Alector Q2 2023 Earnings Call Transcript

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August 3, 2023

There are 11 speakers on the call.

Operator

Good afternoon, ladies and gentlemen, and welcome to the Alator Mid Year 2023 Earnings Conference Call. At this time, all participants are in a listen only mode. After the speakers' presentation, there will be a question and answer As a reminder, this conference call is being recorded. I would now like to turn the call over to Katie Hogan, Senior Director of Corporate Communications and Investor Relations. Please go ahead.

Speaker 1

Thank you, operator, and good afternoon, everyone. Earlier this afternoon, we released our financial results for the Q2 of 2023. The press release is available on our website at www atelector.com, and our 10 Q was filed with the Securities and Exchange Commission this afternoon. Joining me on the call today are Doctor. Arnon Rosenthal, Co Founder and CEO Doctor.

Speaker 1

Sarah Kankari Mitra, President and Head of Research and Development Doctor. Gary Romano, Chief Medical Officer and Doctor. Mark Grasso, Chief Financial Officer. After our formal remarks, We'll open the call for Q and A. I'd like to note that during this call, we will be making a number of forward looking statements.

Speaker 1

Please take a moment to review our slide in the webcast, which contains our forward looking statement disclosure. And we also encourage you to review our SEC filings for more information. I would now like to turn the call over to Arnon Rosenthal, Chief Executive Officer. Arnon?

Speaker 2

Thank you, Katie, and good afternoon, everyone. We appreciate you joining our conference call today. I'll start by highlighting Elektor's key initiatives during the first half of twenty twenty three. Next, Sarah will share the progress we believe we have achieved with our immuno neurology research. Then I invite Gary to discuss the late stage clinical program.

Speaker 2

Afterwards, Mark will provide an update on our financial results and milestone outlook. Today, Alecto is a late stage clinical biotechnology company with an advanced pipeline that includes novel first in class clinical program. We also have world class partnerships in which we retain significant rights as well as innovative research and technology portfolio. Regarding our TRAM2 program, We'll provide more details about our INVOK2 Phase 2 clinical trial with AL-two. The trial is approaching full enrollment and nearly all eligible participants are rolling over into the long term extension portion of the study.

Speaker 2

We're also looking forward to sharing key highlights from the 2 program we In the mouse model of Alzheimer's disease, our antibody AL002C was shown to reduce total tau in the serum, which is a biomarker for normal repair as well as to increase the ratio of EBITDA 42 to 40, which may reflect remodeling of amyloid plaque. Further, we are encouraged that AL-two It was well tolerated in our Phase 1 trial with healthy volunteers. The fact that we are seeing what appears to be incidences of ARIA in VOXX2 2 participants associated with EPO EPO status, we believe is interesting and suggest biological activity. With enrollment in VOQ2 nearly complete, we are advancing closer to potential meaningful data readout. We will also share with you the outcome of our recent productive agency interaction with the FDA and EMA On our INFRONT-three Phase 3 pivotal trial evaluating leprelizumab in frontotemporal dementia, The enrollment in INFRONT3 is also nearly complete.

Speaker 2

We will also provide a brief update on our INFRONT2 Open label Phase 2 clinical trial in frontotemporal dementia with B972 mutation. With that, I will turn over to Sarah to highlight the progress we have achieved with our immuno neurology results.

Speaker 3

Thank you, Arnon. As we look across the space, we are encouraged to see continued advancement in neurodegenerative disease drug development in 2023. The accelerated approval of a new ALS treatment and the traditional approval of an anti amyloid beta therapy for Alzheimer's disease highlights the possibility of progress for patients, families and caregivers affected by these devastating conditions. Moreover, they paved the way for next generation therapeutics that have the potential to work alone all in combination with these novel treatment approaches. At Elektor, we applaud this progress while we Sadly, brain disorders impact more than 1,000,000,000 people worldwide and result in the loss of 6,800,000 lives each year.

Speaker 3

As these figures continue to rise, the urgency to address this immense public health challenge has never been greater. That is why we pioneered the field of immuno neurology and are advancing a broad portfolio of potential first in class treatments for brain disorders guided by our insights into human genetics, immunology and neuroscience. Like immuno oncology, Immuno neurology seeks to harness the immune system as a broad effective and long lasting therapy. Within the brain, microglia are the primary cells of the innate immune system. Our immuno neurology therapies tries to shift Ineffective or damaged microglia into effective and beneficial agents.

