Thank you everyone for joining us here at the Wedbush PacGrow Healthcare Conference. We're gonna have a panel discussion now on antibody drug technologies and maybe some more exotic chemistry and biochemistry here too, given the flexibility of our panelists' platforms. With us today from Mersana, Sutro, and CytomX, we have Anna Protopapas, CEO of Mersana, Bill Newell, CEO of Sutro, and Sean McCarthy, CEO of CytomX. Maybe we can just start with a quick intro from each of you on the highlights of your platform. Just the quick 30 seconds or so on what you think is the best part of your platform, and then we can go into some Q&A. Speaking of Q&A, before we get into that, if you have a question, if anybody in the audience has a question, please type it in the dialogue box that you should have beneath the screen upon which you're viewing this webcast. Without further ado, maybe Anna, we can start with you. Just again, quick intro and highlights of Mersana's technology, and we'll go around to Bill and then Sean in the kind of order of Zoom boxes. Yeah. Thank you, David. At Mersana, since inception, we've been very focused on building the right innovative platforms that address limitations of first-generation technologies, because we think that that's the way one can innovate and really make a difference in patients. At this point, we have three platforms, all with substantial validation, all with scaled up, and two with substantial clinical data, and the third one about to go into the clinic. Two of the platforms carry our proprietary cytotoxic payload we refer to as DolaLock. It is, it has some unique pharmacology that provides for controlled bystander effect. Dolaflexin is our lead platform with a drug-to-antibody ratio of 10, while Dolasynthen allows us to control the drug-to-antibody ratio in a very precise manner, anywhere from 2 - 24. We have found that one size doesn't fit all, and that for a given target, there's an optimal drug-to-antibody ratio. Our Dolaflexin is our lead asset, UpRi, which is in pivotal studies in platinum-resistant ovarian cancer and recently initiated a randomized trial in recurrent platinum-sensitive maintenance ovarian cancer. Dolasynthen, we're about to start dosing B7-H4 Dolasynthen ADC, and we're pretty excited about that. Last, but not least, is our immunostimulatory platform, Immunosynthen, that carries a proprietary STING agonist, and that is about to also go into the clinic. We just cleared the IND for our first Immunosynthen ADC, and that is also the subject of a broad and meaningful partnership we announced on Monday with GSK. Three platforms that we've brought forward. Thanks. We'll get to that partnership in a second. Bill, you're up next. Thanks very much, and it's a pleasure to be here, David. Thanks for inviting us. Anna and Sean, congratulations on all the success you've had in terms of advancing antibody-drug conjugates and other modalities to treat patients. Sutro could take a lot of the words that Anna just said, mimic them, but put a little twist because our technology is a little bit different. We were founded on the basis of some technology out of Stanford that allows us to engage in cell-free protein synthesis. In that case, we are not dependent on cells to make the actual antibody-drug conjugate. We have a cell-free extract that we derive, and then we use that extract to rapidly produce a large molecule like an antibody. We have the ability to insert anywhere in the antibody structure a proprietary non-natural amino acid. That allows us to have exquisite control over both the drug-to-antibody ratio, as well as where the placement of the linker and the warhead are on the antibody structure. We have molecules in the clinic that have a DAR of 2, 4, and our next molecule will have a DAR of 8. We know that where you attach the linker and the warhead matters to the performance of the overall antibody drug conjugate, and so we optimize that pre-clinically before we take it into the clinic. Using our technology, there are now six molecules that are in clinical development. We have two proprietary assets, STRO-002, which is our folate receptor alpha targeting ADC. That is our most advanced asset. That is in the final stages of the dose expansion phase, and we look forward to initiating a pivotal trial that's registration- directed in the near future. We can talk more about that at another point in time. STRO-001 is actually targeting hematologic malignancies, B- cell malignancies in particular, and that is still in the dose escalation phase. We've partnered with Bristol Myers Squibb, formerly with Celgene, on a BCMA ADC that is in two trials. One is as a standalone agent to treat multiple myeloma. That trial started in 2019, and last year they did a combo study with a gamma secretase inhibitor. Those are moving forward. A little over a year ago, our partner EMD Serono took forward our MUC1 EGFR bispecific antibody drug conjugate into phase I clinical development. That's the first time a bispecific antibody drug conjugate has been tested clinically. Most recently, our partner Merck announced, or we announced that our partner Merck had engaged on an IL-2 derivative, moving that forward both as a single agent and in combination with Keytruda. We've also spun out a public company called Vaxcyte, which has a lead program of a 24-valent pneumococcal conjugate vaccine, for which we expect data in the October-November timeframe on their phase 1/2. Last but not least, like Anna, we're interested in adding immunostimulatory agents into the mix with ADCs, and we recently