I am Cheng Li, one of the Biotech Analysts here at Oppenheimer, it's a pleasure to welcome you to our discussion with Wave Life Sciences. It's my honor to introduce Paul Bolno, President and CEO at Wave. Paul Bolno, welcome, and thank you for joining us on a busy day for you, especially you reported 4Q results this morning. To kick things off, Paul Bolno, can you maybe give us a quick overview of the story for those who may not be super familiar with the Wave story, and maybe highlight a few points from your today's 4Q result? That'd be great.
Cheng Li, thank you for having us. I t's a very timely time to be here, in that there's a lot going on at Wave, particularly this quarter. Those who aren't familiar with Wave Life Sciences, what's important to note is we're really at this kind of important point of convergence, meaning we have invested now the last over a decade in optimization of chemistry to improve oligonucleotides and RNA medicine. If we think about these medicines, we have one half is how do we make them better, more potent, more durable? The power point of convergence for us is unlocking human clinical genetics.
If we think about the update and the evolution of the pipeline, it's really been at this dominance of saying: How can we apply these innovations on chemistry and siRNA, in the case of Inhibin βE for obesity, be able to unlock a target that has been challenging for others, that we can do uniquely well? We shared clinical data on that target last year. We'll have clinical data this quarter on the 240 milligram six-month data and the 400 milligram three-month data.
Equally important, unlocked an entirely new category of medicines in the field of RNA editing, and that work that we've done uniquely has been opening up alpha-1 antitrypsin. Again, another program where we had robust clinical data in 2025, and again, this quarter we'll have additional data on the 400 milligram multi-dose. On both hands, really, the advantage of Wave is building best-in-class chemistry to unlock innovation of high-impact, high-value targets.
Great, I think that's a perfect set up for the discussion, and we can just dive into WVE-007, which has gained significant interest since you reported the initial data in December. Maybe just to start off, since you have the data for some time, could you maybe share some maybe initial feedback from the KOLs or the obesity community, how they're viewing the initial data and also the mechanism and the modality?
I think what's important, and it's a great question to get to the data and the KOLs. I think what actually drove our interest in the target came from the community and came from KOLs, who are really looking to address the unmet need in obesity. As we know, this field has grown enormously through the growth of incretin. This idea that if you could dial back appetite, essentially driving it from a central standpoint, so you turn off that food noise, people eat less, their body metabolizes and breaks down fat and ultimately muscle.
Those medicines come not only with a substantial loss in lean muscle mass, we showed in some studies, as much as 50% at the first 3-month time points, can come with tolerability challenges such that nearly 70% of patients can't stay on these medicines for a year. The real need is, how do we drive what's important for obesity therapeutics? This is being driven by the KOLs and the patient advocacy organizations for obesity, which is a focus on improving body composition.
Meaning, h ow do you drive not just total value of weight loss on a scale, but actually, how do you do that through reduction in fat, and importantly, not just subcutaneous fat, but visceral fat, which actually drives the improvements or the worsening in health outcomes. Reductions can drive improvements in health outcomes. Visceral fat drives a high component of that. Realizing that lean mass is incredibly important, people often think about it as a strength concept with muscle, but what's really important is muscle is an endocrine organ, and it's involved in insulin sensitivity, glucose metabolism, body metabolism, and so it's as important in that weight loss phenomenon and importantly, fat loss phenomena.
As we step back and talk to the community and said, "H ere are opportunities," we also have the power, as we said at Wave, not only are we working on innovations in chemistry, but human clinical genetics. Inhibin βE is a target that came out of the UK Biobank. It's a target where there are individuals who walk around with this 50% reduction in Inhibin βE, which leads to a reduction in Activin E. This is a ligand that's produced in the liver. Those people who are heterozygotes have low abdominal visceral fat, they have low hip-to-waist ratio, they have low bad lipid levels, lower triglycerides, lower LDL better hemoglobin A1c and because I t's a human clinical genetic database, the outcome studies have been run.
These people have a low risk of cardiovascular events and type 2 diabetes. When we get to put together a high-impact target that actually addresses the demands for what's needed in obesity therapy, the goal is: How do you tractably treat that? The advantage we have, which this is a target that is in the liver, therefore, with a GalNAc-siRNA, you can potently hit it. We were able to show in preclinical data, the only preclinical data set that showed robust reduction of Activin E in the DIO mouse model, that ultimately translated to weight loss similar to GLP-1s, both on monotherapy. We showed that in combination, we could double the weight loss on GLP-1s, meaning it's an orthogonal approach.
