Great. Thanks everyone for joining us this afternoon. It's my pleasure to introduce our next presenter from Cullinan Therapeutics, Nadim Ahmed, Chief Executive Officer. With that, I'll pass it to you, Nadim. I didn't let you sit for very long. Thanks. All right. Good afternoon, everyone. First live presentation in two years, so thanks for keeping the audience small, easing me back into it. Let me start out by saying a couple of things about Cullinan Oncology. We're a company that's dedicated to creating new standards of care through a very unique approach to the drug discovery and development process. Here are our disclaimer slide, so we'll be making forward-looking statements. One thing you'll notice about our company is that we have a very broad and deep pipeline across multiple modalities, different indications, hematology, solid tumors, and at various stages of development. Then the other thing I would add, when you look at each program, we have assets that potentially at least have the opportunity to be either first in class and/or best in class. Our lead program is CLN-081, which is targeting non-small cell lung cancer patients that harbor the exon 20 insertion mutation, and CLN-081 is currently in phase I/IIa study. We presented an update, updated data presentation December of last year. From the original ASCO presentation, we still see a very well-differentiated clinical profile. Of course, recently, we were very pleased to receive breakthrough therapy designation, which for us was external validation of the differentiated profile that we're seeing in the clinic. In addition to CLN-081, we also have two additional programs that entered the clinic in December of last year, so we're very excited about that. We have CLN-049, which is a T-cell engager targeting FLT3 in AML patients. We also have the pan-cancer potential monoclonal antibody CLN-619, which targets the MICA, MICB pathway. Both of these programs drive the immune activation, as well as having a first-in-class potential. We're very fortunate, and I suppose even more importantly today, to be a company that's very well capitalized. We continue to look for ways to deploy that capital to accelerate our internal pipeline and programs, as well as continuing to in-source innovation where we can find it. Behind our clinical stage programs, three of whom I discussed with you just now, we also have a deep pre-clinical research program of five additional assets, two of which are currently in IND-enabling studies, and we plan IND submissions for those two molecules in the middle of next year. We also continue to in-source innovation. I spoke about how we're deploying capital effectively, as evidenced by a recent collaboration with Mount Sinai for their novel HPK1 degrader program. At Cullinan, we also take a very disciplined criteria-based approach to in-sourcing innovation and advancing our internal programs. First, the asset has to have the potential at least to be first in class and or best in class. We look for molecules that activate the immune system or target key oncogenic drivers. Pre-clinically, at least, we have to see evidence of single agent activity. We use these criteria to really think carefully about in-sourcing assets as well as advancing programs within our internal pipeline. Also at Cullinan, we really innovate without borders. We seek out the most promising clinic-ready assets, either through our internal discovery efforts or through excellence in engagement with external partners. You can see in the top panel of this slide, in the top left, as you look at it, we also position our assets for very early, what we call thriller or killer experiments. This makes sure we're doing early de-risking and only bringing the most promising assets forward into the clinic. We do have a constant flow of deals and opportunities that we look at, and we look at over 100 opportunities each year. Our team is very good at what I'd call scientific ideation, taking something from the concept stage all the way from candidate selection and through to clinical stage development. We're a company that has very deep biologics and small molecule expertise. We also leverage our business model efficiency. We're always looking at the optimal mix of in-house capabilities versus external capabilities as well. When you look at the top right-hand corner of this slide, you can see what I mean within that context of small molecules and biologics, we have a very diversified pipeline of monoclonal antibodies, T-cell engagers, fusion proteins, tyrosine kinase inhibitors, and now also protein degraders. In the bottom panel, on the left-hand side, you can see we also have a focus on unique platforms and novel mechanisms of action, where we often do a lot of engineering or re-engineering of those molecules. Across the broader oncology, Cullinan Oncology team, we have deep scientific expertise that allows us to really accelerate the advancement of our internal programs, as well as tap into an external network of partners in academia and other industry partners. The result of all of these efforts gives you this diversified pipeline that I'm showing you. 8 programs across various stages of development. Our lead program is CLN-081, which I spoke about earlier, targeting EGFR exon 20 mutations, a really important program for the company. Beyond CLN-081, we also have a very deep pipeline following behind, with 8 programs, as I mentioned, 3 now in clinical stage. 