Alector at BofA Securities 2025 Healthcare Conference: Strategic Innovations in Brain Disorder Therapies

On Tuesday, 13 May 2025, Alector Inc. (NASDAQ:ALEC) presented at the BofA Securities 2025 Healthcare Conference, revealing strategic insights into their pioneering brain disorder therapeutics. The company showcased both promising advancements and challenges in their clinical programs, emphasizing a data-driven approach to addressing unmet medical needs in neurological conditions.

Key Takeaways

• Alector’s 3R strategy focuses on removing, replacing, and restoring proteins and cells in brain disorders.
• Latazimumab (AL01) and AL101 are key late-stage programs targeting frontotemporal dementia and Alzheimer’s disease, respectively.
• Cariboo prioritizes CB10 in lymphoma and CB11 in myeloma, extending their cash runway into 2027.
• Both companies emphasize significant unmet needs and potential market opportunities in their respective fields.

Financial Results

• Alector is well-funded for upcoming data readouts.
• Collaboration with GSK on latazimumab and AL101 involves a 50-50 profit share and co-promotion strategy.

Operational Updates

• Alector:

- Latazimumab (AL01) is in Phase 3 for frontotemporal dementia with results expected in Q4 2025. It has received breakthrough, fast track, and orphan drug designations.

- AL101 is in Phase 2 for Alzheimer’s disease, with enrollment completed and data expected in 2026.

- Preclinical programs involve Elektor Brain Carrier (ABC) technology, enhancing drug delivery to the brain.

- Progranulin franchise aims to elevate progranulin levels, improving microglia and neuronal function.

- A beta program targets robust efficacy with good safety profiles in reducing A beta plaques.

- GK program uses machine learning to engineer stable and active enzyme replacements.

• Cariboo:

- Focuses on advancing CB10 and CB11 to critical inflection points, discontinuing other programs to concentrate resources.

- CB10 aims for results comparable to auto CAR Ts in lymphoma, with a partial HLA matching strategy.

- CB11 targets efficacy in myeloma, aiming for a high overall response rate with a "one and done" treatment approach.

- Manufacturing processes are outsourced, with significant scale advantages allowing for large batch production.

Future Outlook

• Alector remains focused on its late-stage programs and early-stage innovations powered by ABC technology.
• Cariboo’s extended cash runway into 2027 provides flexibility for future pivotal studies and strategic developments.

Q&A Highlights

• Discussions highlighted the potential for AlloCAR Ts to achieve durable outcomes, comparable to existing therapies.
• Key efficacy metrics for myeloma include overall response rate and the ability to measure MRD negativity.

Readers are encouraged to refer to the full transcript for a detailed understanding of Alector’s and Cariboo’s strategic presentations at the conference.

Full transcript - BofA Securities 2025 Healthcare Conference:

Alex Strehan, Senior Biotech Analyst, Bank of America: Twenty twenty five Bank of America Healthcare Conference. Thanks for joining this session with Elektor. My name is Alex Strehan. I’m a senior biotech analyst covering Elektor at Bank of America. Sarah Good to meet you.

President and head of research and development at Elektor. So with that, Sarah’s gonna run through a few slides, and I’ll pass it over to you. Take it away.

Sarah Good, President and Head of Research and Development, Elektor: Sound isn’t coming from me. That noise. Oh. That sound okay? Okay.

Great. All right. Thank you. So firstly, just want to say that we’re going to make some forward looking statements here today, so please refer to our disclosures and our SEC filings for further details. Firstly, I just want to introduce Elektor.

Elektor is positioned to drive near and long term value in treating brain disorders. Our therapeutic candidates are, grounded in our 3R strategy. It is a strategy to remove misfolded proteins, replace dysfunctional proteins, as well as restored dysfunctional, immune and neuronal cells. I’m going to touch upon our late stage clinical programs, as well as our early pipeline of preclinical assets. And we are a well resourced team and a seasoned team.

We are well resourced to get through our data readouts. Our development portfolio consists of two molecules, latazimumab and AL101, which are part of our progranulin franchise. And this is in collaboration with GSK in a fiftyfifty profit share, with a co promote. In addition, we have a wholly owned proprietary, preclinical pipeline, that’s powered with our blood brain barrier technology. Talk briefly about our clinical programs.

