Good day, everyone, welcome to Pfizer's Analyst and Investor Call to review oncology business. Today's call is being recorded. At this time, I would like to turn the call over to Mr. Chuck Triano, Senior Vice President of Investor Relations. Please go ahead, sir. Thank you, operator. Good morning and good afternoon, everyone. Thanks for joining us today to provide an update on our oncology pipeline progress, specifically how we are applying our capabilities to move more quickly and utilize cutting-edge science to key programs. As a note, we plan to conduct a series of these sessions across our therapeutic areas as our pipeline progresses and we have new data and insights to share with you all. We'll be making forward-looking statements during this call. Actual results may be different. Additional information regarding forward-looking statements is available in our SEC filings on our Forms 10-K and 10-Q. The forward-looking statements on this call speak only as of the original date of this call. We undertake no obligation to update or revise any of the statements. With that, I'll now turn the call over to Andy Schmeltz. Andy? Thanks, Chuck. I'm Andy Schmeltz, and on behalf of my colleagues, Chris Boshoff and Jeff Settleman, we're pleased to have this opportunity to engage with you today. The three of us have joint accountability for Pfizer's end-to-end oncology presence, inclusive of strategy, investments, and the full R&D and commercialization continuum. Today, we'll spend about 20 minutes on how we're applying the mindset from Pfizer's recent COVID-19 vaccine Lightspeed effort to key clinical programs within oncology. We believe this purposeful, more ambitious approach can make a significant positive impact both for people afflicted with cancer and for Pfizer. We'll open it up to Q&A. Before jumping into the primary focus of our discussion, let me take a minute to highlight Pfizer Oncology today. We have a broad portfolio of 24 medicines across 30 types of cancer that brought hope to more than 716,000 people living with cancer in 2020. We continue to see outstanding year-over-year growth for oncology globally, almost $11 billion of revenue. Even through a difficult year with the pandemic, we delivered 21% operational growth in 2020. IBRANCE, representing about half the revenue of the portfolio, grew 9%, while our other medicines grew a total of 36% operationally, led by our biosimilars portfolio, BRAFTOVI and MEKTOVI in melanoma, BRAFTOVI in colorectal cancer, and XTANDI in prostate cancer. More than 275 clinical trials currently underway and six additional phase I first inpatient clinical program starts since our last discussion with you at Pfizer Investor Day this past September. We've also initiated several new registrational trials in recent months. Two new trials with BRAFTOVI, BREAKWATER in first-line BRAF mutated colorectal cancer, which started in late 2020, and a new phase III trial that started in February called STARBOARD, with BRAFTOVI and MEKTOVI combined with pembrolizumab in first-line melanoma. In prostate cancer, we're expecting data this year from the ongoing phase III TALAPRO-2 trial with XTANDI plus TALZENNA, talazoparib, in men with metastatic castrate-resistant prostate cancer. Bottom line, we're proud of our track record and our future prospects for Pfizer Oncology. Let's now shift gears. I cannot understate just how incredibly proud and excited we at Pfizer are about the Lightspeed development in collaboration with BioNTech that delivered the world's first breakthrough COVID-19 vaccine in less than a year. Our ability to move at such extraordinary speed while always maintaining our focus on quality and safety, was the first powerful display of what the new Pfizer is capable of. Through the vaccine, we found ways to use digital technology to perform tasks in parallel rather than sequentially, and to reduce white space between clinical trial cycle times. All of which we're now looking to apply to transform the way we bring breakthrough cancer medicines to patients faster. These Lightspeed learnings and concepts are something that we within oncology have been focusing on to incorporate into our oncology development approach for some time. Today, we'll walk you through three exciting Pfizer-discovered programs, advancing with this Lightspeed mindset, moving at the speed of science. First, a recent example with LORBRENA or LORVIQUA internationally in ALK-positive non-small cell lung cancer. Our BCMA bispecific candidate, elranatamab, in multiple myeloma, and how we're taking ambitious steps in what is sure to be a dynamic market. Finally, Jeff Settleman will talk about a collection of early development programs in the breast cancer space, building on our already strong position here with IBRANCE. These examples to be highlighted represent just a small subset of our pipeline portfolio. However, we believe they're indicative of how this new breakthrough mindset is being applied and will propel Pfizer Oncology to continue our growth trajectory and to make a meaningful difference for people with cancer. I'd like to turn it over to Chris Boshoff to discuss LORBRENA in more detail. Chris? Thank you very much, Andy. Thank you. As you all know, ALK-positive lung cancer accounts for 3%-5% of all lung