Acumen Pharmaceuticals Q2 2023 Earnings Call Transcript

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August 8, 2023

There are 10 speakers on the call.

Operator

You for standing by, and welcome to the Acumen Pharmaceuticals Second Quarter 2023 Update Call. At this time, all participants are in a listen only mode. There will be a brief overview followed by a question and answer session. Today's call is being recorded. And I would now like to turn the call over to Alex Brunn, Head of Investor Relations.

Operator

Please go ahead.

Speaker 1

Thank you, Lisa. Good morning, and welcome to the Acumen conference call to discuss our business update and financial results for the quarter ended June 30, 2023. With me today are Dan O'Connell, our Chief Executive Officer Doctor. Eric Siemers, our Chief Medical Officer and Matt Zuga, our Chief Financial Officer and Chief Business Officer. Before we begin, we encourage listeners to go to the Investors section of the Acumen website To find our press release issued this morning and related slide presentation, we'll discuss today.

Speaker 1

Please note that during today's Conference call, we may make forward looking statements within the meaning of the federal securities laws, including statements concerning our financial outlook and expected business plans. These statements are subject to risks and uncertainties that could cause actual results to differ materially from those described in the forward looking statements. Please see Slide 2 of the accompanying presentation, our press release issued this morning and our most recent annual and quarterly reports filed with the SEC for important risk factors that could cause our actual results to differ materially from those expressed or implied in the forward looking statements. We undertake no obligation to update or revise the information provided on this call or in the accompanying presentation as a result of new information or future results or developments. After our prepared remarks, we'll open the call for Q and A.

Speaker 1

Now, I'll turn the call over to Dan.

Speaker 2

Thanks, Alex. Good morning and thanks to everyone who has joined us today. A few weeks ago, Acumen presented compelling clinical data in support of ACU-one hundred and ninety three, our asset for the treatment of early Alzheimer's disease. Our positive Phase 1 top line results solidify ACU-one hundred and ninety three's potential as a future option in the Alzheimer's treatment paradigm. The success of our novel target engagement assay, robust study design And committed execution enabled us to demonstrate convincing proof of mechanism inclusive of significant amyloid plaque reduction.

Speaker 2

AC193 was shown to be safe with a broad therapeutic index and with attractive dosing options for our next phase of development. We believe these results substantially derisk our asset beyond our expectations at this stage in its clinical development. I'm extremely proud of our team's achievement I would like to thank our employees, SAC investigators and staff and patients and caregivers for their dedication to advance AC-one hundred and ninety three as a potential best in class treatment in this important field. If you have not already done so, I encourage you to go to the Investors section of our website and view the webcast from July 17 with our full presentation of the INTERCEPT AD Phase 1 top line results. Moving forward, we are firmly committed to harnessing the optionality provided by the Phase 1 dataset.

Speaker 2

We have a knowledgeable and adept Clinical regulatory and CMC team at Acumen with significant large pharma experience in Alzheimer's drug development. Given the positive INTERCEPT AD trial data, including the observed rapid plaque reduction by AC193, our team is working urgently Integrate the findings into both our future clinical plans and our broader strategic priorities. We continue to analyze the data from this study And expect further biomarker data to be available in the Q4. We are also finalizing our doses for our next clinical trial, which Eric will discuss. We have made modest changes to our planned Phase twothree design given AC-one hundred and ninety three's ability to rapidly reduce plaque such as incorporating amyloid PET into interim analyses.

Speaker 2

As previously disclosed, our Phase twothree design incorporates Interim analyses to inform the potential of expanding the size of the study from a Phase 2 to a Phase 3 study, which we believe is the most expeditious route to a BLA filing and potential approval. We continue to anticipate an end of Phase 2 meeting with the FDA to discuss this Phase twothree design in the Q4. As mentioned on our July 17th call, We are investigating the viability of subcutaneous dosing of AC193 as we recognize the potential attractiveness of this mode of administration to expand patient dosing options. We have made meaningful progress on this front and aim to have more details to share later this year. I should also comment that we are continuously evaluating strategic partnerships and are committed to exploring value enhancing opportunities that advance AC-one hundred and ninety three's development and align with Acumen shareholders' interests.

