Good afternoon, everyone. My name is Federica Lussana, and I'm part of the healthcare investment banking team at JP Morgan. It is my pleasure to introduce our next presenting company, Sutro Biopharma. The speaker is Bill Newell, Chief Executive Officer. As a kind reminder, you may submit your questions through the Q&A button listed under the presentation. Thank you all for joining us today. Bill, over to you. Thank you. Thank you, Federica. It's my pleasure to be here today to present Sutro Biopharma at the 2021 JP Morgan healthcare conference. Of course, this conference is very different from the many past conferences that I've been privileged to attend, but some things do remain the same. If you turn to slide two, you'll see a very familiar-looking forward-looking statements. I'm going to be making some forward-looking statements in the course of this presentation, and this page gives you information that you should be aware of in the context of those forward-looking statements and where you can go for additional information. If we move now to slide three, I want to just tell you a little bit about myself. I started as the CEO of Sutro Biopharma at the time of this conference in 2009, really 12 years ago, and what a difference that 12 years has made in Sutro Biopharma. I was the 19th employee at that point in time. Today, we have over 200 employees. We had a very exciting but very early-stage platform technology and no understanding of where the sweet spot for that platform technology would be. We had to grow and develop that platform technology. We had to scale it to a point where today we have a cGMP manufacturing facility, the only cGMP manufacturing in the world that does what we do. We had to focus our efforts on a research basis, and we focused on next-generation cancer therapeutics, molecules that can be highly impactful to arresting the progression of the disease, but that are very complicated to make. Things like antibody-drug conjugates, bispecific antibodies, bispecific antibody-drug conjugates, cytokine derivatives, and more. All of these molecules are really enabled by our unique proprietary platform technology. Our differentiated approach starts with our integrated cell-free protein synthesis technology system. This is a system that has been developed with over 20 years of underlying research. There's a lot of elegant science that goes into making a cell-free protein synthesis work, making it work well, making it be integrated, making it be industrialized, and making it be scaled to GMP. As I mentioned, we have our own GMP manufacturing facility. Why? Because we're the only ones in the world who do cell-free protein synthesis at GMP scale. It's important for us at this stage of our evolution to be able to assure that we can manufacture the molecules that we discover and work through preclinical research and take into the clinic. Today, Sutro has four clinical stage programs. I will talk with you about each one of them. The hallmark of each one of these programs are the molecular design that we put into them. We strive and achieve homogeneous product characteristics. We do not believe in heterogeneous mixtures where performance is, at best, an average of the many species that are in the molecule, in the designed molecule. We want a differentiated approach where we start to understand structure activity relationship because we can make many different variants overnight. We can compete them preclinically to understand what structural basis makes the most favorable drug-like properties. Do we want a drug antibody ratio of two, four, six, eight, or whatever? Do we want a cleavable or a non-cleavable linker? What should be the appropriate site of attachment? What should be the appropriate warhead? These are important questions that have to be answered with precision and have to be answered with a homogeneous molecule in order to ensure that you have best-in-class performance. That's what we strive in every program we take into the clinic. Of course, we've been working on ADCs since 2011, but our protein engineering goes back to the company's founding in 2003. We've been recognized by the industry for the quality of the work that we do and the quality of the molecules that we produce. We count among our partners Merck, Bristol Myers Squibb, and EMD Serono. I'll talk a little bit about each of those relationships and why they're important to us. If we turn to slide four, it's very clear that the company that we've been building since 2009, when I first joined, has really hit its full stride. Starting in 2018, we put the first of our four INDs forward to FDA. That is for our CD74 antibody drug conjugate going for multiple myeloma and non-Hodgkin's lymphoma cancers. Next year, 2019, we put an IND to FDA for our second program, STRO-002, a folate receptor alpha-targeting antibody drug conjugate. Our partner, Celgene at the time, Bristol Myers today, also filed an IND for CC-99712. That is a BCMA-targeting antibody-drug conjugate, the third leg of their BCMA modality stool. In 2020, we were fortunate to have our good partner, EMD Serono, put forward a very novel molecule, the first dual antigen targeting bispecific antibody-drug conjugate. This molecule targets MUC1 and EGFR. That trial has