Thank all of you for joining us today. We're happy to be here to give an update on Annexon Biosciences and all the good work that we're doing. We'll dive in. With no further ado, of course, we'll be making forward-looking statements, and we refer you to our materials that are filed online. Annexon is pioneering an approach in the complement space, targeting the classical pathway at C1Q. For those of you who are familiar with complement, the role of complement inhibition has been well-validated clinically and commercially, with a host of different approaches targeting primarily downstream complement targets, C3 and C5. We're building on those learnings by targeting upstream complement activity, C1Q, the initiator of the classical pathway, to provide more complete or robust protection against aberrant complement activity, both upstream and downstream. With that in mind, we are currently advancing five fit-for-purpose drug candidates to selectively inhibit complement in various compartments of the body, brain, and eye. We're really encouraged on what we've seen thus far. To date, we have demonstrated proof of concept in two different challenging indications, one in antibody-mediated autoimmune disease, which we'll talk about, as well as in a complement-mediated neurodegeneration disease. We're encouraged with the outlook for the company based on these the data we've produced thus far and what's coming down the pike. Indeed, we've got seven clinical trial readouts over the next two years, which we'll talk about this morning. Annexon has pulled together a portfolio approach to complement-mediated neurodegeneration targeting classical pathway across three therapeutic areas, autoimmune neurodegeneration and neurodegeneration in the eye or ophthalmology. We're targeting both rare and large patient populations, and we have the opportunity to treat millions of patients who are suffering from complement-mediated neurodegenerative diseases. Importantly, we are advancing five drug candidates in these therapeutic areas, and we're quite excited about the outlook on each of those. We'll talk about them as we go through the deck, but for now, I'll call out ANX005, our most advanced drug candidate, in effect, a pipeline and a product. This is in two neurodegenerative diseases as well as in two autoimmune diseases, and we do have proof of concept with this drug candidate. With that, we'll turn into ANX005 and talk about the indications for which we are pursuing, both in the autoimmune and neurodegenerative space. Just a bit on ANX005. It really is proving to be a very powerful inhibitor of the classical complement pathway, providing full inhibition of the pathway, both in the serum as well as in the CSF, so across the blood-brain barrier. It's a full-length monoclonal antibody for IV administration with a really high binding affinity for C1Q. In fact, roughly 10 pM. It's been well-tolerated in more than 170 patients to date, and it's shown early consistent improvement on clinical measures as well as biomarkers in the two studies that we've conducted thus far with the drug. Taking a look at the most recent data set that we released earlier this week in Huntington's disease, maybe a bit on the mechanism of action, and then we'll look at the data there. For those of you who are not familiar, what we are targeting with ANX005 in Huntington's disease is the preservation of functioning synapses. Synapses, of course, play a key role in overall brain health and function. When you lose functioning synapses, you have motor deficit and cognitive decline. We're using ANX005 to preserve the loss of functioning synapses, and here's how it works mechanistically. C1Q, our target, again, the initiator of the classical pathway, its normal role is to identify weak and non-functioning synapses in early development, tag these synapses, and prune them so that you have a healthy brain to go forward in life and conquer the world. That's the appropriate role of C1Q. This is a highly regulated process in the development stage, and it then shuts off. As part of the neurodegenerative disease process, however, C1Q recognizes and tags functioning synapses, triggering a neuroinflammatory process that results in damage to synapses and ultimately synaptic death. That, of course, leads to the loss of trophic support of neurons and results in both motor deficit as well as cognitive decline. By targeting C1Q and blocking it right where it binds to synapses, we are preventing the loss of functioning synapses and as a result, slowing or halting the neurodegenerative disease process. In terms of ANX005 and some of its capabilities, we are really quite pleased with the target engagement that's been demonstrated in both this study as well as in other studies. Here we see that C1 or ANX005 providing complete inhibition of C1Q in the serum for roughly four to 10 weeks post its last dose, so a durable effect, and you see that here on the left. It also provided full inhibition of C1Q in the CSF, so across the blood-brain barrier, which of course is very important as you treat neurodegenerative diseases. We're encouraged by the target engagement. We're encouraged