Speaker 2

Before I turn the call over to Eric, I would like to emphasize the degree to which our Phase 1 results have elevated AC193's profile in the field. We believe AC-one hundred and ninety three's high selectivity to bind to toxic soluble A beta oligomers in the brain confirmed by our CSF target engagement assay affords it the potential to differentiate in terms of clinical efficacy. AC-one hundred and ninety three's ability to significantly reduce plaque in only 3 months In line with currently approved and under review anti abeta antibodies, we believe further de risks the asset's potential to deliver efficacy. Monthly dosing provides another important point of differentiation. We intend to drive significant momentum from these timely results and look forward to sharing our progress with you as we execute against our operational and strategic priorities in the weeks months ahead.

Speaker 2

With that, I'll hand the call over to Doctor. Seimers. Eric?

Speaker 3

Thanks, Dan, and good morning, everyone. As I'm sure you can tell, we are very pleased that our INTERCEPT AD top line results for ACU-one hundred and ninety three provided important Clinical proof of mechanism data for a monoclonal antibody developed to selectively target toxic A beta oligomers. We believe these results support our efforts to develop a best in class therapeutic for Alzheimer's disease. In addition to the demonstration of ACU-one hundred and ninety three bound to oligomers in CSF, our measure of target engagement, We were also very encouraged by the rapid dose related amyloid plaque reduction at our higher doses, 60 milligrams per kilogram every 4 weeks and 25 milligrams per kilogram every 2 weeks. Plaque appeared to be reduced at a rate comparable to approved or soon to be approved monoclonal antibodies at a similar time point after starting treatment, In this case, around 3 months.

Speaker 3

The finding of plaque reduction further demonstrates the evidence of 193s activity in the brain and is a positive development given the established relationship between robust plaque reduction and slowing of cognitive decline. You will see in the data we presented that 193 also demonstrated robust dose related target engagement, 193 bound to oligomers as measured by a novel assay developed by Acumen that exceeded expectations. In fact, we observed that our higher doses approach maximal target engagement. This is a finding that we are particularly excited about given that this The first time an oligomer targeted antibody has demonstrated target engagement. Taken together, the decrease in plaque load seen at higher doses and clear demonstration of target engagement with oligomers provides substantial evidence of the intended central pharmacology of ACU-one hundred and ninety three and proof of mechanism.

Speaker 3

With regard to safety, 193 was well tolerated with no drug related SAEs and overall low rates of ARIA E. Interestingly, we did not observe ARIA E in 6 study participants who were dosed with 193 and who were APOE4 homozygous and we will continue to monitor this finding in our next study as a potential point of differentiation compared other monoclonal antibodies for AD. And based on the pharmacokinetic profile observed, monthly dosing is supported. Importantly, INTERCEPT AD provided valuable information required to design the next phase of the program, including dose selection decisions. We are currently in the process of modeling doses for our Phase 2 study arms.

Speaker 3

We have provisionally identified a high dose of Approximately 50 to 60 milligrams per kilogram and are considering a mid dose in the range of 25 milligrams to 35 milligrams per kilogram. These would be every 4 week doses. We are confident in our modeling algorithm and are targeting a mid dose that lies in our target engagement eMAX curve in an area where substantial target engagement occurs. This is because at that location, we can potentially observe robust target engagement with regard to oligomers. Based on our Phase 1 plaque reduction data, we believe it is likely that the Higher dose in our Phase twothree study will result in plaque reduction and at the lower dose plaque reduction could be demonstrated in a longer term study.

Speaker 3

Finally, as far as broader sediment in the Alzheimer's space, we attended the Alzheimer's Association International Conference in Amsterdam this July and the general tone of the meeting was very positive. With 1 monoclonal antibody now having traditional FDA approval and a second antibody likely to achieve traditional approval After decades of attempting to develop disease modifying therapies for Alzheimer's disease, the field is now seeing early successes. While these new treatments are not a cure for Alzheimer's disease, they represent a substantial step forward for patients and families. We at Acumen hope to further advance disease modifying treatments for Alzheimer's disease by developing ACE-one hundred and ninety three as a best in class treatment option. And with that, I'll turn the call over to Matt.

Speaker 4

Thank you, Eric. Good morning, everyone. As a reminder, our Q2 2023 financial results are available in the press release we issued this morning and in our 10 Q that will be filed later today. As of June 30, we had approximately $172,000,000 in cash and marketable Following the announcement of our positive Phase 1 results in mid July, we closed an upsized follow on offering, which brought in net proceeds of approximately $122,200,000 Our cash on hand is expected to support our clinical our current clinical and operational activities into the second half of twenty twenty six. Importantly, we believe that we have enough runway to complete a Phase 2 standalone study.

