Elekto at Goldman Sachs Conference: Strategic Innovations in Neurodegenerative Disease

On Tuesday, 10 June 2025, Elekto (NASDAQ:ALEC) participated in the Goldman Sachs 46th Annual Global Healthcare Conference 2025. The company, led by CEO Arnon Rosenthal, presented its strategic focus on combating degenerative brain disorders. Elekto showcased its promising clinical programs and financial stability, while also addressing the challenges and opportunities in its pipeline.

Key Takeaways

• Elekto is advancing two late-stage clinical programs targeting frontotemporal dementia (FTD) and Alzheimer’s disease (AD).
• The company is financially robust, with a cash runway extending through the second half of 2027.
• Elekto has secured a $700 million upfront payment from a collaboration with GSK, with potential for $1.5 billion in milestone payments.
• The development of a novel blood-brain barrier shuttle technology is a key focus, aiming to enhance drug delivery.
• Elekto plans to proceed with regulatory submissions for its FTD program by the end of the year if Phase 3 results are positive.

Financial Results

• GSK Collaboration:

- Received a $700 million upfront payment.

- Potential for $1.5 billion in milestone payments.

- $160 million milestone for AL001 commercial sales in the US.

- $90 million milestone for AL001 commercial sales in the EU.

- 50/50 profit share in the US for both AL001 and AL101.

- Royalty arrangements for AL101 outside the US, similar to a 50/50 profit share.

• Cash Runway:

- Financial resources extend through the second half of 2027.

- Over $350 million available for clinical and early-stage development.

Operational Updates

• Lenacidimab (AL001) - Frontotemporal Dementia (FTD):

- Phase 3 pivotal study results expected by year-end.

- Received Breakthrough Therapy designation from the FDA.

• AL101 - Alzheimer’s Disease (AD):

- Completed enrollment in a large Phase 2 study, with results anticipated by the end of 2026.

- Focused on early Alzheimer’s disease, measuring the CDR sum of boxes.

• ABC (Brain Carrier) Technology:

- Developing brain carriers for antibodies, enzymes, and nucleic acids.

- Aiming for A beta and GCase programs to enter clinical trials next year.

• Pipeline Expansion:

- Developing siRNA and tau siRNA with brain shuttles.

- Targeting GCase for Parkinson’s disease and Lewy body dementia.

Future Outlook

• Regulatory Submission:

- Plans for regulatory submission based on a single pivotal Phase 3 study if results are favorable.

• Alzheimer’s Disease Treatment Strategy:

- Progranulin-based therapies may complement anti-amyloid treatments.

• Combination Therapy:

- Potential for combining with anti-amyloid treatments.

• Preclinical Program Development:

- Fully owned programs with potential for future partnerships.

Q&A Highlights

• Frontotemporal Dementia (FTD):

- Lenacidimab increases progranulin levels two to threefold, showing a 48% improvement in disease progression in Phase 2.

- Phase 3 study aims to detect a 40% slowing of disease progression.

• AL101 and PK/PD Differences:

- AL101 has a longer half-life compared to AL001, offering convenience in use.

Readers are encouraged to refer to the full transcript for a detailed account of Elekto’s presentation and strategic insights shared during the conference.

Full transcript - Goldman Sachs 46th Annual Global Healthcare Conference 2025:

Unidentified speaker, Host, Goldman Sachs: All right. Good morning, everyone, and welcome to the Goldman Sachs Annual Healthcare Conference. Delighted to be joined by the team from Elektor here today. Maybe I’ll kick it off. I’ll let you guys introduce yourselves and maybe provide a brief overview of the company.

Arnon Rosenthal, CEO and cofounder, Elektar: Sure. I’m Arnon Rosenthal. Welcome, everyone. I was I’m the CEO and cofounder of Elektar. Before that, I was at Genentech for sixteen years as part of the research team.

Then I started Renat Neuroscience that was acquired by Pfizer. One of the drugs that came from this company is AJOVY, the migraine drug that started the CGRP migraine therapeutics. I then started Annexom Bioscience. It’s a publicly traded company. And for the last twelve years, Elekto is my life.

And Elekto was created really with with the vision and mission to to really eradicate degenerative brain disorders, to really make degenerative brain disorders similar to smallpox now. And in order to do this, we really created we build an integrated research organization that involved human genetics, protein engineering, deep understanding of cellular and animal models for neurodegenerative disorders. We build an extensive clinical team, an extensive manufacturing organization. So we are building a large integrated company that can go from ideas all the way to approval. We currently have two programs in late stage clinical development.