2 in IND-enabling studies and some other earlier preclinical assets as well. We're very pleased with the diversification of our pipeline. Let me take a moment now to dig into CLN-081, our lead compound. CLN-081 is a novel oral EGFR inhibitor with a unique chemical structure. That means it preferentially targets the mutant form of exon 20 versus the wild type variant. We believe this contributes to the therapeutic profile that we're seeing in the clinic. As I mentioned, it's in an ongoing phase I/IIa study in patients who have failed prior chemotherapy, heavily pre-treated patients, two-thirds of whom have received two or more prior therapies. You can see from this slide the response rate data that we presented in December. We see a confirmed response rate of 39%, which is at the upper end of agents in this space. We also see 35 of 36 patients who experienced either stable disease or partial response as their best response to elicit an excellent disease control rate of 97%. You also see the data for 150 mg BID. At the higher dose, we actually paradoxically see a lower response rate. I'll explain, but we feel that this is based on that tolerability profile that we see at the 150 mg BID dose. What do I mean by that? You can see on this slide, clearly a differentiated profile at a 100 mg BID dose. In this table, you can see the key toxicities, especially those related to wild type EGFR toxicities. You can see in this slide that at the 100 mg BID dose, we see no cases of grade 3 or greater rash or diarrhea. In fact, the rash or diarrhea we observe at this dose is heavily skewed towards grade 1 as opposed to grade 2 at a 3-to-1 ratio. That's encouraging also. In the protocol, there was no requirement for systemic GI prophylaxis. At the 150 mg BID dose, you do see a step-up in toxicity. In fact, we discontinued enrollment into that cohort after 11 patients. You can see we saw two episodes of grade three diarrhea. We saw pneumonitis. I'll come back to that. We saw transaminitis at both grade three and grade four. You see that step up in toxicity as you go from 100 mg to 150 mg. Just as importantly, you see a significant increase in the rates of dose reduction as well as treatment discontinuation at the 150 mg dose. This is where we think it's contributing to the efficacy profile where we have seen a lower response rate. Let me just say a word about the pneumonitis observed to date. Obviously, a toxicity that has been seen with this class of agent. In both of these cases, there were additional confounding factors, which you can see in the footnote here. In the first slide, I spoke about quantity of response, that 39% confirmed response rate. What we're really encouraged by based on the December data update, this is the first time we were actually able to assess durability. This was in the initial 13 patients that were enrolled in phase I. What we saw based on Kaplan-Meier estimates is a median duration of response of greater than 15 months and a progression-free survival, median progression-free survival of 12 months, which again compares very favorably with the durability of other agents approved in this class or in the clinic currently. A very robust disease control rate at 92%. We're also following on or following up the other patients in the phase II cohort who were enrolled later on, and hopefully we'll be presenting those durability data later on. As I mentioned, breakthrough therapy designation was really important for us on two counts. One, as I mentioned, it provides external validation of our differentiated profile. It also demonstrates that the accelerated approval pathway is still open to us. We were really pleased to receive that. We are planning a regulatory update this month. I would say in summary, the data continues to show that we have a very strong differentiated clinical profile, both in terms of efficacy with quality and quantity of response and a favorable safety profile in a heavily pre-treated group of patients with a significant unmet need. Let me now turn to our other clinical stage assets, and I'll start with CLN-049. As I mentioned earlier on, this is a novel T-cell engager which targets FLT3 in AML patients, and it's currently in a phase I study. Let me start with the design of this molecule. In fact, the chap that designed this molecule is sitting here in the front row. If you have any questions, you can ask him afterwards. CLN-049 is based on an IgG1 construct, the same construct that we've actually seen with some of the newer T-cell engagers in lymphoma, where we're seeing high levels of activity and low levels of CRS-related toxicity. We also have an Fc silent region in this molecule, so that gives you a prolonged half-life, which hopefully should allow for less frequent dosing. Let me spend a couple of minutes on the target now. FLT3 is a proto-oncogene, and it's a very well-validated AML target, as you can see by the approved small molecules in this space. FLT3 is expressed in the majority of AML patients, but with relatively low expression in healthy myeloid cells. The advantage that we have with 049 as a potential first-in-class antibody targeting FLT3 is that we target the extracellular domain of FLT3. That means we target both mutant and wild type FLT3. That means you have a much larger addressable patient population of over 