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spk07: Ladies and gentlemen, and welcome to the Alcator Mid-Year 2023 Earnings Conference Call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star 11 on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star 11 again. 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 Communication and Investor Relations. Please go ahead.
spk12: Thank you, Operator, and good afternoon, everyone. Earlier this afternoon, we released our financial results for the second quarter of 2023. The press release is available on our website at www.elector.com. And our 10-Q is filed with the Securities and Exchange Commission this afternoon. Joining me on the call today are Dr. Arnon Rosenthal, co-founder and CEO, Dr. Sarah Kankari Mitra, President and Head of Research and Development, Dr. Gary Romano, Chief Medical Officer, and Dr. Mark Grasso, Chief Financial Officer. After our formal remarks, we'll open the call for Q&A. I'd like to note that during this call, we will be making a number of forward-looking statements. 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 FPC filings for more information. I would now like to turn the call over to Arnon Rosenthal, Chief Executive Officer. Arnon?
spk10: Thank you, Katie, and good afternoon, everyone. We appreciate you joining our conference call today. I'll start by highlighting Elector's key initiatives during the first half of 2023. Next, Sarah will share the progress we believe we have achieved with our immunoneurology research. Then, I invite Gary to discuss the late-stage clinical program. Afterwards, Mark will provide an update on our financial results and milestones. Today, Alekto is a late-stage clinical biotechnology company with an advanced pipeline that includes novel first-in-class clinical programs. We also have world-class partnerships in which we retain significant rights as well as innovative research and technology portfolios. Regarding our TRUMP2 program, we provide more details about our Invoke2 Phase 2 clinical trial with AL002. The tribe is approaching full enrollment, and nearly all eligible participants are rolling over into the long-term extension portion of the study. We're also looking forward to sharing key highlights from the 002 program we presented at the Alzheimer's Association International Conference, or AAIC, in July. As presented at AAIC, in a mouse model of Alzheimer's disease, our antibody AL002 was shown to reduce total tau in the serum, which is a biomarker for normal repair, as well as to increase the ratio of A-beta 42 to 40, which may affect remodeling of amyloid plaque. Further, we are encouraged that AL002 was well tolerated in our Phase I trial with healthy volunteers. The fact that we are seeing what appears to be incidences of ARIA in INVOX2 participants associated with EPOE4 status we believe is interesting and suggest biological activity. With enrollment invoked to nearly complete, we are advancing closer to potential meaningful data readout. We will also share with you the outcome of our recent productive agency interactions with the FDA and EMA on our InFRONT3, phase three pivotal trial evaluating latiluzumab in frontotemporal dementia. The enrollment in InFRONT3 is also nearly complete. We will also provide a brief update on our InFRONT2 open-label phase two clinical trial in frontotemporal dementia with D9072 mutation. With that, I will turn over to Sarah to highlight the progress we have achieved with our immunoneurology research.
spk11: Thank you, Arnon. As we look across the state, 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 highlight 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 or in combination with these novel treatment approaches. At Elektor, we applaud this progress while we strive to advance transformative first-in-class therapies that enhance efficacy and improve the quality of life for patients. Sadly, brain disorders impact more than 1 billion people worldwide and result in the loss of 6.8 million lives each year. 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 immunoneurology 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, immunoneurology 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 immunoneurology therapies strive to shift ineffective or damaged microglia into effective and beneficial agents. We've translated immunoneurology into a broad portfolio with transformative potential. We are developing letazinamab and AL-101 in partnership with GSP. These candidates are intended to block sultilin, a degradation receptor for progranolins, to boost progranolin levels and enhance microbial activity. In collaboration with AbbVie, we are also developing AL002. With AL002, we seek to increase TREM2 signaling with the intention of stimulating the functionality of microbial. We believe these candidates represent the most advanced immunoneurology 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 technologies which we may selectively deploy on next-generation programs. An additional novel first-in-class program we are excited about is ADP027, which is targeting the GPNMV gene for the treatment of both familiar and sporadic Parkinson's disease. Currently, we are in the process of selecting our lead candidate and look forward to providing updates on ADP027 as we progress the program. Our collaborations with GSK and AbbVie, combined with our clinical expertise and differentiated approach, allow us to advance a broad pipeline with the potential to transform the treatment landscape for brain disorders. With that, I'll turn it over to Gary to highlight recent progress with our late-stage clinical program.
