Alector at Morgan Stanley Conference: Strategic Insights on AI and Neurodegenerative Research

On Monday, 08 September 2025, Alector Inc (NASDAQ:ALEC) participated in the Morgan Stanley 23rd Annual Global Healthcare Conference. CEO Arnon Rosenthal shared strategic insights into the company’s focus on neurodegenerative diseases, highlighting both challenges and advancements in research and development. Alector’s integration of AI and its regulatory strategies with the FDA were central themes, alongside updates on promising drug candidates.

Key Takeaways

• Alector is leveraging AI in research and development to address neurodegenerative diseases.
• The company has over $300 million in cash, ensuring operations through 2027.
• AL001 and AL101 are in advanced clinical trials for frontotemporal dementia and Alzheimer’s disease, respectively.
• Alector is developing a blood-brain barrier platform to enhance drug delivery.
• The company plans to expand its focus to ALS and sporadic types of frontotemporal dementia.

Financial Results

• Alector holds over $300 million in cash, expected to fund operations through the second half of 2027.
• This financial reserve will support the completion of key clinical trials, including the pivotal Phase 3 study for AL001 and the Phase 2 study for Alzheimer’s disease.
• The company aims to advance its blood-brain barrier technology and related drug candidates to the clinic.

Operational Updates

AL001 for Frontotemporal Dementia (FTD):

• The Phase 3 trial data is expected in Q4 of the current year.
• This pivotal study involves 106 symptomatic patients and 16 pre-symptomatic genetic mutation carriers.
• Co-primary endpoints focus on normalizing progranulin levels and improvements in the CDR-SB score.
• A previous Phase 2 study indicated a 48% slowdown in cognitive decline over 12 months.

AL101 for Alzheimer’s Disease (AD):

• The Phase 2 trial completed recruitment in April, involving over 360 patients.
• The study is designed as a placebo-controlled, double-blinded trial, with completion anticipated in 2026.
• AL101 features a longer half-life compared to AL001, with multiple clinical readouts planned.

Blood-Brain Barrier Platform:

• Alector’s proprietary platform aims to improve drug delivery using the transferrin receptor.
• Key programs include an anti-Aβ antibody drug and engineered GCase for Parkinson’s and Lewy body dementia.

Future Outlook

• Alector plans to expand its research to ALS and sporadic forms of FTD.
• The company is focusing on genetic screening as a diagnostic tool and aims to develop a neurodegeneration panel.
• Efforts are underway to educate the clinical community about FTD diagnosis and genetic screening.
• Alector is exploring subcutaneous delivery options for Alzheimer’s and Parkinson’s treatments to enhance patient access.

Q&A Highlights

• Discussions with the FDA focused on statistical plans and approval processes for AL001.
• Rosenthal clarified differences between FTD and Alzheimer’s, emphasizing symptoms and disease progression.
• Concerns about tariffs affecting international operations were addressed.
• The potential market for FTD treatments is significant, with an estimated 15,000 to 17,000 symptomatic patients in the U.S. and EU.

For a detailed overview, readers are encouraged to refer to the full transcript.

Full transcript - Morgan Stanley 23rd Annual Global Healthcare Conference:

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Welcome to the Morgan Stanley Global Healthcare Conference. I’m Sean Lyman, Head of SNiCCAP Biotech, here at the firm. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. For this session, we have the pleasure of hosting Alector’s CEO, Arnon Rosenthal. Welcome and thank you for your time today.

Arnon Rosenthal, CEO and Co-founder, Alector: Thank you for inviting me.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: You’re welcome. Would you like to make some opening remarks, or should we get straight into it?

Arnon Rosenthal, CEO and Co-founder, Alector: Yes, sure. As you said, I’m the CEO and co-founder of Alector. Alector was created to really address the major unmet medical need of now the generation. As you know, one of six people in the world has a brain disorder, and this is really one of the last major unmet medical needs. There are more than 50 million people worldwide with dementia, 10 million people with Alzheimer’s disease, and millions of people with other neurodegenerative disorders. We undertook to really find disease-modifying therapies for these major disorders by really going after the underlying mechanism of these disorders.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Great, thank you. I might just start with some macro questions. We’re doing this for all our companies. With China’s rising biotech innovation, how do you think about the competitive position here and whether it’s influenced your R&D or your business development strategy?

