All right. We'll kick things off. I'm sure people will come in. Good morning. Thank you for attending the conference. Thank you, Jeff, for being here. Pleased to present our next speaker, Jeff, CFO of Cullinan Oncology, ticker CGEM, oncology-focused. We'll see, I think, and hear more about some of the exciting and broad pipeline that they have in their strategic focus in this field. With that, I'll just pass it to you, Jeff, and take your questions. Thanks a lot, Eric. Appreciate it. Just before we begin, a quick note. What we're talking about today, we will have forward-looking statements. Investing in our securities involves risks. Would advise you to please consult with our 10-K and 10-Q to get a better understanding of the risk factors. Let me just pick up where Eric left off. Cullinan Oncology, what are we all about? First and foremost, we like to find high impact targets in oncology. What do we mean by high impact? A target that's either involved in tumor cell proliferation and survival or targets that can really engender and engage a robust immune cell response. We've got examples of both of those in our pipeline. The second thing is, once we've identified those targets, we try to keep an open mind about the modality, figure out really the best way to drug them. Instead of starting from a platform and a technology standpoint, we start for what's the best potential for a therapeutic medicine. We pretty much play across small molecules, antibodies, fusion proteins. The only thing we stay away from is cell therapy. The last point is, we're very rigorous in what we choose to advance and what we don't. We look for molecules that have first-in-class, best-in-class potential, and we run what we call thriller or killer experiments pretty early to figure out what the drug can do. With that, given this is an investor conference, how should an investor be thinking about Cullinan? First and foremost, we've got a really robust cash position. We ended the second quarter with over $650 million on hand, gives us long-term runway. In this market, I think that's a big differentiating factor. The second is, one of our lead programs has produced really good proof of concept clinical data. It's in an area of high unmet need, EGFR Exon 20, which we'll talk about in a little bit. That program is ready to move into a pivotal study this quarter. We've recently announced a partnership with Taiho Oncology to move that forward together in the U.S., we'll look forward to updating you on that shortly. The third point is we've got two other programs in the clinic right behind it with data in the mid-2023, so not too far away. One is CLN-049, which is a T-cell engager, the other is CLN-619, an antibody engaging both innate and immune cells, and we'll talk about those. Behind that, number four, we have a pretty robust pipeline. We have two other programs that are on track for INDs in the first half of next year. Roll forward the clock 12 months from now, we could have 5 clinical stage programs across a number of studies, and I think that gives you a good sense of the breadth and depth of our pipeline. Just so you can see what that looks like visually, we've got our probably eight most advanced programs on the slide here. The top three we covered are in the clinic, the lead one going into a pivotal study shortly, the other two with data expected mid-2023. We're going to spend most of the time today talking through those. Behind that, I'll touch on these other two programs, CLN-617, CLN-978. We don't have a lot of slides in the presentation today, but I could direct you to our website. I'll just give a quick overview of those. CLN-617, there's been a lot of excitement about cytokine development in cancer. IL-2 high dose is obviously approved, but there's been a number of other companies working on different ways to get cytokine into therapeutic reality. With our approach, we're the only company that's combining IL-12 and IL-2 together, and we've got a unique angle to keep those cytokines in the local tumor environment, kind of where they belong to potentiate anti-tumor activity. The other program, 978, a next-gen T-cell engager for CD19, which is obviously a well-validated target in cancer development. Our approach potentially gives advantages of picking up patients that have very low levels of target expression, which could be different settings in the heme space. Both of those programs will have INDs in the first half of next year, but no slides in the deck today, but we could talk about those at another time. Just jumping right into CLN-081. The top half of the slide here, we've got a snapshot of what the molecule looks like chemically. The reason why is that this, I think, highlights what we thought would lead to a differentiated program in the clinic. Number 1, it's a distinct chemical scaffold that's different than all the other TKIs out there. Number 2, we