Good day, everyone, and thank you for joining the H.C. Wainwright 26th Annual Global Investment Conference. My name's Steve Bursey. I'm an Equity Research Associate here at H.C. Wainwright, and I'd like to welcome Willie Quinn, CEO of Bolt Biotherapeutics. Thank you, Steve. I'm excited to be here to talk about Bolt Biotherapeutics. We are harnessing the power of the immune system to improve lives and eradicate cancer. I will be making some forward-looking statements today, so I'll just refer you to our SEC filings for more information on the risks of investment. Here at Bolt, I'm proud of the expert team that we've assembled. We have a team of five senior leaders who are all very experienced, and we're very efficient in how we're executing on our mission. We currently have a staff of just over 50 employees, and everyone is very focused on immunotherapy and cancer. So a quick overview at Bolt to start things off. Currently, we have a pipeline of two wholly owned proprietary innovative products. One is a novel way to target tumor-associated macrophages. This is our 3042 program, and I'll talk a little bit more about that. Currently in clinical development in a phase I clinical trial. The other program is an ISAC, an immune-stimulating antibody conjugate, and we're targeting a tumor marker known as Claudin 18.2, so this is commonly expressed in gastric and gastroesophageal cancers. We're in the process of developing that for clinical trials, which we expect to start next year. We also have a few collaborations. I'll talk a little bit more about both Genmab and Toray. Both of those are leveraging our immune-stimulating antibody conjugate platform, what we call the Boltbody ISAC platform, to develop novel ISACs, and finally, on the corporate front, we're well capitalized. So we have nearly $100 million, which will allow us to fund both of the programs through key early clinical milestones. We have a very simple corporate structure with no debt and no warrants, so going into a little more detail on our pipeline, the Dectin-2 targeting program, BDC-3042, is currently in a dose escalation trial, so this is the first in human clinical trial. It's an opportunity for us to really test the safety and look for activity signs in actual patients, so this one is currently in seven different solid tumor types. We have triple-negative breast cancer, we have renal cell carcinoma, we have head and neck cancer, ovarian, colorectal, non-small cell lung, and melanoma. I'll give you an update on the trial in a little bit, but it's been going quite well. For BDC-4182, our initial indications will be gastric and gastroesophageal cancer, and we are making good progress in clinical trial preparations for that product. And again, we have two strong platform collaborations. Genmab is a collaboration where we are exploring their proprietary bispecific technology in combination with our immune-stimulating antibody conjugates. That's going quite well and can produce up to three separate programs, so we're exploring a number of different targets with Genmab and very happy about our progress with them. We also have a collaboration with Toray. Toray is a global leader in many fields, and they have an interesting biopharmaceutical arm developing, in this case, antibody drugs targeting specific markers on cancer cells. So we're partnering with them to create an immune-stimulating antibody conjugate with their proprietary antibody. I should point out that all of these collaborations are fully funded by our partners through early clinical proof of concept, so it's a way for us to continue to develop our technology, to advance our pipeline and future value, and do that all while conserving cash and doing it very efficiently, so upcoming milestones for us, we're focused on the clinical program. We just announced that we're in our sixth cohort, and we'll continue to update investors on safety and the progress in recruiting patients for that clinical trial, and then in early 2025, we'll be providing an update on the activity signals that we've seen in the trial and giving an update on the next steps for development. For the BDC-4182 program, targeting Claudin 18.2, we're making good progress on activities such as toxicology program and manufacturing, all with an eye to starting clinical trials in 2025. And finally, you know, we will continue to update everyone on our collaborations, and I'll remind people that our cash on hand funds operations through the middle of 2026. So again, that gives us the opportunity to see early clinical data on both 3042 and on 4182. So a little bit more on our Dectin-2 program, BDC-3042. BDC-3042 is an agonist antibody that targets Dectin-2. Dectin-2 is a C-type lectin receptor, so it's on the surface of macrophages, and its function is to recognize certain patterns that are associated with foreign invasions. In this case, it's a fungal surveillance mechanism. So it's looking for mannan, which is the natural ligand, and it's a fungal, sugar protein. What we've been able to do is create an antibody, that also stimulates that receptor and produces an inflammatory response, which can lead to good anti-tumor activity. When we looked at Dectin-2 expression, we looked across a wide variety of, tumor types and a wide variety of different healthy tissues. And what we found, you can see here, different types of tissues, and the normal, tissues are in blue, and the tumor tissues are in red. So across the board, we found higher levels of expression with tumor tissues and lower levels with healthy tissues. And this creates a really good target for an anti-tumor therapy, such as BDC-3042. You'll notice there are a few locations with higher expression in healthy cells as well, such as the lung, and these are cells that often have a lot of macrophage. In this case, it's alveolar macrophages, which are naturally surveilling for potential invasions from your breathing and from your lung. What we're happy about and excited about is that this product has the potential to help cancer patients across a wide variety of cancers, so it's not just looking for a very small subset of a certain type of cancer where you have expression, because macrophages are found across a lot of solid tumors, and we see elevated levels in most of those cancers. The way that BDC-3042 works is by agonizing the Dectin-2 receptor and creating this inflammatory