spk02: Thank you, Sarah. I'll begin with our AL002 program, the most advanced TREM2 program in clinical development for Alzheimer's disease worldwide. AL002 is a novel investigational humanized monoclonal antibody that binds to and activates the triggering receptor expressed on myeloid cells, or TREM2. TREM2 is a phospholipid receptor on the microglial membrane that senses pathological changes in the brain. Binding of TREM2 to its biological substrates, which include ApoE, lipids, A-beta, and other cellular debris, triggers microglial signaling pathways that allow the microglia to adopt a defensive response to disease by clearing pathology and protecting neuronal health. Loss-of-function variants in TREM2 are known to be deleterious. Heterozygote mutations in the TREM2 gene reduce functionality of microglia and increase the risk of Alzheimer's disease. For example, the R47H loss-of-function variant increases Alzheimer's disease risk by threefold. AL-502 binds to TREM2 receptors, resulting in clustering of TREM2 in the microglial membrane and activation of TREM2 signaling pathways, which support microglial survival, proliferation, and function. Microglia are the primary innate immune cells of the central nervous system, 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. 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 AL002 in Healthy Volunteers, which demonstrated both dose-dependent target engagement and activation of microglia. INVOG2 is Elector's Phase 2b study of AL002, which is now ongoing in patients with early Alzheimer's disease. INVOKE-2 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 three doses of AL002 that were demonstrated in phase one to activate microglia. Participants received AL002 or placebo as monthly infusion. INVOG-2 was designed by Elector and Abbey 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 microbial activation and of Alzheimer's pathophysiology. And neuroimaging biomarkers include amyloid and TALPET and volumetric MRIs. To date, we have enrolled more than 300 participants, and the trial is nearly fully enrolled. We expect to complete enrollment in the third quarter of this year with their study reading out in the fourth quarter of 2024. At the Alzheimer's Association Annual Conference, or AIC, in July, we presented an update on INVOK2, which highlighted that early in the trial, three participants had treatment emergent neurological signs and symptoms, and associated MRI findings consisting of focal vasogenic edema, sulcal effusions, microhemorrhages, and superficial siderosis. These MRI findings resemble the area that has been reported following treatment with anti-amyloid antibodies regarding their MRI features, incidence, timing of onset, relatedness to the number of APOE4 alleles, as well as the frequency and spectrum of clinical manifestations. we believe AL002 has the potential to work alone or in combination with anti-amyloid beta therapies by harnessing the broader but beneficial effects of microglia. We expect to report INVO2 data in the fourth quarter of 2024. At AAAIC in July, we also presented a poster on mouse model data demonstrating that TREM2 activation improved Alzheimer's disease biomarkers, including amyloid and tau. I'll now turn to latacinamab, our novel first-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 GenPhi and all FTD cohorts, we plan to meet with regulatory authorities to discuss modifications to the statistical analysis approach for our InFRONT3 Phase III clinical trial of latacinamab in participants with FTD granulins. This is driven by both our and the scientific community's evolving understanding of the variability of FTD granulone disease progression. 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. Our recent interactions with FDA and EMA were productive, and based on agency feedback, we plan to conduct a 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 approximately 90 to 100 symptomatic FDD granulin participants for a treatment duration of 96 weeks. As a result, we plan to complete enrollment in InFRONT3 in the fourth quarter of 2023. Regarding the FDD C9 ORF72 cohort of our InFRONT2 Open Label Phase 2 trial, we confirmed again a two- to three-fold elevation in progranulin levels in CSF and plasma. We have conducted a preliminary analysis of disease progression rates for 14 participants who were treated with latacinamab, compared with baseline matched controls from the all-FTD registry. A high degree of variability in disease progression rates in both groups rendered the analysis uninformative regarding treatment effects. Turning to AL101, our second product candidate in our progranulin portfolio that we are developing in partnership with GSK. AL101 is designed to elevate progranulin levels in a manner similar to latazinamab. Its different pharmacokinetic and pharmacodynamic properties potentially enable dosing regimens for use in the treatment of larger indications, including Alzheimer's disease. Our phase one study in Healthy Volunteers demonstrated that AL101 was well tolerated, an increase for grinding levels in plasma and CSF in a dose-dependent manner. We, in partnership with GSK, plan to initiate a global phase two 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. Mark?
