Morning everyone, and thanks for joining us. My name is Mike Clem. I'm a member of J.P. Morgan's Healthcare Investment Banking team. A quick housekeeping note. To ask a question, there's a blue button that says Ask a Question on the conference portal. Submit questions through there that we'll address during the Q&A session at the end. Without further ado, it's my pleasure to introduce Bill Newell, the CEO of Sutro Biopharma. With that, I'll pass it over to you, Bill. Good morning, everyone, and thank you for having us here today, Mike. It's a pleasure to be here. If you turn to our second slide, you'll see a forward-looking statement disclosure. I will be making forward-looking statements during the course of this presentation, and all the information you need to know about them is on this slide. Turning to slide three. If you thought of Sutro as an antibody-drug conjugate company, you would be partially right. In fact, though, a more complete description would be that we are a next-generation cancer company with four complex cancer therapeutics in the clinic. Our spin-out Vaxcyte is now advancing a pneumococcal conjugate vaccine into clinical development. Our technology truly enables multimodality approaches to cancer therapy on a multi-target basis, and we have a complex protein engineering capability that is world-class and differentiated. We use high science that we've been developing for over 20 years. We have an industrialized research platform that allows us to take advantage of robotics and other high-throughput technologies in order to make many different variants to understand the complexities of structure-activity relationship, and to optimize the molecules we make so that they have the potential to be best-in-class. Our technology platform is scalable, and it is integrated all the way through manufacturing, and we have our own cGMP manufacturing capability in San Carlos, California. Turning to our next slide. What you will see here is a broad cancer therapeutic development pipeline. It is intentionally balanced between proprietary programs such as STRO-002, our folate receptor alpha-targeted ADC for ovarian cancer, and STRO-001, our CD74-targeted ADC for B-cell malignancies, multiple myeloma, and non-Hodgkin's lymphoma. We balance our proprietary assets with our partnered assets, particularly those that are in highly competitive markets, where it makes good sense to get the full value of an asset to have the clinical development and commercial wherewithal of a large pharmaceutical partner. We have a very important program with each one of our partners. With Bristol-Myers Squibb, we have a BCMA-targeted antibody-drug conjugate. With Merck, we are working on cytokine derivatives that can improve the responses of their flagship drug, KEYTRUDA. With EMD Serono, we're working on their EGFR franchise with a MUC1-EGFR bispecific antibody-drug conjugate. These are important relationships, and they are important therapeutic opportunities for patients. Importantly for Sutro, we get robust economics from all of these relationships, and if you total up all the milestones that we could earn from all of our partners, they will approximate $1.5 billion. Beyond STRO-001 and STRO-002, we have a deep pipeline of multiple candidates competing to be declared STRO-003, our third proprietary program to go into the clinic, and I look forward to being able to talk more about STRO-003 later in this year. Turning to slide five. This is a list of where we expect to go in 2022. This is an important value creation year for Sutro, and we are really leaning very heavily on our STRO-002 franchise. We have a three-pronged strategy. First, we want to drive forward aggressively to seek single agent approval in advanced ovarian cancer. Second, we're really looking to broaden the opportunity for this molecule to treat patients who are earlier in their disease progression, and we seek to do that both through combination studies like our bevacizumab combo, which is up and running, as well as other studies that will drive earlier adoption of our molecule as part of the treatment armamentarium. The third prong is to really expand beyond ovarian cancer. We've already started our endometrial cancer study, and we've enrolled the first patient there. In the future, later this year, we look forward to starting a non-small cell and other non-gynecologic cancer study to see if we can have an effect on those sorts of tumor types as well. For our STRO-001 asset, we are moving to do more clinical development across the globe and to really get to a recommended phase II dose so that we can then define the path forward for that molecule. We are also supporting our partner, BioNova, who's working on opening up trials in China in a less heavily pretreated, less advanced patient population, where they can also explore combination therapies as well as perhaps other new indications beyond what we're exploring in the United States. Lastly, it's important to understand that our cell-free manufacturing technology is a strategic asset for us, and it is critical to our partners' success. We really work hard to meet our partners' needs, and as they progress their programs into later stages of clinical development, the importance of Sutro as their manufacturing partner will be even more greatly magnified. Turning to the next slide. I'm now going to discuss our folate receptor alpha antibody drug conjugate