80% of patients compared to the 25% of patients who have mutant FLT3 that are targeted by the current, small molecule tyrosine kinase inhibitors. Also, as I mentioned, relatively low expression healthy myeloid cells, which means CLN-049 should have a better therapeutic index than some of the other targets like CD33 and CD123. As I mentioned, CLN-049 is currently in phase I dose escalation, and we hope to have clinical data provided by the middle of next year. In the next slide, you can see the robust preclinical package we have generated with CLN-049. In the top panel, turning to the left, you can see in a range of AML cell lines that express both wild type and mutant FLT3, we see significant eradication of those tumor cells in vitro. On the right panel, you can see compared to CD3 control antibodies, we see no activation of T cells with 049, which portends potentially for a favorable safety profile in the clinic. In the bottom panel, you can see the efficacy data that we're seeing preclinically. In the bottom left, you can see a nice dose response survival curve in the tumor xenograft model, even at very low doses of 049. On the right-hand side, we actually transfected AML blast, human AML blast into a rodent model, and we saw complete eradication of those cells in the bone marrows of rodent. We're very excited about CLN-049, and as I mentioned, it's currently in the clinic. Our other clinical stage asset is CLN-619, which again is another potential first-in-class opportunity, a pan-cancer opportunity since MIC-A and MIC-B is ubiquitously expressed across various tumors. Starting with MIC-A and MIC-B, it is a ligand for the NKG2D receptor on all NK cells and a subset of T cells. What happens is in stressed cells and tumor cells, you see an upregulation of MIC-A, MIC-B, which then sends a kill me signal to the immune system, especially NK cells, inviting tumor cell destruction. What happens, as we know, cancer is very clever. Within that tumor microenvironment, you often see proteolytic cleavage, which causes the MIC-A and MIC-B to be shed from the cell surface, so those tumor cells are able to evade the immune system. Shed MIC-A, MIC-B is also a poor prognostic marker, and I'll show you that in the next slide. As I mentioned, we have a first in class opportunity here. CLN-619 is the first clinical stage MIC-A, MIC-B antibody with multiple modes of action. I just described how MIC-A and MIC-B is shed on the cell surface to evade the immune system. CLN-619 keeps MIC-A and MIC-B on the cell surface when it binds. That draws in the immune system, especially NK-directed activity. When it's bound to a cell, it also binds to the Fc gamma receptor on NK cells. It has a mechanism of action through ADCC. When you combine these mechanisms of action as well as additional mechanisms of action, you're really invoking both the innate and adaptive immune system in patients. We're very excited about this molecule, especially the potential for pan-cancer opportunity. With CLN-619 specifically, we have very good coverage of the MIC-A, MIC-B alleles of over 95%. We're in an ongoing clinical study, as I mentioned, in phase I. At the same time, we're evaluating monotherapy with CLN-619 as well as combination therapy with checkpoint inhibitors. We plan to have data provided by mid-2023 next year. The next slide shows both the biological and clinical rationale for MIC-A, MIC-B. Starting with the top panel, upper right-hand corner, you can see in a range of NKG2D ligands, MIC-A, MIC-B is more highly expressed and across a range of different tumors relative to the other ligands. Again, there is that pan-cancer potential, as I mentioned earlier. In the top left, you can see how shed MIC-A is a poor prognostic marker. In this retrospective analysis of a clinical study, you see patients that have a high level of shed MIC-A have a much poorer survival outcome. In the bottom panel, you can see the preclinical work we've done with CLN-619 already. In the left graph, you can see complete tumor eradication at all doses of CLN-619 tested. On the right graph, from a pharmacodynamic perspective, you can see at all doses of CLN-619, we see the complete prevention of shed MIC-A, MIC-B. Again, very excited about this program with clinical data middle of 2023. Let me now turn to our preclinical pipeline and speak specifically about our two IND-ready assets. CLN-617 is our first-in-class cytokine therapy, which is a fusion protein containing both IL-12 and IL-2. These are cytokines that are well-described in the literature that have potent antitumor activity. However, the issue with these cytokines is that historically, systemic administration has led to significant toxicities. What we're doing is applying intratumoral administration with CLN-617. This fusion protein allows the co-delivery of IL-12 and IL-2. We also have a collagen-binding domain that allows the cytokines to stay within the tumor, so prevents the leakage out into beyond the tumor to prevent systemic toxicities. Most importantly, we do see preclinically at least, and we'll see the results in the clinical experiments, both memory T- cell response induction as well as an abscopal effect, showing effects beyond the site of tumor injection. What's interesting about this molecule is that we are delivering the wild type version of the cytokine, so we would expect to see reduced immunogenicity. Also, there's