Let me know when you're ready. Go on over. We can start, I think, and people can come in. It's okay. I don't want to keep everyone too long. I know you're all having your lunch, so. All right. Good? All right. Thanks so much for joining us today at presenting on Q32 Bio, where we're hoping to really build the future of immune therapeutics. We're going to focus a bit of the presentation today on our lead clinical asset, bempikibart, and its data in alopecia areata, which is our proof of concept indication. We're really excited about what we're seeing there, excited to walk you through it now, where we're showing durable responses out now seven months post last dose in the program. This is actually on target for what we would expect for this asset, which is a bifunctional antibody that addresses both TSLP and IL-7. We believe we have the potential to transform the AA market, and we'll walk you through the rationale for that. Our Phase 2a has been completed, and we're now moving with an adaptive design to a Part B of that. We have added a Part B on. We'll explain that Part B and what we'll be doing there, as well as an open -label extension, which is a result of patient reconsents and demand getting back into the trial out of Part A. We believe there's broad opportunity to go into additional indications, both Th1 and Th2 mediated diseases. The biomarker data here that we brought in across the Phase 2 program really supports that expansion. We'll speak a little bit about the novel tissue targeted complement platform. Still love this program, but ultimately have made a decision to focus our capital on bempikibart and AA for the time being. We'll be looking for strategic alternatives for that entire set. That includes ADX097, our lead clinical asset, which is Phase 2 ready, as well as the pipeline and our DC candidate, ADX096. Near-term value creation will be around both the open -label extension and Part B, the adaptive portion we've added to the SIGNAL program. We're recruiting into that in the first half of this year, and we anticipate data in the first half of next year. Pipeline shown here, you can see on the top with bempikibart firmly in Phase 2. We expect subsequent to Part B in the OLE, we will move forward into pivotal clinical trials for alopecia areata, and there's opportunity to open additional indications with proper capital. The complement inhibitor program, again, Phase 2 ready for ADX097, and then our additional platform assets, certainly in the discovery and preclinical stage, but a great opportunity, I think, from a partnership standpoint. Focusing now on bempikibart as we go through, this is an IL-7 receptor alpha antagonist antibody blocking both IL-7 and TSLP signaling. The data from Phase 1 has shown a number of favorable components about the asset. First of all, PK and RO spot on where we expected it to be, and PD markers now are showing both target engagement as well as activity in alopecia areata. We've shown minimal ADA in the data set, so we're encouraged by that. You can see these biomarkers on the top: TARC, IgE, eosinophils, as well as CD3 T-cells, all showing responsive rates here as what we would have expected in the program and confirming the mechanism of action is engaging as appropriate for both TSLP and IL-7. A well-tolerated safety profile is seen here, as you would anticipate for a biologic across 130 patients to date, and this proof of concept has been established, as I mentioned, in our AA program with durable hair growth. Before I get into the data sets for that, let me just walk you through what Part A of that trial looks like. This was 24 weeks of dosing for patients. We then followed patients for 12 weeks to see if we could see durability of response as we were predicting it at the time, and we dosed a series of patients in both drug and placebo. Representative case shown here for a patient with severe disease. You can see left to right on the images hair growth starting at baseline and at week 24, last date of dosing for this patient. This was every two-week dosing across that period at 200 mg. Week 36, hair maintenance, encouraging what we were expecting to see and further maintenance now out to week 42 for this patient. I'll come back to why we got that in a 36-week study momentarily, but you can see that continued hair growth. Hard to see if it's maintenance or continued hair growth. The physician treating the patient did show SALT reductions from 10 to 2 during that period of time. Therefore, the patient starting around 46% of their hair coverage and ending at 98% of their hair coverage. Encouraging findings across the study and notable that post-dosing you're seeing that maintenance now out past week 42. Another notable point about this patient, this patient had a four-and-a-half-year episode. Long-duration disease expected to be harder to treat in these populations and encouraging that we're seeing a response here so quickly in the patient. Then again, maintenance out four-and-a-half months after last dose. This is representative of what we saw across the study. You can see in the data sets here both the per protocol and the modified intent to treat, both showing separation from placebo at the 24-week mark. That's the vertical line there for last dose. We're showing separation there encouragingly at week 24. What gets more exciting for us, at least, is this week 36 and beyond where we're seeing that response both deepen and maintain out for a series of these patients in both the per protocol and modified intent to treat. We would argue in alopecia areata, per protocol is the more meaningful population to look at. This is a disease known that you need to get long-duration treatment in order to show response in the hair follicle. Ultimately, we're showing both here just to show you we're