Arnon Rosenthal, CEO and Co-founder, Alector: In general, I think that competition is good for everyone. I know that it’s unpleasant at times, but I think that fair competition really raises everyone to do better. I want to see the best drug for patients, no matter where they are coming from. I think the fact that China is becoming, in a way, more innovative and more focused on pharmaceutical and biotechnology would really force the U.S. to do even better. I really hope that the regulatory environment will become more accommodating for the pharmaceutical industry. I think that just freedom and, in a way, getting out of the way of the pharmaceutical industry will really lead to competitive innovation and will enable the U.S. to continue to be the leader in this field.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Great, thank you, Arnon. How are you currently leveraging AI, if you are? How about AI’s disruptive potential? How do you think about that?

Arnon Rosenthal, CEO and Co-founder, Alector: Yes, we are excited about AI. We think that it’s going to be a significant tool to facilitate both our discovery effort and our clinical and preclinical development, and also generally the way the company is running, even in the administrative aspect. We have a team that’s composed of research and administrative people that are really dedicated to incorporating aspects of AI. We are using all the main tools that are now available, like OpenAI and multiple programs that are dedicated to different aspects of science. I don’t think that AI is going to substitute thinking and science, but I think that it’s going to be a tool to really facilitate science. We are really embracing the opportunity, but we still think that old-fashioned scientific understanding and knowledge are still going to drive innovation in the foreseeable future.

I don’t think that AI for science still has enough information to really substitute scientists.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Yeah, wonderful. I guess over the last period, what’s been the most impactful to Alector from the regulatory side? Would it have been FDA? The phone’s probably a bit too early, but or tariffs?

Arnon Rosenthal, CEO and Co-founder, Alector: At this point, it’s mainly the FDA. We have very sort of close interactions with the FDA. We have a pivotal phase 3 drug that receives breakthrough therapy and orphan designation. That’s sort of going to read in the middle of Q4 this year. If all goes well, we really apply for a BLA and we’ll consider commercialization. Interactions with the FDA on the statistical plans and on the approval process are what keeps us sort of that’s our main focus. We are actually working internationally. Our manufacturing facilities are out of the country. We actually also work with Chinese companies in research. Hopefully the tariffs are not going to hinder our operations longer term because, again, I think that innovation requires sort of global interaction. Basically, you should do the best thing wherever it’s done best.

I think that we should facilitate freedom of interactions and free interchange of both ideas and technologies and reagents. Hopefully the tariffs will not curtail that.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful, wonderful. Thank you. To get to Alector specifically, AL001, which is the company’s program, your own program, APDDRN. Can you give us a high-level overview of the program and what you and GSK hope the AL001 program can achieve?

Arnon Rosenthal, CEO and Co-founder, Alector: Sure. Our most advanced drug, which is in pivotal phase 3 and is going to read in the middle of Q4 this year, is targeting a disease called FTD or frontotemporal dementia. This is the largest type of dementia for people under the age of 60. It’s two to three times faster and more aggressive than Alzheimer’s disease. It constitutes a major burden both for the patients and the caregivers because it is associated with this sort of disinhibition with regard to behavioral, with speech inability and motor disabilities, and some form of cognitive disability. It’s a lethal disease. People are diagnosed before the age of 58 and they die within seven to nine years. It’s a very aggressive type of neurodegeneration. Currently, there are no approved therapies for this disease. One of the underpinnings of the disease is a genetic mutation in a secreted immune regulatory protein called progranulin.

People that have one good and one bad copy of this progranulin gene produce 50% of the normal level of the protein and they invariably develop frontotemporal dementia. We developed a drug called latozinemab or AL001 that elevates the level of progranulin back to normal level in this patient. The way the drug does it is by blocking a degradation cascade of this secreted protein. What happens in patients is they produce half of the normal amount, but the protein that’s produced stays now in the brain two to three times longer because it’s not being degraded. As a result, the reduced production is being compensated by increased half-life. Conceptually, it’s very similar to what all the SSRIs are doing, like Prozac. Prozac prevents the reuptake and degradation of neurotransmitters like serotonin and norepinephrine.

