Morning. I'm Sean Laaman, Head of SMid-Cap Biotech Equity Research here at Morgan Stanley, and welcome to our Global Healthcare Conference. For important disclosures before we begin, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. For this session, we have Generate Biomedicines, and we welcome the CEO, Michael Nally, and President and CFO, Jason Silvers. Welcome to the both of you.
Thanks, Sean.
Thank you.
Yeah. Maybe just for some introductory questions, and we're doing this for all our companies. We have three, and I guess sort of how has the rise of China origin innovation changing your competitive position in R&D vs your business development playbook, if at all?
Yeah. I think China, Sean, has been, I think nothing short of miraculous in terms of the ability to brute force their way to exceptional answers across a broad range of therapeutic modalities and therapeutic targets. Certainly for us, it's forced us to be very thoughtful about how far we push the innovative frontier, because I do think if you're not pushing pretty far out, China can rapidly copy. I don't think it'll stop at just copying. I think they'll continue to push their own innovative frontier. What we've tried to do is actually think about where we can use our machine learning-based platform to drive answers to more complex therapeutic questions. Our TSLP program was largely an affinity maturation program where we basically took the affinity of a molecule like TEZSPIRE and improved it by about 20-fold.
China can get to those sort of answers now. For us, we've started to ask, what complex biological functions are more difficult to brute force your way to answer? Stuff like pH-dependent binding, ultra high selectivity, these sort of things that can combine and answer more and more complex biological questions has been kind of an evolution of our own discovery process.
Sure. Thank you. I think it's one of the most exciting things to me about Generate is that you are an AI-driven company, and we have this question across all our coverage, so it's almost a redundant question for you guys. Is there anything you can share that you think about the adoption of AI across the biopharmaceutical industry?
Well, I think in some ways, the lead times in drug discovery are masking state-of-the-art of AI in drug discovery. For us, I mentioned our anti-TSLP molecule, that was discovered five years ago, and that was on a model that predates the original release of ChatGPT. The state of the art of these generative approaches have progressed on a comparable basis to what we've seen with the large language models. So, where originally we were solving kind of simple questions around binding with these sort of approaches, now we're able to really take on very complex biological functions. The answers we're getting and the speed at which we're getting those answers really is distinguished from anything we've ever seen in drug discovery.
So clearly, I think it's important to note that AI is not a panacea for all drug discovery and development. There are certain parts of the value chain that are probably more prone to disruption, and right now we believe molecular generation is at the forefront of that. We think there's going to be some really interesting use cases in clinical development in terms of taking the waste out of the system. But the complexity of biology is so great that AI is not going to solve biology in the near term. But if you can be discerning and figure out which parts of the value chain can be disrupted, the tools can be extraordinarily powerful.
Sure. Thanks, Michael, and last question before you really get into the meat of Generate, but is there any policy variable that you'd highlight in terms of the outlook for either yourself or the industry that you think would be impactful? FDA, Medicare negotiation, MFN might be a little way away for you guys, tariffs, global pricing, anything.
Well, I think clearly the U.S. industry has benefited from the gold standard regulatory body for the last 50 years. I think the uncertainty within the FDA has not helped anyone in the industry. When you make these sort of long lead time bets, you want to make sure that you have the confidence in the regulator that when you make those bets, if you're successful, they'll ultimately yield medicines for patients. So I think the uncertainty at the FDA has been one in particular. I do think the MFN question is something that is going to be deflationary for the whole industry, right? I mean, the reality is the U.S. economics have covered or carried a lot of the profitability of the industry and with MFN, I think in the first instance it hasn't been too harmful.
Having spent six years leading large parts of Merck's business in Europe, usually when these sort of policies are in place, it's the start of a slippery slope that ultimately the government will see this as a cost savings lever and will continue to turn that crank. It won't be a one-time opportunity. So I do think having the government negotiate prices in the U.S. is a huge swing given the free market dynamics that have underpinned the industry to date.
Sure. Thank you. I've got a few questions here on the strategic framing of your business post IPO. Should investors think about your business as a pipeline with a platform or platform with a pipeline?