program. Turning to the next slide. This is the picture of a next-generation antibody drug conjugate. We created this molecule and used a benchmark of a comparator molecule in order to optimize this beyond what a first generation molecule can look like. We've designed an antibody drug conjugate that we believe is more efficient in killing, perhaps 50-fold more efficient, and it has a dual mechanism for killing the tumor cells. One mechanism is the cytotoxicity of the warhead, a tubulin inhibitor, and the second is immunogenic cell death, which is a byproduct of the molecule and the effect it has on the tumor microenvironment. This molecule is engineered for rapid clearance and gives us the opportunity to have a wider therapeutic window and avoid things like ocular toxicity and avoid lung toxicity as well. Turning to the next slide. This is the design that we've been pursuing for STRO-002. It's a fairly typical dose escalation, dose expansion study design. We took all comers, and in the dose escalation phase, you will see that all comers were very advanced in their disease progression, having had a median of six prior lines of therapy. In the dose expansion phase, they are still with advanced ovarian cancer, but in the main, most of them are platinum resistant and will have had only one to three prior lines of therapy. We saw encouraging preliminary data in our dose escalation study with one CR and nine PRs, four of which were confirmed. We saw good disease control for women on our study during dose escalation, where at six months, 55% of the women at pharmacologically active doses and above had been on treatment for that period of time. In fact, five were on treatment for over one year and three on treatment for over 1.5 years. The safety profile was acceptable and manageable in terms of the toxicities, and we saw no ocular toxicity and no lung toxicity signals. Dose expansion started in January of this year, and we concluded enrollment in November with 44 women enrolled in this phase of the trial. We randomized patients between 5.2 and 4.3, and we were looking to see through analysis of the tissue that these women provided whether there was an enrichment strategy that would be appropriate for this molecule as we move forward into later stages of clinical development. We think we have the initial answers to both dosing and to the enrichment strategy and the data that I'm going to go into now helps us understand that. If we turn to the next slide, where we're looking at patient characteristics, we see that patients were randomized between these two doses. They had virtually identical prior treatment histories regardless of the dose level. About 50% of the women in each arm had one to two prior lines of treatment, and about 50% had three prior lines of treatment. I will note that the standard of care for these women at this stage of their disease is single agent chemotherapy, which has only about a 12% response rate and a durability of around four months. Turning to our next slide. We see that in the dose expansion study, regardless of what dose level you were on, there was good tumor reduction. In fact, 70% of the patients experienced tumor reduction, and there were responses at both dose levels. But it's also of note that there were more responses in the 5.2 mg/kg cohort. Now, this is a reminder that there was no enrichment here. We were just looking at all comers. When we looked at the responses at the data cutoff date, we had seven confirmed partial responses. We had five unconfirmed partial responses. In order to best present this data and understand what happened to those women, we followed those five women to their next scan, and we saw that four of the five women had a confirmed response. As we move forward, we'll be talking about this cohort and this data set referring to 11 women who achieved partial responses with STRO-002 out of a 33 patient cohort. If you turn to the next slide, what you'll see is that we found that a response, an overall response rate of 33% in an all-comers patient population was a very strong signal for this interim data set. Perhaps more striking is the fact that when you look at patients who are treated at the 5.2 mg / kg dose, of which there were 17, fully 47% of them had a response on therapy versus 19% who are at the 4.3 mg / kg dose. This suggests strongly that we should be starting women on therapy at the 5.2 mg / kg dose. Turning to the next slide, which is a spider plot. What you'll see here is that we have robust anti-tumor activity. In particular, I think it's striking that the women who are treated at the 5.2 mg / kg dose and who are responders respond quite rapidly early in their treatment, and then even if they are dose adjusted downwards, they maintain that response and continue to have good disease control. 