Well, good afternoon, good morning to those on the West Coast, and welcome to the next session of the Raymond James Human Health Innovation Conference. I'm Steve Seedhouse. Really, it's a pleasure for me to welcome the next participating company to this session, Annexon. Joining us and presenting on behalf of Annexon, of course, is CEO Doug Love. Very much looking forward to the presentation. Thanks so much for being at the conference this year. With that, Doug, I'll cede the floor and the microphone to you. Thank you so much, Steve. Real pleasure to be speaking with you this morning, and thank all of you for joining us this morning as well. We're excited to share an update on Annexon Biosciences. A lot of good things going on around the company. I will fast-forward through slide two, our forward-looking statements, but invite you to review those on our website at your leisure. Turning to slide three. As many of you know, Annexon is on a mission to unlock the next generation of complement therapies to treat devastating autoimmune and neurodegenerative diseases driven by excess classical complement activity. We're doing so by stopping C1q, the initiator of the classical pathway, to block downstream tissue damage and inflammation in a host of diseases across the body, the brain, and the eye. Importantly, we're leveraging a rigorous beachhead drug development strategy where we're utilizing established biomarkers to produce compelling data in our lead indications while rapidly advancing into beachhead or mechanistically related indications. Our aim is plain, and that is to build a leading complement company. We're really focused on four key pillars in which to do so. First and foremost, we're focused on marrying a strong scientific position with focused execution across the board. Indeed, since our successful IPO in 2020, we've initiated several phase II trials with expected readouts over the next two years, and we look forward to talking more about that as we progress in this discussion. Secondly, we've retained worldwide rights to our portfolio of complement therapeutics, which we think is quite important in driving valuation scarcity as one of very few phase II complement companies that is wholly owned. It's a robust portfolio indeed. We have three diverse drug candidates targeting C1q in the classical complement pathway, currently in the clinic, and we're advancing two next- generation drug candidates to IND later this year. One of which is an oral small molecule approach, which has the potential to be the game winner in the autoimmune space over time. Thirdly, we have de-risked this approach. We've established proof of concept with ANX005, our most advanced drug candidate in our most advanced autoimmune indication, Guillain-Barré Syndrome. That data set importantly showed full target engagement both in the periphery as well as in the CSF or across the blood-brain barrier, as well as meaningful impacts on clinical as well as biomarkers in the program. As a result, this data set is informing our advancement in a host of autoimmune and neurodegenerative diseases in a very informed, de-risked manner. Finally, all of this is being driven by a passionate, proven team to translate the opportunity. We've been able to assemble a group of really strong drug developers and operators across the board who are playing with their hearts and mind to deliver on this opportunity to create value for patients in severe need, as well as value for investors who have supported us on this journey. In terms of the pipeline, it's vast and deep, as I alluded to, with multiple drug candidates in the clinic. Starting with ANX005, this is a monoclonal antibody with IV infusion. There, we've completed a proof of concept study in Guillain-Barré Syndrome. On the basis of that data, we've converted ANX005 in effect into a pipeline and a product, having moved forward into an additional proof of concept study with warm autoimmune hemolytic anemia and two chronic neurodegenerative studies, Huntington's disease and ALS. We'll talk a bit more about those. Our second drug candidate is ANX007. This is an intravitreal infused, intravitreal administered, drug candidate, a Fab for ophthalmic indications. We've also completed a phase I-B placebo-controlled study there in progressive glaucoma subjects. We've embarked upon a phase II study in geographic atrophy that is underway. Our third, clinical stage drug candidate is ANX009. This is a subcutaneous formulation for which we just recently completed a healthy volunteer study. We look forward to advancing it into additional autoimmune indications. Finally, I referred to our next- generation drug candidates. There are two, ANX105, a monoclonal antibody, with enhanced dosing properties that we are advancing towards the clinic later this year, as well as ANX1502, the small molecule oral program that I referred to. We will update on later in the year. In terms of milestones, we have several as it relates to value creating opportunities through 2022. The first half of the year has been quite active from an execution perspective, where we've completed two studies, one a drug-drug interaction study in Guillain-Barré Syndrome, where we dosed ANX005 in combination with IVIG, the standard of care in GBS, although it's not approved here in the U.S. That data set demonstrated that the combined use of the therapies was safe and well-tolerated, as well as full target engagement, as anticipated in the study. We will be presenting that data set on Sunday, June 27th at the Peripheral Nerve Society conference, where we actually have two podium presentations there. Secondly, the first half of this year, we completed our phase I healthy volunteer study, the subcutaneous program in ANX009, which I alluded to. We will release that data set over the summer and also identify additional autoimmune indication or indications in which we will be