by the durability of the target engagement. As a result, we think it's likely to. It's a great tool candidate to assess our capabilities from a clinical perspective. Now, not only does blocking ANX005 block C1Q, the initiator of the pathway, it also blocks downstream components of the complement system. This is very important as, again, there is neural inflammation and toxicity that happens downstream of C1Q. Here on this slide, we show C1Q inhibiting downstream complement activation C3A through the 24-month period of the study, as well as the three-month off-medication pre-treatment period. For an entire nine-month period of time, really, really important and really gives us great confidence in the outcomes that we've seen from a clinical perspective. Now, in addition to blocking downstream complement activity, ANX005 also shows strong evidence of reducing neural inflammation as part of the classical pathway. That's shown here by blocking C3 rather, which is produced by neurotoxic glial cells that are associated with inflammation and tissue damage in neurodegenerative diseases. Three things. We're blocking C1Q right at the start of the pathway. We're blocking the downstream components of the complement pathway, and we're reducing neural inflammation associated with the pathway. All of that has led to what we think are really unique and important clinical findings in this population. We're really pleased to see that in the full cohort of patients in Huntington's disease, we're able to achieve stabilization of the disease process through the entire nine-month study. That's six months on drug and three months off drug, and that's due to the protracted target engagement with ANX005. We're able to measure that in both the composite UHDRS as well as TFC, the two approvable endpoints in Europe and the U.S. This stabilization is against what would be expected natural decline based on 1,600 patient natural history data. You are familiar with neurodegeneration. Patients decline over time, their disease worsens. Typically to get a label, you need to show a slowing of the decline. Here we've shown a stabilization of the decline, so we're really encouraged with the opportunity for this program, as we move forward. Additionally, we went into the study with the hypothesis that patients who had excess complement activity may respond more quickly and more completely with our anti-C1q therapy, ANX005, and that's exactly what we saw in the study. As shown here in the green, these are patients who entered the study with excess baseline complement activity as measured by C4A, a component of the classical complement pathway. As you can see on both clinical measures, starting as early as week six, you see marked improvement and at all time points out to nine months on this study. Improvement on the key approvable neurodegenerative clinical measures early and sustained over the course of the study. We're also quite encouraged that this looks very different than the low C4 group, which is represented in the blue line, which more or less tracks with natural history data. We see this clear separation. It's based on a biological effect, and it's consistent, and it's really encouraging as we look to move forward with a precision medicine type of approach in the neurodegenerative space. We're also encouraged with ANX005's safety profile. This drug has now been dosed in more than 170 patients across multiple studies and been generally well-tolerated across the board. In this particular study of chronic dosing of ANX005, there were no changes in the safety profile from our interim results. The most common, sorry, adverse event seen in this study were initial dose infusion reactions that occurred upon the first dose of the drug prior to full saturation of C1Q. Once C1Q is fully saturated, those infusion reactions no longer persist. It was well-maintained, and there are no discontinuations associated with this infusion reaction. There are also no deaths or serious adverse events or serious infections observed in the study. There were two discontinuations in the study not associated with drug and three treatment-related discontinuations potentially related to drug. In all of those instances, the patients improved or their conditions resolved after we stopped dosing, which we were quite encouraged by. Importantly, we took some key learnings from this study. All of the patients who discontinued for an adverse event entered the study with high levels of ANA titers, which suggested that they had some underlying immunity that was unmasked with the dosing of the drug. No patients with normal ANA titers developed any SAEs as part of the study. With those learnings, we enhanced our screening for ANA autoantibody levels at the baseline in the study and over the course of the study, not only in this program but in three other programs in which we're dosing ANX005, and we've not seen these events since then. We're encouraged overall with the safety profile, and that leads us to kind of the key learnings from the study and our next steps. I think there are four really important takeaways. ANX005 does exactly what we want it to do in terms