I think we think of it as a platform with a pipeline. The reality is that the first program, our anti-TSLP antibody, is an extraordinary molecule. It will do a lot of good for patients. At the same time, it is the first manifestation of what we think is a transformative way of making drugs. We think ultimately every molecule in the future will be generated, not necessarily leveraging random discovery processes like immunization campaigns and screening campaigns. For us, we are at the starting point of this kind of evolution of how drugs are made, and we think clearly it is important for us to constantly show a platform in and of itself is worthless. The platform has to create extraordinary products.
We think if and when Generate's successful, we will have leveraged this platform for a number of different products that will make a big difference in the world rather than be a single asset or kind of therapeutic area company.
Sure. With your lead program, GB-0895, how should investors think about that? Would you credit the platform? It has moved pretty rapidly through trials. You are showing some great data. Would you credit the platform or do you think it is more that you have picked a de-risked biological pathway?
Well, I think it is actually this combination, right? I think if you think about GB-0895, what the technology allowed us to do, and the observation we had from the outset of the company was if you have a good prior generative model, you can actually change the CDRs in more profound ways than any other technology we have ever seen to date, right? Historically, if you had used error-prone PCR or you had used computational techniques like Rosetta, you could only change about 10% of the binding region before you would find no functional variance in a library. What we saw with our technology and with a good prior model is that you could change up to 70% of the binding region, and that allowed you to search the functional space in a much more efficient way. I think the molecule and the molecule design was platform derived.
At the same time, where you direct it was I think a strategic choice by the company. We saw that TEZSPIRE was kind of an emerging medicine with a lot of multi-indication potential. We thought there was an existing liability with both the half-life and the affinity in the initial molecule that could be addressed with our technology. I think what we also did though, and I think critical to the success has been really clever drug development. I think this is going back to the statement, AI is not a panacea. It requires really savvy drug developers to come up with innovative clinical pathways that allowed us to go from phase I to phase III.
Sure. Still on GB-0895.
Yeah.
Clearly a very potent molecule compared to the benchmark, and the long dosing interval for those that might be less familiar is six months. How should investors think about that? Is it a play on convenience or do you really hope to show better efficacy?
Yeah, so efficacy is probably not the direction that we'll take this, although in preclinical studies, we did show a five-time improvement in potency over TEZSPIRE. But in reality, at our 300 mg dose, which is the dose we're in phase III with, we're 99.9% saturating the target, which is very similar to what TEZSPIRE is saturating the target at 210 mg, which is their approved dose. So ultimately, there probably is not an efficacy play in the clinical trials. So this is really a convenience play. Now, every six months vs every one month, we believe is material for patients and for physicians who are seeing their patients every six months anyways.
Now ultimately, the other interesting piece where, Sean, over time you may see an efficacy benefit, not necessarily in the clinical trial, is Glaxo had shown about one year ago that there's only about a 20% adherence rate to biologics for patients. And so if patients are not adherent to their medicines, they're going to, unfortunately, resort back to some of the symptoms that they had and exacerbations. And so with a very convenient play every six months, if the patients are much more adherent in the real-world setting, you might actually see a much better efficacy benefit over time.
Yeah, I think Jason's point there is really important, Sean, because what you see in the sort of domains is massive cost to the health system sure of non-compliance. And the fact that this drug will line up with a severe asthma patient's normal visits gives you a strong underlying driver of maximal adherence that could ultimately lead not only to an efficacy benefit, but also a cost savings to the health system.
Yeah, I think it's a super important point. I just wonder what your view is on how well investors understand that. While you're saturating the target and maybe you can't really improve upon biomarkers and outcomes in that sense, certainly improved compliance does derive better efficacy. Then ultimately better efficacy, less exacerbations, less hospitalizations, less cost to the system. Do you think that's really grasped by investors?
I think it's partially grasped. The nice thing is there's a lot of analogs in both kind of the immunology markets, so markets like psoriasis. We've watched them mature over the last 20 years- 30 years where first-generation therapies were more shorter acting, second-generation, third-generation therapies were longer acting, and you saw these sort of compliance benefits. I can go back to domains like osteoporosis. I worked on FOSAMAX earlier in my career, which was a daily and then a weekly oral pill. Amgen came along with denosumab, a six-monthly biologic. You saw exactly the same dynamic, where in the clinical trials you could not show a difference in hip fracture rates, but in the real world, you saw a significant difference in hip fracture rates.
It's those sort of dynamics that ultimately both, I think, investors need to understand, but also importantly, payers, physicians as well as the patient at the end of the day.
