measure, nearly doubling the overall response rate of TEPEZZA. Ours 75%, 44% for TEPEZZA. We saw 75% proptosis responder rate defined as at least a 2 mm change from baseline proptosis versus but 56% for TEPEZZA. We saw a larger mean change of proptosis from baseline. We saw almost 3x the proportion of patients achieving a CAS of 0 or 1, a complete or near complete therapeutic effect, and double the mean change from baseline CAS 4.0 versus 2.1. Similar in both cohorts. We saw more than double the rate of patients with complete resolution of their diplopia. Ours 75%, TEPEZZA 36%. These results speak for themselves. VRDN-001 is a highly active drug and compares favorably with TEPEZZA, the only approved drug. Let me review the data in detail. One of the key things we were seeking to learn from the 20 mg/kg cohort is if the 10 mg/kg maximized activity as we expected from the PK and the PD data. As we expected, the results are highly consistent between both cohorts. When we look at the individual patient proptosis responses on the left panel, the magnitude of improvement is distributed similarly for the two doses. Majority of patients in each dose cohort had a proptosis response of at least 2 mm reduction from baseline. Further, we observed a similar trend for individual CAS responses shown in the middle panel. Every VRDN-001 treated patient had a CAS reduction of at least two points from baseline with the depth of the improvements, again, distributed similarly between the two doses. Likewise, the IGF-1 increases as in healthy volunteers, which you presented at the American Thyroid Association annual meeting last month. IGF-1 increases in TED patients treated with 10 mg and 20 mg of VRDN-001, and they're no different from each other. Taken together, the clinical activity data and the IGF-1 data confirm that VRDN-001 dose of 10 mg/kg achieved maximum clinical activity. This data confirms our choice of 10 mg/kg as our go-forward dose for our phase III THRIVE program, which is underway. Let's review the proptosis results. We've evaluated proptosis by both PI-administered Hertel exophthalmometry. We have also evaluated proptosis by a more objective orbital MRI, which is read centrally in a blinded fashion by two independent masked readers. This is important because while the Hertel is robust and reliable for studies with large sample sizes, it is a manually applied and read device prone to variability as seen in the literature. In a smaller study, such as our proof of concept cohorts, it's useful to have a second independent and confirmatory measurement of proptosis, such as MRI scans, which have been of course used to assess TED patients. Thus, we set out to implement a robust MRI analysis with a centrally read blinded review. For our study, MRI readers were trained and screened for test-retest reliability. Images were read independently by two masked readers who use imaging software to measure the distance between the lateral orbital rim and the anterior definition of the eyeball. As you can see on this slide, as of today, we have centrally read MRI data available for all four placebo patients. Nine of 12 drug-treated patients. The results are highly instructive and exciting. Here on the left, we show individual patient changes in proptosis as measured by MRI, and you can see all four placebo patients had little change. Actually, three of the four placebo patients had slight increases in proptosis from baseline. Now, if you look at the teal VRDN-001 bars, you can see the majority of VRDN-001 treated patients had proptosis reductions of 2 mm -6 mm. Each of these were also responders by exophthalmometry. We found that two placebo patients and one VRDN-001 patient were proptosis responders by exophthalmometry, but the response was not confirmed by MRI. Shown in the middle panel, in the four placebo patients, proptosis by centrally read MRI slightly worsened at week 6, an average increase of 0.3 mm. In the nine drug-treated patients for whom we have MRI data, proptosis improved on average by a reduction of 2.75 mm from baseline. This is a remarkable reduction in proptosis after just two doses of VRDN-001. As shown on the right panel, the proptosis changes observed by exophthalmometry when adjusted by excluding the responders who were not confirmed by MRI showed a 0.5 mm reduction in the placebo arm and a 2.5 mm reduction for VRDN-001, reinforcing the treatment benefit of VRDN-001 by two independent measures of proptosis, exophthalmometry and MRI. To put the VRDN-001 proptosis response in context, we can compare it to the mean change from baseline proptosis for TEPEZZA at week six in their phase II and III trials, which was 1.8 and 1.9 versus 2.04 mm for all VRDN-001 treated patients. Proptosis responder rate, defined as the percentage of patients who have at least a 2 mm change from baseline proptosis, is shown on the right at week six. 75% of patients who received VRDN-001 were proptosis responders, compared to 55% and 56% for TEPEZZA in their phase II and III study. Let's turn now to clinical activity score or CAS, which is a seven-point composite scale of assessments of patient experience, pain, redness, and swelling. We