cancer. Almost a decade ago, we pioneered the field with the development of XALKORI. lorlatinib was discovered and developed in-house by Pfizer chemists, and it has a unique macrocyclic structure, as illustrated in the center of the slide. Up to 40% of patients with ALK-positive non-small cell lung cancer present with brain metastases. LORBRENA is the next-generation ALK inhibitor targeting most of the known resistant mutations and also covering brain metastases. On the right side is the list of the most common mutations developing to other ALK inhibitors, demonstrating the coverage of lorlatinib to these. We're very proud of the flawless execution and accelerated development of lorlatinib. From first patient dose to first regulatory approval was less than five years. For CROWN and first-line phase III study, from top line report to FDA approval was just over six months. We utilized the latest regulatory tools, including Real-Time Oncology Review pilot and Project Orbis, allowing simultaneous reviews in the participating countries. All submissions are now complete. The FDA approval in first-line non-small cell lung cancer is based on the compelling results from the CROWN trial, which demonstrated a 72% reduction in the risk of progression or death. This study also showed, in patients presenting with intracranial disease, a 78% complete remission, which is the highest ever demonstrated for any ALK inhibitor. For those presenting without any intracranial metastases, the CROWN study also demonstrated a hazard ratio of 0.06 for progression in the brain versus XALKORI. We believe that the CROWN results will position LORBRENA to be highly competitive with second-generation ALK inhibitors in the first-line setting, especially in those 40% of patients presenting with brain metastases. Furthermore, LORBRENA will continue to be a standard of care after second-generation ALK inhibitors in the second-line setting. We are also pleased to still have 27 patients on treatment, more than five years after starting LORBRENA on our phase I dose escalation and expansion study in 2014. Moving now to investigational BCMA bispecific, elranatamab, which we recently announced the initiation of the first pivotal trial in relapsed refractory multiple myeloma. Multiple myeloma remains a significant unmet need, with only 50% of patients surviving past five years with current standard of care. As multiple myeloma progresses, tumors become resistant to the three main classes of therapies, the IMiDs, including lenalidomide, the proteasome inhibitors, and the anti-CD38 antibodies. We believe that the next major pillar of treatment for multiple myeloma will be medicines targeting BCMA, which is highly expressed on multiple myeloma cells. Among the BCMA-targeted therapies, we believe that bispecific molecules will become the next standard of care backbone across the treatment paradigm because of efficacy, their safety profile, combination opportunities, and convenience. elranatamab is a full-length humanized bispecific antibody optimized for binding affinity to both BCMA anti-CD3, enabling more potent T cell-mediated tumor cell killing. elranatamab is being developed as a subcutaneous injection with the aim of reducing the incidence and grade of cytokine release syndrome, or CRS, which is a dose-limiting toxicity, particularly for CAR T-cells. The development program for elranatamab is called MagnetisMM. Shown are data from phase I trial presented at ASH in December 2020. Updates of these data will be presented at an upcoming medical conference. In patients with relapsed refractory multiple myeloma, 83% of patients achieved a clinical response at a recommended phase II dose. Overall, 30% of patients treated achieved complete response or stringent complete response. This was also the first study with a BCMA bispecific to show responses in patients who had received prior BCMA-targeted therapy, including ADC or CAR T. Note, three out of four responses, including a stringent complete remission, were observed in patients with multiple myeloma progressing on BCMA-targeted therapy. Based on these data, we initiated the pivotal Phase II study, MagnetisMM-3, earlier this year. This study is now recruiting patients with triple class refractory multiple myeloma globally. MagnetisMM-3 is enrolling two cohorts of participants, one with and one without prior treatment with a BCMA-directed ADC or CAR T therapy. The primary endpoint is objective response rate as assessed by blinded independent central review. The study's estimated primary completion date is June 2022. elranatamab is one of the key medicines we are prioritizing at Pfizer to apply light speed concepts from the COVID-19 vaccine to accelerate the clinical development program. We are doing this in a variety of ways, including real-time monitoring of blinded independent central review, acceleration of commercial-ready product supply by leveraging internal resources, data review, and analysis powered by machine learning technologies. As an illustration from final approved protocol for this study to first subject dose for MagnetisMM-3 was achieved within 30 days, [audio distortion] from the typical 20 weeks. In addition to MagnetisMM-3, we are initiating a comprehensive development program building