Speaker 3

We've translated immuno neurology into a broad portfolio with transformative potential. We are developing latatinumab and AL-one hundred and one in partnership with GSP. These candidates are intended to block sotenin, a degradation receptor for propranolin, to boost propranolin levels and enhanced microbial activity. In collaboration with AbbVie, we are also developing AL-two. With AR002, we seek to increase TREM2 signaling with the intention of stimulating the functionality of MYCOVIA.

Speaker 3

We believe these candidates represent the most advanced immuno neurology therapies in clinical development worldwide. We also continue to strategically invest in and advance our innovative research portfolio to fuel our development pipeline and to set the stage for our long term success. While our late stage candidates show brain penetration and target engagement, We are developing proprietary versatile blood brain barrier technology, which we may selectively deploy on next generation programs. An additional novel 1st in class program we are excited about is ADP-twenty seven, which is targeting the gcnmd gene for the Treatment of both familial and sporadic Parkinson's disease. Currently, we are in the process of selecting our lead candidate and look Forward to providing updates on ADP-twenty seven as we progress the program.

Speaker 3

Our collaborations with GSK and AbbVie, Combined with our clinical expertise and differentiated approach allow us to advance our broad pipeline with the potential to transform the treatment With that, I'll turn it over to Gary to highlight recent progress with our late stage clinical program.

Speaker 4

Thank you, Sarah. I'll begin with our AL-two program, the most advanced TREM-two program in clinical development for Alzheimer's disease worldwide. AL-two is a novel investigational humanized monoclonal antibody that binds to and activates The triggering receptor expressed on myeloid cells or TRM-two. TRM-two is a phospholipid receptor on the microglial membrane that senses pathological changes in the brain. Finding of TREM-two to its biological substrates, which include APOE, lipids, abeta and other cellular 3 triggers microglial signaling pathways that allow the microglia to adopt a defensive response to disease by clearing pathology and protecting neuronal health.

Speaker 4

Loss of function variance in TRM-two are known to be deleterious. Heterozygous mutations in the TREM2 gene reduced functionality of microglia and increased the risk of Alzheimer's disease. For example, the R47H loss of function variant increases Alzheimer's disease risk by 3 fold. ALS-two binds to TRM2 receptors, resulting in clustering of TRM2 in the microglial membrane and activation of TRM2 signaling pathways, which support microglia survival, proliferation and function. Microglia are the primary innate immune cells of the central nervous And they play a number of important roles in maintaining brain health and function, including clearing of misfolded proteins such as amyloid and other cellular debris And also maintenance of healthy synapses, astrocytes, oligodendrocytes, maintenance of the blood brain barrier and vasculature and immune tolerance.

Speaker 4

Our hypothesis is that boosting microglial function may improve the brain's defenses against age related neurodegenerative diseases. We completed our Phase 1 trial of AL-two in healthy volunteers, which demonstrated both dose dependent target engagement and activation of microglia. INVOQ-two is Elektor's Phase 2b study of AL-two, which is now ongoing in patients with early Alzheimer's disease. Invoke II is a randomized, double blind, placebo controlled, common closed design study of up to 96 weeks of treatment with AL002 in approximately 328 participants with early Alzheimer's disease. It includes 3 doses of AL-two that were demonstrated in Phase 1 to activate microglia.

Speaker 4

Participants receive AL-two or placebo as monthly infusions. INVOLT-two is designed by Elektor and AbbVie to be a biomarker rich proof of concept study. Primary endpoint is the CD arsenal boxes. We're also collecting other secondary clinical and functional outcome assessments. Biomarkers include CSF and plasma biomarkers of microfeal activation and of Alzheimer's pathophysiology and neuroimaging biomarkers include amyloid and Tau PET and volumetric MRI.

Speaker 4

To date, we have enrolled more than 300 participants and the trial is nearly fully enrolled. We expect to complete enrollment in the Q3 of this year with their study reading out in the Q4 of 2024. At the Alzheimer's Association Annual Conference or AIC in July, we presented an update on IMVOQ-two, Which highlighted that early in the trial, 3 participants had treatment emergent neurological signs and symptoms and associated MRI findings consisting of focal vasogenic edema, focal effusions, micro hemorrhages and superficial cirrhosis. These MRI findings resemble the area that has been reported Following treatment with anti amyloid antibodies regarding their MRI features, incidents, timing of onset, related this to the number of APOE4 alleles as well as the frequency and spectrum of clinical manifestations. We believe AL-two has the potential to work alone or in combination with anti amyloid beta therapies by harnessing the broader beneficial effects of microglia.