We have two clinical molecules, latazimumab or AL01 in frontotemporal dementia with the granulin mutation. And this program is currently in phase three in a pivotal study with results expected in Q4 of twenty twenty five. We have breakthrough designation, fast track designation, and orphan drug designation. Our open label phase two showed encouraging results in clinical outcome measures. The other hand, AL101, which is being studied in Alzheimer’s disease, is currently in phase two.

We’ve completed enrollment in the trial in April of this year, with a seventy six week treatment period that’s ongoing. The data on this are expected sometimes in 2026. Our preclinical programs are focused again on the electrode brain carrier, which is our blood brain barrier technology platform, and it’s focused on three targets: removing A beta, replacing GKs, and removing tau. Now, electro brain carrier or ABC is designed for lower dosing, for improved efficacy and safety, and for subcu delivery across multiple cargo types and configurations. Excuse me.

Our electro brain carrier has a number of versatile features. We have ABCs as FABs or SCFBs that bind transferrin receptor in multi specific formats. They are optimized for effective function and for half life and can be tailored to a wide range of affinities and TFR binding epitopes facilitating optimization to multiple cargo modalities. And now we are testing it across either antibodies or enzymes or nucleic acids in multiple different versatile combinations. This is just data from one of our tool compounds that demonstrates deep brain penetration, both in nonhuman primates on the left, where we see up to 40 fold brain uptake to about 18 nanomolar in the brain.

And you can see it across different regions of the brain as compared to the naked antibody. On the right, the same data set, is seen in rodents where again we see real widespread distribution of the electro brain carrier enabled tool compound in the brain. Our ABC also shows superior serum half life and safety and brain penetration in rodents. Again, on the left, you see the serum half life in purple is our naked antibody and our electro binder in pink. In the middle column is brain uptake of our tested antibodies, and on the right, our reticulocyte levels seven days post injection.

And once again, we’re seeing really good features with our molecule all throughout, whether it’s PK, it’s brain uptake, as well as, safety. Moving on to our specific programs, I’m gonna first talk about Elektor’s progranulin elevating franchise for frontotemporal dementia and Alzheimer’s disease. So as I mentioned, we have two molecules, latazimumab and AL101. So firstly, these two programs are based on our pioneering approach to elevating progranulin levels with the potential to enhance microglia and neuronal function and treating FTD and AD. And they are based on a strong genetic and biologic rationale.

Mutations in granulin, which encode progranulin, are deleterious. Now what we know is that when in terms of heterozygous mutations with 50% loss of function, reduce progranulin levels to 50% of normal, and frontotemporal dementia has an onset of about 58 years of age and about ninety percent penetrance. Now, from a biological perspective, we also know that progranulin is a critical immune regulator, sort of a neuronal survival factor, and also important as a lysosomal chaperone. From a mechanism perspective, AL101 and latazimumab binds the receptor sotilin, which is critical for the degradation of progranulin. By binding and blocking the sotilin receptor, we’re able to elevate progranulin levels.

So in patients with deficiency of progranulin, introducing letazanamab or treating with AL101 allows you to replenish these progranulin levels. And we see exactly that. We first studied letacinamab in healthy volunteers. And the data we show here is in INFRONT two, which will trial where we treated 12 symptomatic, subjects with FTD granulin with latazimumab at sixty mg per kg, Q four weeks for forty nine weeks. And what you see is both in plasma as well as in CSF, we were able to normalize, elevate progranulin levels back to what are normal levels in healthy or asymptomatic, subjects.

What we also saw was a change in a number of the disease biomarkers. And what I show here is one of those biomarkers, which is GFAP, which is a biomarker of disease activity of astrogliosis. And what you see in the left, is plasma concentrations right in CSF. And in both instances, we can show that the biomarker of disease activity like GSAB is reduced down to what are normal levels found in asymptomatic individuals. Additionally, we also looked at cognitive decline in these subjects because it was a single arm open label study.