Speaker 4

As highlighted in our risk factors, this timeline could be affected R and D expenses were approximately $9,100,000 in the Q2 of 2023. The increase over the prior year was primarily due to increased costs related Personnel, consulting and other items related to the Phase 1 clinical trial, which we completed during the quarter. G and A expenses were $4,300,000 in the From operations of $13,500,000 in the quarter. We are encouraged by the strong support for the development of ACU-one hundred and ninety three following our positive Phase 1 results and we'll remain financially disciplined as we use our capital to advance our clinical program for the asset and deliver value to patients and shareholders. And with that, we can open the call for Q and A.

Speaker 4

Operator?

Operator

Thank you. And our first question today will be coming from Colin Bristow of UBS. Your line is open.

Speaker 5

Hey, can you guys hear

Speaker 2

me okay? We can. Yes.

Speaker 6

Supa, hey, good morning guys and thanks for taking the question. So I was just wondering, what additional analyses, if any, and sort of referring to CSF And Plasma Biomarkers, have you done since your top line? And anything you could perhaps share with us? And if not, what Additional updates and analyses can we expect over the next 6 to 12 months? And then just maybe since 193 has a mechanistic Profile, which is now closer approximate to lucanumab.

Speaker 6

Can you maybe just again just take us through how you see or what you expect To be the key points of differentiation versus the tadalumab. Thank you.

Speaker 3

Well, Great. Yes. So this is Eric. And as far as the biomarker question, it's a really pertinent question. As you well know, CSF and plasma biomarkers is a rapidly developing field and we've all along said that we are Going to follow the field carefully and send off the biomarkers that appear to be the most promising.

Speaker 3

And so We didn't have all that prearranged at the time we did the study. But what we've now done and we're in the process of finalizing is establishing contracts to look at biomarkers to ship the samples to get the results and those results will come in later in the year. So we'll look at the kinds of things that appear to be promising in the field right now. So As you probably know, the abeta42:forty ratio, especially in CSF, but also in plasma Is receiving a lot of attention, p Tau, especially p Tau217 is receiving a lot of attention. We think that GFAP because it represents astrocyte function could be very interesting along with Neurogranin because it reflects synaptic function.

Speaker 3

So we'll be sending the CSF and plasma Samples out for those assays, in terms of what results we might anticipate, This was a short study. People got at most 3 doses of drug. And so it's possible that we would see a drug effect, but Not necessarily likely. So the biggest reason for doing these assays in this study is to provide experience For the next study, when those biomarkers will actually be very crucial in the development program. So

Speaker 2

We may see a drug effect in this study,

Speaker 3

we may not, but the important thing is we all have then the experience with these assays to apply our next With regard to differentiation, I think I'll just turn that one back to Dan.

Speaker 2

Sure. Thanks, Eric, and thanks, Colin, for the questions. I think in terms of differentiation from leucanumab, we're looking at both The dimensions of safety and efficacy with some basis for that supported in the INTERCEPT AD study, but also most importantly the next Study being the one to really provide clinical proof of concept and maybe a path towards registration. And those would be the ability to push dose and have better therapeutic coverage over ToxiK data ligomers is an important aspect of this. And I think the general selectivity for 193 as we've reported it is 500 fold selective for oligomers over monomer and roughly 90 fold selective for oligomers over fibrils.

Speaker 2

So we think that the approach that we're taking is to demonstrate comparable or better safety profile, but ultimately, we're really looking to drive And that would obviously be a key point of differentiation within the field.

Speaker 6

Great. Thank you very much.

Operator

Thank you. And one moment for our next question. And our next question is coming from Paul Matteis of Stifel. Your line is open.

Speaker 5

Hey there, thanks for taking my question. I wanted to clarify some of the comments you made around the 25 mg to 35 mg per kg once monthly dose that you're planning. What exactly would you expect as it relates to plaque reduction from that dose level? You obviously saw plaque reduction at 25 every other week in this study. And I think in your prior comments, you had talked about CSF exposure data from earlier in this trial Supporting that sufficient drug levels, we're still on board out to, I think, 3 weeks that you were hopeful in monthly.

