Contineum Therapeutics, Inc. (CTNM) September 15, 2026 Conference Transcript

Good afternoon, everyone. My name is Sean Larmann. I'm the Head of US Mid-Cap Biotech Equity Research at Morgan Stanley, and welcome to Morgan Stanley's Global Healthcare Conference. Before we begin, just to make you aware of some important disclosures, please see those disclosures at the Morgan Stanley Research Disclosure website at www.morganstanley.com forward slash research disclosures. And if you do have any questions on that, please reach out to your Morgan Stanley sales representative. For this session, we welcome Continuum Therapeutics with CEO, Carmen Stenjoni. Welcome, Carmen. I hope I pronounced your surname correctly. Close enough. Maybe just to begin with some introductory macro questions. You know, how is the rise of China origin innovation, you know, changing the way that you think, either in a BD sense or an R&D sense or if at all?

Yeah, I think it changes the pace of innovation now. So we have several compounds that are being developed across mechanisms that we see in U.S. and European companies. For us, we see it as a potential advantage. So there is the opportunity for additional BD, as you said. And so as we look to continue to expand our portfolio, we can look towards China and potentially more rational cost metrics around there as well. It also gives us an opportunity in the future to potentially find additional partners for the Asian regions.

Sure. Thank you. And are you implementing AI across your business? And if so, can you point to some specifics on whether it's a cost save, a decision made, or even sort of POS assumptions within your pipeline?

We do. The main focus on this is cost efficiency and being able to generate data in a much more efficient manner. So, for instance, we can generate phase two data sets from our competitors and be able to evaluate that in a much more rapid fashion than had we were building spreadsheets for that, as well as around competitive intelligence and investor interactions and things like that. We see this as a tool for efficiency and ability to reduce costs. We are not using this to synthesize molecules or anything like that. We are very focused on the biology and the team that we have that has been able to generate our portfolio since our inception.

Wonderful. Thank you. And last question in a macro sense, but which policy variable, I'm guessing it's the FDA, but which policy variable do you think about the most? Is it FDA? Is it Medicare negotiation tariffs? What do you think about the most?

By and large, FDA. So we're an early stage company. We're in the clinic. Obviously, we lean on FDA for guidance, for study conduct. It is really the key regulator that we focus on in getting the study up and running.

Wonderful. Thank you. I'm going to focus this discussion on Pipe 791, but just to deal with, you know, can you give us a summary of Pipe 307 and the recent disclosure before we move on?

Sure. So we recently put out data or a press release with our partner Johnson & Johnson for Pipe 307. This program, or this compound, was in a Phase 2A study focused on MDD and really looking into the cholinergic thesis of depression. A well-controlled study, over 100 patients. Unfortunately, like a lot of MDD studies, we missed on the primary endpoint. J&J has been a fantastic partner through this, and as we communicated in the press release, they are investigating pre-specified exploratory endpoints. We don't have any data to speak about today, but we're looking forward to getting more information from J&J and seeing what the next steps, if any, in the development program of Pipe 307 will be.

Thank you, Carmine. To move on to the real meat, which is Pipe 791 and Propel IPF, it's a once-daily LP-A1R antagonist without the same titration burden as Bristol-Myers shot on goal in IPF. But how meaningful is that in older symptomatic population already taking background antifibrotic therapy?

Yeah, I think that it's more meaningful than it sounds like on paper. If you look at the patient population with IPF, generally 65 to 85-year-old patients infirm a lot of comorbidities as well as additional treatments that are on their treatment schedule. So having a dose titration adds complexity to their treatment. It potentially leads to additional doctor's visits and things like that. To be able to identify and advance a compound that can be at its starting dose from the very beginning leads to convenience. And I think in this patient population, that is not lip service. That is something that is meaningful in their adherence and ability to address their disease with 791.