We also showed that it could be used in maintenance, meaning if you dose it and stop a GLP-1, you could see that weight loss sustained without the rebound weight gain. As we step back and say, what did we have before going to the clinic? The KOL community was like, "That's an interesting mechanism. If you can find a way to actually drive fat reduction, that ultimately changes phenotype, but also doesn't, isn't driven off of loss in lean muscle mass, that's a differentiated therapy. Our siRNA is enabling us to do that with a once to twice a year subcutaneous injection, radically changing that treatment landscape. As you alluded to, we saw that translate into the clinic.
At the three-month time point, at the lowest therapeutic dose, after a single dose at the 240 milligram, at that three-month time point, we saw fat loss that was similar to GLP-1, and actually on total fat, we saw that actually visceral fat was higher than GLP-1. We had nearly a 10% reduction in visceral fat. We had sustained lean mass, placebo-adjusted 0.9% increase, and then an adjusted 0.9% reduction in body weight. At the early time point, we're seeing that actually human clinical genetics translated to the DIO mouse model, translated back to clinic. I think the KOL community, and it's a very important part of the conversation, hopefully going forward, which is one that shifts from maximum weight loss to improved body composition. That doesn't mean that you can't lose weight.
That's going to be required for FDA and regulatory guidance. W e fully believe that that's there, but really focus what's on meaningful. We had a KOL recently who was reminding us that there's a really important expression that she uses with her patients, which is: "You want to become leaner, not lighter." The idea that pounds on a scale doesn't equate ultimately to improvement if 40% of that lean mass loss is driving your weight reduction. This idea that you can lose bad fat, ultimately changing that aesthetic value, and sustain muscle, is a really important dynamic in the obesity landscape, and it's clearly addressed through the inhibin pathway.
That's perfect. I guess as we all look forward to additional updates from the INLIGHT study, actually in the coming weeks now, which will include the 6 months follow-up data from the 240 mg cohort and the 3 months data from the 400 mg cohort. How should we frame the expectation and at now which data set do you think will be most informative?
They're both informative, I think we have to go back to the preclinical data that we've seen really nicely translate. I should add that all these advantages we're seeing all happened at a BMI that's lower than a traditional obesity study. We saw this weight loss in a healthy, overweight volunteer study, where patients weren't required to do diet and exercise, where they didn't have comorbidities, and the BMI average was about 32. Again, in these settings, we're able to see that if we think about what we saw in the animal data, which translated nicely to that human data, is we do see a dose response. This idea that as you continue to suppress activity more, that you can increase the slope of those curves, that's what we saw earlier.
We're going to have that in this data set with the 400 milligram 3-month data. Equally important is change over time. The kinetics, when you stabilize muscle and just lose fat, is that curve on weight takes longer to achieve, even though you're losing a substantial amount of fat. The opportunity we have at the 6-month time point is to look at that slope of that curve at the 240. Both become important because it's hard to draw a line and predict out without having multiple points on a slope. Really, what's important about these data in the first quarter is we're going to get the time dependency at the 240 and the dose dependency at 400.
Got it. Just like dig deeper into the time dependency, like for the 6 months data for 240 mg. How should we think about the speed of continuous fat loss? I guess another way to ask the question is that we saw maybe 4.5% total fat loss and over 9% visceral fat loss. Should we expect to see another 4.5 total fat mass loss from month 3 to month 6, or maybe is there some other number?
I think we want to see a continued decline. I think one of the challenges people try to extrapolate from other studies and even trying to look at the DIO is you're talking about higher levels of obesity, so higher BMI, yielding more visceral fat, more subcutaneous fat, and more fat to lose. I think some of the questions that we'll see in this is exactly that.
It should continue to trend lower, and we should see that come. At what expense? Is it straight linear? Is it exponential? I mean, one of the interesting things preclinically in the higher BMI DIO mouse model is to get to that same degree of weight loss as GLP-1s we saw, you actually had to lose more fat than the GLP-1. I think over time, we're going to continue to learn what the slope of that line looks like. What's really important in this next data set is less an absolute value and more a continued trajectory.
We should see continued trending of increasing visceral fat, increasing subcu. What we do know, based on all the studies that actually increase lean mass, and what we do really is stabilize it, is by 3 months they normalize. If you look at the bimagrumab data. T hey had higher lean mass, lower fat loss than what we see, and still had greater than 5% change in total body weight. If we think about kind of those characteristics, we should see stabilization of lean mass decreasing in fat, and all of that should bode well for moving this program forward. The 400 should give us a sense of what the kinetics look like at a higher dose.