progressing it. We anticipate data in that additional autoimmune indication in the back half of 2022. As it relates to the second half of 2021, our lead indications there are Huntington's disease and ALS. Our Huntington's disease program, we're happy to report out, has been fully enrolled more than a quarter ahead of schedule. Both the Huntington's disease and ALS programs are biomarker studies, whereby our primary aim is to demonstrate target engagement across the blood-brain barrier, as well as meaningful reduction of neurofilament light chain. We're quite encouraged by the promise of these programs, given that we were able to both engage the target fully across the blood-brain barrier and statistically reduce NfL in our Guillain-Barré proof of concept study, and we've also done so pre-clinically in the Huntington's disease program. We look forward to unveiling this data later in the second half of the year. As it relates to warm autoimmune hemolytic anemia, we are on schedule to produce that data, if not a bit ahead of schedule, in the first part of 2022. That study has gotten underway, and it really represents a precision medicine approach here at Annexon, whereby we are selectively screening and enrolling patients who demonstrate excess classical complement activity. A really important approach for the warm autoimmune hemolytic program, as well as other autoimmune indications in which we are assessing. I referred to ANX009 and the data set that we anticipate in a to-be-named autoimmune indication also in the second half of the year. Finally, in 2023, we anticipate really very important data sets with a potential pivotal data set in the Guillain-Barré Syndrome in 2023 and our phase II data with ANX007 in geographic atrophy in 2023. We have a nice set or cadre of clinical milestones coming down the pipe second part of this year through the balance of 2023. Finally, I'll just say that as we advance our beachhead approach to developing our portfolio, our lead indications here on slide seven are in red. With compelling data there, we anticipate swiftly moving into later-stage studies in each of these indications while advancing into mechanistically related indications across our three therapeutic areas: autoimmune, neurodegeneration of the brain, and neurodegeneration of the eye or ophthalmology. We have data in many of these indications on this slide, as well as many others. We're excited about the promise for this platform for both in the near term and for the longer term. That brings us to the key question: Why target C1q to treat complement-mediated diseases? Well, the short answer is that C1q, as the initiator of the classical complement pathway, is a key driver of disease processes both in autoimmune and neurodegenerative indications. Indeed, C1q directly binds to and accumulates on tissues in a range of the diseases in which we are pursuing. Some examples of this are here on the right, where we see C1q binding to antibodies on the neuromuscular junction, a hotspot for GBS in green here. Similarly, C1q binds to striatal synapses, the deep region in the brain where Huntington's disease emulates in the second panel. Finally, in geographic atrophy, C1q binds directly to photoreceptor receptors in the eye. By C1q binding directly to the tissue, it anchors complement activation and drives the disease processes in each of these instances. Only by blocking C1q can you block C1q and the downstream inflammation and tissue-damaging aspects of the disease processes in which we are pursuing. This point is further pulled out on the next slide here where we show the classical complement cascade and C1q as the initiator of the cascade. As I alluded to, it triggers activation of the entire cascade, which amplifies as the cascade gets going. By blocking C1q, we are in effect blocking a moving train before it gets started, which is really quite important in the indications in which we are pursuing, because upstream activity in the complement space involves immune cell recruitment and attack. That's both inflammation and tissue damage that can only be fully blocked by blocking C1q at the start of the pathway. Another advantage in targeting C1q at the start of the pathways is that we are solely blocking through the classical pathway, allowing the lectin and alternative pathways to remain intact. We think this is important to allow their normal immune function for chronic dosing in many of the indications in which we are pursuing. We anticipate both a potentially more complete efficacy profile as well as an improved safety profile with this approach. Finally, last slide before moving to some of the clinical programs. We are indeed leveraging established biomarkers to enhance our probability of clinical success. We are using biomarkers to select indications and patient selection. Important to all of our indications is identifying indications and patient populations where there is excess classical complement activity. An example of this is shown here on the left in lupus nephritis, where we've characterized a group of patients who have excess classical complement activity and would be the target for our clinical programs. We're also using biomarkers to set the optimal dose and the dosing regimen. This includes identifying biomarkers that allow us to show inhibition in the periphery or in the blood. An example here in our GBS proof of concept study shows ANX005 in red. As drug levels reach a certain threshold, activity of C1q is completely and rapidly shut down for a period of time until drug levels go back down, and then C1q activity rises back up. ANX005, in effect, is operating as an on/off switch in shutting down complement rapidly and completely. We have also assessed this approach in aqueous humor in the eye, as well as across the blood-brain barrier in the CSF. A very rigorous approach to setting dose and our dosing regimen. Finally, we're