no reliance here on viral mechanisms on nucleic acid delivery systems, so we're really able to control the dose that gets into the tumor. For our CLN-617 presents a pan-cancer opportunity, either as monotherapy or as I'll show you also in combination with checkpoint inhibitors. In this slide you'll see the very robust preclinical package that we've generated to date. Let's start with the top panel. In the top left corner, you can see a very refractory primary tumor xenograft model, where essentially the administration of CLN-617 in the tumor provides complete response in each of the 10 mice tested. Sorry. This has come from someone born in London. Okay. We see complete eradication of the tumors, complete responses. You see a very weak signal with checkpoint inhibition as monotherapy. But even more interesting is when you take these cured mice and you reinject them with tumor without treatment, you see nine out of 10 of these mice completely reject the tumor. Then in one case, you see significant delay in progression. Here you're seeing a really strong T-cell memory effect. In the bottom panel, starting with the left side, what we did here, we transfected two tumors into a mouse model system in vivo. On the left-hand side, you see the administration of checkpoint inhibitor monotherapy, the administration of CLN-617 monotherapy, and the administration of the combination. With CLN-617 monotherapy and the combination, you see complete eradication of tumor at the injected site. However, the more exciting aspect of this study is in the uninjected tumor sites, you see significant reduction or tumor eradication with CLN-617 as monotherapy. Even more interestingly, the combination of CLN-617 plus checkpoint inhibitor completely eradicates tumor. This is why we're very excited about this program and hopefully entering the clinic next year. The last molecule I'll speak about is CLN-978, which is our T-cell engager, which we believe has the potential to be a best-in-class T-cell engager targeting CD19. I mean, clearly CD19 is a very well-validated target, both clinically and now commercially with the CAR-T agents as well as T-cell engagers approved in this space. What we did here is we really looked at the design of the antibody. We engineered it to have a very long half-life, to again allow for less frequent dosing, including continuous infusion. Also engineered it to have very high affinity for CD19, so it's able to be active in very low CD19 expression settings. Why is that important? Well, if you look at current patients, for example, treated with CAR-T, one of the resistance mechanisms we think is taking place is the downregulation of CD19. You can imagine a scenario where you will be able to salvage patients in the post-CAR-T setting with this agent. In other settings, potentially you could see the activity of CAR-T in an off-the-shelf treatment, which then of course opens up a much bigger pool of patients to receive treatment CLN-978. We also think CLN-978 could be competitive relative to CD19 targeted ADCs, where you need a higher level of antigen expression in order to be able to safely deliver the payload. If you look at the bottom right-hand corner of this slide, we did a head-to-head in vivo study looking at CLN-978 versus a currently approved CD19 monoclonal antibody and demonstrated clear antitumor activity. We're really excited to take CLN-978 also into the clinic with an IND submission plan in the first half of next year. Let me just say, 2021, despite COVID-19, has been a really busy year for Cullinan Therapeutics. We have made various achievement of various milestones and progressed our pipeline. Starting with CLN-081, as I mentioned, we updated the phase IIa data in December of this year. We recently received breakthrough therapy designation. With CLN-049, our FLT3-targeted AML agent, we started clinical study in December. CLN-619, our MICA, MICB antibody, again, entered the clinic in December. With CLN-617 and CLN-978, we continued our progression along the IND-enabling study path. Over the next 18 months or so, starting with CLN-081, this month we'll have a regulatory update. We'll also plan to start our pivotal registration study this year. With CLN-049, we expect a clinical update mid-2023, and the same with CLN-619. As I mentioned, these are studies that just started in December, so we're continuing to accrue patients and gather the clinical data. We also are looking at getting CLN-617 and CLN-978 into the clinic next year. A significant number of value creation milestones over the next 18 months. If all goes well, we'll have five highly differentiated molecules in the clinic, which reflects our evolution into a later-stage oncology company, as well as our ultimate ambition to become an end-to-end fully integrated biotech company. The progression of our pipeline, I think, really represents significant value opportunity for our investors, but most importantly, will help us to deliver on the promise of bringing new therapeutic solutions to patients with cancer. In closing, I'd like to say and really thank my teammates at Cullinan Therapeutics who have shown relentless dedication to their work, especially during this global pandemic. I'd also like to thank my colleagues at Barclays who have created this opportunity for me to share the very exciting story of Cullinan Therapeutics. With that, thank you.