Got it. We probably should expect the lean mass to be more stabilized from month three to month, six, which will, I mean, ultimately translate to maybe greater degree of total weight loss at month six.
That's right. I mean is relatively speaking, but yes, it should continue to go down.
Got it. Just for the 400 mg cohort, I think you probably just mentioned that before, but can you just remind us of the baseline characteristic of this cohort? I know the BMI is quite low for the 240 mg cohort, around maybe 32. Should we expect maybe similar baseline BMI for the 400 mg cohort?
We haven't seen the baseline co characteristics yet because we haven't unblinded the data and gone through that. For 400, we'll have that at the time of the data release so that we can compare it. I think what's driving the BMI criteria is really this function of no comorbidities, b ecause it is a healthy, overweight volunteer study, right, and overweight and obese patient study. By being healthy means there's a cap on HbA1cs, there's a cap and threshold for lipid levels. When we think about all of these comorbidities, when they're capped, they tend to be seen when you have higher BMI.
Again, one of the other announcements we made, recently, earlier this year, was that we are accelerating the Phase 2a portion of the study, meaning allowing that to go into higher BMI patients. We'll initiate that this half of the year. What we'll be able to see in that study, by taking off the criteria of allowing patients with comorbidities, is the expectation that we'll also index to higher BMI individuals. Think about 36, 37. The opportunity to still build that in and see those data sets in those patient populations.
Got it. Just one last question for the 400 mg cohort. I think from extrapolating data from the Activin E reduction, I think 400 have maybe 85% reduction compared to maybe 77.8% for the 240 mg, which are kind of a 10% additional reduction. I mean, just like an easy way to think about it, should we maybe expect to see maybe 10% additional, like, fat loss for the 400 mg at the same time point compared with the 240 mg?
When you do something with new biology, trying to extrapolate linearly into humans is something that I'd rather generate the data, and then we'll be able to extrapolate what that does, b ecause I think what's really important is it's not just about a moment in time. I think what's really been interesting is we've looked at comparable preclinical data to emerging peers and competitors, is looking at the fact that we've had this real depth of suppression. The idea that we could do a once to twice a year where others can't be able to keep Activin E, not just knocked down, but suppressed over time. It's really that suppression factor for this target that ultimat ely drives prolonged fat loss.
The ability that we're going to see, not just to get that incremental increase of what do we get between the 240 and the 400, but the speed with which that comes down and the time that that stays suppressed, all will longitudinally contribute to increasing, what we believe to be not just fat loss, but ultimately translating into weight loss.
Got it. I have a question from an investor asking, should we expect to see, like, lean mass increase for the 400 mg at month 3, as we observed with the 240 mg?
This is another, it's a wonderful question because while the mechanism of action doesn't drive, so Inhibin E, Activin E is not driving lean mass production. What we think is happening is you break down fat, you increase free fatty acids and glycerol, the kind of the food source, the energy source for muscle gets larger. There's nothing mechanistically, at least in our belief, that necessarily dose response should lean to increase. Maybe it will. If you free up more fat, you may get a little bit more lean mass. That's what we're going to learn together, is what happens between the 400. What we should see is a corresponding and most importantly, a deeper decline or a faster decline in fat loss, and I think that's the opportunity to have it, looking at those 2 dynamics on lean mass and fat over time.
Understood. As you're planning to start a Phase 2a MASH study, I think first half, and you mentioned you want to just test in a maybe more, like, heavier individuals, maybe with comorbidities, but can you maybe talk about the thinking about the, maybe the trial size and also the dosing strategy, anything you can just optimize further based on your set experience?
I think these two studies are intertwined in the sense that I think we're going to learn, because the follow-up on this study is out to a year. I think we're going to learn about the pharmacology of Activin E reduction, which is really independent of BMI, what the PK looks like over time in this study. That's going to give us kind of the longitudinal piece. Frankly, from an expedient standpoint, so we don't have to make this take longer, we're looking truncating the dosing intervals to maximize the time and efficiency of the study, and would expect reasonably, that these cohorts will look similar in size to the cohorts we're previously studying.
Again, trying to keep as many of the variables similar and really being able to look again at a dose response in a multi-dose way, but most importantly, to your point, being driven off of higher BMI individuals, and that's really the index for us. I think what we'll also be able to learn by having the comorbidities is, we'll be able to look at some of those other biomarker signals.