announced a deal with Astellas, a three-target deal for immunostimulatory antibody drug conjugates. Using our technology, we received $90 million upfront and have opportunities for $1.26 billion across those three programs. Happy to talk about that too in the future, David. We will. Sean, finally. Last but not least. Yeah. Thanks, David, and great to see you, Bill and Anna. At CytomX Therapeutics, we're doing things something a little bit different. You know, we've been the pioneer, now for more than a decade in a new field of therapeutic antibodies that we call Pro Bodies or conditionally activated antibody therapeutics. We have a multi-modality platform. We've applied our Pro Body masking technology across what we think are some of the biggest challenges in oncology R&D today. We're applying our technology to improving the therapeutic window for antibodies and specifically checkpoint inhibitors in IO, to expanding the target space for antibody drug conjugates, to bringing T-cell engaging bispecific antibodies more prominently into the field of solid tumor therapy. Last but not least, the more recent field for us, expanding therapeutic window for very, very potent immunomodulators, cytokines in a wide range of different cytokines. We've built a broad pipeline over the years, multiple programs now in phase II. We have formed a significant number of major alliances with pharma, with BMS, Amgen, AbbVie and also Astellas, friends of ours as they are, friends of Sutro now as well. The clinical pipeline, as I mentioned, includes several phase II programs. We recently reported data on our CD166 targeting conditional ADC praluzatamab ravtansine, showing that we met our primary endpoint in hormone receptor- positive breast cancer, and we're now looking to partner that program to advance it further. We have reported data on another really big idea in ADCs, showing that we can drug CD71, the transferrin receptor. We reported data towards the end of last year showing a 19% objective response rate in squamous non-small cell lung cancer with that ADC, and we look forward to additional data later this year. That program is partnered with AbbVie. We have a very exciting program with Bristol Myers Squibb in the immunotherapy area where we're working to expand the therapeutic window for ipilimumab of Yervoy. They are in a randomized phase II study comparing Ipi/Nivo to Probody Ipi/Nivo in the frontline metastatic melanoma setting. Then earlier in our pipeline, several exciting things moving forward, including our first T-cell engaging bispecific CX-904, which targets EGFR and CD3. That's in a global co-development relationship with Amgen. Two earlier programs we're working to move into IND filing next year, a conditionally masked version of interferon alpha 2b and another ADC targeting a protein called EpCAM, epithelial cell adhesion molecule, which we think has tremendous potential. As with my colleagues here, a lot going on in the pipeline and plenty to talk about over the rest of this panel. Sure. Maybe let's start with Anna on a question. You just signed a deal with GSK, and it was around immuno-oncology target or immuno-oncology program. There's two questions in there. First off, there's also, of course, rumors of a certain ADC-focused company getting purchased at some point in the future. Number one, are pharmas just generally more interested in developing ADCs? And then the second part of that question, are immuno-oncology targets or even pure immunology targets a next big thing for utilizing ADCs or ADC related if you wanna include modified cytokines or things like that as part of the field. You know, how do you feel about that? Are pharmas more interested and are they, you know, is this the next wave here? I have to say we live in an ADC renaissance. I think there is a lot of interest in ADCs, and I think many pharmaceutical companies who have a presence in oncology believe they have to have ADCs as part of their tool set. Yes, there is a lot of interest. We've done two partnerships this year, the one we announced on Monday with GSK. We did an earlier one with Janssen on the Dolasynthen platform. We continue to be engaged in multiple discussions, given the interest and given, you know, the level of validation we have on our platforms. Yes, there is a lot of interest, and it's not, I believe, limited to just IO. I think it's general interest in ADC as an important therapeutic modality. As for the interest of GSK, the data on XMT-2056 is very comprehensive and very compelling. I'm not sure if they're. I wouldn't say their interest is generally in ADCs. I think their interest, this is a single asset deal, and their interest was around our approach with XMT-2056 and the comprehensive data set that supported it. We've seen single agent activity in HER2 high, HER2 low. We've seen combinations with standard of care, PD-1 and HER2 Trastuzumab. We saw a very wide therapeutic index. All of this, as it translates into the clinic, could lead to a very transformative molecule, and I think that's what drove our discussions with GSK. That's fair. Bill, what are your opinions on it? I think Anna's spot on. I think ADCs, as we all know, have been a modality that has had its ups and downs over the last 30 years or so. Now we have 12 approved antibody drug conjugates, and it is our view, much like Anna expressed, that pharma understands the importance of this modality, both as a single agent, but also in combination with other modalities as well. We certainly experience a lot of pharma interest in both the platform technology, as well