Good morning, everyone. Thank you for joining H.C. Wainwright's fifth annual Neuro Perspectives Virtual Conference. My name is Max Maher, and I'm an analyst on the corporate access team. H.C. Wainwright is a full-service investment bank, dedicated to providing corporate finance, strategic advisory, and related services to public and private companies across multiple sectors and regions. We have a total of 24 publishing senior analysts and over 650 companies covered across all sectors. If you'd like more information, please go check us out on hcwco.com. From a logistics standpoint, please make sure to reference your virtual conference online portal that provides your individual links to your meetings and all presentations. With that said, have a productive and enjoyable day, and I'd like to introduce Marc Grasso, CFO of Alector, Inc. Well, thank you, Max, and we appreciate the opportunity to present today at the H.C. Wainwright Neuro Perspectives Conference. I'm gonna give a brief overview of Alector today. I encourage you to review our forward-looking statements and our SEC filings for more information. Alector is founded on a bold vision, where we're looking to address major neurodegenerative diseases in a fundamental way, harnessing the power of our own immune system. And we're doing this in the context of a number of late-stage programs. I'll take you through a few of those today, including our AL002 program, which will have a phase II data readout later this year, as well as our progranulin programs. And I'll touch upon our earlier research platform and proprietary programs as well. Alector has a 10-year history, as this is a very experienced team with global pharma partnerships, including GSK and AbbVie. We're in a strong financial position through major clinical catalysts in the coming years. The intersection of what we're doing is between immunology, our genetics, and neuroscience. One of the founding principles of the company is restoring our dysfunctional or damaged immune cells in the brain, called the microglia, to a healthy, disease-fighting state and a more functional state in the setting of neurodegenerative disease. Shown here is our portfolio. On the top, you can see our late-stage progranulin programs. This includes latozinemab, which is in a phase III pivotal study in the setting of frontotemporal dementia for patients with a GRN mutation. This is a severe unmet need. We'll take you through some of the phase II data we have for this program today. And this is part of a partnership with GSK, and I'll take you through some of the details. And we retain 50/50 profit share in the U.S., where we take the lead on commercial activities in the setting of the orphan indications. And there's also significant tiered double-digit royalties outside the U.S.. Our second progranulin elevating program is AL101. This is currently in a phase II study that we commenced earlier this year together with GSK, and I'll touch on that program today. I mentioned our AL002 phase II program. This is completing a phase II study. This is a TREM2 program, which is partnered in an option deal with AbbVie, and I'll take you through some of the details around this, which is very exciting as we have data coming later this year, as I mentioned. And then you can also see here a number of our disclosed and undisclosed proprietary research programs, and these are advancing towards the clinic and have significant potential in severe unmet needs, including Parkinson's disease, Alzheimer's disease, and other settings. From a cash perspective, at the end of the first quarter, we had $562 million in cash, and this is runway through 2026, and it's through the phase III data that we anticipate on latozinemab towards the end of 2025. We have the anticipated phase II data at the end of this year for TREM2, and we also will potentially have interim data on AL101 on the AD phase II in the timeframe for runway, as well as advancement of the earlier preclinical programs and our blood-brain barrier technology platform. So touching first on TREM2, this is a molecule, it's an antibody, and it's increasing TREM2 signaling. And this is again in the context of neurodegenerative disease in Alzheimer's, whereas we pass through reproductive age, what's found is that the activity, the healthy functioning activity of our microglia tends to wane. And what we're seeking to do with this molecule is restore that activity in a significant way. As noted, this is in a phase II study. We've completed enrollment. We completed enrollment at the end of last year. We're expecting data in the fourth quarter of this year. In addition, we have a long-term extension study for the patients who have completed this study. We've had over 90% of eligible participants who've completed the treatment period extend to the extension study. I should note this is the most advanced TREM2 activating program in clinical development for Alzheimer's disease, and we're modulating multiple biomarkers of microglial activity. So how does this work? So a TREM2 is a damage-sensing receptor on the surface of the immune cell in the brain, the microglia. And this cell type, the microglia, is constantly surveying the neuronal environment, looking for things like m isfolded proteins such as Aβ, other evidence of damage, whether that's myelin damage, cellular debris, et cetera. And when it senses this damage, it triggers a signaling cascade which regulates microglial