Speaker 4

We expect to report IMVO-two data in the Q4 of 2024. At AAAIC in July, we also presented a poster on mouse model data demonstrating that TRM-two activation I'll now turn to latasinumab, our novel 1st in class candidate and the most advanced therapeutic candidate worldwide in clinical development for the treatment of FTD. Previously, we disclosed that based on emerging data on the variability of FTD progression from the Genfi and all FTD cohorts, We plan to meet with regulatory authorities to discuss modifications to the statistical analysis approach for our INFRONT 3 Phase 3 clinical trial of latuzinumab and participants with FTD granuline. This is driven by both our and the scientific community's evolving understanding of the variability of Additionally, as a part of routine monitoring, we in partnership with GSK conducted a blinded sample size re estimation of the INFRONT3 trial, which demonstrated that the variability of disease progression is considerably less than our initial estimates, which were based on limited data at the start of the trial. Importantly, this supports a significant reduction in the number of symptomatic participants required for our primary efficacy analysis in INFRONT3.

Speaker 4

Our recent interactions with FDA And based on agency feedback, we plan to conduct the primary analysis on symptomatic participants in INFRONT3. The agencies also agreed with our proposed sample size re estimation that is anticipated to support a more focused enrollment of As a result, we plan to complete enrollment in INFRONT3 in the Q4 of 2023. Regarding the FDD C9orf72 cohort of our INFRONT2 open label Phase 2 trial, we confirmed again a 2 to 3 fold elevation in progranilone levels in CSF and plasma. We have conducted a preliminary analysis of disease progression rates for 14 A high degree of variability in disease progression rates in both groups rendered the analysis uninformative regarding treatment effect. Turning to AL-one hundred and one, our 2nd product candidate in our progranulin portfolio that we are developing in partnership with GSK.

Speaker 4

AL-one hundred and one is designed to elevate progranulin levels in a manner similar to latasinumab. It's different pharmacokinetic and pharmacodynamic properties potentially enabled dosing regimens for use in the treatment of larger indications, including Alzheimer's disease. Our Phase 1 study in healthy volunteers demonstrated that AL-one hundred and one was well tolerated and increased for granular levels in plasma and CSF in a dose dependent manner. We in partnership with GSK plan to initiate a global Phase 2 clinical trial in early Alzheimer's disease. With that overview, I'll now turn the call over to Mark to provide an update on our financial results and milestones.

Speaker 4

Mark?

Speaker 5

Thank you, Gary. We summarized our Q2 2023 financial results in the press release that we made available after the market closed today. First, I'll highlight that we remain well funded to execute our strategic objectives. We ended the Q2 of 2023 with a strong cash $200,000 compared to $79,900,000 for the same period in 2022. Total research and development expenses for the Q2 of 2023 were $46,200,000 compared to $54,500,000 for the same period in 2022.

Speaker 5

Total general and administrative expenses for the Q2 of 2023 were $13,600,000 compared to $15,800,000 for the same period in 20 For the quarter ended June 30, 2023, we reported a net income of $1,400,000 or $0.02 per share compared to a net income of $9,900,000 or $0.12 per share for the same period in 2022. Turning now to 2023 financial guidance, we are increasing our collaboration revenue estimate to be between $90,000,000 $100,000,000 Our anticipated total research and development expenses are reduced to now be between $210,000,000 220,000,000 And total anticipated general and administrative expenses were tightened to now be between $60,000,000 $65,000,000 In May 2023, Elektor and GSK formally decided to have GSK conduct the initial Phase 2 trial for AL-one hundred and one in Alzheimer's disease, resulting in a contract modification to the GSK agreement. Our guidance updates to revenue and research and development expenses are reflective of this change. Looking ahead, we expect to achieve several important milestones. Namely, we plan to complete enrollment in our 2 late stage trials.