only hit EGFR exon 20. We don't hit HER2 exon 20, I think that's leading to some safety and tolerability advantages in the clinic. The third is we established pre-clinically, it's got a very selective profile of hitting mutant EGFR over wild-type EGFR, and I think that's what is playing out with the therapeutic window we see in the clinic, which we'll talk about in a minute. At the bottom half of this slide, a snapshot of the data that we've shown to date. On the left, very high confirmed response rate, 41%, that sits right on top of the agents that have accelerated approval. At the time of this data cut at ASCO earlier this year, we showed a DOR estimate of 21 months. Hadn't technically been reached, but it was trending in that direction. Also an estimated 12-month progression-free survival. Those three data points in a very relapsed patient population, we are very excited about. They compare very well to agents that have accelerated approval. We also had a favorable safety and tolerability profile, which we can evaluate a little bit here. A little bit more on that study. We dosed almost 75 patients across 5 different dose levels. We've highlighted here the data that we've seen at the 100 mg dose relative to the aggregation of the lower doses below that and the highest dose we evaluated, 150 mg. The top half of the slide has the response rates that we talked about. 100 mg had the highest rate, and it also had the best estimated DOR at the time. What's playing into that, when you look towards the bottom half of the slide, we've highlighted some of the EGFR-associated toxicities, rash, and GI issues. At the 100 mg, we didn't see any Grade 3 or greater events. When you think about some of the approved agents, namely mobocertinib, which has a TKI for exon 20, they saw all grade diarrhea rates above 90% and Grade 3 rates above 20%. We compare very favorably, and we think that's what's playing into the ability for patients to stay on drug, which is encouraging, and supporting the DOR and the PFS rates we've shown here. You can see that all culminated at the bottom, relatively low dose reduction, dose continuation rates at the 100 mg. We've got 39 patients there. Our next steps with the program are to start a pivotal trial, which we'll do on the accelerated approval pathway. We anticipate that study being non-randomized, and in a very similar patient population, which is second-line plus non-small cell lung EGFR exon 20. The last point on 081 is as I alluded to earlier, we did announce a partnership with Taiho Oncology, which is the subsidiary of Otsuka. That was the culmination of a competitive process, a lot of interest in EGFR exon 20, a lot of interest in our molecule after we put out that data at ASCO, and it culminated in this transaction. Financially, we were able to achieve $275 million upfront. We also are eligible for up to $130 million in regulatory-based milestones for EGFR exon 20, very much on brand. The last point in the lower left side of the slide is economically, we share equally in U.S. development and U.S. profits for 081. That's across any indication that the drug is put in. Really nice financial deal that helped us get the cash balance that we talked about over $650 million. Also strategically, Taiho has a good targeted EGFR focus or targeted oncology focus, I should say, in the U.S. The partnership is off and running and going well. Shifting gears to CLN-049. Just quickly on AML, I think it's pretty well understood by the investment community, but where we see the biggest unmet need in AML, I mean, there's been a lot of development with intensive chemo, there's been a lot of development with targeted AML agents, but what remains is the unmet need is for patients who are older, who have the disease, who are ineligible for transplant, ineligible or can't tolerate high-dose chemo regimens, something that's a broad immune-activating approach. That's where we came in with our approach for CLN-049. Just quickly on the target that we're pursuing, which is FLT3, the first and foremost why we like it is it's very validated. There are tyrosine kinase inhibitors approved for mutant FLT3 patient populations. They work well, but they're kind of limited to about 20%-30% of the patient population that has mutant FLT3 expression. By looking at both wild type and mutant, we can address a much broader patient population, potentially 90% of AML patients. The third is FLT3 is expressed both on AML blasts as well as progenitor cells. Hopefully we could see responses that are more durable and deeper. The last point is relative to other T-cell targets like CD33 and CD123, FLT3, the expression outside of AML cells, so on healthy cells, is very limited, very low, and what we hope to see is a nice therapeutic window in the clinic. On this slide 11, you can see on the left the mechanism of action of 049, where we're engaging CD3 on T cells and