We have a phase three program in frontotemporal dementia, which is the largest dementia for people under the 60. The readout is expected to be by the end of this year. It’s a pivotal study. If it’s positive, we will sort of apply for approval and hopefully we’ll proceed to commercialization. In addition to the phase three program, we have a phase two program in Alzheimer’s disease.

We completed recruitment for placebo controlled double blinded eighteen months long trial, which is and we expect data sometimes in 2026. In addition to the clinical programs, we have a significant portfolio of preclinical programs that target Alzheimer’s disease, Parkinson’s disease, Lewy body dementia, and we are integrating our programs with our blood and barrier shuttle to facilitate the entry of both antibodies, enzymes and nucleic acid into the brain. And sort of these preclinical programs are expected to enter the clinic next year also, at least some sort of them.

Unidentified speaker, Host, Goldman Sachs: Maybe we’ll start with lenacidimab in frontotemporal dementia. And you could maybe just set the stage for us on what is frontotemporal dementia. You mentioned this earlier. What do we know about the kind of the pathogenesis of the disease, and what’s the current treatment for those patients?

Arnon Rosenthal, CEO and cofounder, Elektar: So

Unidentified speaker, Unspecified, Elektar: frontotemporal dementia encompasses subtypes that are genetically determined and among those, one of the most common genetic forms of frontotemporal dementia is associated with mutation of the programming gene. These are, loss of function, heterozygous loss of function mutation and roughly five to ten percent of the cases between frontotemporal dementia are characterized by these kind of mutations. Our drug ladocinamab is, it binds to the sorrelin, which is the major enzyme responsible for trafficking of progranulin and degradation of progranulin and through the binding and neutralization of the sorghum receptor, our drug latodinumab is able to increase extracellular levels of progranulin by two to threefold, both in plasma and CSF.

Unidentified speaker, Host, Goldman Sachs: Great. And then I guess what do we, understand about the clinical benefit of increasing progranulin once people have disease? Is that sufficient to kind of drive clinical, clinical meaningful results?

Unidentified speaker, Unspecified, Elektar: Abnormalities and mutation of the programming gene are associated with ninety percent probability of developing frontotemporal dementia by the age of 75. So there is almost complete penetrance of the gene, of those mutations. Frontotemporal dementia in patients with mutational deprogramming gene is associated with roughly 50% decrease of programming levels. Our drug is able to increase programming level two to threefold in CSF and plasma respectively, restoring programming levels to normal levels. And we have the we have seen this kind of data both in, healthy volunteers Mhmm.

As well as in patients with fronto temporal dementia in our phase two study.

Unidentified speaker, Host, Goldman Sachs: You referenced the phase two. Maybe you could spend a bit more time on what you guys saw in that phase two, trial and how did the results there kind of inform your phase three design?

Unidentified speaker, Unspecified, Elektar: Yeah. So the phase two study, was an open label study where we enrolled different types of genetic FTD patients. Among those, we enrolled 12 patients with frontotemporal dementia and mutation of the programming gene and these are the same population that we are enrolling in the phase three study. And, we saw, twelve months of treatment, after twelve months of treatment, besides increases of progranulin that I already described, we saw, changes in lysosomal markers, as well as change in volumetric MRI. And we also measured CDR, NAC, FTLD, sum of boxes, which is the gold standard measurement to track disease progression.

And we compared the change in the CDR sum of boxes, the FTLD version, to the natural progression of disease in match controls from the registry data from the GMPE study. And we observed an improvement of disease progression by forty eight percent using the at one year using this much controls. We also saw a positive effect compared to the natural history of the disease on other biomarkers. We saw a decrease in brain atrophy, in frontotemporal cortices atrophy, as well as a decrease in ventricular enlargement compared to these natural controls.

Unidentified speaker, Host, Goldman Sachs: Okay. You talked about this in in that response, but there was a natural history kind of matched control data set. It’s how how do you think about the fidelity of that natural history kind of matched population in terms of the variability across this patient population? And I guess how much confidence do you have that that will be kind of recapitulated in the placebo controlled study you’re doing here?