Speaker 5

We are on track to complete enrollment in INVOKE-two, our Phase 2 clinical trial for AL-two in Alzheimer's disease in the Q3 of 2023. We also anticipate we will complete enrollment in INFRONT 3, our pivotal Phase 3 clinical trial for latasinumab in FTDGRN in the Q4 of 2023. We are well capitalized with a robust cash position and remain focused on advancing our late stage clinical programs. We look forward to providing additional updates as we advance our work. That concludes our prepared comments for today's call.

Speaker 5

Operator, you may now open the line for

Operator

Please standby while we compile the Q and A roster. The first question comes from Greg Harrison with Bank of America. Your line is open.

Speaker 1

Good afternoon. This is Mary Kate on for Greg. Thank you so much for taking our question. We were wondering about the research program that you mentioned. Could you add additional color behind your CNMB research program in Parkinson's disease.

Speaker 1

And maybe as a follow-up, could this target be used in other neurodegenerative diseases or is it Parkinson's specific? Thank you.

Speaker 3

Yes. Thank you for the question. I'm going to start and then I'll turn over to Arnaud to add more color to this. So of course, we are excited about our program ADP-twenty seven, which is a product candidate targeting GTN MB for the treatment of Parkinson's disease. GPNMB is a risk gene for Parkinson's disease.

Speaker 3

It encodes the transmembrane protein GPNMB, which is The pathological genetic variant of gT NMB disrupts the function of multiple lysosomal proteins Like LERK-two and GBA-one, which leads to an inflammatory stress response and accumulation of alpha synuclein and Parkinson's disease. So we are developing ADP-twenty seven, which is a human monoclonal antibody that modulates gpnmb to mimic the protective genetic variant for both familial and sporadic forms of Parkinson's disease. Currently, we are in early

Operator

The next Question comes from Yaron Werber with TD Cowen. Your line is open.

Speaker 6

Hi, this is Joyce on for Yaron. Thanks so much for taking our question. Maybe just one from us on AL-one. Just double checking timing to data readout for that. I think previously you said early 2025, But with this re estimated primary analysis sample size and enrollment completing in Q4, just wanted to double check if there's any Latest updates on timing to data.

Speaker 6

Thank you.

Speaker 5

Yes, happy to take that. This is Mark. So, as We have noted in the press release today, we had a good engagement with the agencies around our Pivotal and Gary can give some more color on that. I'll just start by acknowledging specifically as it relates to The timelines we anticipate that we're going to complete enrollment for that pivotal study in the Q4 of this year. As the study is designed, it's a 96 week treatment period.

Speaker 5

And yes, Gary, do you want to add a little bit more to that?

Speaker 4

Sure, Mark. Yes. So just to add to the very end there, it's a we're going to finish enrollment in the 4th Quarter of this year, 96 weeks later or that would be approximately Q3 of 2025, we will have last patient out and data shortly thereafter. As I mentioned during the call, We had a very productive regulatory interaction that provided us with guidance to help move this trial forward. We've talked a little bit about FDA Feedback from the past, we've recently received scientific advice from EMA, which is generally consistent with FDA.

Speaker 4

So based on this positive feedback from regulatory agencies, In partnership with GSK, we plan to conduct the primary analysis on the symptomatic participants in FRONTI 3, that's a narrowing of the scope. And the agency has also concurred with our proposed sample size estimation that supports a more focused enrollment on the symptomatic participants, 90 to 100

Operator

Please standby for the next question. The next question comes from Greg Suvannavejh with Mizuho Securities. Your line is open.

Speaker 7

Hey, it's Greg Sivanovich. Thanks for taking my questions. I had one just regards to your Discussions with the FDA and the European regulatory authorities and kind of the changes that you're announcing with the Phase III trial. And I'm just curious as to Whether the topic of looking at biomarkers was specifically discussed on the agency's view around whether you Look at biomarkers as perhaps a surrogate endpoint to maybe also take a look at efficacy. Just Wanted to see, at least in this particular disease, how that discussion went?

Speaker 7

Thanks.

Speaker 4

Yes. So we did discuss the entire trial with FDA and interacted also with EMA. We are this is a biomarker rich study. We will have a number of biomarkers, but I want to emphasize that our analysis Our primary analysis is for a clinical treatment effect that's using the CDR, FEDL, Mac, some of the boxes. And we have had a lot of confidence that we will be able to get a achieve a Full approval or traditional approval based on the clinical outcome measure supported by the biomarker data.