Inhibin βE reduction should have an impact on hemoglobin A1cs, lipid levels. You can't see that in healthy volunteers. We'll have both the opportunity to look at fat reduction, lean muscle preservation, impact of body weight, and other biomarkers. Importantly, and I think this was a really, I think it's a fascinating opportunity with Inhibin βE, is the reduction in liver fat. If we think about the fact that in combination with incretin, with a less potent medicine, I think the data that we share with Ara is 78% reduction in liver fat. With increased potency and suppression, I think there's a real opportunity at exploring liver fat.
What we have done and announced is we've added MRI imaging, along with hepatic imaging for fat, into this higher BMI study, so that we can actually capture in a monotherapy basis, that reduction in fat in the liver. We keep that opportunity open for other indications.
Right. For MASH, is that some, a standalone opportunity for 007, where it's like more like, addressing the comorbidity of fatty liver in those with, in those obese patients?
I mean, we think it's very much a possibility,. You see a substantial reduction. I mean, that combination data that was shown by others was more impressive than, I think, a lot of the MASH data that's out there in other therapies. So the opportunity to bring in, for us, a 1 to 2 times a year sub-Q medicine that can actually drive dramatic decrease in hepatic fat is extraordinarily interesting, in addition to the broader utility for obesity. I think the other applications, and we're hearing a lot of investors asking us about the implications on visceral fat reduction, that's consequential. I mean, if we see the data out on increases in visceral fat, that actually can drive disease outcomes or worsening in cardiovascular disease, MASH, and others.
A 5% increase, 5%-7% increase in visceral fat can drive this. To see a 10% decrease in visceral fat at the , single dose, the lowest dosing interval, I think lets us think about the whole compendium of diseases that can be unlocked if you can meaningfully and substantially reduce visceral fat.
Yep, got it. I guess another maybe popular question is on the regulatory path forward with O seven, and you mentioned you are confident to achieve over 5% weight loss, like, which is a conventional bar for obesity drug, but also the body composition is important. Is there any possibility to incorporate body composition into your, like, clinical endpoint and any just, like, direct evidence you can show, like, improvement in wellness by improving the body composition maybe in the Phase 2a study?
Yeah. No, absolutely, we spend a lot of time thinking about this also from the concept, not at just from labeling, to your point of how to create a differentiated label. O ur conviction is these studies, as you point out, are a year on a optimized dose in a patient population who you intend to treat. Again, as we think about the subsequent study of having a year on therapy at a dose that's selected in a patient population, an obese patient population with a BMI of 36, 37, which is where the historical obesity studies are driven, we absolutely expect that reduction in body weight that would meet a threshold of regulators.
That said, what's interesting, we cite the 5%, and this is actually a lot of what was in the, draft guidance that went out last year, that where it reiterated the 5%, 4,500 patients worth of safety data generated on the compound. There was a lot of time spent on this focus, to your point, on body composition. I think the real opportunity we have in that, in thinking about well-published literature on visceral fat and comorbidities, meaning cardiovascular disease, diabetes, and MASH, the ability to build that reduction in visceral fat and body composition into that label and the impact on preservation of muscle, we see as an important differentiator, both as we think about this as a monotherapy, as we think about this as a combination therapy.
Ultimately, what I think is very important is maintenance. I mean the idea of keeping people on well, 70% of them can't stay on it for a year, but the idea when people are like: "Oh, these medicines should become like hypertensive medicines that you just stay on for a lifetime." The idea of a weekly or monthly injection for fat people to stay on monthly, that continues to deplete lean mass. We know that the anhedonia or loss of joy develops and continues to sustain over time.
Those implications long term, when we can actually shift patients to a once to twice a year subcutaneous shot, where they can maintain their body weight or loss, so the time and money that they've invested in achieving that, we think actually becomes an incredible opportunity to transition patients from incretin therapies onto an inhibin.
I think that's kind of a really interesting point, and that's a question I want to ask. W e're still pretty early in recognizing the full potential of this program, but any thinking, like what is the biggest uptake for the 007 in the future? Do you think it can be used more broadly with GLP-1 combination or in the maintenance, and what is really the ideal patient population for 007?