a wall of clinical studies. This includes other phase III studies in earlier lines of therapy, MagnetisMM-5, 6, and 7, expected to initiate over the coming 12 months. We also initiated MagnetisMM-4, exploring the potential role of novel combinations through an umbrella study with both internal and external molecules. In the future, the appropriate sequencing and rational combinations of elranatamab with other medicines has the potential to transform the outcome of patients with multiple myeloma. I'll now hand it over to Jeff to talk to you about our next-generation breast cancer franchise. Thanks, Chris. As you just heard from Andy and Chris, we're now applying the learnings of the COVID vaccine development experience to our oncology programs, and I'll briefly describe how we're applying these principles as we explore potential new therapies for estrogen receptor-positive breast cancer patients. As you know, the approval of palbociclib, IBRANCE, in 2017 established Pfizer as a leader in the treatment of ER-positive breast cancer, and we've maintained a strong commitment to these patients. One of the most significant challenges still facing ER-positive breast cancer patients is that there's no clear standard of care in the post CDK4/6 inhibitor setting. To address that important unmet need, we've been focused intensively on the development of additional therapies that can overcome drug resistance and potentially provide these patients with more effective and safer treatment options. We've been taking a multi-pronged approach to targeting ER-positive breast cancer. Not only targeting the cell cycle, but also targeting estrogen receptor activity, disrupting signaling pathways that drive breast cancer cell survival, and through immuno-oncology approaches that promote engagement of immune cells with breast cancer cells. Here, I'll briefly highlight four of these programs, including three, which all entered the clinic at nearly the same time last year. First, I'll describe our three most advanced next-generation CDK inhibitor programs, which each enable disruption of the critical G1 cell cycle checkpoint. On the left is our CDK2/4/6 inhibitor, which differentiates from our CDK4/6 inhibitor, palbociclib, with the ability to additionally target CDK2. Since CDK2 activation seems to drive palbociclib resistance in some breast cancers, this molecule has the potential to overcome such resistance. We also see opportunities to develop this inhibitor in other tumor types, including triple-negative breast cancer and ovarian cancer. This molecule is currently in phase I clinical development, and combination studies with endocrine therapy are now underway. It's worth noting that we've been very encouraged by the early responses we're seeing thus far with this inhibitor, even as monotherapy, especially considering that we're treating patients who have previously progressed on CDK4/6 inhibitors, which is consistent with our hypothesis that CDK2 contributes to resistance to current standard care treatments, and that a CDK2/4/6 inhibitor can potentially mitigate such resistance. Next is our CDK4 selective inhibitor, which has been shown preclinically to target CDK4 with more than 10 times the potency of palbociclib, and without the neutropenia sometimes seen with CDK4/6 inhibition. That improved TI potentially provides more opportunity for safer combination treatments in additional cancer types, including lung, colorectal, and prostate cancers. To the right of CDK4 is our CDK2 selective inhibitor, which has been shown in preclinical models to combine with palbociclib or with our CDK4 selective inhibitor to overcome resistance in ER-positive breast cancer and has the potential to drive efficacy in a variety of tumors exhibiting CDK2 activation, especially in combination with standard care therapies. Following the successful acceleration of preclinical timelines for these programs, we were able to move both the CDK2 and CDK4 molecules into the clinic within eight days of each other in October of 2020. It's worth noting that each of these next-generation CDK inhibitors resulted from innovative structure-guided medicinal chemistry efforts from Pfizer scientists that yielded candidates with selectivity profiles that many had predicted would not be possible to achieve. In addition to our robust CDK franchise, we're very excited about the potential for our novel KAT6 small molecule inhibitor, a potential first-in-class agent that blocks the enzymatic activity of the histone acetyltransferase KAT6A, an epigenetic regulator that's amplified and overexpressed in breast cancer. KAT6A is required for expression of the gene encoding the estrogen receptor, ESR1, and we've observed that this inhibitor can overcome endocrine therapy resistance associated with ER mutations in preclinical models of ER-positive breast cancer and shows synergistic activity with CDK inhibition in combination studies. This program also moved into the clinic in late 2020. It's important to emphasize that we've applied light speed principles to the discovery and development of each of these assets that I just described. Our work on both the cell cycle and KAT6 inhibitors has yielded both complementary and overlapping opportunities with multiple shots on goal to deliver