now started, and patients are being screened. In the span of three years, we've created four INDs for ourselves and our partners. As we look to the future, this year and next, we have numerous other opportunities, both for our own proprietary programs, but also for very significant programs that we've partnered with companies like Merck and the Vaxcyte company that we spun out a number of years ago. If we turn to slide five, you will see the breadth of programs and modalities that we have been able to establish. For those of you who were aware of Sutro at the time we went public in the fall of 2018, this pipeline chart would look very similar with one significant difference. All of the arrows showing where the programs presently sit would have been significantly further to the left. All of the arrows would have been there, but they would've been to the left. The only program we had in the clinic a little over two years ago was our 001 asset. What I'm particularly pleased with is that we've been able to drive forward clinical assets that address both hematologic malignancies like CD74 targeting for multiple myeloma and non-Hodgkin's lymphoma, or BCMA targeting for multiple myeloma. We've also delivered solid tumor targeted assets like folate receptor alpha targeted ADC for ovarian and endometrial cancer, this MUC1- EGFR bispecific antibody-drug conjugate for non-small cell lung and esophageal cancer. Of course, we're not just an ADC company. We really are a next-generation protein engineering company doing what other companies simply cannot do. Our Merck relationship, where we're working with them on two programs and cytokine derivatives, is proof of that, as is our spin-out Vaxcyte, which is working on a 24-valent pneumococcal conjugate vaccine, one that could be a game-changer in the industry. We turn to slide seven, skipping over slide six, I'm going to start now talking about our STRO-002 asset. We believe this has the potential to be best in class for ovarian and endometrial cancer. It is without question in our minds that this is a validated target. It's been demonstrated in the clinic, and we thought that the target was an attractive one, but we thought that first-generation approaches were suboptimal in design because they were non-uniform and had average performance, and there were good species that were competing with bad species, as opposed to identifying the single best species to attack this target. That's what Sutro set out to do. We believe that a homogeneous single-species molecule is better than a heterogeneous mixture because all of the molecules that are hitting the target are competent to do their job. We believe that a stable linker is better than one that dissociates early. One that dissociates early creates excessive toxicity that doesn't benefit in terms of tumor kill. We believe that a warhead with a shorter half-life, once it's been released from it doing its job inside the tumor microenvironment, is better than one that has a longer half-life. That's because we don't believe bystander effect plays a great deal of benefit to the cancer patient. We believe it provides excess toxicity, and we want to get rid of that warhead once it's done its job. What we're striving for is a molecule that has a wider therapeutic index than other agents. Why? A wide therapeutic index allows us to choose dosing at an efficacious level to maintain that dosing intensity every three or four weeks and keep the pressure on the tumor. If you dose too high and you have toxicity that causes the patient to be taken off therapy, you're defeating the purpose of the therapy. We would much rather have an efficacious dose where therapeutic pressure can be maintained. Let's move to slide eight. This is a slide that talks about our study design. This study, which I'm going to talk to you about the dose escalation phase, is an all-comer study. We have not enriched for patients for any particular level of folate receptor alpha expression. Importantly, we do not use corticosteroid eye drops to avoid ocular toxicity. We don't see ocular toxicity signals. The patients who are enrolled in this study are late-line patients. Frankly, they would have no other option for care other than palliative care were they not in our study. According to one of our key opinion leaders, most of these patients could be expected to live only six or 12 months longer if they were not enrolled in our study. We explored doses beginning at a very low level, 0.5 mg/kg, all the way up to 6.4 mg/kg. We're now going to be exploring two of those higher doses, 4.3 and 5.2 mg/kg in our dose expansion phase. I'll tell you more about that in a minute. We enrolled 34 patients at the clinically active dose of 2.9 mg/kg or higher. Of those 34, 31 were evaluable. Bear in mind 31 evaluable patients for RECIST responses. These are heavily pretreated patients, as I said. The median number lines of prior therapy was six. Everyone had had platinum. Almost 50% had had three or more lines of platinum. bevacizumab was used for 82% of the patients. PARP inhibitors, patients were treated with PARP inhibitors 60% of the time. That is a very heavily pre-treated patient population with very resistant tumors to new therapeutic modalities. Usually, they do not