then FLT3 on the AML blasts. Unlike the TKIs, we're absolutely lysing the cell and hopefully less vulnerable to any resistance mechanisms that you might see with a targeted approach as well. The other thing, a couple of minor things here that are important, one is we have the two FLT3 binding domains, hopefully that helps us pick up cells that have low levels of FLT3 expression. Also, we have monovalent CD3 binding domains. What we hope to see there is a lack of T-cell activation in the absence of target, which should further support the therapeutic window of CLN-049. This program is in the clinic. We started dosing patients about a year ago, and we expect to show initial clinical data in the middle of 2023. The third program I'm going to talk about today is CLN-619. The pathway we're engaging here and the target we're engaging is MIC-A and MIC-B. We put this in a subsidiary we call Cullinan MICA, because we have gemstone names for our subsidiaries. What you can see here on this slide is the sort of natural evolution of what happens with MIC-A and MIC-B and how that leads to cell lysis. Any cell that's undergoing stress, whether it be from an infection, whether it be from oncology, some malignant transformation, it starts expressing these MIC-A and MIC-B proteins. What those serve as is, as you can see on the right, they're signals to the immune cells, both innate and adaptive immune cell populations, to lyse the cell. They do that through engagement of NKG2D on NK cells as well as T cell populations. You can see on the top right corner of the slide, that's what should be happening. The MICA and MICB is expressed, and the NK cells and the T cells come in and lyse the cell. However, on the bottom right, what's happened with cancer cells is they've figured out ways to cleave MICA and MICB and shed it from its surface, and it effectively hides itself from the immune system. What we're doing with 619 on slide 13 with this antibody is really stabilizing that MICA, MICB expression. Our antibody, what you can see on the right, finds a binding domain on MICA and MICB and protects the MICA and MICB from being shed by the proteases in the tumor microenvironment. By preventing that shedding, first and foremost, they can restore the engagement with NKG2D on immune cells. The second is our antibody has an Fc domain, so it actually directly cytotoxicity. The third is, by stabilizing that binding, we sort of lower the threshold required for killing the cell, and all that's shown on the right. Actually, it was not on this slide, but a very late breaker was yesterday at SITC, we had a poster that elucidated a fourth mechanism of action, which is we actually engage macrophages as well. Multiple pathways to mediate antitumor activity. One thing we like about 619, as we talked about earlier, strategically for us, it's a potential first-in-class play. We're the only program in the clinic in this pathway that's got an antibody. As you can see on this slide, the validation of the pathway as a antitumor activity is growing. There's been other companies that have explored MICA, MICB therapeutically. To our knowledge, nobody's ever gotten an antibody into the clinic. However, at the bottom of the slide, you can see there's several cell therapy approaches that are in the clinic. The most relevant and most on target is Fate Therapeutics, which has a CAR NK that targets MICA and MICB with their engineered NK cells. Nkarta is in a similar pathway, but slightly different. They've CAR'd NKG2D onto their NK cells, and they've shown interesting clinical activity in heme populations. Definitely growing biology, but we're excited that we have a first-in-class opportunity there. On slide 15, what you can see is some of the differentiating points about what we're doing with 619. We talked about the fact that it has first-in-class potential. We talked about the fact that it's got multiple modes of action for antitumor activity. What we don't have today, but what you can see on our website, is we have a very strong preclinical package. We've showed that 619 can mediate antitumor activity as a single agent and have pretty robust tumor reductions at almost any dose level. We've also shown that in non-human primates, we can dose almost as high as we want. We never really reached the DLT, and we got to dose levels that were 10X what we're evaluating in human trials. Hopefully, that portends to a wide therapeutic window. The last thing is even though we've seen monotherapy activity preclinically, there's sort of a natural rationale for synergy with combination therapies. A couple examples are on the slide, but one is any patient undergoing radiation therapy, radiation therapy stresses cells and upregulates MICA and MICB. That could be an interesting therapeutic angle for us, as well as combinations with immunotherapy. Similar to CLN-049, we started dosing patients with CLN-619 