We matched the data to historic controls, from a registry, which is the Gen Phi registry. And based on this comparison, and this was done based on a propensity score matching, what we estimated was that there was a slowdown of the annual disease progression of up to forty eight percent. Now, past the success of Infranche two, we’ve been treating patients in our pivotal phase three study, which is INFRONT three with latazimumab. This study is a randomized double blind placebo controlled study, and it contains one hundred and three symptomatic individuals and sixteen at risk FTD GRN carriers. And they’re being treated with latazimumab at sixty mgs per kg or placebo and for a duration of ninety six weeks.

And we are measuring at the end of this study, the primary endpoint will be the CDR plus NAC FTLD sum of boxes, along with secondary clinical endpoints, as well as a number of biomarkers. Now this study will be reading out, as I mentioned, in the fourth quarter of this year. AL-one hundred ’1 on the other hand is pharmacologically slightly different than latasimumab. It has a longer half life and it is much better suited for larger indications. And we are developing it for Alzheimer’s disease.

AL-one hundred one is currently in a phase two study for Alzheimer’s disease. As I mentioned earlier, we finished enrollment in this study in April, and we anticipate completion in 2026. The grounded basis for AL101 in Alzheimer’s disease is very similar to lacazanamab in FTD GRN. Progranulin deficiency is a risk for Alzheimer’s disease, and there’s sufficient data, in biological disease models that suggests that it’s an important factor, for the course of the disease. Now, this is the design of our phase two study, which is called Progress AD.

In this study, we have two different dose levels of AL101, compared to placebo. And the study, the treatment period is seventy six weeks. I’m going skip this and move on to our wholly owned portfolio, which again is powered by Elektor’s brain penetrant anti A beta antibody. It’s based on our own proprietary blood brain barrier platform combined with A beta as the target. There’s been a long history with A beta based antibodies in the industry from the early 2000s with a lot of failures for a while until we’ve had the approval of drugs like lucanumab and donanemab.

And while it’s really pleasing to see that there’s been real movement, particularly for patients, I think what is still a challenge is that the efficacy for these drugs has been modest. In addition, there are challenges related to ARIA and other safety risks, as well as if you think about the infusion, IV infusion that’s needed for this patient, it is still quite a bit of a burden. Now, the field is moving towards a much more blood brain barrier penetrable approach to A beta, and that’s wonderful because what you’re seeing right now is that there’s rapid A beta clearance with these type of antibodies, this low ARIA, but there’s an additional risk of anemia. So Elektor is trying to develop a best in class A beta, ABC paired molecule as a therapy, and our goals here are to find robust efficacy to have a good safety profile that has low anemia, low ARIA, and in addition, we want to aim for a subcu delivery for patients. So in terms of the design features of our electro anti A beta antibody that is paired with the ABC, the molecule construct has a few features that I want to point out.

Firstly, a really good selectivity. It’s engineered in terms of high affinity and fully human antibody that selectively binds the thyroglut3 epitope on A beta. Secondly, really good potency. We have a active Fc region so it can recruit the immune cells like myeloid cells to actually remove these plaques. And finally, from a safety perspective, we can fine tune the affinity of the TFR region of the TFR part of the molecule in order to reduce the hematologic toxicities.

A little bit of data here showing uptake or internalization of our ABC molecule there on the left in the green signal over a naked antibody, again showing that our BBB transport mediated mechanism really increases uptake into brain cells. This is in a human brain endothelial cell line. We’ve also shown that on the left that if you treat electrodes, A beta ABC with human iPSC microglia, you see enhanced phagocytosis of our program, of our molecule in blue. And then on the right in vivo, in nine month old 5xFERD mice, you see significant reduction of A beta plaques. Also moving on to our second elector, fully owned portfolio molecule, which is again an ABC paired GK enzyme replacement drug.

So GBA1 gene mutations are a major risk factor for neurodegenerative diseases, and GK is critical in the conversion of glucosylceramide and glucosyl sphingosine to its metabolites. When GK is deficient, both of these substrates start accumulating, and when these substrates accumulate, they are actually toxic. In this situation, it’s known that GBA1 mutations, particularly in diseases like Caucher’s disease, they’re causal, and for Parkinson’s disease and Lewy body dementia, they are critical. These GBA1 mutation carriers are a significant part of the population of these diseases. So we’ve now optimized the design of an Elektora ABC for GKs, and we’ll just point out a couple of features here.