clinical benefit for patients. With strategic optimization of resources across programs, we took the approach of developing these Parallel, we were able to deliver three new programs to the clinic within a month and a half of each other in 2020. Going forward, we also plan to efficiently drive acceleration or deprioritization, if appropriate, of individual assets via umbrella studies and by employing specifically predefined go, no-go criteria. This is a paradigm that will continue to guide our oncology research enterprise as we work to bring additional breakthrough therapies to cancer patients in the future. With that, I'll pass it back to Andy to wrap up the presentation. Thanks, Jeff. As you've just heard, we're moving at light speed to advance these programs using enhanced processes, efficiency, and technology. Each of the programs highlighted by Chris and Jeff respectively represents a compelling opportunity for patients and for our business. Here, we're depicting the opportunity for the G7 markets. For LORBRENA, the first line indication will allow us to expand our share of the ALK-positive non-small cell lung cancer market, which we anticipate to peak in the range of 25%-30% share overall. For elranatamab, the multiple myeloma market is large and is expected to reach $34 billion by 2030 due to multi-drug combinations and increasing duration of therapy, as well as the emergence of the BCMA modality. Within BCMA, we believe the bispecifics will become the standard of care, being preferred over the antibody drug conjugates and CAR Ts, offering the potential for the efficacy of a CAR T with compelling safety and convenience advantages. While it's still early days, we believe elranatamab truly has a right to win, not only in the initial triple refractory indication, but also over time in the double relapse in newly diagnosed multiple myeloma settings. We anticipate 15%-20% peak share across multiple myeloma lines of therapy. For our next-generation breast cancer portfolio, we have a strong scientific rationale for our CDK programs as well as for our KAT6A program. We believe there's potential for breakthrough efficacy in the post CDK4/6 setting, where no clear standard of care exists, and also in the first-line metastatic setting to prevent the emergence of CDK resistance. Leveraging our leadership in HR-positive, HER2-negative breast cancer, we believe this multiple shots on goal approach will lead to tremendous opportunity and leadership as a follow-on to IBRANCE. There you have it. Hopefully, our enthusiasm and conviction regarding our future prospects and our light-speed mindset have shown through. Thanks for your time. We'd now like to take questions. Chuck, over to you. Thanks, Andy, and thanks to Chris and Jeff for the presentations as well. Operator, can we please poll the audience for questions? Thank you. Ladies and gentlemen, if you would like to ask a question, please press star one on your telephone keypads. We'll pause for just a moment to compile the Q&A roster. Your first question comes from the line of Louise Chen from Cantor. Hi. Thanks for taking my questions here. The first question I had for you is, if it's approved, where do you see your next-gen CDK inhibitors fitting into the treatment paradigm? You have three, what's your go-to-market strategy? Second question I had for you is, how important is your heme malignancy franchise to you going forward? If it's important, how do you plan to build this franchise out? What type of targets and type of drugs are you most interested in? The last question is just on your early-stage oncology pipeline, which you didn't talk as much about today. What gets you most excited? I know you have a lot of compounds in development. Thank you. Thanks, Louise, for your three questions. We'll try to take them one at a time. I'll talk about the next-gen CDK go-to-market strategy and the heme build-out. Maybe, Chris, you can chime in, and then Jeff, certainly over to you for the early pipeline. With our next-gen CDK franchise, we see clear opportunity here. While CDK inhibitors led by IBRANCE have really established themselves as the modality and standard of care for metastatic HR-positive, HER2-negative breast cancer, that there's clear unmet need. 70% of first-line metastatic patients are on a CDK inhibitor, and so they're going to need options eventually when the cancer wins out. Clearly we're designing this portfolio of early compounds to be able to be effective after prior CDK therapy. Also, as a next generation, we envision them having addressed, as Jeff kind of commented on, some of the toxicities of the current CDKs, and so they certainly could have a strong role in first line as well. We see quite broad opportunity there for the next-gen CDKs. As Jeff also mentioned, there's the possibility with some of these that breast cancer is not the only tumor area that could be applicable, that by having a larger therapeutic window, a broader therapeutic window, that there'll be potential in other tumor areas. Maybe before we go on to the heme question, Chris or Jeff, do you want to add anything there? I'll just quickly add first, and Jeff, this is also for Jeff to expand on. Remember in our PALOMA studies, we show that one of the mechanisms of resistance that was