as in particular product candidates. Certainly, when you have data that is exciting to a pharma partner, there are opportunities for deal-making around that. I think the Janssen deal that Anna did and what we've done with Astellas indicates that there are companies that are willing to take a different and broader platform-oriented approach to try to really generate next-generation therapeutics. In the IADC space, what we're really interested in doing, and what we've pioneered doing, is in a single molecule attaching both a cytotoxic payload. The example that we've given in the past uses a hemiasterlin, a tubulin inhibitor payload that causes a certain degree of immunogenic cell death, and then adding an immunomodulatory agent like a toll-like receptor agonist or a sting agonist in order to actually both kill the tumor cell, but also flag up to the immune system that there's something of interest here and get a one-two punch. The ability to put both of those moieties on a single molecule is a really significant protein engineering feat. We've done it in the past, and we look forward to working collaboratively with Astellas to move our programs with them forward. It's an exciting opportunity. It's kind of a convergence of both the immuno-oncology field as well as the ADC field, but it is something that we think gives an opportunity for the immune system to remain constantly on surveillance for that tumor type that you've been disrupting. Stay tuned. Our field is evolving. Anna, Sean's company are at the forefront of leading that evolution, and I think it's not just a renaissance. I think we're beginning a multi-decade realization of the promise of antibody-drug conjugates writ large. Sean, you have, as you know, as you mentioned, particularly interesting perhaps IO programs like the EGFR, CD3 and your Probody program. I mean, is that you know again, kind of the way forward for you know, the best applications for your technologies or, you know, how are you thinking about the future? Yeah, it's a great question. I think just to take a step back and reiterate some of the comments of my colleagues here. I think the ADC space, you know, it's taken some time to mature. We would all agree that, you know, true innovation takes time. You know, we have to be patient, we have to persevere. With now 12 approved drugs and many in the pipeline, you know, this field is having a huge impact for and on people with cancer. That's what we're all here to do, and it's super exciting to see. It's worth noting that across that multimodality component of our platform, antibodies, ADCs, bispecifics, cytokines, we're still early in the field of bispecifics. We're still early in the field of really harnessing the power of cytokines. The ADC field, and of course, the antibody field before it, but the ADC field is now looking more mature. One of the most exciting things about the ADC field, I think we would all agree, is that the level of clinical validation that has now been afforded by these approved products and the impact that these products are having on patients is opening up the demand from the industry as a whole for new ideas, new targets, new payloads, new strategies. That's our contribution to the ADC field, is opening up new target space. Targets like CD166, CD71, EpCAM. W e've never been shy of taking on these kinds of challenges at the company because we think that in the long run, this is the way that we'll make the biggest difference. Again, happy to talk in more detail about those specific programs in a moment. To answer your question about, in some ways, the programs that flank our ADC work, the masking checkpoint inhibitors on the one hand and masking bispecifics on the other, we do see these as really important applications of the technology. The expansion of therapeutic window for Ipi, if you look at our preclinical work, very clear that masking the antibody can localize the intratumoral activity of CTLA-4 blockade by localizing the modulation of immunobiology. That's what we're looking to translate into the clinic in the phase II work we're doing with BMS. The phase I data that was shared previously at ASCO 2020 showed that we're able to achieve very high doses of the masked version of Ipi. We got to 30 mg per kg monotherapy, 15 mg per kg in combination with full-dose Nivo, with a significantly improved safety profile when you look particularly at immune-related adverse events. That really set the stage for the phase II work that BMS is doing now in real time. We really look forward to seeing that data when it's ready. With regard to the bispecific EGFR CD3 is of strategic interest to a number of companies. It's been of interest to Maverick, to Amunix, to Janux. You know, we all have our different twists. I think it's a great target combination. Our partner, Amgen, was the obvious partner to work with because, of course, they have both an anti-EGFR and an anti-CD3, a CD19, both approved. So it made a lot of sense to try to bring these two technologies together in a masked bispecific, and we're really excited to be now in phase I dose escalation. W e'll be taking it stepwise. I think that's important with these molecules to start low and go progressively through phase I dose escalation, where safety is the key goal in phase I to get to that recommended phase II dose. We do see the potential of our technology to bring T-cell engagers to solid tumors. We heard a lot about this from Regeneron last week as to how important and what the opportunities are in making cold tumors hot with these types of constructs. We're