observed a 4.0-point improvement from baseline CAS after VRDN-001 treatment, far exceeding the placebo response. Given this rapid and sizable change in mean CAS, it's not surprising to observe so many subjects with near total reduction in inflammatory signs and symptoms defined as achieving a CAS of zero or one. 58% of VRDN-001 patients met this criterion. One placebo patient did. Indeed, two-thirds of drug-treated patients had a four-point or greater reduction in CAS. No placebo patient did. Comparing the effects of VRDN-001 on CAS with the data seen for TEPEZZA, we see that the four-point mean change we observed for VRDN-001 compares favorably to the effects reported for TEPEZZA. For our subjects treated with VRDN-001, the percent achieving complete or near complete therapeutic response is two and a half to threefold higher than that seen with TEPEZZA. We've seen dramatic improvements in both proptosis and CAS. What about the combination, the overall response analysis? This is a more stringent assessment of efficacy, as it includes proptosis improvement, but also includes both signs and symptoms of TED that are most bothersome to patients. An overall responder is defined as one who has at least a 2 mm reduction from baseline proptosis and at least a 2-point change in clinical activity score. As you can see, 75% of our subjects were overall responders. 9 of 12 patients, that is, showed a clinically meaningful improvement in proptosis, along with at least a 2-point reduction of CAS, while only 1 of the placebo subjects exhibited this combined change. Our overall responder rate compares favorably to data for phase II and phase III trials of TEPEZZA, which demonstrated overall responder rates of about 46% and 44% respectively. Finally, let's turn to diplopia, the double vision that is perhaps the most disruptive and distressing symptom for TED patients. Similar to the TEPEZZA trials, about two-thirds of patients had diplopia at baseline. For those that do, the most important results and the most stringent endpoint is complete resolution, the complete alleviation of that double vision. Following VRDN-001 treatment, 75% of patients with baseline diplopia experienced complete resolution. Six of eight patients with baseline diplopia demonstrated complete resolution of their double vision after about two infusions of VRDN-001. This is more than double the rate observed in either TEPEZZA phase II or phase III trial. We've just shown compelling improvement in proptosis, CAS, and diplopia, often with complete or near complete resolution of the signs and symptoms of TED. Now, let's review safety and tolerability. There were no reports of hearing loss, drug-related hyperglycemia, or infusion reactions in the 20 mg/kg cohort, and all AEs were mild or severe. Some of the known on-target IGF-I effects were observed as expected. We saw two cases of muscle spasm, both mild, did not require intervention. In fact, one was considered unrelated to drug by the masked investigator. When we look across the safety and tolerability profile of both cohorts, we're very pleased at the encouraging profile, and we look forward to collecting more safety data in our phase III program. I'll now turn the presentation over to John. Thank you, Barrett. As you've heard, for every relevant measure, and in particular for the more stringent measures, we consistently observe signals at least as strong as were reported for TEPEZZA, and in many cases, substantially higher. We now have a clear opportunity to differentiate VRDN-001 from TEPEZZA. We believe we can offer patients a shorter course of treatment to offer them faster symptom relief and possibly greater efficacy, as well as an attractive safety profile. Our phase III program is designed to harness these opportunities. The program consists of two pivotal efficacy studies, THRIVE in active TED and THRIVE-2 in chronic TED. They're expected to read out in the middle and end of 2024, respectively. In support of our global efforts, we recently completed a Type C meeting with the FDA and two scientific advice meetings in the EU, in which we discussed our phase III plans. Based on these interactions, our phase III program is designed to deliver all the data necessary to support successful BLA and MAA filings in the U.S. and E.U., respectively. As Barrett mentioned, we're pleased to share that we've initiated the THRIVE study in active TED patients with sites active and screening patients. The THRIVE and THRIVE-2 trials will evaluate identical dosing regimens, all with a 24-week primary endpoint with three study arms. First, an eight-infusion regimen matching the TEPEZZA regimen. Second, a shorter five-infusion regimen, which would allow patients to complete their treatment course in just three months, 43% faster than TEPEZZA. Finally, a placebo arm. To further improve the treatment regimen, we're using a shorter 30-minute infusion time instead of the 60-90 minutes required for TEPEZZA. One of the reasons we think this shorter course of treatment will work is that published data show little to no benefit from the last two infusions of TEPEZZA. The other reason is that the efficacy of IGF-I antagonists is surprisingly durable post-treatment. We now have our own data for VRDN-001 to support this durability from the 10 mg/kg cohort. We found that at 12 weeks, 9 weeks after the second and last infusion of VRDN-001, efficacy remained largely unchanged. Patients who responded to VRDN-001 at week 6 nearly all maintained that response. Four of five proptosis responders, four of five overall responders, four of five patients with CAS reduced to 0 or 1. For diplopia resolution, all three patients with complete resolution at week 6 maintained that absence of double vision. The fourth patient with diplopia, who had partially improved at week 6, continued to improve between week 6 and 12, achieving a complete diplopia response at that point. 