survival, proliferation, migration, and function in the setting of disease. And what we're seeking to do is restore this activity back to a healthy functioning level in the setting of disease. We know that if you have a mutation in TREM2, it's increasing your risk significantly for disease. In the context of a heterozygous mutation, you're increasing the risk for Alzheimer's disease as much as threefold. In homozygous mutations, you have severe forms of dementia. There's multiple different mutations that have been identified, and it's associated with a risk for other neurodegenerative disease as well. We also know that there's genetic association studies that show if you have elevated TREM2, you have increased baseline microglial activation, and this is associated with slower cognitive decline, including in Alzheimer's disease, for both Aβ and tau pathologies. We think this is fundamentally a very interesting target. This is some of our phase I data, and here you can see a nice dose-dependent activity, and we're using CSF soluble TREM2 as the marker here. And you have a clear evidence of target engagement and also evidence of microglial activation, as shown on the right, with a nice dose-dependent elevation in this case, soluble CSF1R is the marker we're showing. We've advanced this, as I mentioned, into phase II. Here you can see the design of our phase II. This is a randomized, double-blind, placebo-controlled, four-arm, common close study. A common close study just means that the last patient is treated for a specific time period, and all of the earlier patients enrolled are treated for longer, and you take the totality of that data on a proportional analysis as your endpoint. So our last patient is treated for 48 weeks, and you have up to 96 weeks for treatment for the preceding patients. After you complete 96 weeks, you're eligible for going on to the extension study. This is a randomized, prospective, placebo-controlled study with three different dose arms as compared to placebo. So it's a very robust study in design, and we're measuring a number of important endpoints. Our primary outcome measure is CDR S um of the Boxes, the standard for therapeutics in this area. This is the primary endpoint of the lecanemab phase III studies and also for other studies with the Aβ therapies. We have a number of other clinical and functional outcome measures, as shown here. As I mentioned, the primary endpoint is using a proportional analysis, allowing us to use all of the data collected in the common close design trial over the study period. We also have a very rich biomarker package and imaging package. We're measuring a number of different markers of target engagement and microglial signaling. We're measuring CSF soluble TREM2. We're measuring microglial signaling with CSF1R and other measures, including SPP1 and IL1RN. And then there's a number of important measures of Alzheimer's disease pathophysiology, including tau pathology, which we're measuring with amyloid PET, tau PET, and other plasma markers, including plasma phospho-tau and different CSF measures. There's also markers of astrogliosis, an important measure of pathophysiology in this setting, including plasma glial fibrillary acidic protein levels and CSF YKL-40. And there's measures of neuronal and synaptic injury, including NfL. And we'll also be having a pretty rich imaging package. One point to note is that in the phase II, we have seen ARIA, or what appears to be ARIA, in the vast majority of patients. This is an imaging finding. It's important to note this both from a safety perspective, but also as we've seen that this has been associated with the Aβ therapies and as it appears also early in therapy. As you see with the Aβ therapies, it appears indistinguishable under MRI according to radiologists expert in the field, compared to what's seen with the Aβ therapies. And it's also appearing with a correlation as to APOE4 status. If you're homozygous for APOE4, you have a higher incidence. If you're heterozygous, you also have an increased incidence as compared to if you are not APOE4 at all. What this suggests is that there's the potential that this could be an indicator as well as evidence of some biological activity in the phase II. It's important to note that, you know, from an incidence perspective, in the vast majority of patients, it is just an imaging finding. In the patients where there are clinical symptoms, for the significant majority of those, they're mild and transient, and in those cases, we, you know, can remove drug and, you know, there's careful imaging. This is an important consideration as we advance the program, but the i ncidences of clinically serious ARIA, you know, less than 1% and appear comparable and manageable as we have with the Aβ therapies in the field. So, as noted, this is part of an option deal with AbbVie. The way this deal is structured is they've paid significant upfront, so almost $250 million at this point, in terms of an upfront payment, equity investment, and also milestone payments for commencement of the extension study. And then there's a $250 million payment at the end of this phase II, if they choose to opt in. They'll have 90 days after we present them with our proof of concept study package from this phase II study, which we anticipate, again, the data being end of this year, to decide if they're going to opt in. If they do opt in, we receive that payment, and then that payment largely funds our