Sure. Thank you. And Propel IPF, it's now active in more than 55 sites across eight countries. Where does enrollment stand against the 324 patient target, and when should enrollment complete, and when should investors expect top-line data?

Yeah, so as you mentioned, it's a 324-patient study. We actually have, as of ct.gov yesterday, we have 70 sites open. The goal here is to potentially go as high as 150-plus sites. We don't give guidance on individual patient enrollment. We will continue to update clinicaltrials.gov, and we expect to have the study completed in the middle of 2028, and from a runway perspective, we have about $240 million in cash based on our last earnings, and that funds the company for 12 months past the completion of the Propel IPF study.

Wonderful. Thank you. And the primary endpoint is absolute change in FEC through week 26, while Ad Milperant's phase 3 evaluates FEC at week 52. Why is 26-week sufficient, and what placebo-adjusted difference would be both STAT-SIG and clinically meaningful?

Yeah, so there's a difference here with a phase 2 versus a phase 3. The Ad Milperant, And a LOFT-IPF study has over 1,200 patients in it, and obviously they're looking at this as their key component for the registration program. In contemporary studies, 26-week programs for proof of concept have been well accepted, and we're able to see that change in FBC decline. But this is really establishing the proof of concept, evaluating the doses that we could potentially bring forward in a pivotal study. Um, with that MILPRAN, like I said, this is a 52-week study that they will be looking to, uh, include in their pivotal program.

Sure. Thank you. And what proportion of Propel patients are receiving background antifibrotics, and do you expect, uh, PIPE-791's treatment effect to be consistent across, um, across the, the background, uh, regimens?

Yeah, so in most contemporary studies now that include background therapy, typically it's two-thirds to three-quarters on background. For our current study, we include Nintentib and Profenidone as background therapy. Nirondomalast had not been approved by the time we initiated this study, so we will continue to evaluate their script numbers, and there's a high probability that we will include Nirondomalast as a background therapy as well. And, Sean, I'm sorry, I missed the second part of the call.

Oh, yeah, just that, you know, do you expect the treatment effect to be consistent across, you know, whether background therapy or no background therapy?

We do, we do, and we've seen this through the original Edmil-Perant data in their Phase II, as well as near-endomalastin and others.

Sure, thanks, Carmine. And at ATS, you highlighted differences in lung occupancy and vascular pharmacology versus BMS 986278. What does the PET dataset establish about the depth and duration of LPA1 coverage, and how did it inform dose selection?

Yeah, so this is really a critical component of our differentiation strategy versus Ed Milperant. From the non-clinical work, as well as looking at BMS-020, which was the first-generation molecule, it appears that having higher receptor occupancy drives a benefit in the bleomyosin model, but potentially in FBC as well. BMS has added a new dose into their Phase III at 120 mg BID. We believe that they are doing this to attempt to improve target coverage and have an FVC benefit there as well. We ran a positron emission tomography study to set the 50% and 90% receptor occupancy with our molecule. What we were able to demonstrate through the PK that we generated in our multiple ascending dose healthy volunteer study is at all of the doses in the MAD, So 1 milligram, 3 milligrams, and 10 milligrams as a QD dose, we achieve at steady state 90% coverage at the 1 milligram and then multiples beyond that at both 3 and 10. So we think that this is an opportunity to really max out the viability of this receptor and having a positive outcome in this patient population.

Yeah, well, wonderful. And moving on to the involving IPF landscape, so pretty important data point coming up with, you know, BMY's, you know, Phase III Aloft IPF for Ad Milperant. It's expected to read out by year end, so well before Propel. Like, how would you interpret a positive result versus a negative one, and how should investors gauge that data as it relates to the class and to your program and its differentiation?