Sean, I think what's probably not well understood by investors or appreciated to this point-
Sure
with GB-0895 is the fact that we moved from phase I to phase III and did not do a phase II efficacy trial with exacerbation. Some of the points that Michael made earlier kind of justify the move that we made. But in reality, given we are following the same pathway as tezepelumab, we hit the same epitope as tezepelumab. Our biomarker data is as good, if not better than tezepelumab. We have full saturation of the target at our 300 mg dose, and this is not a unique pathway. Glaxo took it with their IL-5, and frankly, is now taking it with COPD as an indication, moving right to phase III without phase II data. It's very highly probabilistic in our view that this will be a strong, efficacious drug.
I think investors have yet to fully grasp the fact that the probabilities of the phase III success are probably very, very high.
Yeah. I'd agree with that. So it brings me to I'll just throw this question out. It wasn't on my list, but it's just given what you just said, Jason, what keeps you awake at night on the trial? What could go wrong?
Whenever you put a drug into humans, there is a lot that can go wrong. The reality of it is, the things that keep me awake are, we have seen you need to have very balanced enrollment geographically. Standard of care of disease like asthma varies by geography, and we have seen in a number of different trials that in Eastern Europe, you are not showing a difference between placebo and active arms in recent trials. Making sure you have the right caps, the right adjudication procedures for entry criteria. The details really matter on these sort of trials, Sean. Making sure that we do that very well, making sure that it is stratified appropriately by EOS level.
One of the benefits that anti-TSLP medicines have is that it works for all comers in asthma, but you want to have the right proportions in the EOS less than 150, the 150- 300, the 300 and greater. How you actively enroll this trial to make sure that you have the right balance ultimately determines the outcomes in these sort of trials.
Sure.
I think that only becomes more and more complicated as you go into other diseases like COPD, where the heterogeneity of the disease is even greater.
Sure.
This is a very competitive space.
Sure.
Speed matters. Getting to patients faster is really important. The speed in which we execute on enrollment in the trial, this is a 52-week endpoint, so getting to enrollment faster will get us faster to market. There are a lot of other companies out there which are behind us on the long-acting molecules. We think we have the best long-acting molecule with a 98-day half-life, which is meaningfully better than any of the other long-acting, next generation TSLP, anti-TSLPs. We do have that binding affinity of 20-fold improved on affinity than tezepelumab, so 100 femtomolar binding. We feel also that in addition to the long half-life, we will be grabbing the cytokine tighter for a longer period of time, which will enable us to have the benefit for patients out to six months, which is not necessarily clear for some of the others. Speed is critical to us as well.
Well, it flows nicely into the next question. SOLAIRIA-1 and 2.
Yep.
What can you tell us about the rate of recruitment and your confidence on completing and getting to top line in, I think guidance is first half of 2028?
Yeah. The studies are off and running. As of Friday, we had regulatory approval in 39 of the 42 countries in which we're recruiting. We're seeing uptake across all regions. The team has done an extraordinary job standing up two replicate 786-patient trials. We feel like we're on track with all of our prior guidance in terms of having enrollment completed by the end of 2027, data toward the end of 2028, given the one-year endpoint. All of those details that I had just mentioned a moment ago, Sean, have been front and center, right? We're making sure we're recruiting broadly geographically, but also making sure that we're getting the right types of patients in the trial.
One of the key entry criteria that we looked very carefully at was having patients have two or more exacerbations, documented exacerbations in the year prior to the start of the trial. Ultimately, we believe that sort of an entry criteria will ultimately show a meaningful therapeutic effect.
Sure. Thank you. What level of exacerbation reduction do you think you may have to show to say you've got a competitive drug? I think TEZSPIRE showed a 70% reduction over 52 weeks. How should investors think about that as a benchmark?
Yeah. I think if you think about the anti-TSLP space, and you mentioned the TEZSPIRE data that was in the EOS greater than 300 cohort, right? They showed a blended rate across all comers of 56%.
Right. Yeah.
70 in the high EOS cohort, 40 in the low EOS cohort. I think that's kind of the TEZSPIRE has set the benchmark as the incumbent, right? I think somewhere in the 50% reduction across all comers. Then pushing up, I think you've seen with the IL-5s and with products like DUPIXENT in the high EOS cohort somewhere in that 50%, 60%, 70% range as well. I think that's the mark that you're going to have to hit to be competitive. I think obviously doing that with also a great safety profile will be key to the success of the medicine.