demonstrated was those tumors that mainly express or overexpress cyclin E. We know cyclin E binds to CDK2. That propelled the development of a next generation CDK2 inhibitor. The CDK2/4/6 could either be to prevent or to manage and treat resistance to the current therapies. Jeff, perhaps you can also expand on why we're specifically interested in the CDK4. Sure. Yeah. The CDK4 selective inhibitor, we see opportunities, as I mentioned, not only in ER-positive breast cancer as a potentially safer molecule than the CDK4/6 inhibitors, but also a molecule that more potently hits CDK4 and therefore, could be more effective in the early line setting, especially when combined with CDK2, as Chris mentioned, to prevent resistance. That's one scenario for a CDK2/4 combination. We also see opportunities, as I mentioned, in other indications outside of ER-positive breast cancer, where clinically that more potent coverage of CDK4 has yielded efficacy in preclinical models that we don't see with palbociclib. Thanks. Let me tackle the heme hematology franchise. Clearly, we're very excited by the prospects of elranatamab in multiple myeloma. We should note that we have an existing, actually, fast-growing hematology portfolio with four medicines. We've got BOSULIF in CML, BESPONSA in ALL, we have two medicines in AML. Collectively, we're approaching $1 billion in revenue with this portfolio. We've got infrastructure globally, most importantly, we understand the dynamics in the blood cancer space. Very excited to bring on and see elranatamab progress quickly, to tap into this infrastructure. Certainly, if there are other opportunities to further expand our hematology portfolio, we'll be primed to do so. Maybe to touch on the early pipeline, the last question, Jeff, anything you want to add about the early pipeline? Sure. Yeah. We're very excited about our early programs. Maybe I can comment on a couple areas that are particularly a high priority. In the IO space, in addition to our approved PD-L1 antibody avelumab and our PD-1 antibody sasanlimab, which is in phase III development in early bladder cancer, we have several NMEs in phase I now, including two different T-cell redirecting bispecific antibodies. You heard about BCMA. We also have a bispecific T-cell redirecting antibody targeting GUCY2C, an antigen that's highly expressed in GI malignancies. We have two different programs targeting the immunosuppressive TGF-beta pathway. We have recently introduced into the clinic a PD-1 antibody conjugated to a modified version of an IL-15 cytokine. We're really excited about that one. Also from our Boulder site, we have a small molecule inhibitor of the TAM kinases. We have a robust early pipeline in immuno-oncology. We also have several promising earlier stage programs that are focused on the PD-1 refractory IO space, a few of which we're expecting to bring into the clinic in the second half of this year, including an oncolytic virus that looks very promising in pre-clinical studies. Another area of scientific emphasis has been on regulators of chromatin, epigenetic modulators. I've mentioned KAT6. We also have an EZH2 program that we're excited about, and our PRMT5 inhibitor, which is differentiated from some of the other programs in the clinic with some very high potency and a unique mechanism of target engagement. Those are a few of the areas that we're especially excited about with respect to our early pipeline. Thanks, Jeff. Great. Thanks, folks. Thanks, Louise, for the question. Operator, please let's move to the next question. Your next question comes from the line of Terence Flynn with Goldman Sachs. Hi, good morning. Thanks for taking the questions. Appreciate you walking through all this today. I guess a couple from me. The BCMA market. You mentioned differentiation versus the ADCs and the CAR-Ts, but if you look at the various bispecific antibodies, what do you see as kind of the key differentiated features there for your asset and what's going to really drive market share shift among those various agents? The second one I had is on your CDK2/4/6 inhib, are we going to see any data there at ASCO this year or potentially maybe another conference later this year? What is the bar? What are you guys looking for in terms of level of activity to really advance that into further studies? The second part of that question is just, can you remind us if you ever saw any activity for palbo in other tumor types beyond breast cancer? Thank you. Thanks for your questions. I'll start and then we'll tag team with Chris and Jeff on these others regarding CDK2/4/6 and palbo activity. For elranatamab role in differentiation within, relative to other BCMA modalities. first- BCMA relative to CAR T, relative to antibody drug conjugates, we believe that the bispecifics are going to be the winners in the long run here. The efficacy of the CAR T, combined with safety and convenience advantages. Elranatamab, from day one, designed to be subcutaneous administration. Many of the other bispecifics started out as infusion molecules and they're trying to make them more convenient into subcutaneous. It's early days in terms of differentiation amongst the bispecifics. We're very excited about the early efficacy results and safety results that we have in