Speaker 4

But in the event that the we're disappointed in the primary clinical outcome measure, We will have a very rich biomarker study and we of course will look to that data at that point to decide whether we have sufficient data for a Accelerated approval approach.

Speaker 7

Okay. Thank you so much. And then, maybe just a follow-up question. If you could just share more details just on the blood barrier technology, blood brain barrier technology that you're advancing and Maybe with a lens on how your approach might differ versus others, including neighbors in your backyard and others on the East Just if you could help us understand that. Thanks.

Speaker 2

Yes. This is Arnon. Thank you, Greg. Yes, we have developed a versatile bladder technology that can be specifically tailored to each cargo That can be used with different types of antibodies, which are active Fc or inactive Fc that can be used with for protein and enzyme replacement And the uniqueness of our technology is its versatility and ability to really tailor The technology to each specific cargo and we will sort of disclose more about this technology in the near future.

Speaker 7

Thank you very much.

Operator

Please standby for the next question. Our next question comes from Paul Matteis with Stifel. Your line is open.

Speaker 8

Hi, this is James on for Paul. Thanks for taking our question. So I believe the original study with FTD was powered around a 40% slowing of disease effect size. What is the effect size of studies powered around now With 100 patients, curious if there's any color you can provide there and if there's anything in the kind of blended analysis That kind of reinforces your confidence in that powering. Thanks.

Speaker 4

Yes, sure. Thanks. This is Gary. So our clinical trial design remains unchanged. That's the clinical endpoint, biomarkers, the duration of treatment, etcetera.

Speaker 4

This meeting we had with FDA about our statistical analysis approach was typical and necessary step before eventually finalizing our statistical analysis plan in the next year. This analysis that we're focusing on is still going to provide sufficient power to detect a 40% treatment effect. The specifics around that will be finalized of course in our statistical analysis plan later next year. In terms of your question about why that is, the real advantage here of focusing The analysis on the symptomatic subjects is that the variance of their disease progression is considerably less than the at risk subjects We originally include and plan to include in the primary analysis. So by focusing on the symptomatic subjects, which by the way, we've also Had it had a somewhat easier time enrolling and nearly complete.

Speaker 4

We can we will have Still adequate power to detect the 40% treatment effect.

Speaker 8

Okay. And maybe just one clarifying. So Is there anything different about the stats plan or the analysis that gives you that it's still powered for 40% effect size with Meaning for less patients beyond just the variance or is it really just that the variance is lower, so the stats are statistically it's still powered 40% with a much smaller sample size. Thanks.

Speaker 4

Yes. That's the it's the main what's really driving this Is the fact that as I think I mentioned we mentioned previously, we had Originally disclosed that based on emerging data on the variability of disease and this comes from both the Genfi and ALLFTD cohorts,

Speaker 2

We wanted to go to

Speaker 4

regulatory authorities to discuss the our statistical analysis approach. So it's really driven by the fact That there is that the variance was significantly less than we Had considered with our initial estimates, which were based on very limited data at the time of the trial nearly 3 years ago. So that's the main driver.

Speaker 8

Makes sense. Thank you.

Operator

Please standby for the next question. The next question comes from Tom Shrader with BTIG. Your line is open.

Speaker 9

Good afternoon. Thanks for taking the questions. You guys seem cautious about calling your effects For TREM2 ARIA, is it somehow different or are you just being cautious because it's new? And Also, are you taking A beta scans in this trial? I think you said you were going to.

Speaker 9

Is that something we will see? Did you take baseline scans? And I have a follow-up.

Speaker 4

Yes, thanks. It's a great question. We're just being cautious. This is a different mechanism. And although the MRI Features are the both the MRI features and the clinical aspects The area that we're seeing is really indistinguishable, if you will, and that's not I'll take it from me, that's from a number of Thought leaders that we've shown that we've discussed the data with.

Speaker 4

So because it's a different mechanism, we don't want to presume that this is related necessarily So amyloid clearance, but of course, clearance in misfolded proteins, including amyloid is one of the functions Of microglia and so boosting microglia function maybe leading to that. We have it will have a rich data set including Plenty of amyloid PET, so we will have certainly learn more about that mechanism when we open the study next year.

Speaker 9

And then abeta scanning, are you doing that?