Given the FDA feedback for our trial, the reason the size of our trial is 786 subjects in two different studies is to be powered to capture the below 300 EOS endpoint. We're 94% powered to capture the less than 300 EOS endpoint in terms of reduction. That means we're basically 99% powered across all comers.
Sure. Can you remind us or tell us what the evidence you have around pharmacodynamic evidence that TSLP suppression is maintained through the 26 weeks?
The data we just showed at the European Respiratory Society actually shows that we're sustaining those biomarker reductions out now up to about a year. Again, Jason mentioned earlier, the 98-day half-life. You're seeing 50% reductions across a number of the key biomarkers like EOS, IL-5, IL-13. You're seeing substantial reductions in FeNO as well. What's really been encouraging is, at that 300 mg dose, you're not seeing a waning effect toward the end of the period. We feel very confident that the medicine is very active for beyond six months, actually.
Great. I guess COPD is the largest swing factor in our valuation. The market will read the ERS poster as a proxy for the multi-billion dollar opportunity of biomarker and PK data alone. Is that a fair basis, or does the real answer need a phase II-B?
No, listen, I think, as we've seen, GSK just took a very aggressive approach going straight to phase III with no COPD data that we're aware of, right? I think TEZSPIRE showed a really interesting signal in their phase II study. If you think about the currently approved biologics for COPD, you have DUPIXENT and NUCALA. They are only approved in the greater than 300 EOS cohort in COPD, which is about 28% of the market. The data that TEZSPIRE showed would take that down to about the 150 EOS cohort, where you would add another about 40%- 45% of the market. Obviously the landscape in COPD is changing with the recent AstraZeneca data for the IL-33, where they were the first medicine to show a benefit in the less than 150 EOS cohort.
But we still think there's a huge opportunity. The COPD market's only 2%-3% penetrative from a biologics perspective. As you know, in these sort of immunology conditions, you usually see when they're mature markets, you have a 40%-60% biologics penetration. There's a lot of room to run. COPD is, depending upon which statistic you look, one of the top five burdens of disease globally. So the cost of the health system is extraordinary. The cost of patients' lives is extraordinary. And we think if you had somewhere, the tezepelumab data in the greater than 150s was about a 37% exacerbation reduction. That is a really meaningful medicine for patients. And so we think the opportunity, as you rightly point out, is profound. We think GB-0895 is very well situated in that.
The other last thing I would just say is the six-monthly dosing may actually be more valuable in COPD given the frailty of the COPD population. COPD patients oftentimes are carrying multiple comorbidities and having a long-acting therapy that almost provides background protection for that population. We get a lot of feedback from doctors and patients that would be very meaningful for their lives.
Thank you. I normally ask these questions towards the end and want to give some time to some pretty exciting oncology programs, the MMAE one in particular. But given SOLAIRIA-1 and SOLAIRIA-2, the data you have shown at ERS in COPD. I think you had $457 million of cash on balance sheet at the end of Q2. How do you think about the balance sheet and funding from this point forward?
So we are funded through the first part of 2028. That will carry us through the phase I trials in oncology. It will carry us through the enrollment in the asthma trial, as well as a lot of the initiatives that we are doing from the platform side and the next generation of molecules that we are moving toward the clinic. There is a number of different paths that we are, I would say, simultaneously pursuing from a capital perspective. Doing partnerships like our Amgen and Novartis partnerships is part of our core strategy, so we will continue to do partnerships like those. We have been very successful in terms of getting toward the end of resolution on most, if not all of those targets, and certainly will be over the next several months. That opens up a lot of capacity for us to do more partnerships.
Those types of partnerships, as well as achieving milestones on the Amgen and Novartis partnerships will bring in non-equity dilutive capital. We will certainly explore equity capital markets, as well as product-specific financing, potential commercial partnerships around some of our products over time. Therefore, we believe over the next 12 months- 18 months or so, a lot of these pieces will carry us through not just asthma data, but beyond.
Thank you. Moving on to GB-4362, so it is your MMAE neutralizing program. Maybe just give investors a snapshot of what that is, because I do not think it might be broadly appreciated, particularly for people newer to the story. What clinical evidence do you need to show toxicity can be decoupled from efficacy?