Unidentified speaker, Unspecified, Elektar: So we these controls were taken from one of the two largest registry data set available. The name of this registry is called Genfi, and we matched the historical controls to our phase two patients according to certain baseline characteristics, such as the severity of disease measured with the CDR and PLASMAC FTLD sum of boxes, as well as we did matching by age, gender, as well as neurofilament light chain baseline So they were very comparable and we use propensity score matching, which is a statistical technique used very often for this kind of comparisons. Our study is, in the phase so the population in our phase three study is very similar to the phases two study and we don’t it’s a placebo controlled trial pivotal phase three study and we don’t expect the placebo response to be, particularly, impactful because according to other studies in neurodegenerative diseases, the placebo response is not very large and it tends to, plateau after the few weeks of treatment. And moreover, we model the magnitude of placebo response in our, statistical powering assumptions.

Unidentified speaker, Host, Goldman Sachs: Okay.

Arnon Rosenthal, CEO and cofounder, Elektar: So just maybe to add two things. the FDA reviewed the phase two open label studies and based on the phase two studies awarded us breakthrough therapy. So they accepted the statistical analysis and the open label studies and sort of all the data in the open label studies were consistent. Again, we saw normalization of multiple isosomal and sort of neurodegenerative biomarkers. We show slowdown in brain tissue loss.

We show slowdown in cognition by 40%.

Unidentified speaker, Host, Goldman Sachs: Mhmm.

Arnon Rosenthal, CEO and cofounder, Elektar: And our phase three study is 10 times larger and twice as long as the phase two study. So we think that we have a very large margin of error. Sure. Means even if the phase three is not exactly as the phase two, we still

Unidentified speaker, Host, Goldman Sachs: Yeah.

Arnon Rosenthal, CEO and cofounder, Elektar: Have a lot of room to

Unidentified speaker, Host, Goldman Sachs: Big cushion.

Arnon Rosenthal, CEO and cofounder, Elektar: Yeah. Yeah.

Unidentified speaker, Host, Goldman Sachs: Have been some other progranulin directed agents that were discontinued. What distinguishes ladasenamab in the way it works versus some of these other programs targeting the same mechanism?

Arnon Rosenthal, CEO and cofounder, Elektar: So, basically, what discontinued are transcriptional activators, like what’s called HDAC

Unidentified speaker, Host, Goldman Sachs: Mhmm.

Arnon Rosenthal, CEO and cofounder, Elektar: Activators that was supposed to increase expression of the progranulin from the progranulin gene, and they ended up not really working. Mechanistically, they never really worked. Nobody was really able to show in human or even in nonhuman primate that there is a meaningful elevation of progranulins. So I think that just the mechanism of action of the mainly one previous drug was just not working. Now there are other therapeutic approaches.

As as you know, there’s gene therapy. There’s enzyme replacement therapy.

Unidentified speaker, Host, Goldman Sachs: Yeah.

Arnon Rosenthal, CEO and cofounder, Elektar: And and we are I mean, we think that what’s unique in our approach is that we are elevating the endogenous physiological progranulin in the right places and exactly in the right amount. Like progranulin is a mitogen, it’s a growth factor. If you elevate it more than you need, I mean, the risk of cancer, basically. Mhmm. And if you look at other growth factors like insulin, insulin like growth factor, human growth hormone, all these factors, like, there is a sort of Goldilocks optimal level that sort of you want to elevate it.

If you elevate too much, you start getting diseases. Sure.

Unidentified speaker, Host, Goldman Sachs: Okay. So you’ve got the phase three results coming up here soon. Maybe speak to us about the key endpoint to watch and what your power to detect in terms of difference between, the treatment and the placebo arm.

Unidentified speaker, Unspecified, Elektar: Our phase three study is powered to detect forty percent, slowing of disease progression in the active treatment arm as compared to placebo. And, however, we if we are observe a slowing of disease progression as low as twenty five percent according to our statistical, simulations, this study will be positive.

Unidentified speaker, Host, Goldman Sachs: Okay. And then what comes after kind of a positive result in this trial?

Unidentified speaker, Unspecified, Elektar: So the we are well positioned to deliver meaningful clinical data by the end of twenty twenty five in fourth quarter. And, our studies are weatherly powered and to detect a meaningful effect by the drug and the clinically meaningful I mean, clinically meaningful effect by the drug. And if, the study is positive, we plan to proceed with this regulatory submission based on the single pivotal, phase three study.