The GKs enzyme has been engineered with, you know, machine learning. Over 1,400 mutations were engineered and slewed, and it’s more than tenfold active and stable than the wild type GK’s enzyme, which actually does not get into the brain. In addition, a safety perspective, the Fc portion of the antibody is silent, so this allows for minimal safety risk and hematologic risk. And a brief data set on the left shows that our ABC molecule has over tenfold stability and activity over the naked GKs. And on the right is just an in vivo experiment in nonhuman primates suggesting that we are seeing about 10 to 100 fold elevation in GKs activity in nonhuman primate CSF.

So overall, just want to come back to saying that Elektor is focused on opportunities to drive near and long term value, And currently, our goals and our focus remain on our two late stage programs, latazimumab in Phase III and AL101 in Phase II, and the early programs which are powered by our oligoprine carrier.

Alex Strehan, Senior Biotech Analyst, Bank of America: Thanks. All right. So flipping straight into the next session. Thank you for joining this session with Cariboo. My name is Alex Stranahan.

I am senior biotech analyst at Bank of America, covering Cariboo, and I’m pleased to be joined by Rachel Horowitz, president and CEO of Cariboo. Thanks for being here.

Rachel Horowitz, President and CEO, Cariboo: Thanks for having us. We really appreciate it.

Alex Strehan, Senior Biotech Analyst, Bank of America: We’ve got time for a mini fireside here. And maybe just jumping in straight into it, Rachel, maybe at a high level walk us through sort of the current pipeline strategy and sort of the refined approach, balancing the cash and pushing the assets forward.

Rachel Horowitz, President and CEO, Cariboo: Yeah, absolutely. So just a few weeks ago, we disclosed a number of critical decisions we’ve made prioritizing the continued development of CB10 in lymphoma and CB11 in myeloma. In concert with this, we discontinued two phase one programs in AML and in lupus. We’ve also discontinued preclinical research and that allows us to really meaningfully advance, these two programs ten and eleven to critical inflection points and to significantly increase our runway. We’re able to revise guidance from funding our operating plan into the second half of twenty six, all the way now into the second half of twenty seven.

And Alec, I should share, of course, are all open label phase one studies. So we are able to learn real time what’s happening in these programs and ultimately make data driven decisions. And so doubling down on 10 in lymphoma, eleven in myeloma, this is really driven by the data and our enthusiasm for what we’re seeing and what we’ve shared through these discussions is that we’re seeing encouraging efficacy in both of these programs. And in particular with CB10 seeing continued evidence that it has the potential to be on par with auto CAR Ts. So encouraged about the future of these programs.

Alex Strehan, Senior Biotech Analyst, Bank of America: That’s great. And obviously that’s the goal, right? Is alleviate the logistical burden of auto while delivering comparable or better on the efficacy side. So maybe starting on CB10, eagerly awaiting the updates in the second half of this year. I guess what sort of classifies success here or would maybe dictate a gono go to a registrational study?

Rachel Horowitz, President and CEO, Cariboo: Yeah, absolutely. What are we looking for? We are looking for an AlloCAR T that drives results just like the auto CAR Ts. So that’s really the full picture. It’s overall response rate, it’s complete response rate, and it’s duration of response.

So the data we’ve committed to for the readout in the back half of this year are really laser focused on this 20 patient cohort that we’re enrolling, where we’re intentionally applying our partial HLA matching strategy. So for each of these 20 patients, we’re ensuring that they receive a dose of CB ten, where they and the donor share at least four of the 12 HLA alleles. This will allow us hopefully to confirm what we’ve thus far seen retrospectively that modest HLA matching can drive outcomes that look to be on par with auto cars. And what we’ve done by pushing out some of these timelines is ensuring that we have sufficient follow-up to really answer that durability question. And in particular, we’ve committed that for those 20 patients, a majority will at least be at the six month mark.

Some will be meaningfully beyond the six month mark. So we’re really looking for an overall profile that looks and smells and sounds like an auto CAR T.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay, that’s great. I guess what can you share sort of about the patient characteristics in the antler trial and how these have maybe evolved over time?

Rachel Horowitz, President and CEO, Cariboo: So our dose escalation work going back to the very beginning of this program was in third line and later patients. We enrolled 16 patients in dose escalation. And based on the very encouraging data, we went to the FDA then to seek permission to really leapfrog directly into the second line setting and they granted that. So everything since then has been exclusively in second line patients. That has allowed us to work in our target population.