immune response, so the tumor-supportive macrophages, these are in the tumor microenvironment. You can see the little stylized depiction of our antibody here, and when the antibody engages the Dectin-2 receptor, it creates cytokines and chemokines. Now, these are good ways for us to monitor the activity. So in our clinical trial, we're looking for these biomarkers of activity, and these also attract other immune cells to the tumor, and they lower the activation threshold and help the immune system fight the cancer. So those cytokines and chemokines can have an impact on the tumor cell. The macrophage can also kill tumor cells, and ultimately, it attracts T cells and trains those T cells to recognize the cancer cells. So that's the mechanism. It's both innate immunity at the beginning with our macrophage focus, as well as an adaptive immune response later on. I've been very happy with the progress the team has made in this clinical trial. We have a small number of sites in the U.S., and they've been very successful in recruiting patients into our clinical trial. We're currently in cohort 6. The drug has been safe and well-tolerated to date, with no dose-limiting toxicities, so we're very excited about the safety profile, which is consistent with what we were expecting in the clinic, and we are continuing to monitor those biomarkers I talked about, as well as tumor response, and we'll be able to give an update in early 2025. So before I talk more about BDC-4182, I wanted to talk a little bit about our next-generation ISAC platform, so immune-stimulating antibody conjugates are comprised of an antibody and a linker payload. In our case, we've learned over time that the combination of both the antibody and the linker and the payload are all vitally important to having a good immune-stimulating antibody conjugate. So Boltbody ISACs take advantage of active Fc regions. So these are the regions that trigger phagocytosis. And if you think about an antibody attaching to a target on a tumor cell, the end of the antibody sticking out is the Fc region. And once you have the antibody coated around the tumor cells, you can trigger phagocytosis by the immune cells, and that's how we kick off our mechanism. So the tumor-targeting antibody is important for locating the tumor and then also triggering that next step in activity. The payload is what really kicks off the immune response. So what we've found in the next-generation payloads is that we've increased the magnitude of activity, and we've increased the potency. All of this while tailoring this to pattern recognition receptors that will have the best anti-tumor effect. So we've explored different types of agonism, including Toll-like receptors, such as Toll-like receptor 7 and Toll-like receptor 8, as well as STING and other methods for kicking off a strong immune response. We also have spent a lot of time with conjugation chemistry, making sure that we have just the right combination of, in our case, non-cleavable linkers, to keep the payload on the antibody so that we're only stimulating the immune response in the very specific anti-tumor context that we want. As a result of all these innovations, we see enhanced immune system activation and superior anti-tumor efficacy, all the while maintaining the safety profile we've seen with earlier generations of ISAC. So to give you a sense of the improvements we've generated over time, I have here a few different examples of next generation ISACs, and all of these are going against slightly different targets. So HER2 is a target that we know well from our extensive work with our first generation product called BDC-1001. In this case, we looked at two different models of HER2 positive tumors. On the left here, you see a model that has very high levels of HER2 expression, and in this case, both the first generation ISAC and the next generation ISAC completely clear that tumor. This is in marked contrast to a naked antibody, which does not clear the tumor, and you can see the black line growing out on that. By contrast, when you have fewer HER2 markers on the surface of the tumor cell, it becomes more difficult to have anti-tumor activity. And what you see here in this second panel is that the antibody still does not impact the tumor. The first generation ISAC is not strong enough to get a significant response, but when we have our next generation payload, we start seeing significant anti-tumor activity. Similar story when you look at a target such as TROP-2 or a target such as CEA. So we're excited about the potential of these next generation payloads. Mechanistically, this is slightly different from the agonist antibody I walked through before. In this case, we're coding the tumor cell directly, so the antibody is targeting an antigen on the surface of the tumor cell, and it's the Fc region on the end of the antibody here that triggers the phagocytosis by the immune cell. Once that happens, the receptors for the immune response are on the inside of that immune cell. And so presenting the tumor cell, which is being chopped up, in the same area and the same context as the immune signal from the Toll-like receptor agonist, that's what creates that very tumor-specific anti-tumor effect. Similar to the other product we have, it also bridges to an adaptive immune response once you've started this innate immune response by targeting those myeloid cells. And just a little bit about the types of immune stimulants we use. We've explored a lot of different ones. We've found that a combination of both Toll-like receptor 7 and Toll-like receptor 8 gives us the best results. We believe this is because Toll-like receptor 7 is the only, good pattern recognition receptor on a certain subtype of dendritic cells called plasmacytoid dendritic cells. These are important to produce interferon alpha, which is one of those, cytokines that are really, good at producing an anti-tumor effect. Toll-like receptor 7 and 8 are both present on conventional dendritic cells, monocytes, and macrophages, and then Toll-like receptor 8 is only present on neutrophils. So you do not have Toll-like receptor 7 on neutrophils. So across the spectrum, we think that stimulating both of these is the best approach, and we've seen that empirically in our preclinical work as well. So recently, we discontinued our phase II program, known as BDC-1001. This was