Speaker 5

And so Certainly encouraging that you're pursuing monthly, but I guess what's the gap there for why you wouldn't expect this dose to match As well on plaque reduction as some of the other A beta antibodies?

Speaker 3

So, yes, I guess I can take that. This is Eric. We've spent a lot of work obviously looking at doses for the next study and we are narrowing down the ranges as you point out, but We haven't finalized those. So one of the things to be aware of and this is a little bit of an anecdote, but when we first designed the INTERCEPT study or Phase 1 study. There was a post dose PET scan in there and a few people that Acumen said, well, why do you need that?

Speaker 3

We don't target And my reply was, that's the theory, let's find out what happens. And so when we got the data, We saw we did see this plaque reduction at the higher doses. And I think it's just an important lesson for drug development generally is, Don't expect that you know what the results are going to be, but you have to look for those results. And so that's really exactly what we're going to do Actually even for both doses in our next study. So I think at the higher dose based on our INTERCEPT data, we have a Pretty high likelihood that we'll see plaque reduction at that higher dose.

Speaker 3

At the lower dose, we really will see what we get. We got some plaque reduction at 25 mgs per kg, but every 2 weeks, so a total of 50 mgs per kg every month. But that was only with 3 administrations of drug. So the next study will be 18 months. So it will be a longer study And we'll see what will happen to plaque at that lower dose.

Speaker 3

Now again, our target is actually All of them are original target. The plaque reduction is not it's not a bad thing, But it's not necessary for us to have efficacy or at least that's our view. And so I think it's this is why you do the studies to get the results. And so whether we'll see plaque reduction at the lower dose We're not, I think is an open question at this point. But either way, once you get into a Phase twothree study, It's all about clinical efficacy and that's what you really need to be starting to focus on.

Speaker 3

So it's a great science experiment. We're going to do it. But we're also sort of shifting to where the emphasis is going to be on some of the clinical measures.

Speaker 5

Okay. Thanks, Eric. Appreciate it. And then just one question on the subcu. I know it's early, but based on some of your preliminary modeling work, What do you think you might be looking at in terms of the range of different drug volumes you might test and also the frequency of potential injections?

Speaker 2

Yes. Thanks, Paul. I'll hear that. I mean, I think it's a little early for us to comment on Those are the details. Sorry, there's a little feedback.

Speaker 2

So in the Q4, this work is ongoing. We've got good insights into where we're headed. I do think that the We do not anticipate a high dose of 50 mgs or 60 mgs per kg to be amenable to subcu format. I think we could be Clear on that, but I do but we'll have more details that take on precisely the plan and how we expect to proceed with the subcu in the Q4.

Speaker 5

Okay. All right. Thank you.

Operator

Thank you for your question. One moment. For the next question, And our next question will be coming from Tom Schroeder of BTIG. Your line is open.

Speaker 3

Good morning. Thanks for taking the call. Given the robustness of your oligomer binding How interested are you in the level of 193 you need to saturate a ligamer once plaque is gone? And do you think you'll get those data from the next trial? And then a second inclusion trial is how appealing is to do some screening for tau?

Speaker 3

I think Lilly has shown or suggested you can really increase the separation between treated and untreated if you screen for tau? Thank you.

Speaker 7

So yes, thanks Tom for

Speaker 3

the question. In terms of essentially being in antibody excess Versus oligomers, I mean that's something that we've spent a lot of time thinking about. One Sort of detail, but I think it addresses the point is that if you take 193, the antibody and just spike it into Spinal fluid from a person with Alzheimer's, you get a little bit of a signal on that target engagement assay, but not very much. But when you give it to people intravenously and then it obviously goes through brain interstitial space and whatnot, you get a much Bigger signal. So it tells us or at least that I would think that that means that it's going through a compartment where the oligomer concentrations Or substantially higher than in CSF, which I think intuitively makes a lot of sense.

Speaker 3

So in terms of when are you really in antibody excess, so you're talking about antibody excess In a compartment bringing interstitial fluid that you can't directly sample. So it's a tricky thing to figure out. We do know that and we are constantly doing additional analyses on these data. But if you look at plaque load With regard to target engagement signal, there's no relationship there. There was some thought that maybe the oligomers were sort of attached to the plaque And the more plaque you had a baseline, the bigger target engagement signal you would get.