at the beginning of last year. It was in a solid tumor trial in all comers, we will be reporting initial clinical data on that program in mid-2023 as well. We have two clinical readouts next year. Here's a little bit of the study schema. It's a little bit busy, I'll just orient you on the top half. This is the monotherapy evaluation of CLN-619, then in parallel at the bottom half, we are evaluating in combination with checkpoint inhibitor, specifically pembrolizumab, given the breadth of its approvals. On the right, you can see that once we have established enough dose escalation and get to dose levels of interest, where we've established the safety and clinical activity of the drug, we could expand into tumors of interest. Specifically, non-relapse patients in non-small cell lung, in cervical cancer as monotherapy, just given the unmet need there for an IO agent. On the bottom half, looking at targets of interest where we could potentially improve the efficacy seen with checkpoint inhibitors. Given our safety profile, hopefully, just adding efficacy without adding any safety or tolerability issues. Like I said, that study is ongoing, we expect to have data in the mid-2023 timeframe. Just to conclude on our five most advanced programs that'll hopefully all be in the clinic by mid-next year. You can get a snapshot of our milestones on our lead program with Taiho, where we anticipate starting a pivotal study in CLN-081 very shortly, we'll look forward to updating folks on that when that is in the pivotal study phase. CLN-049 and CLN-619, as we've talked about, expecting to have clinical data in 2023 for both of those programs. CLN-617 and CLN-978 are tracking for IND submissions in the first half of 2023, which would hopefully enable trial starts shortly thereafter in 2023 as well. Pretty catalyst-rich period for Cullinan, luckily we've got the capital and the cash to take it forward. We look forward to updating people on our progress in the future. Pause here for any questions. Yes. The deal that you did. Thank you. Is the model to replicate, for some of the key assets that you have, to partner at a certain stage when you feel comfortable that the economics and the synergies make sense? Would you want to retain more of your lead assets going forward? That's a great question, Eric. Thanks for asking. Yeah, I think we're going to continue to take things on an asset-by-asset basis. We're excited about the Taiho deal. I think it made a lot of sense for EGFR exon 20. When you look at the competitive landscape, I think given the strategic benefits of working with Taiho and the financial benefits of the deal, the fact that that came out of a very competitive process, I think it all lined up for a partnership. Going forward, now with the resources we have in the company, both financial as well as some of the leadership changes we've made, a CEO who was a head of commercial at Celgene, Chief Medical Officer who's developed oncology drugs. I think we're very well put to take programs forward ourselves. We're going to continue to make that on an asset-by-asset basis and do whatever's best for shareholders. Thank you. Yes, Ivo Stein, HBM. Question on your corporate structure. Is that working out for you with these various subsidiaries that are developing the single assets? Yeah, that's a great question. The company was set up historically, where each drug was put in its own subsidiary. We always kept all the financial and human resources up at the parent level, and it worked from a scale perspective because we were only focused on oncology. Today we have three subsidiaries, one, Amber for our cytokine program, Florentine for our T-cell engager, then MICA for 619. We own approximately 95% of the equity in each of those. Going forward as a public company, we're probably going to shy away from creating new subsidiaries and try to keep things wholly owned. CLN-978 is a good example of that. That is sitting in the parent company, and it's 100% owned. I think it made sense when we were private and we were trying to preserve cash, we would give equity to some of the originators. I think going forward, we're going to probably move away from that. On the MICA programs, is that monotherapy possibility there, or if you want to combine with what? Yeah, it's a good question. I think monotherapy activity is possible, and we've seen it pre-clinically. We're in a very relapsed refractory patient population in this all-comer study, the primary goal is establish that the drug is safe, establish the right dose. We're going to look at the PK and PD biomarkers of MICA and NK cell engagement and tumor microenvironment, et cetera, to guide the dose selection, and efficacy will be a part of that mix. The trial's set up that we can look at efficacy, both monotherapy and combination. TBD on what the ultimate plan is. There's a possibility for either. Okay, thanks. Thank you.