our trials, and we'll have to see how this plays out. Given our intent to move quickly and to generate robust data across different patient segments, we're quite confident that we're going to be primed and have a right to win over time. Chris, anything to add there? I have just two other points of differentiation is the molecule itself. The molecule was designed for optimal affinity to both BCMA and CD3, which resulted in a very favorable PK profile for us. As Andy pointed out, we're starting in the trial with weekly and then two weekly subcutaneous dosing, but we're also now starting to test in MagnetisMM-9, four weekly subcutaneous dosing, which of course could be differentiated. The overall risk benefit profile, as mentioned, the safety, we so far only have grade 1 or grade 2 cytokine release syndrome, and specifically, we were the first to notice observed responses, including a stringent complete remission in patients previously exposed to either ADC, BCMA ADC, or BCMA CAR T. We certainly believe we will be in the first wave with elranatamab. Jeff, over to you for CDKs. I think there was a question about the path for CDK2/4/6. I think while we don't have a specific plan for the presentation of the data, as I mentioned, what we're especially encouraged by is seeing responses with the monotherapy treatment in patients who have progressed on CDK4/6. Again, this does seem to support our hypothesis around the role of CDK2 in driving resistance. As I mentioned, we're also exploring the endocrine therapy combination, which is already underway. I think as far as where the bar is, we don't have a specific metric to point to at this time, but I would say that we do see the CDK2/4/6 monotherapy if there is transformational efficacy as our first path to an approval with our next generation CDK molecules. I think there was also a question about palbociclib in other tumor types, and maybe Chris, I'll hand back to you for that one. Thank you. We did observe the number of some of the rarer tumors or the rarer lymphomas and sarcomas, soft tissue sarcomas, where we did observe single agent activity with palbociclib. One of the challenges has been in combinations, apart from hormonal therapy, has been either DDIs or the therapeutic index, especially with cytotoxic therapy. Although we've noticed in some of the phase I studies significant activity with palbociclib in combination with cytotoxic therapy, that has always been hampered by hematological toxicity, and we hope that that can be overcome with the CDK4 specific inhibitor. Having said that, we still have ongoing pediatric studies in new sarcomas and other types of sarcomas with a combination of palbo plus cytotoxic therapy, which appears to be better tolerated in the pediatric population. All right. Thank you. Thank you all for those responses. Operator, can we move to our next questioner, please? Your next question comes from Vamil Divan from Mizuho Securities. Great. Thanks so much for taking my questions. One, maybe I may have missed it, but just on the earlier stage assets, your HER2 ADC, we get questions on that periodically. I'm wondering if you can just give any update on when we might see some more data on that product, HER2 ADC. Then maybe just, you talked a lot about encouraging the learning from the COVID situation, how you're transferring over. I'm wondering if you can just talk more specifically around sort of mRNA technology and how you sort of maybe see that any further development you look to doing on that in terms of oncology vaccines or otherwise, would be helpful. Thanks. Jeff, I think both of these are squarely in your shop. Sure. Yeah. For our HER2 ADC, we've recently stopped that program. We had seen robust clinical responses, we just felt that the therapeutic index wouldn't quite be adequate to move into earlier line indications when considering the competitive landscape. We decided to prioritize other programs where we see greater potential. Also worth mentioning, though, that from our Boulder site, we have a small molecule program that targets HER2 exon 20 mutations. As far as the RNA technology in cancer vaccines, absolutely. This is something we're looking at very carefully. We do have an interest in cancer vaccines. We've seen how the power of RNA as producing immunogens that seem to be quite effective in the preventive vaccine setting. We think that that technology may very well translate into therapeutic cancer vaccines, we're excited about that possibility. That is something that we're actively investigating. Right. Thank you, Jeff, for those responses. Let's move to our next question, please. Your next question comes from Geoffrey Porges from SVB Leerink. Thank you very much for taking the question and for all the information. Chuck, I hope they let you out of the witness protection program soon. It looks a little rough there where you are. Two questions, both related about earlier lines of treatment. First, on the CDK4/6, do you have any insight yet as to why IBRANCE was not successful in the adjuvant setting? Then secondly, which of the CDKs that you outlined do you believe has the best opportunity to move into the adjuvant setting? Related to that, are there any principles from Lightspeed that you think can accelerate the path to either