Unidentified speaker, Host, Goldman Sachs: Okay. Understood. Addition to ladazimumab, you also have AL one zero one. It it’s also targeting progranulin, but how is it designed to differ from the ladazimumab agent?

Unidentified speaker, Unspecified, Elektar: So, both AL zero zero one and AL AL101, target, the enzyme. Sorry, Lynn.

Unidentified speaker, Host, Goldman Sachs: Sure. Yeah.

Unidentified speaker, Unspecified, Elektar: And, AL101 differs from AL001, for, PK as well as PKPD characteristics, characteristics, which makes it better suited to treat, more common diseases such as Alzheimer’s disease as well as Parkinson’s disease. We, as Arnon said, we just completed the enrollment in a really large phase two study in April 2025 and we are expecting the results by the end of twenty twenty six. This seventy six weeks long study and primary outcome measure is the CDR, some of the boxes. And we are, we have enrolled patients with early Alzheimer’s disease.

Unidentified speaker, Host, Goldman Sachs: Okay, maybe, sorry.

Arnon Rosenthal, CEO and cofounder, Elektar: Yeah. Just it’s interesting that sort of proglanolin is is one of the few universal risk genes for neurodegeneration. Like, most of the risk genes are specific for given diseases. So there’s a set of rich genes for Alzheimer’s disease, Parkinson’s disease, ALS.

Unidentified speaker, Host, Goldman Sachs: Okay.

Arnon Rosenthal, CEO and cofounder, Elektar: And and progranulin is one of the very few genes. There’s maybe one or two additional genes that appear in all. It’s loss of function is a risk for frontotemporal dementia, for Alzheimer’s disease, for Parkinson’s disease, for late, which is another type of late onset dementia typified with TDP 43. It’s a risk gene for ALS. So a universal risk in the every time you see even a modest loss in the level of proglanolin, even fifteen to ten percent, you increase risk of disease.

So we we are developing, again, a franchise of multiple drugs that elevate progranulin for multiple indications, and that’s really what was the excitement around.

Unidentified speaker, Host, Goldman Sachs: So you mentioned that the differences on PK and PKPD. I guess what were some of the key things you needed to optimize for as you think about setting this up for a larger indication?

Arnon Rosenthal, CEO and cofounder, Elektar: So we try to optimize for convenience of use. So the 101 is a two to three times longer half life compared to zero zero one. So you can either deliver it sort of less frequently. One is being delivered once a month, so we can deliver 101 every two or three months. Okay.

Or you can reduce the dose and eventually convert it to subcutaneous delivery. Understood.

Unidentified speaker, Host, Goldman Sachs: And then in terms of the ongoing Alzheimer’s disease study, I guess, what was the decision for Alzheimer’s disease And could you talk about some of the, like, preclinical and clinical data you’ve reported on this agent that supported that decision?

Unidentified speaker, Unspecified, Elektar: So, as Arnon just said, mutation of the progranulin genes are ubiquitous in many neurodegenerative diseases. And through our collaboration with GSK, we thought that besides frontotemporal dementia, Alzheimer’s disease would be a very good, indication to pursue. And, especially in light of the progress made in the past decade and the identification of, very valuable biomarkers that can help with decision making and speeding up the development process. We, in the ongoing phase two study, we use several of those biomarkers, including fluid biomarkers that get markers of Alzheimer’s disease such as the different p tau species, but we also have amyloid PET and tau PET. So, we decided with with GSK to pursue, these larger indications.

Unidentified speaker, Host, Goldman Sachs: In, frontotemporal dementia, you’re stratifying or you’re selecting for patients who have specific progranulin mutations, but in the case of Alzheimer’s disease, are there biomarkers or any other features that help you for the patients most likely to respond?

Unidentified speaker, Unspecified, Elektar: So, the population enrolled in the phase two study is very consistent, with the population enrolled in other Alzheimer’s disease trials. So these are patients with early AD who have evidence of amyloid pathology. We don’t specifically select for patients with mutation, any specific genetic mutation, because the penetrance in Alzheimer’s disease is much lower versus a frontotemporal dementia, where as I said, patient with the programming mutation have more than ninety percent chances to develop the disease. In Alzheimer’s, the link is not, is like different. The population is, as I said, are patients with early AD with the presence of amyloid pathology.