100% of patients were free of double vision at week 12. When we look at mean change in proptosis shown on the slide, we observe the same thing, maintenance of efficacy between week 6 and week 12. This durable response further suggests that a short three-month course of treatment will provide durable efficacy to the 24-week endpoint and beyond. We're excited to have launched the VRDN-001 phase III program and look forward to updating you on our progress. I'd like to close by summarizing what we've learned and what's next. VRDN-001 continues to deliver significant improvements in the signs and symptoms of TED. In both cohorts of TED patients, we've observed rapid, profound improvements on all the key signs and symptoms of disease. Based on this data, we're extremely excited about our phase III program, which we initiated earlier this month. Separately, we've also initiated our proof of concept cohorts in chronic TED, with initial data expected in the first half of next year. We're on track to launch the THRIVE-2 phase III trial in chronic TED shortly thereafter, around mid-year next year. This puts us on track to read out both pivotal studies in 2024. We're also excited to share data in early January for our final acute TED proof-of-concept cohort, evaluating 3 mg/kg, which has completed enrollment. Data from this cohort will inform the feasibility of an every four-week subcutaneous dosing paradigm for our subq programs, VRDN-002 and VRDN-003. These next-generation subcutaneous auto-injector programs are also advancing rapidly. We now have final PK data for VRDN-002, establishing a half-life of up to 43 days, better than the 30 to 40-day half-life we estimated at the interim analysis in August. This means that VRDN-002 has about 4x the half-life of first generation antibodies like Teprotumumab. We're on track to have VRDN-002 subcutaneous proof-of-concept data in TED patients using every two-week and every four-week dosing in the second half of next year. VRDN-003, which is VRDN-001, but incorporating the same half-life extension technology as VRDN-002, is also advancing quickly to IND in the second quarter next year. Non-human primate data supports a half-life at least as good as VRDN-002. By the end of next year, we expect to have all the data we need to choose either VRDN-002 or VRDN-003 to advance to pivotal studies and plan to initiate phase three in early 2024. Together, our intravenous and subcutaneous programs would represent the most complete commercial offering for TED patients. We'll initially enter the IV market, projected to exceed $4 billion globally with VRDN-001, followed shortly thereafter by our subq auto-injector product. We believe a new entrant with a differentiated drug and a simpler dosing regimen will be highly competitive in a nascent market. Every year, 20,000-25,000 new active TED patients in the U.S. and 35,000-40,000 in the E.U. will choose a therapy, and we believe our products can be a choice for many of them. In summary, we're thrilled with the new data we presented today, confirming the profound treatment benefits of VRDN-001 in a growing number of TED patients. These results increase our confidence in our phase three program, and we're pleased to have just started our phase three THRIVE trial earlier this month. We're well-funded and moving rapidly to advance the most complete portfolio of TED assets toward a market projected to exceed $4 billion and in need of better therapies. Before we open the call for questions, Kristian will review our financials. Thank you, John, and good morning, everyone. I'd like to give a brief summary of our Q3 earnings. Cash, cash equivalents, and short-term investments were $431 million as of September 30, 2022, compared with $197 million as of December 31, 2021. We believe that our current cash equivalents and short-term investments, excluding our $75 million credit facility, will be sufficient to fund our operations into the second half of 2025. As of September 30, 2022, Viridian had approximately 56.2 million shares of common stock outstanding on an as converted basis, which included 40.2 million shares of common stock outstanding and an aggregate of approximately 16 million shares of common stock issuable upon the conversion of 188,000 and 51,000 shares of Series A and Series B preferred stock, respectively. Please refer to our earnings press release for a more detailed Q3 financial update. With that, we can open the