Yeah, so I would tell you that the Continuum team is the biggest cheerleaders out there for the BMS data. We're very bullish on this, right? I think unlike other mechanisms that have failed in phase twos, there is a high degree of clinical validation that BMS has generated, 500 patients, two different studies, three different cohorts, all demonstrating an improvement in FVC decline. So we think that the clinical validation there is pretty indisputable at this point. For their phase three, again, if this is positive, this is further validation for the class and will make us even more bullish on our differentiation story. If they miss, one, we would have to know what that was. Was it insufficient target coverage? Is it a tox profile? Is it actually mechanism-related or is it drug-related? And that is something that we would have to dig through and see if it is drug-related. We believe that we have a best-in-class, if not best-in-disease approach to IPF.

Sure. Can you make some commentary around the potential differences in hemodynamic profile between your drug and Ad Milperant?

Yeah, and credit to BMS. They have been very upfront that they have seen hemodynamic signals across their studies, starting at the Healthy Volunteer into the Phase 2, and they were looking to mitigate this in the Phase 3 in a dose titration. So, and it looks like this has worked because, from what we understand, the 120 mg dose got through that cohort one, but they did implement a dose titration that, from what we understand, can take anywhere from 7 to 16 days to get to the 120 mg dose. That dose titration was not evaluated in the phase two, so, you know, we're questioning whether a dose titration will be required in a commercial setting or not. We have not seen the hemodynamic signature that BMS has, so we are confident in not having to do a dose titration, and we actually generated data and presented it at ATS, nonclinical data obviously, demonstrating why a compound with a fast on and off rate and a high peak to trough may have a hemodynamic signature, whereas the pharmacokinetic profile of pipe 7.9.1 prevents that.

Right, sure. You've kind of made a case already for the next question, but I'll ask it anyway. So assuming Edmil Perrant reaches the market first, what's the commercial case for a second LPA1 antagonist?

You know, I think that their commercial case right now is that they're first in class. And I don't think it's a bad position for A smaller biotech to have pharma start to build the market. What we believe is that a more safe, tolerable QD dose, potentially with a benefit in FBC and a potential benefit in quality of life around CNS penetrants, will overtake a first-in-class approach. And we truly believe that the LPA class will serve as the backbone for combination therapy. We also truly believe with what we have seen so far with our compound that we have the potential to be best in class and the backbone of therapy across IPF.

Sure. Thank you. Still on involving competitive landscapes, so United Therapeutics are advancing their drug through a non-antifibrotic mechanism. If successful, does it change the standard of care Pipe 791 would be added to, or the efficacy bar it must clear?

I don't know that it changes the efficacy bar that must be cleared, and I didn't answer your question before. We think that a 50% reduction in FVC decline is the barrier here. With Tyvaso, I think it's a different mechanism. It is certainly something that we would look to combine with, but I don't think that it changes the landscape. Even if you look at the data between nirindomalastin and Tyvaso, the 95% confidence intervals overlap. And in speaking with KOL, something that we have heard is that a compound that has a slightly smaller FBC decline but is tolerable is more ideal than a compound like we have with OFEV, where 50% of patients don't take the drug and the majority of patients roll off the drug because of tolerability. So if we can have, with this class or any other class of compound, a sizable reduction in FEC decline, but also have a side effect profile that makes patients adherent to it, is really the benefit that we want to show so then patients can actually extend their life.

Sure. And how should investors compare the data that we have seen so far from Silico Medicine and their program?

To be frank, I haven't seen any data. Yeah. I'm sorry. I haven't.

Yeah, fair enough. So longer term, do you view LPA1 antagonists as replacements for existing antifibrotics or combination partners or treatments for patients unable to tolerate current therapy?

So our hope is that this, we've had a kind of renaissance in IPF, right? There was dark days a few years back, but now we have not only profenadone and nintetanib, but we have nirondomilast, which is, it looks like a very good drug, and from what we understand, the scripts have been pretty impressive, and we'll have Tyvaso coming. I think we need to think about IPF like we thought about the antivirals in HCV and HIV. It really changed the treatment paradigm in patients and the lifespan of patients when combination therapies came around, similarly with drugs in oncology. So we look forward to the opportunity to combine with near-endomalast, with Avalyn's drugs. I think we're all in this to extend the lives of patients and give them a healthier existence. To do that, it's not going to be a one-drug treat-all.