Yeah, it's a great question, and thanks, Sean, because GB-4362 is a program that is very unique. We talk a lot about medicines, and you started the conversation with China. We are not aware of anyone else pursuing a concept like this. The beautiful thing about GB-4362 is the dose-limiting toxicity for MMAE-based ADCs has been peripheral neuropathy. This has been seen in pretty extraordinary rates in the clinical trial setting. enfortumab vedotin, PADCEV, Pfizer's extraordinary molecule for urothelial cancer shows about a two-thirds rate of peripheral neuropathy in that trial, which leads to about 20% of patients discontinuing, leads to down-dosing, and it leads to dose holidays. Ultimately, what we are trying to do with this molecule is selectively bind the cleaved payload without interrupting the intact ADC.
We have a molecule that can distinguish the cleaved payload from the intact ADC because it binds the cleavage site, and that cleavage site is only exposed once the payload is circulating systemically. We think this has a huge opportunity to not only address this core dose-limiting toxicity, but also extend the utility of all MMAE-based ADCs. Pfizer had some really interesting data at ASCO in June, which showed a direct correlation towards survival on drug and overall survival. If you are able to keep people on these ADCs, you are seeing extraordinary survival rates, and that is ultimately what we hope to be able to show is that by reducing the neuropathy, you are reducing that dose-limiting toxicity. We think the endpoint that the FDA will look for is a reduction in neuropathy.
Right.
What you will try and show is a non-inferiority from a survival perspective, because you rightly point out what you do not want to do is interrupt the bystander effect. We are partially through the design of the molecule, partially through the work we have done in terms of dosing in a line to the second dose of MMAE. We think there is a way to actually thread that needle nicely.
Sure.
What we have done until pre-clinically, what we have shown is we can reduce free MMAE by up to 80% in non-human primates and mice without impacting tumor killing, but with getting substantial reduction in skin toxicities and neutropenia, which are other toxicities that occur in additional peripheral neuropathy. Our phase I trial is designed to find the dose of our antibody that reduces free MMAE by 50%. The feedback from the FDA, which this has gotten Fast Track designation and is in first line therapy, has been you can go up to 80%, but we think 50% reduction is the right. It gives us enough room to not impact the bystander effect, but to reduce the peripheral neuropathy and other toxicities meaningfully enough that patients can benefit from continuing on the drug longer.
Sure. Thank you, Jason. What milestones should investors look for in terms of data release around that program?
We have completed dosing the first cohort of subjects in the dose escalation portion of the phase I. We believe, and again, the dose escalation portion is to find the dose that reduces free MMAE by 50%. We believe we will have that dose toward the beginning of 2027. Once we have that, we are going to do a dose expansion study or cohort expansion where we will take somewhere between 40 and 60 subjects, let's say, who already have Grade 1 peripheral neuropathy on PADCEV and KEYTRUDA that are urothelial cancer patients. They will receive our drug, the MMAE neutralizer, commensurate with the cycles of getting PADCEV and KEYTRUDA to see if we could reduce the progression of Grade 1 peripheral neuropathy going to Grade 2. Because once you hit Grade 2 peripheral neuropathy, it is irreversible for the patients.
That over the course of 2027, we believe we will have the data, which is the safety and efficacy data we are looking for to be able to potentially move directly to registrational trials, as Michael mentioned, where safety would be the endpoint.
Sure. What relationship might you have with PADCEV and how do you fill out or unfill further MMAE-containing partners?
Yeah. There is no formal relationship. The beautiful thing is in the U.S., standard of care for first-line urothelial patients is KEYTRUDA plus PADCEV, right? This is just simply layered on top of that standard of care. As we look forward, though, I think there are two different pieces, Sean. You point out ultimately the way you will develop this, we have done it with PADCEV because that is the leading MMAE-based ADC. You will do a basket trial likely with all MMAE-based ADCs to kind of show that this works across the whole continuum. Then I think in the future, there is an opportunity to potentially co-formulate, which would be I think really interesting as well, where you could co-formulate GB-4362 with the MMAE-based ADCs.
Sure. Is there anything specific about PADCEV that might mean that compared to other MMAE-containing ADCs, that might make it more robust in combination with GB-4362 about just soaking up the free MMAE, or you think it's broadly applicable, your confidence level around that?