of full target engagement in both the brain and the body for a durable period of time through the off-treatment period into the off-treatment period, fully stabilized the disease progression in the full cohort for the entire nine months of the study, showed rapid clinical benefit in patients who entered the study with excess baseline complement activity, which matches on all fours with our mechanism of action. It was generally well-tolerated over the course of the study. One of the important things about Huntington's disease is that there is a very clear development and regulatory path. From a next steps perspective, we will be engaging the U.S. and E.U. regulators to assess the conduct of a confirming study in Huntington's disease, leveraging the learnings from the precision medicine approach we saw in patients with high baseline complement activity. Turning to ALS, this is the second neurodegenerative disease that we are pursuing with ANX005. You guys are undoubtedly familiar with ALS. It's a fatal neurodegenerative disease that involves loss of central and peripheral motor neurons caused by, among other things, the loss of functioning synapses. Here C1Q binds the synapses, triggers their removal by, again, initiating this neuroinflammatory process, and synaptic damage and ultimately synaptic loss. We're simply blocking that approach by targeting C1Q right at the start. We have a significant amount of evidence which gives us a great deal of confidence in our likelihood of success in this study. We have a robust preclinical package in ALS that includes protecting muscle function in a very aggressive SOD1 model of ALS. We've seen clinical outcomes in our two prior clinical studies that suggest a higher likelihood of success. In our Guillain-Barré study, which we will talk about, we saw early and rapid improvement both in motor or muscle activity as well as cognitive function. I just showed you, we've seen similar outcomes in the Huntington's disease study. We're operating this study very effectively, and we anticipate data in 2023. Turning to autoimmune conditions as it relates to ANX005, our lead indication there is Guillain-Barré syndrome. This is an acute antibody-mediated autoimmune disorder, and it really is a very severe disease. These patients here have paralysis in their lower and upper extremities. 25% of the patients actually go on a ventilator in the ICU, and 5% of Americans die from this disease annually. Very significant disease. Autoantibodies drive this disease, and C1Q is the key effector of the disease, and our approach is simply to block C1Q right at the start of the pathway and stop this entire process. As a result, we would expect a rapid, meaningful improvement on all of the key measures, and that's what we saw in our proof of concept, placebo-controlled study. There we saw improvement on muscle strength as measured by MRC and objective measurement one week into the study. We saw a statistical reduction of neurofilament light chain two to four weeks into the study. That's a measurement of death or damage to peripheral nerves. On the clinical readout, the GBS disability scale, the approvable measure, we saw improvement across the patients in all of the studies, and we saw a whopping effect in about a third of the patients with perhaps more aggressive disease versus zero in placebo. To put that into context, what that means is patients who entered the study in the ICU and were bed bound within eight weeks were able to walk unassisted after treatment with ANX005. We've been really quite encouraged by this program. We've met with the regulators, and we're now well underway into a phase II phase III, potentially pivotal study that'll read out in 2023. Also in the autoimmune space, we're targeting Warm Autoimmune Hemolytic Anemia. This is another antibody-mediated autoimmune disease, this time targeting red blood cells that results in anemia. Now, this disease has a fair amount of heterogeneity from a patient population perspective. We're using a precision medicine approach here, whereby we are screening and only enrolling patients who have excess classical complement activity as a key driver of their disease process. We know quite a bit about that. We know that excess complement activity is really the underpinning of what occurs in Cold Agglutinin Disease, a sister disease to Warm Autoimmune Hemolytic Anemia. We've identified patients in a feeder study to enroll into the phase II study that meet that profile. As a result of this precision medicine approach, we think this is a highly enriched, higher POS program, and we're quite excited by the outlook for that. We'll have initial data from this study in the second half of this year. With that, I'm gonna turn to our second drug candidate, ANX009, again, targeting C1Q in the classical pathway. This drug is a subcutaneous formulation targeting C1Q in the vascular space or in the blood. We like it specifically for a host of autoimmune conditions that involve hemolytic conditions or highly vascularized conditions. The drug has completed a healthy volunteer study where it was well tolerated and has demonstrated twice-weekly dosing with a