Speaker 3

And there's no real clear evidence that That's the case. So these oligomers are in a compartment that it appears to be independent really to plaque, But it's different than spinal fluid. So the team is working on an assay now to look at Free oligomers in spinal fluid with all the caveats that spinal fluid is not really the compartment where the action is. But the team is working on an assay to do that. It's technically really difficult.

Speaker 3

Oligomer concentrations in spinal fluid are really low. They're less than 2 picomolar To start with and then with the antibody, they'll become even lower. So it's technically a difficult thing to do, But the team is working on that. And then the other thing just briefly in terms of tau and Using that to select patients, that again, which obviously is what Lilly did, It's a really wonderful science experiment. I'm not sure how that will play out in terms of clinical medicine, Because that means that people have to be amyloid positive based on a PET scan or spinal fluid.

Speaker 3

And then on top of that, you have to be tau positive, but right in the right Range of tau positive and basically it means that 1 out of 10 people that you screen for the therapy will be essentially eligible for it. So it's really interesting from a scientific standpoint. I'm just not sure that practically that would be something you could do in the clinic. So we're going to obviously look at tau at baseline and see if that co varies with efficacy and all that. But we have Made the decision not to include tau as an inclusion exclusion criteria.

Speaker 3

We will of course make Amyloid positivity and inclusion exclusion criteria, but we're not going to specify a certain level of tau. Great. Thanks for the thoughtful answers.

Operator

Thank you. One moment for the next question. One moment please. Our next question will be coming from Pete Stavropoulos of Cantor Fitzgerald. Your line is open.

Speaker 8

Hi, Dan, Matt and Eric. Thank you for taking our questions. So now that you've had several weeks to socialize the data internally and externally, Just curious to hear if your thoughts have evolved in terms of possible reasons from a mechanistic standpoint on the lack of ARIA In APOE homozygous and observed only in females, is it by chance or is there some plausible mechanistic reasoning? And thank

Speaker 2

you. Yes. Eric, go ahead.

Speaker 3

That's a great question too. In terms of it just I honestly don't have a good explanation for that. It could be chance. We'll see. I mean, Alzheimer's disease is a bit more Common in females, but still I don't have an off the top answer on that.

Speaker 3

In terms of the APOE homozygous, There was a preprint of a paper that just came out this week that actually showed that people who were APOE4 carriers had a different more to their plaque than people who were non carriers, which would suggest that one possibility Is that AC193 targets an epitope that's maybe a little bit different than the plaque targeting Antibodies that have this relationship between ARIA and APOE. So the first thing, well, and the other thing, even in terms of the homozygous Observation, I mean this is small sample size Phase 1 study, we need to see if it replicates. But if it does replicate, I think that is a clear point of differentiation For ACU-one hundred and ninety three and we'll have to have a lot of further discussions about what the mechanism might be, But it clearly would differentiate ACU-one hundred and ninety three.

Speaker 8

All right. Thank you for taking my questions.

Operator

Thank you. One moment for the next question. And the next question will be coming from Judah Frommer of Credit Suisse. Your line is open.

Speaker 7

Hey, guys. This is Nick on for Judah. Thanks for taking our question. So With leucanumab reimbursement and post infusion monitoring seemingly getting more traction recently, we're just wondering what's the read through for 193, The safety profile that we saw last month holds up. I know we were just talking about differentiation from mucanumab, but I just wanted to just to confirm, is the ARIA occurrence that we see with leucanumab, is that the right bar that you'd be looking to be with 193?

Speaker 2

Thanks. Yes. Thanks, Nick. I mean that I think clearly that we do think that the ARIA rate for lukanumab is Benchmark for sort of a safety profile in this indication and we think 193 can be as good or better on Score. So that is our intent to demonstrate that in a longer duration study.

Operator

Thank you. And our next question? Our next question is coming from Charlie Yang of Bank of America. Your line is open.

Speaker 9

Hello.

Speaker 2

Hey, Charlie.

Speaker 9

Hi. Oh, hey, sorry. I think I missed that earlier. Yes. Thanks for taking the question.

Speaker 9

This is Charlie for Jeff. I have two questions, please. First, can you clarify regarding the reason For not specifying the tau level, I mean, I understand that it's scientifically interesting, but I think given the Consistency in terms of what Lilly has shown with the trial as well as, I guess, somewhat more of a Preliminary or post hoc data with lekadalumab that also shows some Favorable in terms of the efficacy in the kind of lower to intermediate tau patients. I'm just wondering, Would it make sense to have that as an inclusion or exclusion criteria to improve the probability of success? That's number 1.