Speaker 4

Yes. I'm sorry. So we do have abeta PET and This study includes both amyloid and tau PET studies, substudies and so we will have that data to certain.

Speaker 9

And then housekeeping for the 1 trial, how many asymptomatic patients did you get? Are you just going to continue to treat those? And what do you do with patients that progress while on treatment? Are they counted in the bucket of symptomatic?

Speaker 4

Yes. So we have a relatively smaller much smaller number of at risk subjects Then we do symptomatic subjects. And those at risk subjects are, in fact, we could see this with a blinded sample size re estimation Are not progressing very much. So that hasn't really been an issue. I think The second part of your question was how many of the symptomatic patients have been enrolled?

Speaker 9

How many of them became symptomatic, but it sounds like it might be none.

Speaker 4

Yes. It's from what we can tell by sample size re estimation, it doesn't look Like we're seeing progression in those patients yet.

Speaker 9

Okay. Thanks for the detail.

Operator

Please standby for our next question. The next question comes from Myles Mentor with William Blair. Your line is open.

Speaker 10

Hi. Thanks for taking the questions. Just on the InPran III analysis here, just on a blinded basis, Are you seeing the same variability on a symptomatic patient population as What you saw or what they saw in GenFee II, specifically looking at the analysis that you did With the n equals 12 in front 2 patient population versus the 10 patients you picked from Gen 5 2, Like is it that sort of level of variability that we should be looking at, that you're seeing on a blinded basis in IMPROXX 3? Thanks.

Speaker 4

Yes. Thanks for the question, Myles. So when we speak about the variance and as a basis of the A change in the statistical analysis plan for the Phase 3 study, we're speaking about variance In that study, which is, as you said, we're enrolling 90 to 100 patients and we're nearly finished. So That's we're talking about sample size reestimations based on that data. The data sets for the Phase 2 study, which I think I heard you reference, These are very small cohorts and 10 up to 14 in the C9 cohort, very, very small, really too small to really draw any conclusions about disease progression.

Speaker 4

That study was really designed to be a biomarker proof of concept study, was not designed or powered to determine treatment effects and Really, so you can't really say much about looking at those very small cohorts about overall variance.

Speaker 10

So you'd caution against extrapolating that and saying that in the placebo arm, patients are going to decline like 12 points on CDR on placebo over 2 years.

Speaker 4

No, no. I mean, I would say we've looked very carefully at the Gen P and OFTD data and we sat down with the people who are running those And the variance actually, the reason we thought about this in the first place was reading through that their recent paper that came out in fall of last year With Adam Stafferoni as the lead author that and studying that where he in that paper he suggested that Future trials in FTD could potentially be significantly smaller than our original study design. And when we looked at the variance, They shared their data with us and we've looked at that and it was considerably less than our original estimates for our own trial and that's where we went in and looked And found with our sample size estimation that in fact our variance was, as I said, much less than we originally anticipated Conservatively based on the original whatever data was available 3 years ago.

Speaker 3

Miles, I'd like to also maybe qualify A little bit, I think you are asking about the variability in the Phase 2 study, but that's in the C9 population and not the granuline population.

Speaker 2

I mean the variability in the granular population in the Phase 2 study is similar to the Phase 3 study. I mean, the increased variability means if you look just as symptomatic, if you look at pre symptomatic or at least the variability is much higher. The conversion rate is much less predictable. So the variability in Phase III in the symptomatic only is Significantly smaller than if you combine symptomatic and at risk and symptomatic in Phase 3 similar to the symptomatic in Phase 2.

Speaker 10

Okay. Quick one on InvoTUR. Were there any patients that were Positive or potentially positive for cerebral amyloid angiopathy that may have been played at those ARIA signals? Thanks.

Speaker 4

Not that we know of, no.

Speaker 10

Thanks for the question.

Operator

I show no further questions in the queue. I would now like to turn the call back to Mark for closing remarks.

Speaker 5

Thank you, operator. And before we end the conference call, I'd just like to share that Elektra will be participating in a number of upcoming Conferences, including BTIG's Virtual Biotechnology Conference on August 7, Citi's 18th Annual Biopharma Conference on September 7 in Boston, Morgan Stanley's Global Healthcare Conference on September 11 in New York, and H. C. Wainwright's Global Investment Conference on September 12, also in New York. Thank you again for your time and attention today.

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