spk14: Thank you, Gary. We summarized our second quarter of 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 second quarter of 2023 with a strong cash position of $630 million, and our runway extends through 2025. Collaboration revenue for the second quarter of 2023 was $56.2 million compared to $79.9 million for the same period in 2022. Total research and development expenses for the second quarter of 2023 were $46.2 million compared to $54.5 million for the same period in 2022. Total general and administrative expenses for the second quarter of 2023 were $13.6 million compared to $15.8 million for the same period in 2022. For the quarter ended June 30th, 2023, we reported a net income of $1.4 million or two cents per share compared to a net income of $9.9 million or 12 cents 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 million and $100 million. Our anticipated total research and development expenses are reduced to now be between $210 million and $220 million. and total anticipated general and administrative expenses are tightened to now be between $60 million and $65 million. In May 2023, Electro and GSK formally decided to have GSK conduct the initial Phase II trial for AL101 and 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 two late-stage trials. We are on track to complete enrollment in INVOKE-2, our Phase II clinical trial for AL002 and Alzheimer's disease, in the third quarter of 2023. We also anticipate we will complete enrollment in INFRONT-3, our pivotal Phase III clinical trial for laticinib and FTD-GRN, in the fourth quarter of 2023. We are well-capitalized with a robust CASP 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. Operator, you may now open the line for questions.
spk07: As a reminder, to ask a question, please press star 11 on your telephone and wait for your name to be announced. Please stand by while we compile the Q&A roster. The first question comes from Greg Harrison with Bank of America. Your line is open.
spk13: Good afternoon. This is Mary Cato 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 GPNMV research program in Parkinson's disease? And maybe as a follow-up, could this target be used in other neurodegenerative diseases or is it Parkinson's specific? Thank you.
spk11: Yeah, thank you for the question. I'm going to start, and then I'll turn over to Arna to add more color to this. So, of course, we are excited about our program ADP-027, which is a product candidate targeting GPNMB for the treatment of Parkinson's disease. GPNMB is a risk gene for Parkinson's disease. It encodes the transmembrane protein GPNMB, which is selectively expressed in microglia and oligodendrocytes, and regulates lysosomal function. Our hypothesis is that the pathological genetic variant of GPNMB disrupts the function of multiple lysosomal proteins like LRK2 and GBA1, which leads to an inflammatory stress response and accumulation of alpha-synuclein and Parkinson's disease. So we are developing ADP027, 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, it's part of our early portfolio.
spk08: We are looking forward to a lead selection soon. Please stand by for our next question.
spk07: The next question comes from Yaron Werber with TV Cowan. Your line is open.
spk01: Hi. This is Joyce on for Yaron. Thanks so much for taking our question. Maybe just one from us on AL001. Just double checking timing to data readout for that. I think previously you said early 25, but with this, you know, primary analysis sample size and enrollment completing in Q4. Just wanted to double check if there's any latest updates on timing to data. Thank you.
spk14: Yeah, 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 timelines, we anticipate that we're going to complete enrollment for that pivotal study in the fourth quarter of this year. As the study is designed, it's a 96-week treatment period. And, yeah, Gary, do you want to add a little bit more to that?
