Some of the recent milestones you've had. Sure. First, Emily, thank you to you and to the company for having us today. It's a pleasure on behalf of all my colleagues here at Jasper to present the company today. Jasper Therapeutics, our lead program is based on an antibody, briquilimab, that specifically targets the epitope on the receptor of c-Kit on mast cells. We are currently in two clinical trials in urticarias. One is in chronic spontaneous urticaria, and that study is known as the Beacon study. We have another clinical trial known as the Spotlight study in inducible urticarias. We also have a third clinical trial in asthma, in allergic asthma. Three important clinical trials that we're operating with our antibody, all targeting mast cell diseases. Those clinical trials, we had a readout initially at the end of last year on the first two cohorts from the Spotlight clinical trial in inducible urticaria, which showed dramatic responses there and complete resolution of disease for a period of time with a single dose at the 120 milligrams. On that clinical trial, the Spotlight clinical trial, we will have an additional readout from the 180 milligram cohort patient population in the first half of this year. On the Beacon study in chronic spontaneous urticaria, we had an initial readout from that clinical trial in January of this year. Those data were then presented at Quad AI as the late breaker for that section. We will have another significant amount of data that will come in midyear. Awesome. As you mentioned, briquilimab targets c-Kit, which plays a significant role in mast cells. How might this target be advantageous for urticarias relative to other targets that are being developed, like IL-33, BTK, and IL-4 receptor? Yeah. Maybe to start out at the 20,000-foot level, there are two approaches to a mast cell. Mast cells in these diseases are healthy, but there is something in the immune system that is triggering the mast cell. Otherwise, the mast cell is normal and healthy. There are two approaches to targeting a mast cell. One approach is inhibition, and that is with drugs like omalizumab or remibrutinib or even a small molecule, wild types. They cannot deplete the mast cell. On the other hand, there is the approach like we are taking that actually depletes the mast cell. What is known about the mast cell is that c-Kit is the primary survival pathway. If you shut down c-Kit, you shut down all phosphorylation, which then controls FOXO3A. When FOXO3A is shut down, BIM is then upregulated and initiates apoptosis, making the mast cell die. All of the other approaches can't do that. They're not able to initiate apoptosis. We believe a superior approach here is to deplete a mast cell and give a patient a long and durable response, as opposed to inhibition, where with those therapies, they need to maintain 24/7, 365 inhibition, or as soon as they fall below a concentration to inhibit the mast cell, the symptoms will come right back for those patients. Great. We have started to see a significant amount of data from c-Kit inhibitors with briquilimab, omalizumab, and also oral kit inhibitors. How does briquilimab differ from these other assets? Now that you have seen some clinical data, where do you see potential for differentiation? Sure. Maybe I'll start with the wild type c-Kit small molecules. While it's encouraging that there might be another therapy available for CSU patients sometime in the future with a small molecule, from the initial data read from those data, again, even when they're dosing at levels above IC90, they were not depleting the mast cell. How do we come to that conclusion? It's based on their data. As soon as their drug cleared, the tryptase came right back, thereby meaning that those mast cells were only inhibited and not depleted. Significant amount of drug on board to get above an IC90, but not depleting the mast cell. From a safety standpoint and a product differentiation, that could be a challenge for them as well. With the small molecule, they observed 64% graying within the first 14 days, which means that they're really saturating those other c-Kit presenting cells like the melanocytes to see that level of graying in 14 short days. Now, if we switch over to the antibody side and comparing our approach to barzolvolimab, structurally, the antibodies are really different. They share three common characteristics. They're both humanized IgG1 aglycosylated antibodies. However, at that point, the similarities really end from how the antibodies are constructed to nullify the FC. We've only made one single change to our antibody to nullify the FC. They've made six. May end up conferring a difference in ADAs. It's known in the antibody field, the more structural changes you make, the higher likelihood you are of having ADAs, and the early data suggest that. I think more importantly than that, though, is their antibody is an anti-dimerization antibody, which means that they have the possibility of not fully shutting down that signal because SCF can still bind in the presence of barzolvolimab, where with briquilimab, we have a higher affinity and avidity than the natural ligand. So we know we shut down all downstream signaling. I think the last piece, though, is really the half-life. They engineered their antibody to have a longer half-life. Their antibody, their half-life is 21 or 22 days. Our antibody half-life is only about nine days. In a drug like, in a disease like CSU or depleting