seeing it both in the MITT and the per protocol. This is where things got pretty exciting and led us to really double down in alopecia areata. The top patient here inbound to the company, subsequent to completing the study. We received a note from this patient saying, "Listen, I was in your trial. I showed very modest hair growth at week 36 at the end of study, about 10% hair growth at that time. Since that time, I've had substantial hair regrowth, and I'd like to get back on the drug. Notable that this is coming from a patient who has eligibility and access to JAK inhibitors but is choosing not to go on those and wants to get back onto our program. We first sought out to reconsent the patient and confirm this finding, which you can see we did at week 57 now with almost a full head of hair. They're 92% of scalp coverage at this point based on the PI's assessment. This patient started with less than 2% of her hair. We then have now reconsented a series of other patients as a result of this finding. We reached out to other centers and said, "Do you have patients showing a similar occurrence?" We do, in fact, have a series of those patients. We now expect those patients to recruit into the open -label extension that we've added on to Part A. You can see an example case down below. This is a severe patient with a duration of nine months. Baseline, you can see that whole left side of the head missing hair. Again, a little bit of growth at week 24 when we completed dosing, more growth at week 36, but again, not substantial, much more substantial as we get out now past the year mark. Again, both of these cases showing the substantial hair growth seven months after last treatment. This is paradigm shifting in alopecia areata, and it's a key reason why we've decided to focus all of our resources moving forward on the alopecia indication for the time being. Is it a fluke? Would you expect to see this? Absolutely, we would expect to see this. This was predicted in the data sets that exist in the literature over the course of a decade or so. Ultimately, we designed the clinical program for SIGNAL specifically looking for this phenomenon. Of course, we were only looking in the first 12 weeks. We weren't expecting to look out to seven months and see it there, but we designed the study for three months of follow-ups for these patients after dosings for exactly this reason. This is not unexpected that we're seeing this. Some great examples of the preclinical evidence for this are shown here with long-term durable effects following this antibody treatment. You can see type 1 diabetes here, three weeks of dosing and 14 weeks of maintenance of the response. You're seeing it also in collagen-induced arthritis here with a separation that goes out 108 days after about 35 days of dosing. In the tuberculin challenge model, this is a pretty notable one. A single dose, right? Single dose of IL-7 alpha, markedly reducing the tuberculin-induced DTH response in baboons for a year. Single dose. This is an extremely powerful mechanism. We now have the first clinical evidence in patients of this type of a remittance effect in patients. We are really excited about what we're seeing there. We believe the mechanism of this is a rebalancing effect of the T effector memory, and we're really excited about what we can do here for patients with alopecia areata and beyond. The maturing SIGNAL-AA data package is really supporting a very differentiated profile in AA. While we think we're already aligned in the range of what you would see for low-dose JAK inhibitors, ultimately this is a complete shift from that paradigm. If you know JAKs, you know that these have black box warnings. These are challenging for patients. Penetration has been limited. The second you come off of them, within weeks, your hair starts to fall out. What we're seeing here is a very different profile that's emerging. We're seeing durable hair regrowth, which is preserved here in the study showing the potential for this transformative paradigm. The mean SALT scores continue to improve from week 24 to 36 and now beyond out to seven months past last dose. The response is being observed in hard-to-treat populations. We're seeing it in both severe and very severe patients, and we're seeing this in long duration of episode out to four and a half years in the one example that I provided you. The safety profile here is supporting a competitive positioning with the ability to drive more patients to treatment. Ultimately, this is the one JAK market in autoimmune where there is not a biologic competitor. Where you do see JAKs and biologics, AD, RA, biologics take the frontline position every single time. You have an upside-down market where alopecia areata is wide open for biologic entry and for the ability of that biologic entry to take a frontline position. We believe we will be the lead in that process. With the remission effect we're seeing, we'll have a completely different approach for these patients long-term. What are we going to do next? We've decided to do an adaptive approach, taking our SIGNAL-AA program and adding a Part B to this study. We're utilizing the majority of the centers that were in Part A for expediency. Ultimately, we'll have 20 evaluable patients coming out of this. We will recruit more, but we're assuming we'll have some dropout rates. We'll have 20 evaluable patients in this data set. We will look to compare these patients with a different regimen to what we saw in Part A. What are we going to do differently? We're going to add a loading dose in order to get to steady state quicker and hopefully see the response sooner. We're going to dose longer. We're going to dose for 36 weeks, looking to see if we can deepen that effect over that period of time. Subsequent to that, we may look at