Arnon Rosenthal, CEO and cofounder, Elektar: I mean, the rationale for going with all comers is that, for example, in animal models, overexpressing proganolin beyond normal level is protective in multiple Alzheimer’s disease models.

Unidentified speaker, Host, Goldman Sachs: Okay. So in terms of the phase two study, what would you look to see? And maybe also this is a question sort of for how the partnership works, but what what will you look to see to proceed forward with phase three studies in this indication?

Unidentified speaker, Unspecified, Elektar: So the, the primary outcome measure is the CDR sum of boxes

Unidentified speaker, Host, Goldman Sachs: Mhmm.

Unidentified speaker, Unspecified, Elektar: Which is the gold standard, one of the accepted clinical and functional measures to determine whether the drug is effective in Alzheimer’s disease. We also collect a number of meaningful biomarkers. So overall, we and it’s a study which is it’s an adequate length to detect, an effect is, one year and a half duration, which is, according to, prior data, it’s enough to see, where a meaningful effect of drugs that, in Alzheimer’s disease. So at the end of the study, we’ll review all the clinical data as well as all the biomarker data and make, you know, them decisions about the next steps in the program.

Arnon Rosenthal, CEO and cofounder, Elektar: Yes. Again, so we are measuring PET imaging for I beta, PET imaging for tau, CSF and and serum biomarkers, I beta forty, forty two, multiple phosphatals, neurofilament

Unidentified speaker, Host, Goldman Sachs: Yeah. GFLP. The gamut.

Arnon Rosenthal, CEO and cofounder, Elektar: Yeah. And and it’s, like, five different clinical readouts. So if there’s a movement in any of them that’s meaningful, we will proceed.

Unidentified speaker, Host, Goldman Sachs: Okay. Understood. And then how do you envision the Alzheimer’s disease landscape will kind of evolve with things like new mechanisms coming to bear? Do you expect this would be used in, like, a polypharmacy sense and sequential therapy? And how does that inform the way you think about phase 3s?

Unidentified speaker, Unspecified, Elektar: Yeah, I so the data from anti amyloid treatments, that have been approved are very encouraging and they represent a significant milestone in the treatment of Alzheimer’s disease for the medical community. However, there is still loss to be done. This treatment improved, this is progression, by twenty five to thirty five percent and doesn’t do not, there is room for, even larger improvement. They also, they, we also know that there are some patients, especially patients with more advanced disease, which do not benefit as much from anti amyloid treatments.

Unidentified speaker, Host, Goldman Sachs: Moreover,

Unidentified speaker, Unspecified, Elektar: as we all know, there are significant hurdles for the implementation of those treatment in the, you know, in the field which are driven by the frequency of ARIA, especially in patients who are APO, E4 homozygous. So there is definitely a lot of room to, improve the current treatment in Alzheimer’s disease. Our, drugs, AL-one hundred one, our drug AL-one hundred one is a different mechanism. It, modulates progranulin which above physiological levels and we think that progranulin is a very important modulator of the immune function as well as, neuronal survival. So we think that it may be as well as complementary mechanism to existing amyloid treat anti amyloid treatments, which target only, the amyloid plaques.

Regarding the mode of use, as you ask, sequential treatment combinations, I think these are, the best approach will be data driven. And, as we can see from the Alzheimer’s field, there are different ways of administering, drugs with different mechanism of action that are being tested if we think about, you know, all the way that our, acaemulate treatments are, combined with anti tau treatments. So we still don’t have the best answers, but, but what is the optimal way to combine treatment with different mechanism of action? However, we think that given the diversity of AL101, there is plenty of room, for the drug to coexist with anti amyloid treatments, either in a sequential way or even as a combination treatment, as our drug doesn’t so far has been shown or other side effects profile or similar side effects profile is anti amyloid.

Unidentified speaker, Host, Goldman Sachs: Okay. And then maybe last question on this program. Just remind us the parameters around the GSK collaboration, and what gets triggered with positive phase two results?

Arnon Rosenthal, CEO and cofounder, Elektar: So means the whole franchise is a, you know, a fifty fifty profit share collaboration. We received when the collaboration was established, we received $700,000,000 upfront payment. It’s a total of $1,500,000,000 milestone, which includes for zero zero one, like, commercial sale in The US is is a $160,000,000. Mhmm. Commercial sales in The EU is $90,000,000.

Mhmm. And we we have commercial leadership in The US, so so we are the commercial lead in The US.