subcutaneous format. The initial study in which we are exploring from a efficacy perspective is Lupus Nephritis, another antibody-mediated autoimmune disease. Their autoantibodies attack or amplify kidney inflammation and damage. Again, C1Q being the key effector of this autoantibody activity. Our role here is very much like what we're doing in the warm autoimmune hemolytic program and what we saw in the Huntington's disease program. That is, we are only targeting patients with excess complement activity where we have clarified that that is the key driver of the disease process. Importantly, very much like Huntington's disease, as well as in the warm autoimmune hemolytic program, this excess complement activity correlates with disease progression. We've enriched the study whereby we are, again, only targeting those patients. We're excited by the outlook on this program with ANX005. We'll release initial phase I-B proof of principle data in the second half of the year in this program as well. That leads us to ANX007. ANX007 is another Fab-formulated drug candidate for intravitreal administration of C1Q in the eye. It's localized inhibition of C1Q in the eye. There we've completed a phase I-B sham-controlled study demonstrating that it was well tolerated with full target engagement in the eye, and we are now progressing it in Geographic Atrophy. We really quite like this Geographic Atrophy indication. There's downstream validation of the role of complement in this particular disease, and we think we have the potential to have an enhanced outcome by targeting C1Q and the initiator of the disease process. We've produced a robust preclinical package demonstrating that. What I wanna point out for you today is really what we see with regard to C1Q and the classical pathway in all of the diseases in which we are pursuing. That is, C1Q is localized on the diseased tissue. It anchors the complement cascade, triggers its activation, and amplifies its destructive nature. Here, as it relates to Geographic Atrophy, you could see C1Q is ripe on photoreceptor cells, as shown in green in the top panel. C4, which is just downstream of C1Q, is also on the outer segments of photoreceptor cells, so both sides of the photoreceptor cells are coated with classical complement activity. As it relates to drusen, a hotspot for Geographic Atrophy, C1Q completely coats that as well. Only by blocking C1Q can you block all of the upstream and downstream aspects of the disease. We know that inflammation occurs upstream of C3 or C5, for example, in Geographic Atrophy. We're providing a more complete approach to this aberrant complement activity by blocking C1Q and activity downstream all the way through C3, C5, and C9. We're currently conducting a phase II proof of concept study there, a multi-site randomized study. We've completed enrollment early on that program, we anticipate data in the first half of 2023. Looking ahead at, you know, the balance of 2022 and 2023 and our priorities, just wanna highlight a couple of additional drug candidates that we're bringing forward into the clinic. One is ANX105. It is next generation to ANX005 with enhanced dosing properties. It is a full-length monoclonal antibody designed to inhibit C1Q in the body and the brain, and it's designed as such so that we anticipate it'll be less frequent dosing in both autoimmune and neurodegenerative conditions. What we think is kind of the coup de grâce in the complement space is ANX1502, first-in-kind small molecule in this space. We're really quite excited about this. We've been working on this program for many years. It's an oral administration, and it is targeting the peripheral C1Q activity, so we are targeting autoimmune indications. We are just advancing that into the clinic, and we're excited about the potential here to go after diseases for which there are other indications that have validated the role of complement but are IV types of presentations or indications where there are no, drugs currently approved based on this oral presentation and that we are blocking full upstream and downstream complement. We also continue to work on a host of mechanistically related diseases. I won't go into those, but suffice to say, in all of the disease areas that we're in, and in all of the indications for which we are pursuing, we actively characterize the role of the classical pathway as a key driver of the disease, and we look to block that activity right where it starts for enhanced efficacy outcomes. That brings me to the end. Really excited with the progress that we've developed to date and what looks, what's ahead for us. We have a really engaged, talented team of drug developers across the board, and we're excited by the catalysts that are coming over the next two years. We're funded into 2024 to achieve these catalysts. Having just released the Huntington's data earlier this week, we will next release the warm autoimmune hemolytic data and lupus nephritis data, and then a cadre of data over the course of 2023. With that, we thank you and happy to take any questions that you might have. Or none at all. All right. Thank you all. Appreciate your attention.