have a good prognosis for a dose escalation study. If we turn to slide nine, we'll talk about some of the safety characteristics. Fully 86% of the treatment-emergent adverse events were grade one and two. That's a really good safety profile. As I indicated, no ocular toxicity signal has been observed, and it hasn't been observed in our other program as well, but I'll get to that in a moment. As we move through the dose levels, we saw activity and patient benefit beginning to emerge at 2.9 mg/ kg, clearly establishing that that was the dose that starts to show benefit for patients. We kept escalating. When we saw a certain degree of toxicity at the 6.0 mg/kg or 6.4 mg / kg level, we understood that we weren't going to be able to sustain dose intensity at that level, even though the toxicities could be managed. We spent more time exploring 5.2 mg/kg and 4.3 mg/kg, as those seem to be much more tolerable dose levels that allow us to maintain dose intensity, and that dose intensity keeps the tumor under control. As I said, most of the treatment emergent AEs were grade one or grade two. We did see neutropenia, but in 22 of the 23 neutropenic cases, there was no fever associated with it, and the neutropenia generally recovers in about a week. That means you're delayed one week from three to four weeks in your dosing cycle. Otherwise, there was no significant consequence to the neutropenia. Neuropathy did show up. That's really not surprising. We enrolled patients who had up to grade two pre-existing neuropathy into this study. We know that tubulin inhibitors and our warhead is a tubulin inhibitor. It's a hemiasterlin. We know that warheads that are tubulin inhibitors can cause neuropathy. Certainly, it's seen in the label for Adcetris and Kadcyla. We were able to manage the neuropathy with dose delays and dose reductions. These patients continued to experience benefit even with those dose delays and dose reductions. We really want to avoid both of those things. Moving forward, we're going to be looking at dose levels that we think allow us to maintain a consistent dose intensity every three or four weeks. Moving to slide 10, I want to talk about some of the encouraging efficacy data that we've seen. I want you to remember that these are late-lying patients with progressive disease at the time that they enroll. If you think about other agents, other ADCs that have been studied in dose escalation in ovarian cancer, I think you will come to see that there are very little response by RECIST criteria that you're generally going to see in this patient population. What we see from this waterfall plot is broad evidence of tumor control. In fact, we had one complete response. We had nine partial responses out of our 31 evaluable patients. Of those nine, three are confirmed, three were unconfirmed at the time that the data cut was made, which was October 30th. They remain on study, the potential for confirmation continues to exist. Then there were three who were not able to be confirmed. We had, importantly, 18 patients for whom there was stable disease. This is remarkable tumor control when the tumors were progressing at the time of study entry. The deep responses, we think, are seen at 2.9 mg/kg, 4.3 mg/kg, and 5.2 mg/kg because we could maintain dose intensity at those dose levels. Turning to slide 11 now. This spider plot really looks at the amount of disease control that we're able to gain. We see a deepening of responses in the lines that are not hashed. These are the patients who either had a partial response or a complete response. They start down quickly after beginning study treatment, and they continue to deepen and extend. Even the patients for whom there was stable disease, it is quite clear that there was a high degree of tumor control beginning early on in the treatment process for these patients as well. This is very encouraging because these patients are very refractory when they enter our study. If we move to slide 12, what we see is a swimmer's plot. Really the thing that I think is most remarkable about this swimmer's plot are the four patients at the top. These are four women who came onto our study having no other treatment alternative for whom they enjoyed a year or more on study. Three of those four were on study as of October 30th, and one of those three was one of our complete responders. Today, we still have, or as of October 30th, we still have 10 patients on study. There's an opportunity for this data set to look even better. If you take a look at our disease control rate, fully at the 12-week mark, fully 74% of the evaluable patients by RECIST were still on study at that point in time. If we go out to the 16-week mark, a benchmark many others point to. You see that 58% of this heavily pre-treated patient population was still on study. In fact, the median time on study as of October 30th for all of our RECIST evaluable patients was 19 weeks. Given the number of patients who were still on treatment, we believe that that number will go up, and we believe this bodes well for calculation of a progression-free survival statistic and is a good signal of how this drug is very active in maintaining disease control. If we move to slide 13, I really want to emphasize that this is a study