4.3 shows disease control as well, but it's on a much slower trajectory and therefore, again, providing additional supplemental evidence to suggest we should be going to the 5.2 starting dose. If you turn to the next slide, which is our Swimmer's plot, you'll see that it's really too early to make a determination on the durability of this treatment, which we understood to be the case. When your last patient enrolls in November, you really can't start to judge durability for another six months after that last patient is enrolled, and we'll be doing that later this year. We were encouraged that 12 patients had reached 16 weeks, although there were 19 still ongoing, and that four patients had reached 24 weeks of treatment, with 23 still ongoing. It was really too early to tell. We do note that the dose adjustments that took place did not affect confirmation of the partial responses, and we continued with disease control. Our next slide is really an example of one of these women. She was dosed at 4.3 mg/kg, and she had a tumor proportion score of 85, which one might think means she has a high score from a target expression standpoint. In fact, on the strictest standards of the PS2+ scoring algorithm, this woman would not be characterized as a high expresser because she has cells that only express at a 1+ scoring intensity, not a 2+ or a 3+. What you can see is significant disease control after several lines of treatment. She was very close to a response on her first scan, and it took some subsequent treatment for her to achieve her response, and it deepened to a 72% reduction in tumor volume. Turning to the next slide. When we think about our second question in this study of whether or not there's an enrichment strategy, we concluded early on that the PS2+ scoring algorithm was going to be too restrictive for our therapy because it excluded many women who we believe can benefit from our therapy. We have selected the tumor proportion score algorithm, where you count the percentage of cells that stain positive regardless of the intensity in which they stain positive. Using this TPS scoring algorithm, we see a clear breakpoint and that women who are at 25%, above 25% in terms of cells that stain positive, have a significantly greater response than women who are at 25% or lower. You see a 40% response for those women who are above 25% TPS. This correlates to, we believe, about 70% of the addressable market for our therapy. Now importantly, when you actually put these two data points together, what's the optimal starting dose and what's the right enrichment strategy? You see out of 13 patients that we improve the response rate up to almost 54%. Turning to the next slide. We've now treated 83 patients in dose escalation and dose expansion. We believe our ADC safety profile is now well-characterized, and it is manageable with 85.5% of the treatment-emergent adverse events being Grade 1 or Grade 2. We saw no new safety signals in this dose expansion phase. Importantly, again, we saw no ocular toxicity or lung toxicity signals. The leading treatment-emergent adverse event is asymptomatic neutropenia. Fortunately, this generally recovers in one week and can be managed, if need be, by courses of G-CSF or a dose reduction. All in all, this is a safety profile with a toxicity profile that oncologists are used to managing and one that creates no particular issue in the main for the women because it is asymptomatic. Turning to slide 17. This is our summary slide, and what you see here is an all-comers efficacy of 33%, an improved efficacy when you focus on patients starting at 5.2 mg/kg to 47%, and an even greater improved efficacy when you look at those women at 5.2 mg/kg who have a TPS score above 25%, leading to a 54% response rate. Turning to our next slide. As I indicated early on, we are leaning in on our STRO-002. We are working hard to get to our dose expansion near final data set, which we expect to be able to present in the second half of this year. We're looking forward to having a conversation with FDA in the first half of this year about what can be a pivotal trial. Based on that conversation, we'll be looking to get a pivotal trial started potentially by the end of this year. As I said earlier, our combination study with bevacizumab is open and enrolling patients, our endometrial cohort is open, and our non-small cell lung cancer trial is on the way. In the final minutes that I have here, let me just talk briefly about our next program, CD74 targeting antibody-drug conjugate, which begins on the next slide. Going to slide 20. This is a molecule that is a similar design approach, but a very different molecule because it's a very different cancer. We have a drug-to-antibody ratio of two. We use a non-cleavable linker and a catabolite, and the catabolite is designed to minimize the bystander effect. Turning to slide 21. We talk about our dose escalation scheme here. We are still in the dose escalation phase of this trial. Currently, we are at 4.2 mg/kg for our NHL and 5.0 mg/kg for multiple myeloma. In order to really conclude this dose escalation phase, we've recently moved to activate sites outside of the United States to find patients who can help us understand the recommended phase II dose in both of these indications for this drug. We're also working with our partner, BioNova, in China to develop this molecule in a less heavily pre-treated patient population. When you go to slide 22, what you'll see is that many of the patients who we've been treating have very advanced disease. In non-Hodgkin's lymphoma, which is what these tables refer to, patients had a median of 5 prior lines of therapy, and in fact, some of them had even been through CAR- T therapy as well. We see a very encouraging safety profile for this molecule. There are no ocular or lung toxicity signals, and the vast majority of treatment-emergent adverse events are Grade 1 or Grade 2. Turning to slide 23. We really looked here, and this was data that was presented at ASH in 2020 