spk02: Sure, Mark. Yeah, so just to add to the very end there, it's a 96- We're gonna finish enrollment in the fourth quarter of this year, 96 weeks later, or that would be approximately third quarter of 25, 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 in the past, we've recently received scientific advice from EMA, which is generally consistent with FDA. 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 FRONT3. That's a narrowing of the scope. And agencies also concurred with our proposed sample size estimation that supports a more focused enrollment on the symptomatic participants, 90 through 100. symptomatic participants for a treatment duration of 96 weeks.
spk08: Please stand by for the next question.
spk07: The next question comes from Greg Souvenaya with MIZU Securities. Your line is open.
spk05: 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 three trial. And I'm just curious as to whether the topic of looking at biomarkers was specifically discussed and the agency's view around whether you could 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. Thanks.
spk02: Yes. So, you know, 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 is, our primary analysis is to use, is for a clinical treatment effect. That's using the CDR, FEDL, NAC, some of the boxes. And, you know, we have a lot of confidence that we will be able to get, achieve a full approval or a traditional approval based on the clinical outcome measure. supported by the biomarker data. But, you know, in the event that 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, you know, sufficient data for a accelerated approval approach.
spk05: 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 Coast, just if you could help us understand that. Thanks.
spk09: Yes, this is Arnon.
spk10: and thank you greg yeah we have we have developed a versatile blood and bio technology that can be specifically tailored to each cargo that can be used with different types of antibodies which are we have active fc or inactive fc that can be used with for protein and enzyme replacement and the uniqueness of our technologies is versatility and an ability to really tailor
spk09: the technology to each specific cargo, and we will sort of disclose more about this technology in the near future.
spk05: Okay, thank you very much.
spk07: Please stand by for the next question. Our next question comes from Paul Matase with Stifel. Your line is open.
spk04: 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%, you know, 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, you know, anything in the kind of blended analysis you did that kind of reinforces your confidence in that powering. Thanks.
spk02: Yeah, sure. Thank you. This is Gary. So our clinical trial design remains unchanged. That's the clinical endpoint, biomarkers, the duration of treatment, et cetera. You know, this meeting we had with FDA about our statistical analysis approach was typical and necessary step before eventually finalizing our statistical analysis plan 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, you know, 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 that 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 a somewhat easier time enrolling and nearly complete, we can, you know, we will have still adequate, you know, adequate power to detect the 40% treatment effect.
spk04: Okay. Maybe just one clarifying. So is there anything different about the stats plan or the analysis that gives you, you know, that it's still powered for a 40% effect size with, you know, meaningfully less patients? beyond just the variance, or is it really just that the variance is lower? So, you know, the stats are, you know, statistically, it's still powered for 40% with a much smaller sample size. Thanks.
spk02: Yeah, that's the main, what's really driving this is the fact that, as I think I mentioned, we mentioned previously, you know, we had originally disclosed that based on emerging data on the variability of disease, and this comes from both the GEN3 and OFDD cohorts, we wanted to go to regulatory authorities to discuss the, you know, our statistical analysis approach. So, it was really driven by the fact that there is, you know, 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 three years ago. So that's the main driver.
spk04: Makes sense. Thank you.
spk07: Please stand by for the next question. The next question comes from Tom Schrader with BTIG. Your line is open.
spk03: 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. Is that something we will see? Did you take baseline scans? And I have a follow-up.
spk02: Yeah, thanks. It's a great question. We're just being cautious. You know, this is a different mechanism, and although the MRI – features are, you know, both the MRI features and the clinical aspects of the area that we're seeing is really, you know, indistinguishable, if you will. And that's not going to take it from me. That's from a number of thought leaders that we've shown that we've discussed the data with. So, you know, because it's a different mechanism, you know, we don't want to presume that this is related necessarily to amyloid clearance. But, of course, You know, clearance of misfolded proteins, including amyloid, is one of the functions of microglia, and so boosting microglia function, you know, may be leading to that. We'll have a rich data set, including plenty of amyloid PET, so we will certainly learn more about that mechanism when we open the study next year.