maintenance dosing for these patients, call it monthly, call it quarterly. We'll look at that as we get closer and once we assess the pharmacokinetics coming out of this new dosing regimen. In addition, we've added on an open -label extension based on patient demand to allow patients back in from Part A to continue their dosing. We'll put them back on a regimen of dosing every two weeks for a period of time and then follow those patients through the trial as well. Let's talk a little bit about the population. I touched on this earlier, but important to note, there's 700,000 patients living with alopecia areata in the U.S. alone. These patients are typically diagnosed in their 40s. This is a young, relatively healthy population. Their only critical option right now is JAK inhibitors. JAK inhibitors come with black box warnings for cardiotox and cancer risk, right? You are talking about patients who are relatively healthy having to stay on JAKs indefinitely for decades if they want to keep their hair. That is not a good trade-off for patients, and I think that is being reflected as we think of the penetration in the market on the next slide, right? 30,000 patients roughly JAK-treated based on claims data out of the eligible 300,000 on those labels, right? You are talking about 700,000 overall with only 30,000 being treated with the JAKs. The market is believed to be roughly approaching $1 billion with the expectation of it to get up to $2.6 billion by 2030. Substantial market and again, no biologic entry at this point. We think we have a huge opportunity with the safety profile we're seeing amassed across 130 subjects to date. We believe we have the biologic profile that physicians and patients are waiting for. You can see on the next trial a Guidepoint interview with a KOL. There's another one out there unrelated to the study just looking at our data sets as they emerge. The feedback from investigators, both independent and associated with the company, are consistent. Docs and patients are looking for safer alternatives to JAKs, and they're looking for opportunities for subcutaneous dosing. That being said, remittive effect is obviously of high priority to these patients. If there's an opportunity to have something that's going to have a long-tail response that's going to be of high interest, an infrequent dosing will be of high value. Beyond AA, right, with this data in hand, we've got a lot of opportunity. The biomarker data here supporting the opportunity to go to Th1 and Th2-driven diseases. Obviously, the data coming out of the biomarker supporting that TSLP side, the opportunities to go to asthma, COPD certainly on the table. On the other side, certainly alopecia will be our key indication, but ulcerative colitis with the OSE data certainly something we could contemplate in the future. You're seeing another IL-7 alpha there. The emerging data there encouraging. We continue to believe pharmacologically we have the better asset here, and we can certainly speak more to that. Ultimately, there's celiac, vitiligo, MS, RA, many, many indications we could go to over time. That being said, we're going to focus on AA for the time being with our current capital, continue to drive more data and better safety profile data so that we can move into those indications when the time is right. Spend a few minutes on our tissue-targeted complement therapeutic program, and then I'll come to conclusion and take questions. This approach, this is actually originally what the company was founded around. We still have a lot of love for our complement program. We think there's a great opportunity here to really change what the unmet needs are for patients and really address the limited activity that's being seen, the high doses, frequent administration of therapy that is required with the complement inhibitors that are out there, and the infection risk in some cases with black box warnings for Neisseria infections. The opportunity here really is to enhance activity with a tissue-directed approach, reduce the treatment burden, and improve risk-benefit profiles. We do this through a fusion protein, a bivalent fusion protein that goes directly to the tissue surface and then catalytically degrades the convertases at that location. The ADX097 lead asset is doing this on the alternative pathway. You can see though by doing so, we're taking command of the amplification loop and ultimately shutting down all three pathways through that methodology. Our Phase 1 data for this already supports that we've confirmed the planned Phase 2 dose, the route, and the schedule. We've evaluated and shown proximal proof of mechanism of the mechanism engagement. We've characterized the safety profile, and we've characterized the immunogenicity risk. Collectively believe this modality has high value, and both ADX097, ADX096, and the platform nanobodies have great potential beyond the ADX097 program in vascular, ophthalmology, renal, and dermatological indications. We are currently seeking strategic alternatives for this, looking for partnership or sale for that program to bring non-dilutive capital into the company. Quick summary on the financials, and then I'll stop for questions. Ultimately, we ended Q3 with $89 million. We will report out in another week for year-end financials, so you can wait for that. We will give you more information then. Ultimately, next year will be our readout for Part B and the open -label extension. That being said, both are open label. We will look for opportunities if they present themselves to present that data early. We expect to start recruiting here in the very near term and excited to get these underway so that we can move forward on this asset we believe has huge potential to transform the paradigm for AA. I'll pause there and take questions.