excited about the prospects there too. Got you. This is again a little bit of a field question, but when you think about your technologies and the targets that you've chosen Anna, with your lead product NaPi2b or Bill with the folate targeted STRO-002. When you think about developing those programs, is it better to develop a novel target maybe NaPi2b, a relatively novel target that Genentech explored a little bit before, or should you really be looking to that new target space and as the best way to apply your technology? I know both have risks and you know, you made your choices, but maybe help us out on the ideas and thoughts that went behind those choices. Maybe we'll start with Anna, since we seem to be stuck in that circle. We ultimately it's about bringing products to the market that make a difference to patients. What's important is can you come up with a target product profile that you believe is actually truly differentiated and delivers a benefit? In the case of NaPi2b, we were very fortunate in that there was validation of the target by Genentech, but we had a platform that when we tested it head-to-head with the Genentech molecule, we could convince ourselves it was superior, both from an efficacy and a tolerability standpoint. We were very fortunate there, and we continue to be not only first in class, but only in class there. We try in each case to really convince ourselves that this is something differentiated and not a me too. I think as we move forward, we're gonna see increasing pricing pressure in our industry, and I think bringing meaningful therapies forward is going to be incredibly important. You know, on the HER2 Immunosynthen, we know it's differentiated, even though it's in a space and on a target that's well validated, 'cause we are delivering a differentiated payload, an immunostimulatory payload, and we have a unique antibody that binds to a different epitope. It's a proprietary antibody, and it's not competitive with Trastuzumab or Pertuzumab or Enhertu. That gives us a very differentiated product profile. I think that's what's important. We have not pursued novel, completely novel targets. That requires a set of, you know, capabilities and resources that we don't have at this point. We definitely look for targets that are well-characterized biologically and where we can convince ourselves that our ADCs will be differentiated in a way that's really meaningful for patients. Bill, maybe thoughts o n why folate and why again, how the regulatory pathway plays out, when you choose a known target and not with an approved ADC in particular, but others as Anna alluded to, you know, there are other HER2 approved targeted antibodies and things like that. H ow do you think about those choices and regulatory pathways and going forward? Anna makes a number of important points. I wanna really build on what she has said. I think, you know, we're all building companies that started much smaller. In my case, I was the 19th employee in this company, and we were a long way from being able to make a drug that could be of benefit to patients. Sean's been on a journey, and Anna with Mersana as well. As you think about the approaches that each of us have taken, we're really trying to find the right fit for the platforms that we have to make a differentiated product for a patient. If you're gonna go after an established target, a validated target. As Anna said, you really do need to have conviction that you are making a molecule that is meaningfully more impactful than a competitor's molecule may be. In our case, we have primarily biased at the outset of our clinical development journey towards validated targets because there was a lot of question, as there are for emerging companies, about the platform technology, the scalability, the risk associated with it. It's not an antibody that's people know how to make and have known how to make for 25 years. We're pioneering in our own technology spaces, new ground, and so it's important to be able to give investors confidence that not only do you see the target opportunity and the commercial opportunity clearly, but you also know how to execute on it in a differentiated way. When we looked at the ovarian cancer space, and, we're really focused on another company that is not on this panel today, but is also known for their ADCs, we thought, let's look and see if we can make a better molecule, not just incrementally better, but meaningfully better than the one that they have been developing and are pursuing, to treat ovarian cancer patients. What we wanted to do was design something that was homogeneous, not a heterogeneous mixture. I think the three of us can agree that homogeneity is preferred, not by a little bit, but by a lot. We wanted to find something that was really, in the main, minimizing of the bystander effect because we didn't think that was going to be helpful from a toxicity standpoint as well. We went after the folate receptor alpha target. We had a different approach from a linker and a payload standpoint. Pre-clinically, which was some of the data that we shared when we went public, we felt like we had a better molecule, more potent and probably with less off-target toxicity. Importantly, we wanted to avoid the ocular toxicities that many ADCs seem to have. So far, we've been successful in our clinical development of our two programs, and we'll let our partners speak to theirs, in terms of avoiding the ocular toxicity signals that are a problem for other antibody-drug conjugates. For us, it was really, can we do something that's more