Speaker 9

And number 2, can you just discuss the kind of like the cash flow that you have? I think just given how long the trial will run for Phase 2, It seems like by the end of cash runway, that's how around the timing when You'll end up with your cash. So what's the I guess what's the outlook in terms of How do we get another raise or perhaps having some sort of partnership prior to the actual readout?

Speaker 2

Yes. So thanks, Charlie. If you want to hit the first one, I can Matt or I can take the second.

Speaker 3

Yes, yes, exactly. So yes, again, in terms of using tau as an inclusion exclusion criteria, which essentially and we'll see what the label ends up Being for denanimab, but more than likely you'll have something in the label that will track with that. Again, I think it's a great science experiment. I don't think I think it will be a real challenge in terms of making that work in the world of clinical medicine. Now what we are doing in our study and so our patient population is in early Alzheimer's And so these are people with either MCI or mild dementia, but not beyond that.

Speaker 3

So the lowest Many mental score you can have is 22, for instance. We've also and this is some ongoing analyses that we're doing is In our INTERCEPT study, we actually used a hybrid model of looking at amyloid positivity. So it wasn't just based on A PET scan SUV are, it could also be based on a visual read, which may actually Be able to allow you to pick up people who are amyloid positive, but not So blatantly that they cross a SUVR threshold. And so that I think will help us dial in with this Milder population without having to take the extra step of a tau PET scan. Now looking to the future, And I don't think the field is there just yet, but there may be some time in the future when one of these plasma tau PhosphoTail assays could be useful and we'll obviously continue to track that.

Speaker 3

But in terms of our next trial, which is a Phase twothree, so if it becomes a Phase 3 trial, that's a registration trial. We have to make that mere clinical practice As it exists more or less today. And so that was the overall thought process in terms of the design of the Phase twothree trial. So for the cash question.

Speaker 2

Yes. Thanks, Eric. So Charlie, at the current time, we have runway through In room readouts anticipated for our Phase twothree study. Based on our current assessment today, we believe that we have enough runway to finish a Phase 2 standalone Study should be not expanded to Phase 3 following a positive interim analysis. Of course, the timeline, this could be affected by the pace of Clinical site initiation, enrollment rates, etcetera.

Speaker 2

But generally, based on our current planning, we do have a cash runway through A standalone Phase 2 study subject to the qualifiers that I mentioned. In terms of partnering, we think the optionality of I'll be using a Phase twothree design with the potential to expand the Phase 3, as I mentioned earlier on the call, is that The fastest potential path to a BLA filing and potential approval. And we would anticipate and continue To have engagement from prospective partners as to potentially working with us on particularly in terms of the Phase 3 portion The development of AC193. So those things are kind of part of our bread and butter of our strategy and will continue to evolve and over the course of the next year itself.

Speaker 9

Great. Thanks so much.

Operator

Thank you. This concludes the Q and A session. I don't see any more questions in queue. And I would like to turn the call back over to management for closing remarks.

Speaker 1

Great. Thanks, Lisa. Thank you, everyone, today for listening in. We here at the company are always available if you have further questions.

Operator

This concludes today's conference call. Thank you all for joining. You may now disconnect. Everyone have a great day.

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Key Takeaways

  • Positive Phase 1 results: ACU-193 demonstrated convincing proof of mechanism with significant amyloid plaque reduction in only three months and a broad therapeutic index supporting attractive dosing options.
  • Phase 2/3 trial planning: The team is finalizing a mid dose (25–35 mg/kg Q4W) and high dose (50–60 mg/kg Q4W), adding amyloid PET in interim analyses to enable a potential seamless Phase 2 to Phase 3 expansion and a BLA filing path.
  • Phase 1 safety was favorable, with no drug-related serious adverse events, low ARIA-E incidence and, notably, zero ARIA-E in six APOE4 homozygous participants, supporting monthly dosing.
  • The company is advancing subcutaneous dosing evaluations to broaden patient convenience and remains open to strategic partnerships to accelerate ACU-193’s development and enhance shareholder value.
  • Q2 financials showed $172 M in cash and marketable securities plus $122 M net from a follow-on offering, providing runway into the second half of 2026 and funding for a standalone Phase 2 study.
A.I. generated. May contain errors.
Earnings Conference Call
Acumen Pharmaceuticals Q2 2023
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