And that is the population that we would be making that go no go decision for the pivotal trial. As we first started that work, we’re inherently working at sites that have ready access to auto CAR T cell therapies. And so necessarily our trial has been selecting for patients who have disease characteristics, they are too sick to wait. They are part of that vast majority of patients for whom auto CAR Ts can never be the answer. Actually, commercially, it’s only twenty percent of patients who are getting auto cars.

And there’s a big chunk of that eighty who auto As we’ve continued to work and accumulate data that not only we are excited about, but physicians are excited about and been able to leverage ex US geographies where access to AutoCAR T looks different. It’s allowed us to, I’d say modestly shift the profile of patients. And we’re seeing some who look a lot more like the commercial AutoCAR patients, and some for whom think Allo will always be the answer.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay. And is there maybe a particular threshold on ORR CR rate, that you’d maybe put out there to help frame expectations or that you’d want to see versus other options in the second line setting?

Rachel Horowitz, President and CEO, Cariboo: Yeah, that’s a great question. I would say a good way to measure and visualize what we’re looking for is to look at, say, PFS curves from the auto cars and some of the data that we’ve put historically, I imagine that is a way we will continue to visualize some of this because it captures so much of what you just asked about in one graph, right? It’s really looking at the total number of patients who respond and critically how durable those responses are. Even what we’ve done historically is do our best to plot our data on top of some of the auto curves to really paint that picture of similarity and outcomes. And I expect we’ll use proxies like that going forward as well.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay. Do you think PFS is still kind of the gold standard for as an approvable endpoint in this setting?

Rachel Horowitz, President and CEO, Cariboo: Doctor. It’s a really great question, which probably leads me to we are actively discussing the potential trial with the FDA. Stay tuned. We expect that when we put out these data, we would be in a position to describe the pivotal study at that point in time. I will say the two approvals in the second line setting for the auto cars, the primary endpoint was EFS.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay. Okay. So slight slightly different. Got it. Got it.

Okay. The the other update we’ll see second half is CB 11. May maybe talk about this asset and, you know, sort of how the competitive landscape here for BCMA directed therapies has evolved, in multiple myeloma.

Rachel Horowitz, President and CEO, Cariboo: Yeah, the unmet need for cell therapy in myeloma is even more severe than lymphoma, right? I just said a moment ago, only twenty percent of lymphoma patients are getting auto CARs. Only about ten percent of myeloma patients are getting auto cars. And so when we talk to myeloma physicians and ask them, what does an aloe car need to look like to be relevant and appropriate for your patients? They always point us to the bispecifics.

That’s the only other asset class that is readily available and broadly available off the shelf to this much larger patient population. So what they’re hoping to see from CB11 or any AlloCAR would be efficacy on par with a bispecific. So let’s call that at least sixty percent to seventy percent overall response rate. We think a baked in expectation that the one and done nature of an AlloCAR is superior to a bispecific, where you are stuck on this repeat dosing for months, as long as you can tolerate it, with the really quite profound prolonged infection risk that comes

Alex Strehan, Senior Biotech Analyst, Bank of America: with it. I

see. I see. And that kinda leads me to my next question, which is how would an off the shelf option maybe ease adoption of cell therapies? You mentioned that they’re quite effective, right, on ORR, but ten percent penetration is is pretty low and probably lower than a lot of people would have expected based on the the data. Do you think an off the shelf option is really the the solution here if you can get in the ballpark?

Rachel Horowitz, President and CEO, Cariboo: I think it’s a critical piece of the puzzle, right? Because it solves for both rapid access and scale altogether, right? Even in our myeloma work, where we are doing clinical trials at the sites that have ready access to KERVICT and ABECMA, we’re still rapidly enrolling this study. And I think it’s truly demonstrative of just how significant that unmet need and therefore opportunity is.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay. And I think you maybe already kind of touched on this, but do you think on par efficacy versus auto is required here or maybe something in between, say, a bispecific or the cell therapies could be actionable given the increased convenience?