using biomarkers to assess our drug's impact on the disease processes themselves in our early clinical studies. Here on the right is an example, again, in our GBS program, our proof of concept study, where we show a 30% reduction in neurofilament light chain, a key measurement of neuronal damage upon dosing with ANX005. Again, we are using this approach in other programs such as warm autoimmune hemolytic anemia, Huntington's disease, and the like. With that, I will turn towards the clinic and profile our lead indications with each of our drug candidates, or at least ANX005 and ANX007. Here I'll talk about Guillain-Barré Syndrome and Huntington's disease. Guillain-Barré Syndrome is an acute antibody-mediated autoimmune disease, and it's really quite devastating. In fact, it is the number one cause of neuromuscular paralysis in the world. It is caused by autoantibodies attacking the peripheral nerves that trigger complement activity and downstream inflammation and tissue damage. Our approach simply is to shut off complement activity rapidly and completely to provide complete protection or more complete protection for this patient population. A quick summary of our proof of concept data in GBS is we did provide rapid and complete target engagement both in the periphery and the CSF. In the GBS patient population, which is important for both GBS as well as for other indications such as in the neurodegenerative space. We had early and statistical decline of serum NfL, key marker of neurodegeneration. Again, very important for GBS as well as neurodegenerative diseases such as Huntington's disease and ALS. Although not powered for statistical significance, we were quite pleased to see that on all of the key GBS clinical measures, including MRC and GBS Disability Scale, really strong positive trends across the board, which has encouraged us to advance this program further. We have received Fast Track and Orphan Drug Designation for this program as we continue to prosecute it. Slide 13 just highlights some of the data that we produced in the GBS program. On the left here is a panel showing full target engagement of C1q in the CSF, so across the blood-brain barrier at the higher doses, at 18 mg/ kg and higher. Importantly, those doses at 18 mg/ kg and higher translated to a statistical reduction of neurofilament light chain in the middle panel of roughly 30% by week four, which we were quite encouraged by. This had not been seen before in prior GBS studies, that, again, has given us reason to be excited about the opportunity here. Finally, on the right, as it relates to clinical measures, we saw roughly a third of the patients on the GBS disability scale show a whopping 3-point improvement on the scale. What that means in tangible form is that patients who have come into the hospital or the ICU who were bedbound or on ventilators after eight weeks were able to walk unassisted or run with treatment on ANX005 versus zero patients being able to do so in the placebo arm. An early data set for us that has encouraged us to advance this program forward into a potential pivotal program, our phase II/III GBS trial that is underway. This is a well-powered, placebo-controlled study of roughly 180 patients. The GBS Disability Scale is the primary endpoint, which we have confirmed with the FDA. Importantly, we are stratifying patients in this study based on their baseline muscle strength as well as from time from treatment onset to increase the likelihood of success in the study. We anticipate data in 2023. Shifting to the other side of the house in our approach in neurodegenerative disorders, we're really encouraged by the role of C1q and the support for it as a major driver of synaptic loss and neurodegeneration in a host of diseases. This approach was discovered by Annexon scientific co-founder, the late Ben Barres, the former chair of neurobiology at Stanford, who discovered the role of C1q in driving the removal of functioning synapses and ultimately neuronal death in a host of neurodegenerative diseases. Since Ben's discovery, a whole field has been spawned of research in this space. Some of the papers are depicted here on the right side of this slide that have come out just over the last three or four years in a range of indications, including Huntington's disease, FTD, geographic atrophy, and Alzheimer's. Each of these studies have been run in separate labs with separate models and have shown the consistent result that average C1q activity drives the loss of functioning synapses and neurodegeneration. By inhibiting C1q, one is able to protect functional synaptic activity and increasingly improvement on functional measures. A snapshot of some of that data here on slide 16 shows in three different models. The first on the left in a model of Alzheimer's, where A-beta was induced in the model, we're able to demonstrate by administering our antibody systemically, we were able to protect functioning synapses in the face of active A-beta activity. In the middle, as we've pushed forward, we are now seeing improvement on function and survival in many of these different models. The middle here is in frontotemporal dementia, where inhibiting C1q in this model it prevented obsessive behavior in the animals in FTD, which is quite important. Then finally, on the right, by administering our antibody systemically, animals are able to gain motor function in a model of SMA. Again, three very distinct models run out of three different labs showing very consistent results that inhibiting C1q protects functioning synapses and results in functional benefit in the different neurodegenerative indications in which we have studied. Digging a bit deeper into Huntington's disease, we're really quite excited by this opportunity. You are undoubtedly familiar with Huntington's disease, a progressive movement disorder which involves dementia and psychosis. C1q is