portion of the phase III. Our portion of the phase III is capped, and there's a global 50/50 profit share. If we choose to maintain that, we also have the option to move that to a royalty arrangement at our election, if we so choose, and that royalty would approximate the 50/50 profit share. So, the time remaining, I'm gonna switch to a number of our progranulin programs and touch on our pipeline. So we're excited about the progress of TREM2 and that data that's coming later this year. We're also very excited about our progranulin franchise. These are late-stage programs. Our most advanced, as I mentioned, is latozinemab. This is currently in a phase III study for FTD-GRN. This is frontotemporal dementia. This is a poorly understood form of dementia that's often underdiagnosed, but it's a very severe form of dementia, and there's no current therapies for this disease. And it can be confused with Alzheimer's disease, and is a significant area of need. So elevating progranulin is seeking to basically restore deficient levels of progranulin in the case of patients with a GRN mutation. We're treating patients that are heterozygous mutant for GRN. They have about half the normal levels of progranulin, and we're seeking to restore that back to normal levels, and I'll take you through how we're doing that with latozinemab. This is the most advanced progranulin elevating candidate in clinical development for frontotemporal dementia. We recently received breakthrough designation from the FDA, and we also have orphan drug designation and have fast track status for this program. As noted, this is completing a phase III. We've completed enrollment towards the end of last year, and it's a 96-week treatment timeframe for the phase III. We also have a second progranulin elevating program. This is AL101. They're both latozinemab and AL101 are monoclonal antibodies. The AL101 program is in a phase II study in early Alzheimer's disease, and, again, it's the most advanced progranulin elevating program, in development for Alzheimer's disease. So just touching briefly on frontotemporal dementia and, the opportunity in the setting of latozinemab. We see the initial indication being frontotemporal dementia patients with a GRN mutation. Again, these are patients that have about half the normal levels of progranulin, but there's other forms of frontotemporal dementia as well, where we see there's, an association from a genetic perspective, where you have-- where progranulin is associated with, you know, significant risk for frontotemporal dementia if you don't have sufficient levels of progranulin. And there's also associated risk in other settings, including ALS, Alzheimer's disease, Parkinson's disease, and other areas of neurodegeneration. So we see the opportunity for elevating progranulin as a broad opportunity that can begin with FTD-GRN, expand to other settings, including other frontotemporal dementia settings, and then to additional indications, such as Alzheimer's disease and others over time. So how is this working? So in the setting of a GRN mutation, again, if you have two bad copies of GRN, you die at a very young age with almost 100% penetrance. Progranulin is a well-conserved protein in evolution that you need to have sufficient levels to survive. If you have half the normal levels, you have frontotemporal dementia with about a 90% penetrance by age 60. So a very significant disease if you have half normal levels in almost all patients. And then if you have other mutations, you have increased risk for these other severe neurodegenerative diseases, including ALS, Alzheimer's disease, and Parkinson's. Progranulin is a key immune regulator, a neuronal survival factor, and a lysosomal chaperone. So what we're doing with latozinemab and AL101 is blocking sortilin. And this is a pathway that regulates the degradation of progranulin, and by blocking this pathway, we can restore levels of progranulin, both in, as measured in the CSF and plasma, back to normal levels. We're currently in a phase III, but let me take you through some of the data that we have for our open-label phase II study. You know, we've studied this in frontotemporal dementia patients in an open-label study for multi-dose over 96 weeks, and we measured safety and tolerability, PK/PD. We measured CSF plasma biomarkers, imaging, and also clinical outcome assessments. And you can see here some of the measures we looked at, including target engagement, measuring progranulin levels, both in the CSF and plasma. Different measures of biomarker activity, including lysosomal function, inflammation, brain health, brain atrophy, and I'll touch on some of our clinical outcome assessments as well. So what you can see here is a nice restoration back to levels of age-matched controls of progranulin, both in the plasma and CSF. Shown here is an important indicator of disease in the brain, glial fibrillary acidic protein levels, both in the plasma and CSF, returning back to more normal levels, levels seen in asymptomatic patients, over the treatment period. And then here you see a range of other lysosomal and inflammatory biomarkers on the left-hand side of the slide, returning back to normal levels. In the right-hand side of the slide, some indication based on brain imaging, that you can also have an improvement in what can be significant brain atrophy in these patients back to less atrophy, and that you can see most dramatically in the context of ventricular