mast cells, where c-Kit is present on other cell types, like melanocytes, taste buds, stem cells, that we believe you follow the biology. The biology of the mast cell is that that irreversible apoptosis will happen within hours. Those mast cells are all cleared from the system in 7-14 days. It takes a while for those mast cells to come back. You don't need to have the antibody on board. If you do, that antibody is just going to hit those other c-Kit presenting cells. We think play into our rapid Tmax, high Cmax, clear the drug out and not bring the drug back on board. Celldex, on the other hand, is dosing more to an AUC model. What you see is it's starting to now play itself out in a difference in a safety profile that they get the early adverse events to c-Kit, but then they see an increase in those adverse events over time because they're never giving those cells a break, and they're constantly saturating these other c-Kit presenting cells with no advantage or increase in efficacy. Great. Maybe you can summarize the recent Beacon data that you presented and also kind of walk us through what we should be expecting for the update in mid-2025. Sure. The Beacon study was designed to test this optimal biologic dose hypothesis. In the Beacon study, we have a number of different dose levels and dose intervals. What we observed through the first seven cohorts there through the 240 milligram as a single dose is that briquilimab demonstrated that it can rapidly get out of the SubQ compartment and get to the mast cells. What we observed is that in our doses above 120 milligrams and above, so 120 milligrams, 180 milligrams, and 240 milligrams, within a week, we saw substantial reduction in the UAS7 scores of these patients. Within a week, we saw tryptase levels drop below LLOQ. What we saw in the case of the 240 milligram was that within a week, we drove the UAS7 score to zero, so a complete response in three out of three patients. With a single dose, that complete response was maintained through eight full weeks of the drug, which again matched the half-life and the clearance of the drug. It tells us that we have a drug that can drive complete responses in these patients with an associated tolerable safety profile, a safety profile that when we do see these c-Kit related adverse events, they're mild, transient, and self-resolved before the next dose. Obviously, the data you observed in the 240 mg cohort was very positive, but also the small cohort of patients. What do you think would be positive and competitive in a larger patient population at such a dose? What are you kind of hoping to see with more patients added in the update later this year? Yeah. Let me first talk about the data that'll be coming midyear. In the midyear, we'll have more patients in the 240 single dose. We'll have a total of eight patients. The N of three will go to eight on 240 as a single dose. We also went up to 360 as a single dose. We'll have eight patients in the 360 as a single dose. We'll also have eight patients on a 240 Q8 week dose. We'll be able to see what happens when you repeat dose the 240. We'll have eight patients at the 240 as an induction dose followed by 180 Q8 week. In addition to that, all the patients in the Beacon study are now eligible to roll over into the open label extension. The open label extension is 180 milligram Q8 week dosing. We would anticipate midyear having 20-25 patients on the open label extension that have had multiple doses at the 180 mg level. There will be a significant amount of data that will be coming that will show us at these dose levels that are probably the higher efficacious doses. We will be able to see in repeat dosing with the 240 mg, importantly, are we able to maintain those complete responses, the durability of the disease, as well as the safety profile of repeat dosing? Yeah. We've talked quite a bit about long-term efficacy and safety for barzolvolimab. What would you be hoping to see longer term with briquilimab in terms of efficacy and also safety? Yeah. We would, based on the properties of the antibody and our dose and schedule, that the 240 milligram level, so even at that highest level to date, now we'll need to see the 360, but the 240 is cleared at eight weeks. We won't be having drug accumulation. What we would anticipate seeing with longer-term follow-up on these patients is not having the drug accumulation. Not seeing what barzolvolimab saw when they had their 16-week data and then their 52-week data, there was a significant increase in these AEs because they were having drug accumulation and never giving these c-Kit cells a break. We would anticipate that we would either not see that or have a reduced amount compared to what barzolvolimab has observed. We would also expect to see a continued trend of what we've seen so far through the 240 milligram is that all of these adverse events were grade one, so mild, transient, self-resolved before the next dose. None of these patients required a drug holiday, a drug dose adjustment, or had to discontinue their dose. That's a meaningfully different experience than what patients see with barzolvolimab. Okay. Great. You also recently announced your phase 2b/3 strategy. Can you discuss your plans there and how far that leaves you behind barzolvolimab's phase 3 program? Sure. Based on all this data we'll have at the midyear, we will be able to select the two doses to take into our phase 2b. Our phase 2b that we've proposed to the