call up for Q&A. Thank you. At this time, we'll be conducting a question and answer session. If you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment, please, while we pull for questions. Our first question today comes from Rami Katkhuda of LifeSci Capital. Please proceed with your question. Hey, guys. Congrats on the updates and thanks for taking my questions. A couple of quick ones for me. First, can you provide more color on the discrepancy in the percent of patients who achieve a CAS of 0 or 1 between the 10 mg/kg and 20 mg/kg cohorts? Sure. Thanks, Rami. Hi, as you saw, both cohorts had a percentage of patients achieving that CAS of 0 or 1 higher than either of the TEPEZZA studies. In both cohorts, that looked great. You're right. We had five of six patients in the first cohort and two of six in the second cohort. There is a difference there. Now, if you look at the baseline characteristics, you'll note that the baseline CAS in the 20 mg/kg cohort is a little higher than in the 10 mg/kg cohort or indeed the TEPEZZA cohort, the TEPEZZA phase II and phase III trials. We think that explains why we're seeing very similar magnitude of CAS improvements, 3.7 and 4.3 points in the two cohorts, showing up as what appears to be a bigger difference in that percentage of patients getting to a CAS of 0 or 1. In fact, if you look at the individual patient data, there are two patients of interest. One in the 20 mg/kg cohort had a 7-point score at baseline. Seven out of seven. Had a 5-point improvement, a huge change in CAS, but of course, that took the patient to a two. Large improvement didn't get to the CAS of 0 or 1. Likewise, the second patient started at six. Had a 4-point change, got to a score of 2. We're consistently seeing a tremendous improvement in clinical activity score. It's just a slight difference in the baseline characteristics across the two cohorts. Got it. Makes sense. Can you touch upon if we've seen variability in proptosis change with the Hertel exophthalmometer in other studies? Sure, yeah. The TEPEZZA studies, if you look at the New England Journal phase III supplements from 2020, you can look at the individual patient responses over time. If you look at the 12-week data, you can see that the average change with placebo is very close to zero, but the range is from +3 to -4.5. Now, that's fine when you've got a large sample size, and the study size was about 40 patients per arm, same as our phase III. When you have a smaller sample size, you're gonna be more sensitive to that noise. It's not surprising. This is a manual device applied to the patient's face by the investigator. The question is how do we deal with that in a smaller study? You wanna use an independent orthogonal and ideally more robust confirmatory measure. That's why we turn to MRI. As you heard, this is a centrally read process where two blinded reviewers in parallel measure the data, so it's extremely rigorous. Most of the time, the MRI confirmed the exophthalmometry results. But what do you do when it doesn't? Which do you believe, right? The manual exophthalmometry, which we know can be variable, or the more rigorous MRI? We, I think, sensibly view the MRI as more accurate. That confirmation step is what enabled us to clearly assess the performance of our drug in the small sample size. Going forward, in phase III, we're gonna have a similar sample size to the TEPEZZA studies, so that variability of the exophthalmometer will average out. It's a great endpoint for larger sample size. The MRI is useful in this smaller study. Of course, we'll include MRI measurements going forward. It's a great measure. May actually deliver some differentiating data for us. Makes a lot of sense. Congrats again, guys. Thank you. The next question is from Gavin Clark-Gartner of Evercore ISI. Please proceed with your question. Great. Thanks for taking the question. I had two. First, is there any scenario where you would consider adding a weekly dosing cohort for the subcutaneous TED proof of concept trial, which I guess can be viewed like an induct- Based on what we know of the performance of VRDN-001, the half-life we've seen for VRDN-002, we're really confident in the every other week dosing paradigm. Really the question is can we get to even less frequent than every other week? We'll learn about that with the upcoming 3 mg/kg cohort. If that shows positive data, then we'll know that lower doses, lower exposures are required, and hence we can spread out the dosing paradigm. Really we're looking at already in hand having every other week, and the question is can we get to every four weeks? Yeah. No, got it. One on the commercial side. Do you know roughly what percent of covered lives have site of care restrictions for TEPEZZA and require infusions to be given outside of the hospital outpatient setting? We actually don't have that information now. As you can imagine, we're ramping up a large amount of commercial work, given the very strong data we reported in August and now again today. You'll be hearing a lot more from us on the commercial front going forward. Sounds great. Thanks. The next question is from Thomas Smith of SVB Securities. Please