first line or to adjuvant short of showing an overall survival benefit? If you could address that for both the CDKs and for the BCMA, because as you allude to, the first line indication and/or the adjuvant indications for both of these diseases are by far the majority of the revenue opportunity. Thanks. Thanks for the questions. Chris, I think that you're probably best positioned to speak to our early breast cancer experience with IBRANCE and how we would apply learnings to next gen CDKs, perhaps for early breast cancer as well as our Lightspeed approach with elranatamab. Thank you very much, Andy. We're obviously very disappointed in the data from our early breast cancer studies, especially PALLAS. Overall, it's very difficult to compare the various studies in early breast cancer because of, obviously, demographics. I need to point out as well that these were not Pfizer-sponsored studies, so we're working with the sponsors of those trials, so the cooperative groups who conducted those studies. As you would have noticed in the presentations last year, there was a high percentage of patients that discontinued palbociclib during the study. That was also disappointing to us. Having said that, we have collected both tissue samples as well as plasma samples during that study, and that is starting to reveal a lot of interesting data for us and data that could be applied to our future studies. Specifically for our CDK4 and our CDK2/6 programs as we could potentially developing them into earlier settings. Early breast cancer, we believe, will become molecularly fractionated between different risk groups. Not everyone will benefit from adding a CDK2/6 or CDK4 or CDK4/6. Using those translational data, I think, is going to be enormously helpful to us. I do want to point out quickly another study we just initiated that's being led by Yale University as a CRC or collaborative research study, is in the early setting called M0. What this study is doing is a very novel study in breast cancer. Patients very early on, we sequence all their samples, then determine the genetic drivers of their specific disease. Those genetic drivers are then detected in plasma with circulating tumor DNA, and as soon as they become detectable, patients are randomized to either continue their standard of care hormonal therapy or to be randomized to be added a CDK4/6. That study, which has just opened, a randomized trial, we also believe will give significant insight how to develop the best combination and at what time point in the treatment paradigm. Thank you. Chris, do you want to comment on applying Lightspeed to our elranatamab? I think, as you's seen from the slide we've shown with the nine studies that's now in initiation, and some of them already started, MagnetisMM one to nine, a lot of things are done in parallel. We're using the latest digital tools, virtual tools for virtual site initiation, getting data in from sites using artificial intelligence and machine learning pattern recognition to see if there's any regarding AEs or any other information we're collecting from the sites. Particularly also the acceleration of our CMC. Commercial ready product will be ready to be launched. As you've seen, the current primary completion date is June 2022 for our first study. We're very excited to do things in parallel and apply the latest digital technologies in that program. Great. Thanks for that, Chris. Operator, let's take our next question, please. Your next question comes from Steve Scala from Cowen. Thank you. Two questions. I think CDK4/6 inhibitors overall have been studied unsuccessfully in lung, pancreatic, and prostate cancer. I think you mentioned interest in triple-negative breast and ovarian as targets now. Is that the totality of the other tumors that you plan to pursue? Secondly, why did Pfizer out-license the PI3K/mTOR, given its promising clinical response post CDK4/6 inhibitor failure? Thank you. Thanks, Steve, for those questions. Jeff, let me hand it to you first for other opportunities for our CDK franchise. Based on preclinical data, we've been exploring each of these next generation CDK inhibitors in a broad panel of preclinical models across many indications. For the CDK2 and CDK2/4/6 programs, there are clearly settings where CDK2 activity is driven by, for example, increased cyclin E expression or amplification, loss of RB, such as is seen frequently in small cell lung cancer. That would be one. Triple negative breast cancer, endometrial cancer, ovarian cancer. These are places where CDK2 activation seems to play an important role. In terms of CDK4 activity, as I mentioned briefly there, with the greater potency we can achieve in the absence of the CDK6 associated neutropenia, we can push the coverage of CDK4, and at least based on preclinical modeling, we can see activity in settings like lung cancer, colorectal and prostate cancer, where with palbociclib at similar concentrations, that is lower exposures of CDK4, we're not seeing that kind of efficacy. That gives you some sense as to how we're thinking about positioning each of these molecules in other indications beyond ER-positive breast cancer. Thanks, Jeff. I don't know, Chris, you want to take the out-licensing of gedatolisib? Yeah, I'll be quick. Thanks, Andy. As