regulators is an operationally adaptive design. That study will run. At the conclusion of that study, we'll be able to roll seamlessly into our phase 3 the dose that we choose from the phase 2b portion of that study. We'll save anywhere from three to six months in the normal transition and maybe even longer. If we look at the barzolvolimab timeline from finishing their study to getting into the phase 3, that was more like nine plus months. We'll be able to roll directly into that study. It's also important to note that that phase three clinical trial, because we'll only be taking one dose into that study, will likely be required to enroll significantly less patients than what they did. Their safety database is requiring 2,200-2,300 patients, where we would anticipate we would need to enroll somewhere between 1,300 and 1,500 patients. So 500-700 patients less than what they need to enroll. That's a significant time advantage as well. When we put all of that together, we think we're 12-18 months behind barzolvolimab. Okay. Great. Maybe a question for Herb. In terms of capital for these phase 2b/3 studies, maybe just touch on how much cash you have on hand and ability to finance these trials. Sure. Absolutely. Thanks, Emily. As of year end, we had about $71 million in cash on hand and kind of current guidance on that has been consistent that that represents cash through the third quarter of this year and into the fourth quarter. I think as we sit today, obviously in somewhat challenging capital markets right now, I do not think anybody would contest. I think we are really looking at a couple of different mechanisms to fund that. Obviously, equity capital is certainly on the table, and we may very well choose to bolster the balance sheet in advance of that midyear data update. I think maybe the potentially better approach, or maybe an approach used in combination with equity capital, would be non-dilutive capital. I think we have had significant interest for a long period of time now from pharma and big biotech investors on the strategic side in this asset. I think they recognize how compelling this mechanism can be and the potential size of the markets that this mechanism can address. I think a broader collaboration could not only obviously help address the ongoing spend from a cost split perspective, but we would expect would bring a meaningful upfront as well that would help fund that next kind of stage of development. I think we view both of those as being on the table. In markets like this, we're really focused on kind of finding the right window and picking the right approach to manage dilution for our existing investors, but to make sure that we're putting the asset in the best position to be able to get this thing to market as rapidly as possible. Okay. Great. Maybe for our last few minutes, we could touch on the asthma program. Obviously, that's also in phase two currently. Maybe just spend a couple of minutes talking about how briquilimab could be an effective treatment for asthma and how c-Kit plays a role in asthma exacerbations and also maybe sets of expectations for the data later this year. Sure. We're really excited about that program and the data that this trial can provide us with. That study is being conducted in mild asthmatics. I'll come back and talk to you about that. To your question about the mechanism of action in the mast cells, it's known that mast cells are sort of the conductor in the orchestra. In the release phase, the initial phase of asthma, mast cells are responsible for releasing histamine, prostaglandin, R2, a whole myriad of things that the mast cells release to really create an asthmatic attack. We think that it holds promise if we're able to deplete the mast cell and thereby reduce or even potentially eliminate that release phase. That could be significant in this disease. Mast cells are also known to be an important immune cell in the recruitment phase. One of the things that they recruit are eosinophils. If by reducing or eliminating the mast cells in the lung, can we block or reduce the recruitment of eosinophils? That could be really interesting and important as well because, as you know, the endotypes currently for treatment are driven by eosinophil levels. That could be really interesting as well. By extension, all of that and mast cells are involved in remodeling that this could then be really interesting in diseases like COPD. This first readout will be really interesting and important here to see if we can deplete the mast cells at the same level that we're depleting them in the skin. Tryptase levels from the Beacon study and the Spotlight study would tell us that because if you're driving tryptase below LLOQ, tryptase is a total measurement of total body mast cells, not just skin mast cells. That tells us that we are depleting the mast cells in the lung for a period of time. This study will be really interesting. The primary endpoint is six-week EAR and LAR in mild asthmatics. We will also be looking at an additional six-week or 12-week endpoint follow-up on these patients as well. That study will read out in the second half of this year. Okay. Great. A lot of updates coming up this year. It should be a very exciting year for you. I guess we will end it here. Thank you very much, Ronald and Herb, for joining and everyone else for listening and tuning in. Please enjoy the rest of your days. Wonderful. Thank you, Emily. Appreciate the support. Take care. Thanks.