Unidentified speaker, Host, Goldman Sachs: Okay.

Arnon Rosenthal, CEO and cofounder, Elektar: For the zero zero one Mhmm. And there is a similar sort of situation for 01/2001. It’s a fifty fifty profit share in The US and royalty, which mimic fifty fifty ex US. Okay.

Unidentified speaker, Host, Goldman Sachs: Great. Maybe we could spend some time on your pipeline. Last summer, you introduced a suite of electro brain carrier ABC candidates. Maybe you can speak to the brain carrier technology that you’ve developed

Arnon Rosenthal, CEO and cofounder, Elektar: Yes. So we are developing brain carrier that should enable us to deliver drug more efficiently to the brain, and we are going after antibody drugs, enzyme drugs, and nucleic acid drugs. So it’s a pretty versatile technology. We are using, means, the Trojan horse technology that sort of other people are using, basically hitchhiking on either the transcellular receptor or the CD 98, which is a amino acid transporter. Mhmm.

What’s unique in our technology is the sort of the the degree of versatility, means, we have a very large range of of affinities to the receptors. And and the technology in general is not plug and play. You have to really tailor the technology for the given drugs. It means that you have to play between efficacy and safety.

Unidentified speaker, Host, Goldman Sachs: Because

Arnon Rosenthal, CEO and cofounder, Elektar: for for specifically, for example, for the transferring based technology, means that the target mediated adverse effects are are hematologic because there is a lot of transferring receptor on on red blood cells. There’s actually 100 times more red set red concerning receptors on red blood cells compared to the blood and barrier endothelial cells. And and if you are somehow buying red blood cells and recruit the immune system to attack red blood cells, you you lead to anemia, and that’s sort of an intrinsic problem with this technology. So you really have to play with, the affinity with the binding epitope for each drug to to optimize the safety and efficacy. And we have, I think, unique ability to do that.

We have a thousand fold range of affinities that we can play with. We have unique epitope that actually may exclude simultaneous interactions with red blood cells and immune cells to increase safety. We have, we can use multiple configurations to optimize for the different drugs. So we have a different technology for antibodies, and even this depends on the antibody, like whether if you need the full effect of function, if you want the antibody to recruit the immune system, You use a certain type of of affinity and epitope of transferring. If you do enzymes and you don’t need a full effector function, you can use a different technology with maybe higher affinity Yeah.

And the same for nucleic acid. So for example, if you want to remove beta amyloid with an anti anti A beta antibody, you need to recruit the immune system because Yes. The anti A beta antibody just tag the site. You need the excavator. You need the immune system to really dislodge the so you need to recruit the immune system.

But if you recruit the immune system to an to a beta plaques, you also recruit the immune system to red blood cells. So there is really a very delicate balance that I think we can really optimize better than most other technologies.

Unidentified speaker, Host, Goldman Sachs: Okay. How do you think about the context where transferrin versus CD98 are the most appropriate target?

Arnon Rosenthal, CEO and cofounder, Elektar: So, so far, the sort of transferring is more validated. It’s been in the clinic, both in the context of enzyme replacement therapy and in the context of antibodies. And although there are cases of anemia, especially again, if you have full effect of function as in the case of trantunamab with Roche

Unidentified speaker, Host, Goldman Sachs: Yeah.

Arnon Rosenthal, CEO and cofounder, Elektar: It sort of seem to be manageable. So transferring the limitations are known and they’re really mainly safety associated with hematologic side effects. With CD98, there is still less understanding of the safety profile, so we are working very extensively to really establish the safety profile of CD ninety eight. I mean, there is there are differences, like, in the kinetics of entry to the brain, in the cell types that express the

Unidentified speaker, Host, Goldman Sachs: Mhmm.

Arnon Rosenthal, CEO and cofounder, Elektar: The different shuttle that may again impact brain distribution. So ultimately, it will be good to have more than one shuttle.

Unidentified speaker, Host, Goldman Sachs: Yeah. But

Arnon Rosenthal, CEO and cofounder, Elektar: so far, everyone is using transferring. It’s a lot more validated.

Unidentified speaker, Host, Goldman Sachs: Right. How did you think about selecting an antibody for your ABC brain shuttle or ABC candidate?