Jeff mentioned earlier, by the end of 2021, we'll have 21 new molecular entities in the clinic. In 2020 alone, we had five First-in-Human, first in humans, and already three achieved in 2021. We really have to prioritize across our portfolio. We agree that's an active medicine. It's an intravenous PI3K inhibitor and mTOR inhibitor, and we're very pleased that there's a home now with Celcuity, and they will take it on and develop it further. It's still an active molecule, you're correct. All right. Thanks, Chris. Operator, if we could take our last question now, please. Your final question comes from the line of Seamus Fernandez from Guggenheim. Oh, great. Thanks for the question. Just a couple of questions here. First off, in terms of the interest in other mechanisms on the breast cancer side, I was just wondering if you guys could update us, if you're doing work on oral SERDs or if you're watching that space relatively closely. If not, what are the issues that you see with regard to the oral SERD class? Is it just sort of the hurdle of stepping above fulvestrant, or other dynamics in that regard? The second question, just in terms of protein degrader technology, would you guys mind updating us on the work that Pfizer is doing in this space, whether it be through the Arvinas collaboration or otherwise, and when might we see some more products from Pfizer on the protein degrader side of things? The last question, in terms of feedback that we've gotten so far, can you just update us on when we might know the sort of ultimate dosing regimen for your BCMA? I believe you'll start with kind of a once a week dosing profile, follow that with expansion to kind of every two week and then pursue every three week. Just wondering when we might have good visibility on the treatment duration. Thanks so much. Thanks for your questions. We'll try to tick them off one at a time. In breast cancer, you asked about additional mechanisms of action, specifically oral SERDs. Clearly, this is an interesting space where it looks like if they can actually have significant improvement upon fulvestrant, that they'll have utility in the breast cancer setting. We're actually working with many of the companies that have oral SERDs today because it's about combination studies, and IBRANCE palbociclib is the combination agent of choice. We're closely monitoring this space to see how it plays out and if there's really a true winner that can establish a new standard of care for hormone therapy. Chris, do you want to answer that? I think you said it. Importantly, those companies that you're all very well aware of, that's now got in hurdle studies starting or started with the SERD. Those in the earlier lines have been combined with IBRANCE, and we're partnering with them, with IBRANCE for those SERDs, at least three. Okay. The next question was about protein degrader technology, how that's playing out. Jeff, do you want to take that? Maybe to Chris? Thanks, Andy. As was mentioned, we have an active collaboration with Arvinas on protein degraders. It's a research collaboration. We have several programs that are part of that collaboration. We haven't yet disclosed the targets that we're working on. Just fair to say that we've been very thoughtful about choosing targets for which we think that PROTAC-type technology is especially relevant, and we're excited about how that collaboration is going. We also have internal programs focused on similar technology. We've developed that capability in-house, and we have a few complementary programs that we're driving internally that we're very excited about. That's what I can say about the degrader technology. It's really opening up the difficult to drug space, and so we're excited about what we're doing there. Great. Chris, on to you for dosing with elranatamab. Thank you. You're absolutely correct. The current study is, that's the phase I study, is weekly. All our PK modeling has indicated that we can move to two weekly. The pivotal trial that is now ongoing, MagnetisMM-3, therefore has a regimen of weekly with step-up dosing to further reduce any cytokine release syndrome, and then after a couple of months, moving to two weekly. We've also just initiated MagnetisMM-9, and again, from PK modeling, inferring that this molecule can be moved to four weekly, since later probably more, I would say in 2022, you'll see data emerging with moving from two weekly to four weekly. You ask about duration of response. As I mentioned, we'll update later this year. You'll see updated data from our phase I study. Just to point out that the data I've shown, of all those patients that's responding, there's only one that has progressed, and that was at the lowest dose during dose escalation. All the other responses are currently ongoing. It's highly encouraging for us. Thank you. Terrific. As you can all hear, a lot going on in the oncology portfolio and broadly at Pfizer. We will look forward to periodically hosting similar sessions like this to highlight other parts of our portfolio. I'd like to thank everyone for their attention this morning and to Andy, Chris, and Jeff for their insights. Have a great day. Ladies and gentlemen, this concludes today's conference. Thank you for your participation. You may now all disconnect.