By that, it increases the level of these neurotransmitters in the brain, leading to the antidepressive effect. We are doing the exact same things. We increase the level of the proteins and the residence time of the progranulin protein in the brain two to three times longer. That’s how we elicit the therapeutic benefit.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful. How does frontotemporal dementia differ from normal age-onset dementia?

Arnon Rosenthal, CEO and Co-founder, Alector: Yes. Frontotemporal dementia is different than Alzheimer’s disease in the way that it’s not really mainly short-term memory loss. It’s more associated with behavioral abnormalities, disinhibition, inability to control behavior, and also with inability to articulate yourself, to speak. Eventually, these people are unable to communicate, unable to control their behavior. They have extravagant behavior. They can go to people in the street and hug them and harass them. It’s more behavioral and speech abnormalities as well as motor deficiencies, which is different than Alzheimer’s disease. It’s mainly short-term memory deficiencies.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Got it. Thank you. I’m just moving to the phase 3 and phase 3 top-line data, the readouts expected in Q4. Could you give us an overview of the trial design and what you expect to report in the top-line results?

Arnon Rosenthal, CEO and Co-founder, Alector: Sure. As I mentioned, we are at the end of a phase 3 study with this drug. It’s a placebo-controlled, double-blinded pivotal study with 106 symptomatic patients and 16 genetic mutation carriers that are still pre-symptomatic. It’s going to be a significant package of clinical and non-clinical readouts. We have the primary, the co-primary readouts are elevating progranulin back to normal level or statistically significant elevation in the plasma. The second co-primary is the CDR-SB for FTD. This is a clinical readout that contains eight different domains of cognition, activity of daily living, behavioral, and speech that we agreed with the FDA would represent the clinical readout. We have two co-primary, progranulin elevation in the plasma and the clinical readout. In addition, we are measuring multiple biomarkers, including neurofilament and GFAP. We are looking at changes in brain tissue loss in the brain with volumetric MRI.

At sort of the end of this year, we’ll have a fairly extensive package that will tell us conclusively whether we have a drug. We agreed with the FDA that this single trial together with the biomarker will be enough to get approvals.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Thank you. Just to really double down on that, maybe talk about your alignment with the FDA on the endpoints and what gives you that confidence that you know the answer will be the answer.

Arnon Rosenthal, CEO and Co-founder, Alector: Yeah. We, again, because we receive breakthrough therapy and orphan designations, have very close interactions with the FDA. Recently, we agreed with the FDA that we’ll have, again, two co-primary elevations: statistically significant elevation of progranulin, which is the disease-causing missing protein in the plasma. Based on our open-label phase 2 study, we think that there’s more than 99% chance that we will reach this co-primary. We agreed with the FDA that the CDR-SB, which is, again, tailored for FTD, will be the clinical co-primary. There is alignment that these two co-primary will really drive approval of the drug. Based on our phase 2 study, we did show two to three-fold elevation of progranulin throughout the disease, throughout the treatment period. We now have patients that have been treated for over two years.

As long as the drug is applied to these patients, the progranulin level is restored back to normal level and indistinguishable from what you see in a healthy individual. With regard to the clinical readout, in the open-label studies, we were able to show a 48% slowdown in cognitive decline over 12 months with 12 patients. Our phase 3 is 10 times longer with like 106 patients. It’s twice as long with two years versus one year here in the phase 2. We think that we have significant room for variability. Even though in the phase 2, we showed 48% slowdown in cognitive decline, we think that even if we show 25% slowdown in cognitive decline in the phase 3, it will still be statistically significant, clinically meaningful, and in our view, approvable.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful. Thank you. Could you mention the timelines? You know, how long have patients been on therapy in the clinical trials and the timeframes around sort of measuring those endpoints?

Arnon Rosenthal, CEO and Co-founder, Alector: The trial is a two-year-long trial, like 96 weeks long. We decided to really follow these patients for almost two years to make sure that we can capture the disease progression and both the biomarkers and the imaging readout. We are measuring in the plasma. We are taking samples monthly. Every time the patient is coming for treatment, we are also taking samples of plasma. The clinical readout is every six months, and the imaging is also every six months.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful. Thank you. You presented the impromptu baseline characteristics at the International Society for FTD in September last year. I’m looking at those baseline data. How would you describe the FTD GRN population involved in terms of at-risk versus asymptomatic and other clinical distinctions?