Arnon Rosenthal, CEO and cofounder, Elektar: So, yeah, we are sort of aiming to really develop the best in class anti abeta antibodies with brain shutters. So we are optimizing each of the components. And the the lead program now is is the trantunamab from Roche. But they are for their naked antibody actually was inactive, like the gantenerumab, which was the the the precursor for trantunamab was inactive as a naked antibody. So we are choosing epitope that is very potent as a naked antibody, most similar to the Lilly antibody, danunumab.

Also Roche saw incidence of anemia. They claim that it’s manageable, but so far patients were not treated for that long. So I think anemia, it’s a cumulative effect. It will become worse with time. So we are we have a different, transferring technology, which we think will have much less anemia risk.

Unidentified speaker, Host, Goldman Sachs: Okay.

Arnon Rosenthal, CEO and cofounder, Elektar: And compared to other technologies, like, people are trying to solve the anemia problem in different ways. For example, Aliada and and AbbVie are inactivated. They don’t they have an inactive effect or function, and they hope that the transferring receptor will somehow recruit immune cells. We think that this approach is less likely to fully recruit immune cells. I think that we will have an optimized antibody that has the best epitope Yeah.

As a naked antibody, the best transferring technology with to minimize anemia. Mhmm.

Unidentified speaker, Host, Goldman Sachs: The other program that you have using the ABC technology has a GKS enzyme. I guess why did you select that, and sort of could you give us the high level on that molecule?

Arnon Rosenthal, CEO and cofounder, Elektar: So so GK is a lysosomal enzyme that’s mutated in over ten percent of Parkinson’s patients. It’s like ten percent of Parkinson’s patients. It causes up to thirty percent of Lewy body dementia. It’s a validated enzyme replacement modality because if complete loss of function of GKS leads to Gaucher disease and there is there are good enzyme replacement therapies for Gaucher disease. So it’s a relatively validated enzyme replacement target.

The only issue until now for Parkinson’s disease and Lewy body dementia was that it didn’t enter the brain. So we basically now engineer the enzyme to become significantly more stable, more active, and we integrated the blood and bear shuttle. So we think it would be a good drug for Parkinson’s disease and eventually Lewy body dementia.

Unidentified speaker, Host, Goldman Sachs: What are the next steps for those programs in terms of getting into the clinic? And to what extent does, like, one program validate the technology for multiple?

Arnon Rosenthal, CEO and cofounder, Elektar: Yeah. So we are targeting both the A beta and G case to be in the clinic next year. Yes. Each one of them will validate the technology. But as I mentioned, like, there are actually different variations, and we are also developing siRNA, tau siRNA with brain shutters, which will also have a tailored technology.

So so I think, each of these drugs like the antibody, a beta antibody, the GKS enzymes, and the tau siRNA will validate maybe the drug modality.

Unidentified speaker, Host, Goldman Sachs: Sure.

Arnon Rosenthal, CEO and cofounder, Elektar: But they will validate the technology in general if there is little safety issues and and good brain penetration.

Unidentified speaker, Host, Goldman Sachs: Okay. Maybe in our last minute, you can just talk about, kind of, your, like, strategic and and overall approach to thinking about capital allocation across early stage portfolio versus the later stage programs?

Arnon Rosenthal, CEO and cofounder, Elektar: Yeah. So we have sort of resources. Like, our runway is through the second half of twenty twenty seven. We have over $350,000,000 Our clinical programs are already fully funded, like our phase three Mhmm. Drug is fully funded.

Our phase two drug is fully funded, and we have resources to develop a beta, GKs, and tau to sort of start the clinic. So we think we will have a like, in the next two years, we will have a really good portfolio of clinical programs and and Mhmm. Earlier stages clinical programs.

Unidentified speaker, Host, Goldman Sachs: And maybe since I have thirty seconds, I’ll ask you one more question, which is you guys had partnered a lot of your early programs. If you look to the ABC candidates, will you take a similar approach, or do you want to wholly own those?

Arnon Rosenthal, CEO and cofounder, Elektar: Our preclinical programs are currently fully owned. Yes. If there is a proposal that we can’t refuse, we will explore it absolutely. But at this point, we are developing it as as a fully we are developing the preclinical programs as fully owned.

Unidentified speaker, Host, Goldman Sachs: Perfect timing. Thank you so much for joining us. Really appreciated the discussion this morning.

Arnon Rosenthal, CEO and cofounder, Elektar: Thank you so much. Thanks.

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