where we took all comers. We weren't able to get tissue biopsies from everyone. That was not permitted by FDA. We asked for tissue samples to be forwarded to us. At the time of the analysis that we did on October 30th, we had received 13 tissue samples from patients who were evaluable for RECIST. We've used the same assay, the Ventana assay, and the same PS2+ scoring system that others use to categorize those patients into patients who have high expression, moderate expression, or weak or absent expression. We also show the H-scores, which is a calculation of the frequency and intensity of staining, on the axis on the left as well. Interestingly, we see that patients who are in the weak or absent expression level or the moderate expression level benefited from our therapy, even despite the highly refractory nature of their disease. We see that stable disease patients who had weak or moderate expression also benefited from therapy. In fact, one of those weak or absent expression patients, weak patients, has been on our study for over a year. This is very encouraging. We will need more samples, and we expect to collect a few more from the dose escalation study. I'll tell you how we're going to treat this differently in the dose expansion study. We'll need a few more samples to really understand whether or not our drug works in a much broader patient population than is presently being studied by any other investigational antibody-drug conjugate. This is a very encouraging start, and we look forward to updating this data and providing more data on expression levels and RECIST responses later on in this year. If we turn to slide 14, I want to pick up on what I said earlier, and that is we're moving forward with our dose expansion phase. The trial is open. We're screening patients, and we look forward to having our first patient in January of this year. We are going to, again, allow all comers into our study, regardless of folate receptor alpha expression levels. We will be requiring either a tissue biopsy or an archival sample or a fresh tissue biopsy so that as the study proceeds, we'll be able to look at correlations between responses and expression levels to determine whether the information that I've shared with you today continues to hold the case in a larger treated patient population. We also want to work with a less heavily pre-treated patient population that is more reflective of the patient population we would expect to go after in a registration-directed study. This is a very typical approach as you move from your first-in-man study to a more selected patient population that is less heavily pre-treated and therefore may be more amenable to therapeutic intervention because you're getting to them earlier rather than when they have no other line of therapy available to them. This is a very similar patient population to what is being studied by at least one other company. Like them, we are not allowing in frontline platinum refractory patients, and we are also excluding anyone who's got peripheral neuropathy that is grade two or higher. We're going to study two dosing cohorts, 4.3 mg/kg and 5.2 mg/kg. This will be a random assignment to those dose levels because we really want to understand which one provides us the best efficacy and safety profile to move forward in a registration-directed opportunity. We're increasing the number of sites that we have open, and we plan to have 35 sites for this portion of the study. They will be in the United States, and importantly, they will be in Europe. We expect that by the second half of this year, we will have our preliminary data from the dose expansion phase of this study, and we look forward to sharing that at a future conference. We also believe that before the end of the year, we'll be able to take the dose escalation data and the interim dose expansion data and have a conversation with FDA about whether or not a registration-directed study, single arm, is appropriate. We know two companies have been able to persuade FDA to allow them to go forward in that fashion and also then to have a confirmatory study that is a controlled study. We're hopeful that we'll be allotted the same opportunity, and I look forward to discussing that further with you once the data has matured, and we've had a chance to have our conversation. Slide 15 lets you know that we're moving on to our second program, the CD74-targeted antibody-drug conjugate. This is a different target. It's a different molecule, but it is the same approach to designing a best-in-class molecule. We think that CD74 is a very interesting target. It gives us a chance to be first in class in patients that need additional therapies because they are working their way through everything that exists today. There have been other antibody-drug conjugates that have been attempted and failed, targeting this very interesting target. We think we understand why they failed, and we believe that the design that we put together here is really ideal for this rapidly internalizing target. Again, this is a homogeneous antibody-drug conjugate. We are using a maytansinoid linker. Why? Because we think it is the optimal killing mechanism for this hematologic malignancy. As I said, Celgene's BCMA ADC, now Bristol's, uses