heavily localized on synapses, and the patients in this population have high and sustained NfL levels, as have been reported in literature in multiple studies, in longitudinal studies. Our approach is simply targeting the loss of functioning synapses to protect neuronal health and against neurodegeneration. Some of the data that has us excited about this is on slide 18. The top row involves patient data, and the bottom row involves animal data. What we see here on the far left column is patients with Huntington's disease, as they progress, have increasingly higher levels of classical pathway activity. Beneath that, we show that by administering our antibody, ANX005, we're able to normalize complement activity in this population. In the middle panel, we also show in published papers that NfL increases with the stage of progression of Huntington's disease. Just beneath that, we show that by administration of ANX005, again, systemically, we're able to meaningfully reduce NfL in mouse models of Huntington's disease. This is indeed the first known data set we are aware of any therapeutic intervention reducing NfL in a model. Finally, on the right, as patients progress with disease, they lose functioning synapse in Huntington's disease. By again administering our antibody, ANX005, in a separate model, we are able to protect against the loss of functioning synapses. We're encouraged by this overall data set, and these are indeed the types of measures that we are reviewing in our phase II study shown here on slide 19. As I said, this study has completed enrollment. It involves a six-month treatment duration and a three-month off-treatment follow-up. The key measurements in this study are full target engagement across the blood-brain barrier in the CSF, as well as a meaningful reduction of NfL light chain. We anticipate having data in the second half of this year, which we are encouraged by. Finally, I'll turn to ANX007 and our approach in geographic atrophy, where we're tackling blindness in retinal diseases. In effect, neurodegeneration of the eye. Now, we quite like our differentiated approach. Indeed, C1q, by blocking C1q at the start of the pathway, we are blocking C1q's localized impact on the disease process throughout the eye. As depicted here, C1q and early complement components are deposited in multiple layers of the retina, including photoreceptor synapses shown in green on the left, photoreceptor cells here in the middle shown in red. That is C4, an activating component of the classical pathway. Again on the right, C1q shown here on drusen, a key hotspot for geographic atrophy. So C1q really serves as the potential initiator of the neurodegenerative disease process in geographic atrophy, and our approach is to stop this activity right at the start. By doing so, we've been able to demonstrate in models of retina damage that C1q protects against photoreceptor cells. We have an example of that here on the right in some of our preclinical data. I've alluded to what I think is some of the potential efficacy advantages of doing so. We have the potential to provide more complete protection by blocking not only C3, but C4 and C1q ahead of C3, which has the potential to provide more complete protection against inflammation and nerve damage or tissue damage. We also like by selectively blocking C1q in the classical pathway, we are allowing the normal immune function of the lectin alternative pathways to remain intact, including the vascular function of C3a and C5a, which in the literature has been associated with higher rates of CNV. In terms of our drug candidate, ANX007, as I noted previously, we studied it in a phase I-B placebo-controlled study in progressive glaucoma subjects, and we were quite pleased by the profile. There, we took the extra step of pulling aqueous humor out of patients' eyes to ensure that we could have full target engagement in this patient population, and we were able to demonstrate that at both our low and high doses, 2.5 mg and 5 mg, both out to a month. We did not pull aqueous humor beyond a month simply because patients wouldn't allow it. Based on our preclinical data, coupled with the data that we have here, we're encouraged that at 5 mg we have the potential to dose this patient population every other month. With that data set, we have advanced into a phase II study in geographic atrophy with two arms of dosing. We have 5 mg dosing once a month and 5 mg dosing every other month. This is a well-powered study, randomized, double masked of roughly 240 patients. The primary endpoint is fundus autofluorescence, an effective biomarker that we know quite a bit about and are encouraged by. We are, of course, leveraging the experience from related complement trials in the enrichment and conduct of this study. Enrollment is going quite well in this study, and we anticipate data in 2023 in this program. I've covered a lot, and I'll bring this to a close. We're really encouraged and excited by the opportunity here at Annexon over the next 24 months. By stopping complement activity at the start of the cascade, we think we have a potential for an improved next-generation complement approach with enhanced efficacy and safety benefits in the indications in which we are pursuing. We have several data readouts ongoing over the next 12- 24 months, each of which are important in their own right and will also unlock opportunities in mechanistically related diseases. We have a team, as I alluded to at the outset, that is playing with their hearts and minds and a great deal of experience in translating this potential game-changing opportunity in the complement space. With that, I will bring it to a close, Steve, and turn it back over to you. Thank you. Thanks so much, Doug, for the great presentation. Really terrific to have you at the conference here and looking forward to following the progress going forward. Thank you