Rachel Horowitz, President and CEO, Cariboo: Yeah, look, what physicians tell us is they’d love to see an AlloCAR that’s at least on par with the bispecifics. And that that for them would be a really meaningful tool in the toolbox for their patient population. Shoot for the moon, right? Better would be better. But we think that that profile alone would be incredibly attractive for this patient population.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay. And when you think about sort of the efficacy metrics that’s maybe most important, we talked about PFS maybe taking over in the LBCL setting. Is that kind of the metric here too or is response still sort of the?

Rachel Horowitz, President and CEO, Cariboo: Yeah, it’s a great question. I think there are a few pieces of the puzzle to highlight here. Of course, overall response rate, I think it’s important to look at the fraction of patients who have a VGPR or better, certainly the fraction of patients who have a CR or a stringent CR. And on top of all of that is the ability to measure MRD negativity. We know that’s really critical in the myeloma setting.

It demonstrates critical depth of response and can be prognostic of long term outcomes. And so our update will include all of those metrics and we know MRD negativity rates are critical.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay. Okay. That makes sense. And one question we’ve received from investors is just on the manufacturing and supply side of an allo program. Presumably, it should be much easier to scale for a launch, but it’s also not an antibody.

There’s a little bit more complexity. How do you see manufacturing sort of evolving at Caribou? And how do you sort of scale up and how quickly could that happen if you do get good data?

Rachel Horowitz, President and CEO, Cariboo: Yeah, I think scale is absolutely one of our advantages. For example, with CB10, our process today results in enough cells from just one run for two hundred to three hundred doses. So it really just immediately changes the equation from the end of one auto CAR T strategy, where instead a turn of the crank is two hundred to three hundred doses And they have a long shelf life. Typically cell therapies can sit in the freezer for years and maintain their activities. It really gives us the opportunity to completely change the game as we think about supply.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay. And that’s kind of the skill today in house at Caribou, right?

Rachel Horowitz, President and CEO, Cariboo: Actually, develop the processes in house. We do not do our own manufacturing. We have outsourced that. And again, we’re able to leverage great expertise in CMOs who we partner with. We don’t have to invest in our own brick and mortar to do this work.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay. Okay. That makes sense. That gives you flexibility on the capacity side as well. I guess, you know, you you talked about sort of the refined pipeline strategy.

Maybe talk about the updated cash runway, I think is into second half of twenty twenty seven now. What sort of contemplated within this guidance and what sort of steps of derisking does this kind of encapsulate?

Rachel Horowitz, President and CEO, Cariboo: Yeah, great question. So yes, our guidance is into the back half of twenty twenty seven. It allows us to deliver on all the things that we’ve been talking about in terms of these critical data updates. It does not contemplate say running the pivotal for CB ten or doing dose expansion for CB eleven. However, there’s sufficient flexibility that we could do some of the setup work for a pivotal study at risk ahead of raising the capital necessary to execute on the pivotal study.

Alex Strehan, Senior Biotech Analyst, Bank of America: Okay. Okay. That makes sense. And I guess in the last few seconds we have here, is there maybe one key focus point that you get from your investor conversations, you know, here at the conference or or elsewhere that, you know, would would be helpful for people to hear? Just maybe something that’s misunderstood about the story or a differentiation point, that you think is underappreciated?

Rachel Horowitz, President and CEO, Cariboo: Yeah, I think a big question that people often bring to the field, especially when they’re new to the field is will AlloCAR Ts ever result in durable outcomes for patients? And we’ve been doing this long enough now that for some of these patients, we know the answer is yes. For example, our very first patient dosed with CB ten almost exactly four years ago and he remains in complete response. And there are an increasing number of additional patients who are past a year or past multiple years still in complete response. And I think it’s really encouraging not only for our work, but for the field to demonstrate that AlloCARS can drive durable responses.

Alex Strehan, Senior Biotech Analyst, Bank of America: Yeah, that’s the sense I hear as well. There’s folks that were maybe in the initial wave of interest and are now revisiting things. And it’s crazy to think that the first patient dose with CB10 is four years out. So great to see the progress. Looking forward to the second half updates.

I think we’ll have to leave it there for time, but please join me in thanking Rachel for the great discussion.

Rachel Horowitz, President and CEO, Cariboo: Thanks, Alec. Really appreciate it.

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