In the pre-clinic, it's very clear that it's broadly applicable.
Awesome.
So we think that again, it's partially tied to the linker and the payload. So a lot of the early Seagen ADCs all use the same sort of core technology there.
Sure. Philosophically, at the beginning of the conversation, we're talking about platform, pipeline, platform that I think many people might look at Generate and think it's a respiratory company- and not really an AI company, and that the molecule could have come from the wet lab, could have come from AI. We don't care as long as it works and you get a payback. The way I'm thinking about this is potentially a step in the validation of the platform to investors. Maybe put some meat around the bones on that.
Yeah. I think one of the things that we've spent a lot of time thinking about, Sean, is actually, I think it's easy sitting here today to think, "Oh, well, where is the AI?" The real question we had to answer with GB-0895 was would computationally generated molecules be immunogenic? That was the unanswered question that nobody had ever tested because there had never been a truly computationally generated protein that entered the clinic. What we've seen now across the five programs that have entered the clinic is that these are very well-behaved molecules. The ADA rates have been very low, and so in some ways, for us, from a platform perspective, GB-0895 de-risked that question across all of our programs.
Now, as you rightly point out, where we're going is to these more complex biological tasks, like distinguishing this intact ADC from the circulating MMAE, and you'll see that, I think, across the next generation of programs. They're taking on more and more complex domains of biology that I think traditional tools have not allowed us to drug.
Sure. Maybe an opportunity, just given we've got limited time here, I just sort of wanted to touch on your Novartis and Amgen partnerships and maybe give investors a flavor on those partnerships and what could we expect in milestones, et c., or announcements on candidates.
Yeah. The way these are structured, each of Novartis and Amgen back at the end of 2021, Novartis late in 2024, almost a couple of years ago, we agreed on select number of targets. We generate molecules that ultimately would get to either lead candidate criteria or DC nomination based on some pre-specified criteria. Then once we get them to that level, they take time to verify it, and once they verify, they pay milestones, and then ultimately they have the choice to move them forward into the clinic, and they would pay milestones over time and potentially royalties. Milestones are in the mid to upper $300 million on each program, and the royalties are some mid-single digits up to low- double digits on each of those programs. We have been extraordinarily successful in prosecuting across all of the targets.
There are a total of nine targets between the two of them at this point. Some of them we will get to the criteria, but they will not be moved forward because frankly, biology that they could not test for a decade, let's say, or more, we finally were able to get them a molecule to test the biology, and the biology doesn't work. I think we were very successful in getting there, but ultimately, if the biology doesn't work, they are not going to move them forward. We have received the first milestone on the first program from Amgen already. We believe we will hit multiple more programs on theirs, and on Novartis, we have been extraordinarily successful, even much faster, just given we had signed that deal a few years after Amgen, so had many more people at the company and a lot more capabilities.
We believe we will also hit multiple milestones. The timeline on verification is the biggest impediment to receiving those milestones, but now we believe over the next 12 months- 18 months or so, we will receive multiple milestones on both of them.
Sean, one of the really cool things, though, about the partnerships is Amgen and Novartis are probably two of the best protein engineering companies on the planet, right? Certainly in the top 10, right?
Sure.
When they hand you tasks that they can't solve, this goes again to this question of China. If the best in the world can't solve these sort of things, you're basically finding complex biology questions that if you solve them for them, we then have the right to apply that across other domains. One of the tasks that both of them had given us was can you stabilize a native hormone and drive a thousandfold improvement in selectivity? Neither of them had solved that for almost a decade. We gave Novartis 40 molecules that had over a 10,000-fold improvement in selectivity in four months.
Wow.
The power of these technologies, once you get them up and running, is really profound.
Well, gentlemen, we're right at time. Is there anything I didn't ask that I should have or any message you would like to leave investors with before we call a close?
I think we've covered a lot of ground here today, Sean. I think the most important thing is, I think the point you made at the outset. Generate is a company that with our first manifestations, we're showing clinical proof of concept for these AI design molecules, but we're really only scratching the surface. I think, as we continue to push the frontiers, what we're going to find is that there are a whole series of undruggable domains that we have never had the tools to prosecute that will unlock biology in really meaningful ways, and we're excited to be part of that journey for the industry.
Awesome.
Thanks.
Well, thank you, Michael. Thank you, Jason.
Thank you.
Appreciate your time.