Arnon Rosenthal, CEO and Co-founder, Alector: In general, the features of the patients that we recruited to the phase 3 trial represent the general population based on what was reported in the major FTD consortia, both the European consortia and the U.S. consortia. The general features of the symptoms, the stage of severity, levels of biomarkers. What we recruited to the patients is really the presenting real-life patient population. In the trial, we recruited two types of disease severity. 70% of the population that we recruited is early-stage disease, like in CDR-SB global score of between 0.5 and 1 out of a 3-point scale. About 30% is a scale between 1 and 2. We have really very early patients and early medium patients. We want to see if the drug could work at these stages. As I mentioned, we also have 16 patients that are still pre-symptomatic.

In this case, we want to see if we can prevent conversion from pre-symptomatic patients to symptomatic patients. So far, the drug appeared to be very well tolerated. It seemed to be a really safe drug. Our ultimate goal is to really do prevention, to really capture patients before they become symptomatic and prevent the conversion to symptoms.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful. Thank you. Inflammatory is powered to show 40% slowing of disease progression. KOL feedback suggests about a 25% slowing of CDR-SB would be clinically meaningful. Given that, what would be your expectations at the 96-week time point on CDR?

Arnon Rosenthal, CEO and Co-founder, Alector: Based on our phase 2, we did show 48% slowdown in cognitive decline over 12 months. Hopefully, the phase 3 will reproduce this. As you said, even 20 to 25% slowdown in cognitive decline according to the KOLs that we talked with will be clinically meaningful. This is a lethal disease. There are no approved drugs for this disease. It hits people at the prime of their life, like when they are sort of between 30 and 60. It’s a major burden on the family because of the behavioral disinhibition. We think that any sort of even modest clinical benefit will be meaningful for these patients.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful. Maybe giving the answer to the nuts and bolts of building out a market model. You could talk about what the patient opportunity is here. If the drug does prove successful, sort of the touch points and how you go through the launch process, just to start.

Arnon Rosenthal, CEO and Co-founder, Alector: Yeah. There are an estimated 50,000 to 60,000 FTD patients in the U.S. and about 110,000 FTD patients in the EU. Up to 10% of these patients carry the progranulin mutation. In the U.S. and EU, there could be 15,000 to 17,000 symptomatic patients. Because the disease symptoms occur at the age of 50 to 60, there may be five times more pre-symptomatic mutation carriers. We think that it’s a very meaningful market opportunity. It’s a rare disease, lethal, and with complete unmet medical needs. We think that there is a very meaningful market for us.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: In that, sort of accessing the physician network, maybe talk about the types of physicians both coded in academic centers and how do you see that unfolding?

Arnon Rosenthal, CEO and Co-founder, Alector: Yes. We are already spending a lot of time educating the scientific community, the clinical community. It’s going to be both psychiatrists and neurologists. We are working with advocacy groups. We have KOLs in all the major clinical centers. Our clinical trials are already done in dozens of clinical centers, both in the U.S. and EU, where we have close interactions with the KOLs. It will require educating the clinical community because not everyone knows how to diagnose FTD and what to deal with it. We are going to introduce genetic screening as part of the drug. The genetic screening is conclusive and relatively simple. We are engaged in very extensive education, again, through scientific meetings and through direct interactions with KOLs. We think that once the community knows that there is a drug, the level of interest and awareness will grow significantly.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: It seems like you’ve got enough runway in symptomatic patients, but on the genetic screening part, how do you ensure that you get proliferation of that screening to access the patients that aren’t symptomatic?

Arnon Rosenthal, CEO and Co-founder, Alector: Yes. Even for the symptomatic patients, we want to have genetic screening because you want to make sure that the frontotemporal dementia is caused by the progranulin mutation. It will be a lot of education that genetic screenings are available and are easy to do; basically, it’s a blood sample. The genetic screen will be easily available. We’ll have to educate the KOLs, the treating physicians, and the scientific community in general that the genetic screen is the way to conclusively diagnose this disease.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Sure. You could make it part of a bigger screening panel at some point?