impactful? As our interim data and our dose expansion demonstrates, we're able to have a broader patient segment that is amenable to our therapy than the competitor's therapy is. They're gonna be limited by their own account to about 35% or 40% of the platinum-resistant ovarian cancer patient population. We think based on the interim data that we've seen, and we'll talk more about this at the end of the year when we have our full complete data set, that a patient opportunity that is approximately 2 x that is a much more meaningful therapeutic for patients who have platinum-resistant ovarian cancer. Now we wanna have a strong response profile, and we've certainly seen that, as the interim data demonstrates, where if we go at our highest starting dose and we look at those patients who have a tumor proportion score above 25%, that they have a 53.8% response rate. That's a great response rate. We'd love to see good durability of that and stay tuned for later in the year in terms of what that is. As we've gone through, we wanted to differentiate the molecule. We wanted to broaden out the patient opportunity because the more patients who have access to therapy, the more benefit you can derive. We've thought about that. Now we love novel targets too. It's just cutting our teeth initially on targets that are more validated, a better strategic opportunity for our company and our technology platform. Sean McCarthy, I know, has a different view, but he's also got a different technology. Yes. Sean, how do you think about it? I did wanna follow up too with on the EpCAM program. I believe you have a little bit different toxin or change in the toxin from some of your earlier programs. Maybe, you know, again, some of the thinking behind choosing a target and toxin in that program. It 's a great key question, and, you know, we talk about this all the time at CytomX, in terms of how to. I mean, there are so many different dimensions to how we think about target selection in the context of the product concept and the overall modality that we're using to engage a particular target. I think it's also important to think, you know, we believe in a portfolio construct. You know, really from the early days of the company, as we began to move towards the clinic, we thought it was important to build a balanced portfolio where we took on different levels of risk in terms of target and modality. Where we've taken, I would say, the most target risk is in ADCs. Where we've taken the least target risk has been in our immunotherapy\- type of programs, like with PD-L1, CTLA-4, more recently with interferon and to some extent with the EGFR program. But with ADCs, you know, our view has been, you know, why not really push the envelope with our technology to see how far we can get? In a way, you know, stress test the system to see what the technology can deliver because, and I completely agree with Anna and Bill that we're gonna be living in the next 1-2 decades in an increasingly price-constrained price-controlled environment, and differentiation is so crucial to, you know, to have successful products. So the differentiation can come from various places, but certainly can start with the target, and that's how we've been thinking. So CD166, CD71. First-in-class targets. We've validated these targets for the first time, and you therefore have an intrinsic differentiation from the outset. Doesn't mean it's always easy, and it doesn't mean anything necessarily happens fast, but you know the. The payoff in the end is you know clear in terms of the differentiation from other mechanisms and modalities. We should talk also a little bit about payloads because of course and this is from Bill and Anna. I think a lot of the innovation at Mersana and Sutro on the payload side of things does present opportunities for known target, new payload being new drug, right? There's an intrinsic differentiation there. That certainly can work, and it's an effective strategy. Our approach on payloads it was to not take payload risk because we were taking target risk. For the CD166 program, we've used the DM4 payload from ImmunoGen, which is well understood, and at the time that we moved into the clinic, there was a substantial, now there's even more, a substantial body of clinical data so that we knew what the tox profile, the tolerability would be of the payload, so that if we saw any surprises from the target, given that our targets are present on most normal tissues, we would be able to to tease out the payload tox from the on-target tox. That's actually worked out very, very well in the clinic with the CD166 program because we can say with a high degree of confidence that the NCD related toxicities that we see are all attributable to the payload and their ocular toxicities and neuropathy. Similar with the CD71 program, which is in many ways an even bigger idea, trying to turn the transferrin receptor into a drug target. People have been trying to do this for decades. We took a very deliberate approach on the payload there to go with MMAE, so VC-MMAE. That's also played out well where our principal toxin in the clinic is heme tox. MMAE is known to induce heme tox, particularly anemia. Again, we can kind of begin to tease out what's payload toxicity, is there a target component? That helps us thinking about the overall development strategy and ultimately the differentiation of these molecules. Now, with regard to EpCAM, it's a target of sort of high interest to us and others for a long time. It does have clinical validation. Probably the clearest clinical validation