Sure, sure. Maybe a bit of market-sizing question. So how do you think about the market size in the U.S.? How many patients are annualized that are diagnosed with IPF, the existing prevalent base? You know, how do you frame that, and how do you assess the addressable population?

Yeah, from an IPF side, you have about 130,000 to 140,000 prevalent patients. The incidence rate, I believe, on an annual basis is around 30,000, and that kind of fits with the current lifespan of patients. So from diagnosis, generally the lifespan is about three to five years. So, really, as you think about this disease, it's comparable in terms of lifespan with some of the more virulent cancers, and I think people need to understand that that is a big component of this is patients are refusing therapy right now, despite the fact that it may be able to extend their life given the tolerability and safety issues, and this is where we believe that LPA1 really excels. If you look at the BMS Phase II data, the major side effects were primarily around the background therapies of OFEV and profenadone.

Sure, sure. And how is it typically diagnosed, and what's the diagnostic algorithm?

Yeah, it's usually diagnosed very late in the disease progression. It's generally people going to their primary care and then to a pulmonologist to see if they have a UIP signature, and then that starts leading to the treatment regimen.

Right, and is it better to diagnose early? Do we know that data?

I don't know that there's prophylactic treatment, but yes, I would assume that it is much better to diagnose this early. Okay.

And how do you think about sort of pricing and reimbursement? It might be a bit early in the day for...

Oh, it's early for us, but it's certainly something that we think about.

Yeah, maybe give us some context around that, medical care versus private, et cetera.

Well, from what I understand, the average price in the United States for OFEB is about $135,000. And Nir Endomalast, I think, is closer to $200,000, and Tyveso is already on the market for pH. That is a little bit more than a quarter million, so, yeah.

Yeah, and what would you think about the pricing for your drug against those?

I don't think that I'm ready to take an estimate there. No problem. Thankfully, we do have a big pharma coming ahead of us.

Yeah, you'll know. Okay, fantastic. Moving on to capital and portfolio strategy. So, you know, we've propelled the principal value driver. How are you balancing investment in that study against preserving optionality and chronic pain and CTX 343?

Yeah, so we have a nice balance sheet right now. But as we look at resources, the number one resource that is going to be pushed is into the IPF franchise, and specifically on the phase two. That being said, we are excited about CTX343. This is a peripherally restricted LPA1 receptor antagonist that could potentially move into additional indications. And as you mentioned, we have a pain portfolio or a pain program here as well where we tested pipe 791. Right now, we are laser focused on Propel IPF, getting that study completed, well, fully enrolled and then completed. But we will opportunistically use resources to advance other programs, as well as we have bulked up our translational division at Continuum. So looking at the LPA1 mechanism, not only in pulmonary fibrosis, but potentially other fibrotic disorders.

Interesting. And what milestones does the current balance sheet fund, and is the next major capital decision expected before or after Propel?

I'm sorry, Sean, I missed that.

Sorry, what milestones does the current balance sheet fund, and is the next major capital decision expected before or after Propel data?

So we are funded through the middle of 2029, which that means about 12 months after conclusion of the Propel IPF study. From a capital perspective, obviously there's BMS data coming up. We're going to be opportunistic in terms of capital raises moving forward. We want to make sure that the company has the appropriate capital to not only complete this phase two, but run the ancillary DDI studies and everything else, and then start to think about a phase three program.

Sure. Great. Well, I've run through all my questions. So is there anything that I didn't ask that I should have? No. We've covered it?

Yeah, I think we're good.

All right. Well, we might call a close proceeding there, but thank you for participating and appreciate talking to you next time, Carmine. No, it's fine.

I appreciate it.

Thank you, everyone.