proceed with your question. Hey, guys. Good morning. Congrats on the data, and thanks for taking our questions. I guess just first on the 20 mg/kg data for clarification. I know it's small number of patients, but can you clarify what the mean proptosis reduction was in the placebo patients with this updated dataset? The mean proptosis when we exclude the patients that we couldn't confirm by MRI, the mean change was an improvement of a half a millimeter, very consistent with what was seen in the TEPEZZA study. Thinking forward here to the 3 mg/kg data set, can you talk about, I guess, your expectations for efficacy there? Are you expecting roughly equivalent efficacy based on what you've seen on the PD effect in healthy volunteers, or should we be expecting a moderation in efficacy with the lower dosing? Yeah. The pharmacodynamic measurements, the increases in plasma IGF-I that we reported for healthy volunteers in August does suggest that there's a full receptor engagement systemically. While we can't draw a direct line between systemic target engagement and efficacy, I'd say it's a strong hypothesis that we will see robust efficacy at 3 mg/kg. The question is what does it mean for us, right? We think the 10 mg/kg dose for VRDN-001 is the right dose to carry forward in phase III, best balances perspective, potential benefit and risk, so that's why we're moving that forward in phase III. What the 3 mg/kg data will do, again, is really inform what we think we'll be able to achieve with a subcutaneous product. Is it going to be every two weeks, which would be, commercially compelling, or even better, once a month or maybe even longer? Okay, got it. Then just maybe, lastly, I know when you had the 10 mg/kg top-line data, you were able to give a little bit of color on the, safety and tolerability you were seeing in the 20 mg cohort. I guess, what can you say about the ongoing 3 mg/kg cohort at this point? Any color on safety or tolerability? We haven't seen any data from that cohort, safety or otherwise. The only thing I can say is that there have been no SAEs reported. That's all we know so far. Okay. Got it. Thanks, guys. Appreciate you taking the questions and congrats on the data. Thanks, Tom. The next question is from Laura Chico of Wedbush Securities. Please proceed with your question. Hey, good morning, guys. Thanks for taking the questions. I guess I had one on safety and then one related to the phase III study. First, could you offer any additional color on the hyperglycemia event in the 20 mg/kg cohort? And just, you know, was this exacerbated in response to treatment? Maybe how high did glucose levels increase? Apologies if I missed that earlier. Sure. I'll ask Barrett to comment on that, please. Thanks, Laura. Because we wanted to study the same population that Horizon studied, we allowed for the enrollment of patients with known diabetes and known glucose intolerance. In this cohort, we actually enrolled a patient with known diabetes and let's just say less than elegant diabetes management. The patient came in with known hyperglycemia on an oral agent for their control. Step back for a minute and say, what's the hallmark of diabetes? The hallmark of diabetes is glycemic variability. This patient, during their time with us, showed some variability of their glucose measures. The investigator who is masked was following and taking care of this patient and felt that variability was entirely consistent with the underlying disease of the diabetes and the expected variability of glucose levels, which, as you know, are influenced by what the patient eats, when they eat it, times between meals. The PI made the decision that any change in this variability and bouncing around of glucose in this known diabetic was in fact due to the disease itself and not drug-related. That's super helpful. Thank you, Barrett. Maybe one follow-up question then. I think, Jonathan, you mentioned you completed the Type C meeting with FDA around the phase III design. I just wanted to confirm then no comparisons to active drug would be required. Then related to the current THRIVE design, where you've got the five-cycle and the eight-cycle course arms, would you anticipate the potential for hearing impairment might diminish over a shorter infusion cycle? Thanks, guys. Sure. Thanks, Laura. Correct, the dosing, the arms of the study that I described are what we're moving forward with, and of course, were discussed with the agency. Two active arms, one placebo arm. With respect to the potential of this shorter course of treatment, the answer is yes. One of the reasons we're excited about this is not just that it's more convenient for patients and prescribers. There's potential that by limiting the duration of exposure to drug, you might limit the incidence of adverse events. Now we don't know that. The adverse event profile that we've seen so far is extremely encouraging, and we're excited to collect more safety data as we move into phase III. Thanks very much, guys. The next question is from Kalpit Patel of B. Riley Securities. Please proceed with your question. Yes. Hey, good morning. Thanks for taking the questions. On slide seven, I