about the initial patients who have been in our non-Hodgkin's lymphoma cohort. Focusing specifically on diffuse large B-cell lymphoma, where we had seven patients who were treated, as of the time of this data cut. We saw that of those seven patients with DLBCL, one had a complete response, and there were two partial responses. Importantly, worth noting that these two partial responses occurred in patients who had already been treated with a CAR- T therapy and had had a subsequent therapy as well. Now these are at lower doses than where we are currently studying the drug, so we continue to look for safety and efficacy at these higher doses to understand what the recommended phase II dose is and what the path forward should be. Turning to our next slide 24. We have a strong financial basis on which to continue to progress the development of our assets and our partners' assets. At the end of the third quarter, we had $254 million in cash or equivalents in which to continue to operate the company. We had guided to a runway through into the second half of 2023. Now, since the time of that presentation of those financial results, we have now done a deal with a company to license STRO-002 in the Greater China market. Our partner, one who we're proud of, is a company called Tasly Biopharmaceuticals. They have a deep history in developing and commercializing drugs in the Greater China market, and they're taking our molecule STRO-002 forward for that development market as well as the commercial opportunity in that market as well. We received a $40 million or will receive a $40 million upfront payment with them, subject to some minor withholdings. That cash will augment the capital that we reported at the end of the third quarter of last year. Importantly, we also have a significant investment interest in our spin-out Vaxcyte. Today, we own 1.6 million shares of Vaxcyte, and importantly, we have a 4% royalty on all of their programs, including their lead program, a 24-valent pneumococcal conjugate vaccine. We've been fortunate to receive generous funding from Merck, from Bristol-Myers Squibb and their predecessor, Celgene, and our partner, EMD Serono. We've been able to finance the company not only with investor capital but also with the capital provided by our partners. We hope that in the future, we'll be able to augment that partner-provided capital with additional deals like the one we did with Tasly at the end of last year. Final slide, please. This is our leadership team. Joining me will be our CSO and President of Research and our CMO for the question-and-answer period. This team is deeply experienced, and I am confident in our ability to take STRO-002 forward to make it both a clinical success, to make it a commercial success, and to benefit women who have ovarian cancer and other solid tumors. We're excited about the prospects for our internal pipeline as well as our partner pipeline, and I look forward to updating you more as the year goes on as to the progress that we are making. Michael, that's it for me. I think we can be open for questions, please. All right. Great. Thank you, Bill. Bill had introduced or mentioned the leadership team, but just wanted to quickly introduce Trevor Hallam, the Chief Scientific Officer, President of Research, and Arturo Molina, the Chief Medical Officer. They'll be here to answer questions as well. Just to reiterate the method to ask questions, there's a little blue button to ask a question. Without further ado, we'll get started. Can you discuss more about the IHC method and the scoring method? ImmunoGen saw a variability in FR expression depending on the scoring method used. How do you ensure consistent FR scoring? My internet is a little spotty right now, Michael. Arturo, can you answer that question, please? Sure. Yeah, just to clarify that the IHC process uses the same assay by Ventana. The main difference is the scoring algorithm. In evaluating our patient population, not only dose escalation but also dose expansion. When we applied H-score and PS2+, we saw that our patient population is skewed toward low expressers, and therefore, we started to evaluate TPS, which is percent positive. TPS is commonly used in clinical practice. It only relies on the presence or absence of staining and does not have to further differentiate between intensity of staining of one plus, two plus, or three plus. When we evaluated the TPS score and assessed it by quartiles, where we looked at 25% positive or less, greater than 25%, greater than 50%, greater than 75%, we saw that there was a cutoff point at the 25th percentile, where the responses seemed to be higher in patients who have a percent positive score of greater than 25%. It increases if we go to 50% or 75%, but the separation is not as striking as the separation between less than 25% versus greater than 25%. We're confident that with this approach, we will vet this approach with the FDA and CDRH. It's an approach that's been used before. This approach seems to identify patients who are more likely to have objective responses. With longer follow-up, we'll be able to confirm if this approach also identifies patients who are more likely to have durable responses, and that would be the focus of a follow-up presentation probably in the second half of the year. Thanks, Arturo. Yeah. Thank you, Arturo. We are getting close on time, but perhaps just one more. Can you touch again