spk03: And then A-beta scanning, are you doing that?
spk02: Yes, I'm sorry. So we do have a beta PET, and this study includes both amyloid and tau PET studies, sub-studies, and so we will have that data for certain.
spk03: And then housekeeping for the 001 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 patients?
spk02: Yeah, so we have a relatively smaller, much smaller number of at-risk subjects than we do symptomatic subjects. And those at-risk subjects are, in fact, you know, we could see this with a blind sample size estimation are, you know, 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?
spk03: Well, how many of them became symptomatic, but it sounds like it might be none.
spk02: Yeah, from what we can tell by sample size re-estimation, it doesn't look like we're seeing progression in those patients yet.
spk03: Okay, thanks for the detail.
spk07: As a reminder, to ask a question, please press star 1-1 on your telephone. Please stand by for our next question. The next question comes from Miles Minter with William Blair. Your line is open.
spk06: Hey, thanks for taking the questions. Just on the Infront3 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 GENFEED2? specifically looking at the analysis that you did with the N equals 12 in front two 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 saying on a blinded basis in front three? Thanks.
spk02: Yeah. Yeah. Thanks for the question, Myles. So when we speak about the variants and as a basis of the a change in the statistical analysis plan for the phase three study, we're speaking about variance in that study, which is, you know, as you said, we're enrolling 90 to 100 patients and we're nearly finished. So, we're talking about sample size re-estimations based on that data. The data sets for the phase two study, which I think I heard you reference, you know, these are very small cohorts. up to 14 in the C9 cohort. Very, very small. Really too small to really draw any conclusions about disease progression. You know, that study was really designed to be a biomarker proof of concept study. It was not designed or powered to determine treatment effects. And really, you know, so you can't really say much about looking at those very small cohorts. about overall variants.
spk06: 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 two years?
spk02: No, no. I mean, I would say we've looked very carefully at the gen P and all FTD data, and we've sat down with the people who are running those studies. And the variants, actually, the reason we thought about this in the first place was reading through their recent paper that came out in fall of last year. with Adam Staffaroni as the lead author that, and studying that where he, you know, then 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, you know, they shared their data with us and we 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, you know, and found with our sample size estimation. And in fact, our variance was, as I said, much less than we originally anticipated conservatively based on the original, whatever data was available three years ago.
spk11: Miles, I'd like to also maybe qualify a little bit. I think you are asking about the variability in the phase two study, but that's in the C9 population and not the granuline population.
spk10: I mean, the variability in the granuline population in the phase two study is similar to the phase three study. If you look just at symptomatic, if you look at pre-symptomatic or at risk, the variability is much higher. The conversion rate is much less predictable. So the variability in phase three in the symptomatic only is significantly smaller Then if you combine symptomatic and at risk, the symptomatic in phase three is similar to the symptomatic in phase two.
spk06: Cool. OK. Quick one on invoke two. Were there any patients that were positive or potentially positive for cerebral amyloid angiopathy that may have inflated those ARIA signals? Thanks.
spk09: Not that we know of, no. Cool.
spk06: Thanks for the question.
spk07: I show no further questions in the queue. I would now like to turn the call back to Mark for closing remarks.
spk14: Thank you, operator. And before we end the conference call, I'd just like to share that Elector will be participating in a number of upcoming conferences, including VTIG's Virtual Biotechnology Conference on August 7th, CIDI's 18th Annual Biopharma Conference on September 7th in Boston, Morgan Stanley's Global Healthcare Conference on September 11th in New York, and H.C. Wainwright's Global Investment Conference on September 12th, also in New York. Thank you again for your time and attention today.
spk07: This concludes today's conference call. Thank you for participating. You may now disconnect.
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