Yeah, i t's been wonderful since the data's come out, the number of conversations we've had with various strategics who are deeply embedded in the obesity landscape, that have lots of ideas for the program. I think what's affirming for us is the conversations go to all three areas. I think there's a recognition that even in frontline monotherapy, there's going to be segmentation based on patients , perimenopausal women, older patients with a risk of loss of lean mass. Again, what we saw from the BELIEVE data is that you see about a 50% reduction in lean mass on GLP-1s at early time points. I think there's lots of opportunity in the monotherapy for fat loss, muscle stabilization, and doing that with a once to twice a year sub-Q medicine. I think in the combination, there's a lot of opportunity.
We've had some suggest to us, maybe you start with inhibin and titrate the incretin on, therefore can be really deliberate of pushing patients on incretins, and how do you titrate that? I think there's a lot of ways to think about patients who aren't a goal, how you help people achieve that based on the combination. A s we were alluding to and speaking about later, I think there really is a recognition that long-term maintenance a medicine that doesn't drive caloric restriction and ultimately lean mass loss, is going to be an important medicine in long term.
I f we really think about the 1 billion patients living worldwide with obesity, the idea of really providing access where you can think about a medicine again once to twice a year, the accessibility that can be provided on that is pretty enormous for patients who don't have to come in for a weekly or a monthly shot. I think the data is still yet to be seen on orals of whether or not that becomes real maintenance in terms of tolerability and in terms of patients really staying compliant with therapies to see weight loss.
Maybe a last question on 007 is, I guess it's, again, early days, but any thinking about the pricing strategy for 007, especially in the very, very dynamic GLP-1 landscape, and also how to think about the scalability of 007, given the billions of addressable population in the future?
Yeah, I think on that last part on scalability, what we've watched in the emergence of RNA medicines is where do we see them? We see RNA medicines being developed for cholesterol, right, with inclisiran. We see them moving into hypertension. We are seeing this movement into large disease areas. The benefit of more of these medicines moving into bigger indications is actually at the very beginning of what's required. Starting material costs, there's continued improvement of accessibility and decrease in the cost of all the starting materials, so kind of the raw material side of building oligonucleotides. I think what we're also seeing is the scalability of synthesis.
The yields of these are getting better and better. With those investments in scale, innovations and novelty in terms of synthesis, the shift from solid support to liquid phase synthesis. This, again, you can increase yields, you can increase scale, you can decrease the cost of starting material, all ultimately contribute to the end product. If at the end product, you're giving that once or twice a year, again, you get kind of exponential advantages that come not just with scale, but ultimately in enabling you to think about pricing. w e do see these as innovation engines. This isn't about trying to piggyback off of the GLP-1. We think there's a distinct advantage to a medicine that substantially reduces fat, preserves muscle, and provides that outcome. O bviously, that could be priced differently. Accessibility, scalability is there to meet the demand.
Got it. Maybe we can just move to 006. I think that's another pretty exciting program, being the leading company in RNA editing. I mean, again, we are expecting data from the 400 mg MAD cohort in the coming weeks. Again, the same question, how to think about the update and how to frame the expectation? Especially, I think, the 400 mg.
Yeah.
You are using the Q4W dosing strategy. Kind of how to think about that, the dosing strategy?
I think before we just talk about this data, I think to take a step back, because I think oftentimes we think about these data in a linear way, I don't mean we Wave, I mean the broader community. I think, those who are listening, who are thinking about, what RNA editing does versus IV protein replacement. In protein replacement, we're used to this very linear. You give more drug, you have a higher NATER that gets consumed during these events. If we think about a disease that's a chronic disease of acute exacerbations, the real treatment for alpha-1 antitrypsin deficiency is correcting people back to a heterozygous phenotype so that when they have their acute exacerbation. You have this acute phase response, you can actually produce protein into that acute phase response to protect them.
We have already shown at our early time point, 200 milligrams, 2 weeks after a single dose, that a patient could mount a 20 micromolar response into an acute phase response, meaning they could be corrected at greater than 11 micromolar, 11 micromolar, more baseline, we think to see up to 13 micromolar. They're over 50% corrected M protein, they can rise to meet that challenge. That challenge is the ultimate treatment paradigm. When we think about the data that's coming, we expect it to continue to affirm the things we're seeing, which is: how do we think about durability in frequency of having to administer this? Is it monthly? Is it potentially quarterly, less frequent? What happens over time as you get liver healthier? Is there more M protein? I think what's encouraging is we already saw the data earlier says we announced.