on the efficacy profile of the STRO-002 asset, how you think that differentiates you? Thank you, Mike. As we indicated, when you look at an all-comers patient population that is unenriched, we see that 11 of 33 women had a response. That's a 33% response rate, which is quite significant given that the standard of care for these women would suggest a 12% response rate. For women who are dosed at the higher dose levels, we saw a 47% response rate, so a step up of another 14% from the all-comers statistic. If you then select for the patients that Arturo was talking about who have a tumor proportion score of above 25%, you now see that the enriched patient population at the higher starting dose has an almost 54% response rate. Another 21% increase over the all-comers response rate. We think these are very important indicia of the disease control that we are getting with this molecule, and we look forward to the data maturing, showing us what the durability of these responses is, and then identifying the patient population to take forward into a pivotal study, which we hope to begin before the end of this year. Great. Thanks, Bill. I think I was a little premature on the time frame. We do have a little bit more here, so. Okay. How do you view partnering in the future? I know we touched on the China deal. If you could touch on where you see future opportunities for the company, that would be great. Absolutely. I indicated earlier that Sutro has always had a partnering strategy embedded, as part of the company's DNA. Really, with the relationships that we struck with Celgene, now Bristol-Myers Squibb, with Merck, and with EMD Serono, we really have been carving a path forward in doing broad platform-oriented partnerships. Now, the last one that we did was our deal with Merck, and as we've been moving their programs forward, and we hope that they will have something to talk about in the cytokine derivative space, with our lead program later this year. As we've moved their programs forward, we've realized that we still have additional capacity to find a win-win partnership with a larger biopharmaceutical partner. We're in active discussions about broad-based platform deals that can really allow us to take advantage of the expertise that those partners have in terms of their understanding of the tumor microenvironment and particular target biology, and marry that up with our protein engineering skills in order to deliver a molecule. Now, for our three collaboration partners, so far, we've delivered two high-value assets to them into the clinic. For Celgene, now Bristol-Myers Squibb, they have a BCMA ADC that is a very important tool in their next-generation multiple myeloma strategy. For our partner EMD Serono, to complement their Erbitux franchise, we have a next-generation MUC1-EGFR bispecific antibody-drug conjugate that they're very excited about. That's a high-value asset for them as well. as I indicated, for Merck, we're working on cytokine derivatives that can, we hope, improve the responses seen with their flagship drug, KEYTRUDA. It's that sort of relationship where we're focusing on high-value opportunities and large opportunity and market opportunities that we look to strike deals with, companies, and I'm hopeful we'll be able to move forward with a significant collaboration this year. Of course, we've done some deals now in the Greater China market with Tasly for STRO-002 and BioNova for STRO-001, and there may be selected market opportunities for us to consider partnering one or more of those assets this year as well. In the main, we're focused on trying to find that right partner for a broad-based, multi-target collaboration, looking to provide the next-generation cancer therapeutics for them that meet their needs from a development and a commercial perspective. Perfect. No, that was great. Can you confirm which molecule is subject to the enrichment program? Yes. The folate receptor alpha ADC STRO-002 is the one that we've been looking at the enrichment strategy for. Okay. Maybe it makes sense just would love to get your thoughts on, you know, the corporate roadmap for 2022, what gets you the most excited for the year coming up here? Well, I think, having now presented our interim STRO-002 data, there's going to be a lot of enthusiasm to see, the final or near final data set, from STRO-002. As I indicated, last patient was dosed in November, was first dosed in November of last year. If you project out six months, that would get you to the May timeframe. We look forward to a scientific conference in the second half of the year, where we should have a really good handle on what the durability of our treatment has been. This development of that molecule in the fall of 2019. That program has really been in the clinic for over two years. Last year, they had indicated an intent to present to the scientific conference. It didn't happen last year, but we do hope it will happen at a major scientific conference this year. Now, they've started a second study, again, a secretase study, but you know, we're waiting to see what will happen as we move forward. That's great. That's incredibly exciting. So I think with that, we can conclude the session here. I wanted to thank you for your time, Bill and team, and everyone for attending. I hope you guys have a great rest of your conference here, and have a great rest of your day. Thank you, all. Thank you, Michael.