targeting HER2-positive cancers, and I just wanted to talk briefly about some of the lessons we learned from that effort. One is that our Boltbody ISACs can drive anti-tumor activity. We saw a number of patients with partial responses. We saw one patient with a complete response, so we know these drugs can help patients. We also saw very clear correlates of the activity in terms of the immune cells coming into the tumor environment, upregulation of markers showing that the macrophages were working, antigens were being presented, the T-cells were getting inflamed, and we also saw really good safety. So we know this can work, and what excites us is that the next generation of ISAC is much more potent, and we believe that w e can maintain a safe approach while getting a much better effect in terms of activity. So let me talk a little bit more about BDC-4182, so BDC-4182 is a Claudin 18.2 targeting antibody conjugated to a TLR7/8 agonist. And again, this is a next-generation payload, so it's much more potent than our first-generation payloads, and it produces a much stronger activity, both against TLR7 and against TLR8. We've clinically validated the target by looking at the development going on in Claudin 18.2 space. Zolbetuximab was recently approved and really highlights the ability to target this antigen and produce anti-tumor activity. We're excited about this because as we develop new therapies with our next-generation program, we're looking early on at our ability to compete against antibody drug conjugates. ADCs use cytotoxic payloads, and it's a way to deliver chemotherapy in a much more efficient way. In order to be competitive and really bring patient benefit, we need to be just as effective. And so our preclinical work is largely shifting towards showing our competitive advantage versus ADCs, and we'll be showing some of that at the upcoming SITC conference in the fall. So just a little bit about Claudin 18.2. You can see here expression patterns are very high in the stomach and not nearly as high in other tissue types. It is often seen in gastric, esophageal, also in pancreatic cancers. So we're gonna be starting with the gastric and gastroesophageal cancers as we start development of our Claudin 18.2 targeting ISAC. What we've seen in our preclinical work is dramatically enhanced immune activation. Here, you can see a Claudin 18.2 ISAC we created with our first-generation payload in blue. It is hard to distinguish from the antibody itself, which is in black, also on the axis here. And then with the next-generation payload, you get a dramatic increase in cytokine secretion. And we saw this in a number of cytokines and chemokines, so this is one example of what we see, but it's why we're so excited about the next-generation payload. We've completed toxicology, and we believe that the maximum tolerated dose will be 12 milligrams per kilogram or higher. The changes that we saw in toxicology were consistent with Claudin 18.2, so you can have some gastric irritation, nausea, things like that. And that's what we're gonna be watching for in the clinic as we develop this program. But we're excited 'cause very strong signals of immune activation and a very different profile from what you'd see with a toxic ADC. A few more preclinical models that we've done. This one on the left is in high Claudin 18.2 expressing tumors. So IHC 3+ is a proxy for how much claudin is being expressed, whereas one plus is a much lower level of expression. You can see in those higher-expressing models of gastric cancer, we perform quite well. And if you look at the naked antibody or a controlled ISAC, it doesn't really impact the tumor at all. We continue to have activity even at lower expressing, harder to treat tumors, such as this pancreatic tumor model, the PaTu model. So we're very excited about that potential. And I mentioned a little bit about some of the work we're doing comparing our drugs to ADCs, and here you can see a great example of that. On the left is a high antigen density model, and in this case, the isotype antibody doesn't have any impact on the tumor. So you can see the tumor growth there. When you have an MMAE ADC, and that's a certain type of cytotoxic payload, that's in blue, you can see you actually get pretty good tumor control. And then in the ISAC in red, we get about the same tumor control, maybe a little better. But the difference is really striking when you go to that medium antigen density model. In that model, the ADC loses activity, starts to look like the antibody itself, whereas our Claudin 18.2 ISAC maintains very strong anti-tumor activity. This is what we're excited about, is the ability to compete, and to go up against lower antigen tumors and still have a meaningful anti-tumor effect. Finally, I should mention the memory. The immune activation produces a very durable anti-tumor effect. To explore this in preclinical models, we first cure animals with our treatment, and then we rechallenge the animals. You can see here that the T cells present in those animals prevent the tumor from regrowing. If you deplete the T cells, the tumor grows out. We know that the T cells are the component of the immune system that is surveilling and preventing recurrence. And when you do not deplete them on the green line, you can see you get no tumors growing out. Similarly, another point here is that we see epitope spreading. So in these models, we engineer in Claudin 18.2, but in the rechallenge, we used a tumor that did not have Claudin 18.2 engineered in, so it was the parental tumor line. And once again, T cells are required, so without T cells, it grows out. But the immune response has spread beyond Claudin 18.2 to locate other antigens within that parental tumor line. So even without that Claudin 18 expression, it fights off the rechallenge. So we're excited about the potential for immunotherapy, both to treat that tumor and also to prevent recurrence and to not allow the tumors to escape. So that's really the story of Bolt Biotherapeutics. We're well capitalized, we have an interesting pipeline, we have some great partnerships, and we're harnessing the power of the immune system to improve lives and eradicate cancer. So thank you for the opportunity to present today. Thank you, Willie, for taking the time to present, and thank you to everyone joining in to listen. Have a great day. Thanks, Steve.