This year that with full control of the program and being able to go to regulators and have the discussions around potential pathways to accelerated approval, I think that data is already that discussion can already be predicated off of the data and supportive data we have, with the 400 continuing to reaffirm for us where we can continue to build and grow from there.
I think, w e're in a, in a really wonderful position in RNA editing because we only create the edited protein, so we only create the endogenous human protein. We don't have bystanders with a discussion with regulators, the impact of M+1 proteins, of which in DNA editing, you have over 50% of that protein is a different protein than that which is not naturally produced. I think the other interesting phenomena is we don't have to use delivery vehicles. We can use GalNAc.
One of the things I think people need to be prepared for is the LNPs that we watch that evolve in this space, and we've seen it with others in the LNP space, do cause systemic and hepatic inflammation. That inflammation causes increased CRP and IL-6, which actually causes a transient elevation in alpha-1 antitrypsin protein. I think as we think about the opportunity in RNA editing to selectively and specifically create that improved protein, gives us a very distinct opportunity as we think about the 400 milligram data coming, and can look at that in the context ultimately of building out the profile.
Got it. Just moving to maybe the regulatory path, I think there are some, like, maybe favorite comments by the FDA Macquarie. Recently, I think in the past few days, I think he used the word like, poster child...
``Poster child.
... ``alpha-1.
Yeah, he did.
Yeah. Especially, he kind of treated the ATD patient before, so kind of, some additional credibility to what he said. Just with that said, how to think about the path forward as you are planning to have, like, regulatory engagement, and what kind of the key alignment you are hoping to achieve?
It's always nice when they say that we'll continue to drive this because the data should support that accelerated pathway. And the data that we have is truly being able to demonstrate that conversion to what would be seen in an MZ-like phenotype, meaning you cross those thresholds. We're doing that with the native endogenous protein. The discussion that we would expect to provide feedback on in the middle of the year is not just that, which is: How do you get an accelerated approval and on the market with the existing data set? Most importantly, what does then subsequent study and labeling need to look like to make sure we can address the alpha-1 antitrypsin market?
We do see this as a substantial TTR-like opportunity that we can continue to build and grow, meaning you've got liver and lung patients, so the opportunity to think about unlocking a label that really supports the holistic treatment of ATD patients. How do you continue to grow that with genetic testing? Meaning the vast majority of patients could be diagnosed that are non-responsive to COPD therapies may actually be Alpha-1 antitrypsin patients, and the same with patients who are misdiagnosed with asthma. I think there's an opportunity to grow the market through genetic testing, and then there's the opportunity to look at the MZ patients. I think the step 1 is figure out the path to registration on the biomarker strategy and assure that we've got a clear pathway for what a confirmatory study needs to look like to open up liver and lung.
Got it. I think we're slightly short on time, but I really want to ask a question on your early discovery work. I think there are some pretty exciting work you're doing, as you maybe shared some of the work at R&D Day, including, like, bifunctional modality that can combine knockdown and editing in a single molecule, along with some, like, delivery capability into additional tissues like fat and kidney. I guess the question is: how should we think about the next wave of your pipeline or early-stage program, and how the pipeline to evolve in a few years? I think related to that, is there any potential to incorporate Inhibin E into your bifunctional modality in the future?
The short answer to that last part is absolutely. The opportunity we have, both on the bifunctional side, is bifunctional silencing, so the ability to think about knocking down two targets and, as you point out Inhibin E and t hen editing, so again, the same thing of knocking down targets and increasing them. So playing with that upregulation, silencing, and really the efficiency that comes with that.
To this point, the idea that instead of having to synthesize two medicines, run trials with two medicines, and then think about them as either fixed-dose combination or as two drugs that you give simultaneously, the idea to have a single synthesis with a single medicine where we can measure two biomarkers that ultimately exert effect, we think long term, particularly in the cardiometabolic arena, has an incredible opportunity from thinking about trial dynamics and cost dynamics. Lots of opportunity there. More to talk about the next wave of WAVE as it relates to that.
You pointed out an interesting phenomena there, which is our ability to target not just hepatocytes, but being able to think about adipocytes and dual targeting, even besides having one molecule that goes to both that does both modalities, being able to think about a single drug that can go to two cell types, meaning go to adipocytes and liver. I think as we think about the axis of potential therapeutic opportunities within cardiometabolic, there are a lot of them, so it's an exciting time.
Great. I thank you so much, Paul Bolno, for your time today. I think we can wrap up things here, and, yeah, looking forward to the updates and catching up with you soon.
Great. Thank you.
Thank you.