comes from the toxin fusion, Vicineum, oportuzumab monatox, which is the drug that Sesen Bio has been advancing. It has clear single- agent activity in non-muscle invasive bladder cancer. Actually, very impressive response rate. The product has to be administered intravesically. It's a local administration because the drug is too toxic to administer systemically. Why is that? Well, because EpCAM is present, as the name of the target might suggest, epithelial cell adhesion molecule. EpCAM is expressed on all epithelial structures in normal tissues at high levels. It's an undruggable target with a systemic therapy. Our strategy is to turn it into a drug target for an ADC by using our masking technology, our Probody platform, and being really thoughtful about the overall construction of the molecule, including the payload. We haven't disclosed the payload yet on our lead candidate, which is called CX-2051. We will be doing that in the relatively near term. We're super excited, and we see EpCAM as, you know, potentially a real sweet spot for our technology moving forward. Maybe to follow up on a couple of points that you raised with Anna and Bill, do you, Anna or Bill, think that we need more development in the toxin realm, or you know, kind of do we have enough ways to kill cells? I mean, you know, how do you feel about you know, the kind of level of investment development put into you know, novel payloads or toxin payloads? And we can start and finish up with Bill. I definitely think there's room for more innovation, and I think the toxin or the payload, because in the case of Immunosynthen, it's not a toxin, it's a payload, I think is there's lots and lots of opportunities. What I think we should avoid is more and more me-too payloads. I think ever since we saw the Enhertu data, which we all agree is changing the standard of care in breast cancer, the number of companies that have rushed out to do very, very similar me-too topoisomerase payloads is. I just can't count them on the fingers of my two hands. How many of those are actually going to be me-too? How many of those are going to actually run into IP issues with Daiichi? Of course, there's incredible room for innovation, and we've demonstrated that by taking, you know, a very orthogonal approach with Immunosynthen. I just hope all of us focus on real true innovation rather than pursuing me-too payloads. I have a different spin on that. Although I think the core point that Anna makes is exactly right on, which is, there is no one payload that works for all ADCs. Like, you know, I think originally it was thought, oh, there's the maytansinoids, then there's the auristatins. We're done. That's all we need. The history of our industry has been to innovate both on linkers and on payloads. I don't wanna disrespect linkers because linkers are also an important point for innovation. For me and for Sutro, we think about what's the right linker, what's the right payload, and importantly, what's the right DAR and sites of attachment to actually derive the most out of the molecule that you're making. We are pretty much agnostic as the payload because we can test- All of the different payloads that are available. We've tested PBDs, we've tested a lot of other things, and there are features of each payload and each linker that make it appropriate in a particular instance, and HER2 is a great example. That's a lovely constructed molecule. It is not without its liabilities, but it really represented an advance in our industry and unlocked some thinking in that regard. Really gotta look hard at the linkers, you gotta look hard at the payload, and importantly, from our perspective, where you attach them and what the numbers are. That's the equation. It's gonna be a different answer for every different tumor type that you're going after. I wish that it was one size fits all, then Anna's technology could rule or Sean's could rule, or maybe ours could. The fact of the matter is we have to break these down one by one, and having a broader toolkit, and I believe the industry is gonna continue to work on linkers and payloads because we've got a nice toolkit, but it can certainly be expanded broader. You have to figure out what's the right tool for the right disease that you're trying to modify. That's the magic in drug development. Bill, I totally agree that it's not just the payload, it's the linker, it's the antibody, it's the target, it's how you attach it. I totally agree with that. I just want to make sure, my point was more in response to Dave's question around payloads, and I said there's lots of room, but let's not. It would be good if we saw some real diversity in those payloads. As an industry, so. No, I agree with all that. I mean, I would add that, you know, when we think about the paradigm of how we do drug development in oncology these days, you know, we all tend to start in the same place, which is an all-comer phase I dose escalation, understandably, right? Because we wanna try to get to our recommended phase II dose as quickly as possible and then expand. You know, I think increasingly trying to find ways to get to relevant patient populations earlier in the development cycle is going to be really important. If that's the way to think, and I'm talking just this is a sort of cross-industry kind of comment I'm making right now, not specifically CytomX. It requires a product design and a product conceptualization approach where with regards to payloads, you know, Bill, you touched on this, you know, you have to think very carefully about which payload might be