enlargement. So, if you're reducing the ventricles being the windows in the brain, if you're reducing the size of those windows, it suggests you're having less atrophy. Here shown is some of our matched historical control data from a clinical perspective. What we're doing here on a blinded basis is comparing the treated patients from a disease progression perspective, as compared to the controls. These are controls selected from a longitudinal registry. GENFI is the registry being compared to here. And we're measuring what's called CDR-NACC-FTLD Sum of the Boxes, which is an adapted CDR Sum of the Boxes, specific for frontotemporal dementia, looking at domains of behavior and language, which are key components of frontotemporal dementia, in addition to the other domains in the Alzheimer's CDR Sum of the Boxes. And what you can see is that over the treatment period here, looking at 12 months, you can see an approximately 50% slowing of disease progression over the treatment period as compared to the age-matched historical controls. So it's exciting data that we've taken into a phase III. Shown here is the design of the phase III. The treatment arm has 60 mg/kg IV every four weeks for a 96-week treatment period, as compared to placebo. You have an extension as well, and safety follow-up. As noted, we've completed enrollment in this phase III study. We completed enrollment with 103 symptomatic patients, ahead of our target of 90 to 100 patients, and we also have 16 at-risk or pre-symptomatic patients as well in the phase III. We'll be looking at this primary endpoint, the CDR plus NACC-FTLD, Sum of the Boxes, as well as a range of secondary outcome assessments and important biomarker endpoints and imaging endpoints. That study, as noted, earlier in the presentation, we anticipate data could be towards the end of 2025, perhaps early 2026. It's a 96-week treatment period. We'll, we'll provide more specific guidance around the expectations of timing there. And I wanna touch on our second progranulin elevating program, AL101, which is advancing in a phase II study. This study is a multi-dose study in early Alzheimer's disease patients as compared to placebo. It's a randomized, prospective, 76-week treatment period, also with a safety and a follow-up as well. You can see here some of the key inclusion criteria. The primary endpoint, as we see in other Alzheimer's studies, is CDR Sum of the Boxes. We're looking at this across weeks 52, 64, and 76 weeks, and we have a number of key secondary endpoints, and it's a rich biomarker study as well, looking at amyloid PET, tau PET, other CSF and plasma biomarkers. This will be a rich data set to understand the importance of progranulin elevation in the setting of Alzheimer’s disease. As noted, it’s the most advanced program elevating progranulin in Alzheimer’s disease. We’re conducting this together with our partner, GSK. So just touching on the GSK partnership, this is a significant partnership for Alector and $700 million upfront paid. There’s $1.5 billion in potential milestone payments. It’s a US 50/50 profit share with tiered double-digit royalties outside the US. There’s a $160 million payment for the first commercial sale in the US, a $90 million payment to Alector for the first commercial sale in the EU. So a rich partnership, and we’re working closely with our partners, GSK, on these programs. So in the moments remaining, I want to touch briefly on our exciting blood-brain barrier platform. This is advancing with our proprietary program, some of them disclosed, some of them undisclosed. This allows us to get best-in-class brain penetrance and do this in a very customized way. We're achieving tenfold increases in brain concentrations, deep brain penetration. We can optimize for different targets and different mechanism of actions and cell types. We have versatile formats, and shown here are some of those formats. And we can adapt for optimizing effector function, half-life. And there's also the opportunity to use different modalities, including monoclonal antibodies, oligonucleotides, proteins, and we're advancing a portfolio here that we think is proprietary and differentiated. There'll be more coming on this platform in the coming weeks and months. So in summary, today, I wanna just recap. So significant accomplishments for the company to date, including advancing some firsts for patients, including the first anti-sortilin molecule in the setting of FTD-GRN in a pivotal phase III study, where we've completed enrollment. We've completed enrollment, are advancing towards data on the phase II TREM2 antibody, which is the most advanced of its kind, and we continue to progress a rich pipeline of first-in-class approaches for a number of different neurodegenerative diseases. We have significant upcoming data events for the coming years. We are anticipating delivering data, as I mentioned, for AL002, phase II study, for TREM2, later this year, and our phase III data for latozinemab, towards the end of 2025, early 2026. We are advancing our AL101, AD phase II study, as well as advancing our blood-brain barrier platform and proprietary programs. So we're doing this from a strong cash position and with significant opportunities from a downstream economics perspective for our late-stage clinical programs and our proprietary programs. We're looking forward to continuing to update you on our progress as we advance. Thank you very much for your time today.