Arnon Rosenthal, CEO and Co-founder, Alector: Yes, there is a sort of neurodegeneration panel that could build, yes.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Yeah. Wonderful. Thank you, Arnon. Moving on to AL101, can you describe the changes in PKPD relative to latozinemab and which make you feel AL101 is more amenable for a broader population like AD?

Arnon Rosenthal, CEO and Co-founder, Alector: The unique feature of progranulin is that it appears to be a universal risk gene for neurodegeneration. Whereas many risk genes are disease-specific, like SOD is specific for ALS, alpha-synuclein is specific for Parkinson’s disease, and presenilin is specific for Alzheimer’s disease. In contrast, progranulin reduction in the level of progranulin appears to be associated with practically every neurodegenerative disease that’s been tested. A 50% loss of function in progranulin leads to frontotemporal dementia, but a 10% to 15% decrease in the level of progranulin is associated with Alzheimer’s disease, with Parkinson’s disease, with ALS, with LATE, which is another prevalent form of dementia that’s typified by TDP-43. Based on this, elevating progranulin either back to normal level or even to supraphysiological level could have therapeutic benefit in many neurodegenerative diseases.

Because of this hypothesis, we initiated a second clinical trial with a progranulin-elevating drug, which is a drug called AL101. This is in Alzheimer’s disease. We completed recruitment in April in Alzheimer’s disease. It’s a placebo-controlled, double-blinded phase 2 with over 360 patients with our second progranulin-elevating drug. The clinical trial for this Alzheimer’s study will be completed in 2026. We have selected this second drug, this AL101, because it has different pharmacokinetic features. It has a half-life two to three times longer than the 001 or latozinemab. This will enable us either to reduce dosing frequency or reduce the dose level and maybe make it more amenable to subcutaneous delivery. We think that for the prevalent diseases like Alzheimer’s or Parkinson’s, subcutaneous delivery could be a lot more convenient and will enable much better patient access.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Sure. Maybe you should talk to Alector.

Arnon Rosenthal, CEO and Co-founder, Alector: Yes, we are.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Unlike our frontotemporal, you know, AD patients, I believe, have relatively normal PGRN levels. You know, given that, what’s the rationale supporting AL101 and increasing PGRN for having a clinical benefit in AD?

Arnon Rosenthal, CEO and Co-founder, Alector: Yeah, that’s a great question. The scientific rationale is twofold. Genetically, progranulin was shown to be a risk gene for Alzheimer’s disease. If you look at the 70 or 80 risk genes that have been identified for Alzheimer’s disease, progranulin is one of them. The risk gene is associated with a 10% to 15% slowdown and decrease in the level of progranulin. It’s hard to measure this modest reduction, but even modest reduction in progranulin leads to increased genetic risk. There is a genetic rationale for elevating progranulin in Alzheimer’s disease. The second rationale is animal model-based. There are multiple studies showing that elevating progranulin to super physiological levels in disease models of Alzheimer’s leads to therapeutic benefit. Our hypothesis is that in Alzheimer’s disease and eventually Parkinson’s disease and ALS, elevating progranulin to a super physiological level, like two to three fold above normal level, will be therapeutically beneficial.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Yeah. Wonderful. Maybe you’ve touched on this already, but maybe just to remind us the overview of the study design in progress in the phase 2 trial. I believe enrollment’s just completed. You know, when can we expect first data?

Arnon Rosenthal, CEO and Co-founder, Alector: Yeah. Enrollment was completed in April of this year. It’s a study with 300 patients. It’s a placebo control, so there is a placebo arm, and there are two dose drug arms. It’s an 18-month long study. The readout will be the CDR-SB, as well as like four additional clinical readouts for activity of daily living and other cognitive measures. We are also measuring levels of A-beta and tau by PET imaging. We are measuring multiple biomarkers, again, A-beta 40, A-beta 42, multiple types of phospho tau in the plasma and MCSA. It will be a fairly extensive data package that will tell us whether the drug is working and if it makes sense to continue to phase 3. The trial will be completed in 2026. If you calculate from April, like 76 weeks, it will be the end of 2026. We expect to have data shortly after that.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful. Wonderful. Let’s talk about AL101, but maybe we talk about the blood-brain barrier platform. We’ve seen several advances in the field. Could you briefly touch on Alector’s proprietary BBB platform and how it’s positioned within the current landscape?