best suited to a particular tumor biology. We know, for example, that microtubule inhibitors are less proven and less likely to work, for example, in CRC. Well, what would you choose and how would that be paired up with the overall target strategy and the DAR and so on and so forth. All the, you know, the levers that we've got as we design our molecules. I think this is very open debate with everybody in clinical development as to, you know, how quickly can you get to relevant patient populations with these types of strategies because you don't want to, you don't wanna miss a signal, of course, in phase I. B ut do you really wanna do a two-year, you know, phase I dose escalation to find out rather empirically why your drug works if you can avoid it with more bespoke sort of targeted strategies. I think that's something that we're all thinking about in the particularly in the ADC field now, where the field is more mature than, like I said, the bispecifics or cytokines where maybe more targeted strategies could be employed. Gotcha. One last lightning round question. Just any quick thoughts on the effects of the recently passed legislation on, you know, pricing, negotiations or, I don't know if negotiations is the right word, but pricing, abilities of Medicare. You know, any direct effect? No effect, just any immediate quick thoughts on it? Anna, we can start with you. Start with me, but I'll look to Bill, who I think is quite active in the bio council. I understand, and I'm still working on digesting. The very large bill, that it will have less of an impact on our kind of drugs than on small molecules. But that being said, as I said earlier, I do think all of us should be thinking about a world in the future where there is more pricing pressure, and we should all be thinking about how can we make the most difference in patients, and how can we deploy the funds that are in our industry invested to maximize the innovation we have. You know, we've seen companies go after. And I'll give PD-1 as an example, how many PD-1s do we have? And I think the future should look different because we should take our resources as a collective industry and apply them where we can make the most difference. It will be more successful and the system will be more efficient if we do that. I think it's clear that for many Americans, drugs are unaffordable, particularly as they're at the prescription counter trying to get their refills for the innovative medicines that we all toil so long and hard to bring forward. The system is broken. It's broken in a variety of different ways, and I think Congress is having a reflection, a knee-jerk reaction to the system being broken and thinking that there are easy ways to fix it. There are no easy ways to fix it. This will have some benefit for some patients. What I'm particularly encouraged by is that if the bill passes as written, there will be an out-of-pocket cap on the cost of medicines for patients at $2,000 per year, which I think is great, but not a lot of people have the ability to even pay that $2,000 a year. I would have liked to have seen the cap be lower. I think the price negotiation is really more price control because there's not much room for negotiation when the government can just say, "Hey, if you don't take it, you know, there's gonna be a huge penalty on you, or you're gonna pull all your drugs out of Medicare, all of your drugs, not just the one we're trying to negotiate." I think it's gonna harm innovation. I think the estimates of the number of new drugs that are not gonna come to pass because of this legislation are far underestimated. I think we've got to find ways then to live within the system that's created and then find ways to attract capital to the smaller companies. The big companies will be able to fend for themselves. I never try to defend them. They can do a good job on that. We need to make certain that we've got a vibrant ecosystem of innovative companies, smaller companies, smaller than even the companies that are represented on this panel. I'm continually thinking about ways in which we can incent investors to make the long-term investments that are necessary to bring to fruition these next generation cancer and other therapeutics. I'm a little discouraged by it, but you know what? Our industry is one where we take a step back, we absorb it, and we move forward. That's just who we are as an industry. Yeah. We're all oncology companies. You know, the devastating impact of this disease and all of its horrendous manifestations needs us, needs the companies like ours to make a difference for our friends and family and the community as a whole. You know, I'm an eternal optimist. I think that I totally agree with Bill that this legislation does have the potential to harm innovation, but innovation will continue. We have to stay laser-focused on bringing value forward, bringing differentiation forward. You know, we've got so much more work to do to impact the diseases that we work on. I think it's, you know, it's a development, but it's, I think we just got to keep our eyes down and keep innovating. Gotcha. All right. That will be our time for the day. I really appreciate everyone participating and everyone in the audience for watching. I hope you have a great rest of your afternoon if you're on the West Coast, or I guess it's still afternoon on the East Coast, but we just hit afternoon here, so. Thank you, David, and thank you for inviting us to the conference. Thanks. Thank you, David. Great to see you guys. Thanks, David. Good to see you all. Bye. Bye-bye.