guess, John, do you have any thoughts on why the IGF-I increases were lower for the 20 mg/kg versus the 10? Also, I think, there's five patients worth of data instead of six. Was there anything about that one patient, that wasn't reported? Yeah. Great. Yep. We have data from five patients because the IGF-I data just takes a little while to come in. As you heard, the last patient's six-week visit was just last week, so we just don't have the IGF-I data for that last patient yet. In terms of the levels of IGF-I across the two cohorts, honestly, we think they're quite similar. You're right, numerically, they're a little lower. We've seen that before. Mechanistically, there's no basis for thinking they're anything different between these two cohorts. Once you get to full receptor occupancy, you should be maximizing the effects of the drug. That's why we think the conservative approach, the right way to look at this is to consider these two doses equivalent, and that's why we're discussing the data for all 12 patients. I think you guided to choose either VRDN-002 or VRDN-003 for phase III development by early 2024. You know, based on your timelines, I don't think you'll have any patient data for VRDN-003 by then. I guess, you know, what gives you the confidence for selecting, you know, either of these candidates by early 2024? Yeah. Thank you. Keep in mind that VRDN-003 is the exact same antibody as VRDN-001, except for the half-life extension technology. The way these antibodies work, the variable domain drives target engagement, and then these half-life extending modifications are in the Fc domain, the other end of the antibody, and they do not affect the antigen binding function of the antibody. We've proven that with VRDN-001 and VRDN-003. They bind the same affinity, drive the same receptor antagonism. What that means is that VRDN-003 works just like VRDN-001, just with much better PK in non-human primates, and again, we're expecting similar PK to VRDN-002 in humans. The cool thing about that is that we can take the exposure response data from VRDN-001 and use that for VRDN-003. When we have PK from healthy volunteers, we'll have everything we need to know based on the VRDN-001 exposure response to pick doses for phase III. That's why this bake off between VRDN-002 and VRDN-003 works so well. We'll have VRDN-002 proof of concept. We'll have its own PK/PD, and then in parallel, the healthy volunteer data for VRDN-003, which can leverage the VRDN-001 patient data, set us up to make a very robust choice of which molecule moves forward into phase III, and we'll be phase III-ready and ready to kick off pivotal studies early 2024. Okay, very helpful. Thanks for taking the question. The next question is from Jason Butler of JMP Securities. Please proceed with your question. Hi. Thanks for taking the questions, and let me add my congratulations on the data as well. I guess first, if you get to greater than every two weeks, i.e., every four weeks with VRDN-001, can you just talk about the overall, you know, product portfolio, thinking about VRDN-002 and VRDN-003, and how commercially they would all fit together? Sure. We're moving VRDN-001 forward as the IV product offering. When we talk about every two week dosing, that's what we know we have in hand already for VRDN-002 and VRDN-003. VRDN-001 might also work as a subcu. We'll learn about that with the 3 mg/kg cohort. But honestly, we want to bring the best product forward, and the half-life extension is working so well that our subcu offering will be either VRDN-002 or VRDN-003. Again, as we just talked about, we'll pick at the end of next year which molecule moves forward. That the portfolio we'd bring forward is VRDN-001 IV and then either VRDN-002 or VRDN-003 sub cu. and VRDN-003 are the only half-life extended antibodies in development and really seem to deliver an optimal profile for an IGF-1R antibody, we think those, either one of those will be a best in class that's very hard to beat. Great. I think the answer is largely mechanistic, but can you talk about now you have a larger sample size, the non-responders and if there's anything in, you know, about the baseline characteristics of those patients or anything that could help you know, target patients in the future? Honestly, the results are so consistent. When we have a patient who doesn't reach responder status for proptosis, they're usually showing substantial changes in CAS, or diplopia. We haven't identified a true non-responder population. This drug works very well across the population. It's one of the things we like about it. Great. Thanks for taking the questions. Thanks, Jason. There are no additional questions at this time. I would like to turn the call back to Jonathan Violin for closing remarks. Thank you. I'd like to thank the investigators, patients, and Viridian employees who have contributed to our programs. Our data provides an incredibly strong foundation to advance our programs rapidly and with purpose to create valuable new therapeutics for thyroid eye disease. With that, we'll close the call. Thanks for joining us. This concludes today's conference. You may disconnect your lines at this time.