Arnon Rosenthal, CEO and Co-founder, Alector: Yes, absolutely. As you know, large molecules like proteins, enzymes, and nucleic acids do not penetrate the brain well. If you can have a shuttle that can improve brain penetration, you could have a more effective drug. We, as several other companies, have developed a brain shuttle that uses a receptor that’s present in the blood-brain barrier that usually transports iron to the brain. This is the transferrin receptor. You can use the transferrin receptor as a Trojan horse to bring large molecules to the brain. We are using this technology to transport antibodies to the brain, to transport enzymes to the brain, and to transport nucleic acid to the brain. With each of these drug modalities, we have a specific drug that we are advancing.

In the antibody realm, we are developing an anti-Aβ antibody drug with our blood-brain barrier shuttle that we expect to reduce the side effects, the area side effects, and to increase efficacy. We think that our unique blood-brain barrier technology will also reduce anemia compared to other technologies, which is a side effect associated with this technology. For the enzymes, we are developing an engineered GCase. GCase is a lysosomal enzyme that’s mutated in up to 10% of Parkinson’s patients and up to 30% of Lewy body dementia patients. There are hundreds of thousands of neurodegeneration cases that are caused by loss of function mutations in these lysosomal enzymes. We developed an enzyme that’s a lot more stable, a lot more active than the natural enzyme, and linked it to the blood-brain barrier technology.

We are able to restore enzyme deficiency in the brain of Parkinson’s and eventually Lewy body dementia patients. Finally, we are also developing siRNA in conjunction with blood-brain barrier technology. Here, we are focusing on tau siRNA and on alpha-synuclein siRNA. Both of these proteins are hallmarks of Alzheimer’s disease and Parkinson’s disease, respectively. Because a lot of the pathology is caused intracellularly, antibodies do not seem to be very effective in counteracting these misfolded proteins.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Of these technologies, thinking about the ability to maximize penetrance, is there a trade-off between efficacy and concentration? How do you think about that?

Arnon Rosenthal, CEO and Co-founder, Alector: Yes. I mean, like this technology in general, you really have to thread the needle. It’s not a plug and play. You have to really find the right configuration of that transferrin binding domain that really optimizes brain penetration, but minimizes adverse effects like anemia. The blood-brain barrier, the transferrin receptors are expressed on the blood-brain barrier, but they’re also expressed at very high level on red blood cells. If you bring too much of your drug to red blood cells, you can damage them. You have to really play with the binding domain to the transferrin receptor, with the affinity of the binding, with the configuration of the rest of the drug to really optimize, again, the safety to efficacy.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful. Thank you. I’ve just got a couple of minutes left. I’ll jump forward to this question that you’ve recently updated guidance. Can you touch on some of the updates and remind us how much cash you have and how far that will get you?

Arnon Rosenthal, CEO and Co-founder, Alector: Yeah. We have over $300 million in cash. We announced that this will be sufficient to get us through the second half of 2027. This will enable us, again, to complete our pivotal phase 3 study, to get readout of our phase 2 study in Alzheimer’s disease, and to take at least two of our blood-brain barrier-linked technology drugs, the anti-Aβ drug and the GCase drug, to the clinic. We are expected to have at least four shuttle goals within our runway.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful. With that said, is there anything that I didn’t ask that you’d like to highlight or that’s of particular importance?

Arnon Rosenthal, CEO and Co-founder, Alector: I just want to highlight, again, that we have a really good mixture of late-stage program, a phase 3 program for frontotemporal dementia, phase 2 program for Alzheimer’s disease, as well as a portfolio of preclinical programs that will get into the clinic in 2026 that are linked to our proprietary blood-brain barrier technology. We are addressing both rare and major neurodegenerative diseases, frontotemporal dementia, Alzheimer’s disease, Parkinson’s disease, and we are going to expand to also ALS and sporadic types of frontotemporal dementia.

Sean Lyman, Head of SNiCCAP Biotech, Morgan Stanley: Wonderful. We’re just perfectly on time. Thank you for your time today and thank you for coming to our conference. We really appreciate it.

Arnon Rosenthal, CEO and Co-founder, Alector: Thank you. Thank you for the great question.

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