the same linker warhead for myeloma, another B-cell malignancy. The drug-to-antibody ratio here is two, because we felt, based on preclinical data, we got very good cell kill, and two gave us a better safety profile than a drug-to-antibody ratio of a higher level, like four. We use a non-cleavable linker because we really want to minimize the bystander effect. We don't want to screw up the bone marrow while we're going after the malignant B cells. That non-cleavable linker means that you have the non-natural amino acid, our proprietary one, the linker, and the warhead, very potent inside the tumor microenvironment. When it gets released, it's hydrophilic and doesn't cross cell membranes easily. If we move to slide 17, I'll talk a little bit about the study design. We really thought it was advantageous to look at two different dosing cohorts, given the differences in the diseases. A multiple myeloma dosing cohort and a non-Hodgkin's lymphoma dosing cohort. At ASH last year, we updated on the non-Hodgkin's lymphoma dosing cohort, and I'm going to share some of that information with you. We started at a very low dose in this study, and we've now worked our way up so that at the time that we did the data cut, again on October 30th of last year, we were active at the 3.5 mg/kg dose level and still continuing in our 3+3 dosing paradigm. We have not reached an MTD, and I look forward to updating this program as 2021 moves on. Last year, at lower doses, we did see one pulmonary embolism. We had to really dig deep to understand whether this was drug-related or whether there was some other cause for this. We've come to conclude that this was most likely caused by the very bulky disease that this patient had. We set about instituting a protocol amendment. This was done around the middle of last year, in which we screened for patients who might have bulky disease. We looked specifically to see whether there were any emboli that could be seen. We were able to actually find a number of patients who had emboli. They were allowed to be anticoagulated per standard of care. They came on treatment. I'm pleased to say we've not had another instance of pulmonary embolism. If we move to slide 18, I want to reflect on the heavily pretreated nature of this patient population. They had a median of five prior lines of therapy, and many of these lines of therapy are combination therapies. For NHL, we reported on 21 patients. Seven of those were DLBCL patients. Of the DLBCL patients, we saw that two of them had CAR -T therapies. In fact, three patients in this part of the study at this time had CAR -T therapies as well. There were other autologous stem cell patient transplants in our patient population as well. The safety profile looks very promising. Most of the AEs, as you can see on the table on the right, are grade one or grade two. As I said, there is no ocular toxicity. There's no neurological toxicity. This is a drug that's performing very well from a safety standpoint. Encouragingly, we are seeing efficacy. As we move to slide 19, this is the data we shared at ASH. We had one complete response in DLBCL, two partial responses in DLBCL. Meaning out of the seven DLBCL patients we enrolled, three of them were responders. We had three stable disease instances in marginal zone and follicular lymphoma. Two of those were in follicular lymphoma. It's interesting to note that the two PRs in DLBCL both were patients who were treated with a CAR -T, who had about a five or so month response to the CAR- T, and then they progressed. They were treated with a subsequent treatment to which they did not respond, and that subsequent treatment included lenalidomide. Then they came on our study. The duration of time that they were on treatment in our study was approximating the duration of time that they were responding on a CAR -T. This is a very interesting finding, one that we're going to be looking forward to understanding more as we get more patients and we're treating patients at higher dose levels. If I move on to slide 20, I want to reflect for a moment on the great collaborations that we've been able to achieve. We have some of the best names in the business as our partners. We have Bristol Myers Squibb working with us to develop our BCMA antibody drug conjugate CC-99712. Based on statements they made last year, they expect to report clinical data on the dose escalation portion of this study in 2021 this year. Of course, we love working with our partner, Merck. They've been a very good partner to work with over the last two and a half years. There's been a very symbiotic research relationship. We've made very good progress on both of the cytokine derivative programs that we have with them. Stay tuned. I look forward to talking more about this this year. Our partner, EMD Serono, is thrilled to be putting the MUC1 -EGFR bispecific antibody-drug conjugate drug into the clinic. They have now opened that trial. You will find it on clinicaltrials.gov. We look forward to seeing their results as they treat non-small cell lung cancer and esophageal squamous cell carcinoma patients. Of course, our spin-out Vaxcyte is doing well too. They went public last year. We still have 1.6 million shares of their stock that we own, as well as a 4% royalty on all of their programs. They are progressing their pneumococcal conjugate vaccine, VAX-24, towards IND. We anxiously await to see how that vaccine performs. That could be a very significant drug in the pneumococcal conjugate vaccine space. If we turn to slide 21, I want to offer a perspective that buttresses my earlier statement that we're not just an ADC company. Over the course of the last 10 years or so, as we thought about where is the sweet spot for this technology, we thought about complex molecules that can make important differences in patient care. We profiled and presented antibody-drug conjugate information today. We've also talked about the bispecific antibody-drug conjugate that's in the clinic today. Obviously, we can make bispecifics if we can make a bispecific antibody-drug conjugate. Stay tuned for more understanding of what we're doing there. We've also been working and had a chance to present data on a very exciting concept, an immunostimulatory antibody drug conjugate, where in one molecule we combine both a cytotoxic warhead and an immune modulator. You get a one-two punch to the tumor microenvironment. It's a very exciting concept. I look forward to having opportunities to talk about that in the future as well. Then, as I indicated with Merck, we've been working on cytokine derivatives. When you think about Sutro, don't think about us only as an antibody drug conjugate company. Think of us as a protein engineering company. We are reinventing how these very complex molecules are made, and because we're the only ones in the world who have access to this cell-free protein synthesis technology, we're the only ones who can make best-in-class molecules in this fashion and do it consistently and across multiple modalities. Now, for those of you who are wondering how we're doing for capital, I'll point you to slide 22. At the end of the third quarter last year, we had $202.4 million in the bank, and we subsequently raised net proceeds of almost $136 million in December. This translates into a robust cash runway, taking us into the second half of 2023. Importantly, that runway does not include any value associated with the shares of publicly traded Vaxcyte that we own. We built this company with the collaboration capital, almost $400 million that we've received from our partners, as well as investor capital. I'm pleased that we have such a strong financial position to really drive our existing programs that are in the clinic, and new programs to create better options for patients and better value for investors. If we turn to slide 23, this is a summary slide that articulates what we think are some of the key drivers of value this year. Of course, 002 is a big program for us, and so we look forward to a couple of different data presentations as well as new events in the 002 program. As I said, as of October 30th, 10 women were still on study in the dose escalation phase. We think we'll have final or near final results sometime in the first half of this year and look forward to presenting them at a scientific conference in the first half of this year. I indicated we've started the dose expansion trial, we look forward to having our initial dose expansion data shared at a conference in the second half of this year. Importantly, we want to study this molecule in endometrial cancer. That'll be the next cohort that we get moving, and then we also believe that it's important to start to begin combination studies. Look for us to start our first combination study in late 2021. For 002, we expect to initiate dose expansion in the second half of this year. What that also means is that we will be in a position to talk about our phase I dose escalation data as well. Stay tuned for STRO-003. For our partner programs, we expect that Bristol may have data on our BCMA-targeted molecule. EMD may have updates on the M1231 bispecific antibody-drug conjugate. Vaxcyte is expected to have updates, and I look forward to talking about Merck as well, all in 2021. Lots of different value drivers for us. Lastly, if you turn to slide 24, this is a very experienced team. Everyone on this page has multiple years of industry experience and is really an expert in their field. Trevor Hallam has been with us for over five years as our Chief Scientific Officer and the architect of many of these molecules. Arturo Molina has been our Chief Medical Officer for almost five years. Shabbir Anik heads our technical operations function, also about five years. Linda, Nicki, and Ed are also very experienced senior leaders. This is a great team of a lot of industry experience. We've been building this company, as I said, and I look forward to sharing with you the other successes that we have as 2021 continues. I want to thank you all for your time and attention today. It's been a pleasure to present Sutro. In any remaining time, if there are any questions, I would be happy to take them. All right. It seems like it's been a long week for all of us. I'm pleased to be here and talk about Sutro today. It's a very exciting journey that our company has been on since I joined in 2009, 12 JPM organs ago. Thank you for your attention, and we look forward to speaking with you when we can later this year. Thank you, everyone.