My name's Herb Cross. I'm the Chief Financial Officer of Jasper Therapeutics. I'll be walking through the corporate presentation today, and if we have a few minutes at the end, happy to field any questions. So safe harbor, I will be making forward-looking statements. We're a public company. I'd refer you to our filings and our risk factors to make sure you're aware of everything associated with the company. So, Jasper is focused on development of our lead asset briquilimab. It's a monoclonal antibody, an aglycosylated monoclonal antibody, that we're developing in mast cell driven diseases. Currently, we have studies underway in chronic spontaneous urticaria as well as CIndU, chronic inducible urticaria. And we announced a couple weeks back via a KOL event that we're actually also going to be starting a clinical program in asthma with briquilimab later this year, and so I'll touch on each of those indications as we step through the program. So currently, from a portfolio perspective, as I indicated, we're in phase 1b/2a studies in both CSU and CIndU, asthma starting later this year. The company did early on begin developing this asset in stem cell transplant conditioning regimens for transplant. That has been deprioritized at this point, and our primary focus is on mast cell-driven diseases. So mast cells, for those that maybe aren't as familiar with the space, they're very potent drivers of inflammatory responses kind of throughout the body, in the skin, which is a main driver for urticarias, as well as in the lung, which can drive asthma, atopic derm, and other respiratory diseases, and the gut. They are triggered by allergens, viruses, other environmental factors, that can often be confounding when trying to diagnose and treat these indications. The reality is, specifically in the skin, mast cells are somewhat antiquated cells. They were originally kind of there to address poisonous stings and other things like that that don't happen as often nowadays in the more modern world, and so they are somewhat antiquated, and we believe you can actually live very comfortably without mast cells. So when we really look across the diseases that mast cells are drivers, you know, there's a list here: asthma, atopic derm, chronic rhinosinusitis. There's probably north of 30+ potential indications where mast cell inhibition or mast cell depletion, our focus is on depletion, could be a viable therapeutic mechanism. And there are a number of therapies targeting mast cells that are already approved. However, most of those are inhibitory. The truly depleting mast cells, which is something we believe we can achieve with briquilimab, is a relatively novel mechanism in most of these indications. So again, depleting mast cells. So our antibody targets c-Kit. It hits the ligand binding domain for stem cell factor on mast cells, and by binding that domain and preventing stem cell factor from binding to the mast cell and depriving the mast cell of SCF, you actually drive the mast cell down an irreversible apoptotic pathway. And so it goes into apoptosis, it dies, and it's cleared by phagocytosis, so it actually truly is depleted and removed from the system. You know, the recovery of mast cells, again, they are very energy-dependent cells as far as what it takes to regenerate them. Data actually released by Celldex in this space has shown that mast cells can take three to maybe as many as four-five months to regenerate in the skin and in other areas of the body. So once you've depleted them, they stay depleted for a fairly long period of time, which gives you a nice window of disease relief to the extent they are the primary driver of disease. So looking at mast cells, again, as I articulated earlier, you can see here there's a number of different companies with a number of different molecules targeting a number of different aspects of the inflammatory pathway related to or around mast cells. Again, with the exception of Barzo, which is Celldex's antibody and briquilimab, which we're developing, these are all, for the most part, inhibitory. They're inhibiting the mast cell from degranulating in one way, shape, or form, but they're not actually eliminating the mast cell. They're not actually eliminating the source of the disease. Our approach of targeting c-Kit and driving the mast cells into apoptosis actually eliminates, in many cases, the disease driver at its source. So Celldex has shown here, this is Barzo data. We're still in our phase 1b/2a, but one piece of data here that Celldex showed, as I mentioned earlier, when you actually dose with an anti-c-Kit antibody, and you drive mast cells into apoptosis and deplete them, it actually takes a significant period of time for those mast cells to return. Tryptase, which is on the right graph, right from my perspective and yours, is actually a biomarker that is a leading indicator of the return of mast cells. As you'll see in the left panel, the skin mast cells specifically, it was as much as 18-24 weeks before those started to return to pre-dose levels, and this was based on a single dose of their anti-c-Kit antibody. The tryptase increases that we start to see a little earlier at 12 or 18 months, we believe are likely due to increases in the gut and the lung mast cells, which are frankly more active and more used mast cells, and so those we believe repopulate first, driving some of that tryptase, but again, the skin mast cells, we generally don't see them repopulating until as much as 18-24 months, which again, provides a really nice therapeutic window, for potential what we refer to as optimal biologic dosing. This is our own healthy volunteer study that was done by Amgen with briquilimab, our model, which is, we did acquire briquilimab from Amgen many years ago. What we showed here is, as you can see, we have a nice dose-dependent mast cell depletion curve. And so as we kind of look at this data, this actually helped us target in on our dose that we're using in our initial urticaria studies. As you can see, lower doses in kind of the 42 mg didn't have a profound effect. At 84 mg, you start to see some significant mast cell depletion, and you really start to see a dose-dependent drop at 158 mg and when they got out to 280 mg. So again, you know, with very reasonable doses and doses that could be a single injection here, we've seen significant mast cell depletion that we think can drive therapeutic benefit. So I referred earlier to optimal biologic dosing, so this is a schema that gives a little visibility into that. In diseases like the urticarias, where the mast cell is the primary driver of the disease, our optimal biologic dosing approach is to dose with briquilimab, deplete the mast cells down to a level where you have relief from the disease, and then let the drug clear. Let the patient proceed with kind of a drug-free interval until the return of those mast cells, and then redose at that point to drive the mast cells back down again. The primary reason for this approach is, you know, like anything else, you do have other mast cell... Or sorry, c-Kit is presented on other cells in the body, and so there are on-target side effects like graying of the hair, impact on the taste, that patients dosed with depletion of mast cells do see that are dosed with c-Kit antibodies. By taking this optimal biologic dosing approach, we believe we can hopefully minimize those side effects for patients, while at the same time giving them durable disease control and a manageable dosing regimen. From a safety perspective, again, there are, as I mentioned, there are other cells that, anti-c-Kit, that do, present c-Kit, and so anti-c-Kit antibodies do hit. Stem cells is one. If you block SCF on stem cells via blocking c-Kit, you actually drive, ultimately will drive stem cells into more of a, down a platelet lineage. It is not a single survival, pathway for stem cells, so you actually don't drive stem cells into apoptosis. Those are very important cells, and so they have multiple redundant survival pathways. Things like melanocyte that drive melanin production, you know, you do see some transient reduction in those, and at high enough dose levels, you can start to see graying of the patient's hair. So a side effect that we're obviously watching, and Celldex has seen in their study and, and you know, we may see in ours, and but that's manageable. You know, spermatogenesis can be impacted by this, but again, you're not impacting the pre-spermatogonia stem cells. You're basically causing very reversible reductions in sperm count. So going off drug or having a dose-free interval via optimal biologic dosing can actually address that. And then again, from a taste perspective, you do see some potential impact there. But again, all these impacts we've seen are mild, transient, and they are reversible either during a dose-free interval or if you come off drug. So the safety profile to date, again, you know, relatively low frequency of ADAs. You know, we did a NHP chronic tox study, and you know, saw some of the side effects that I mentioned, the graying hair, but only at very high doses. So overall, a solid safety profile at this stage of development, and again, we're now actively developing it in CSU and CIndU and soon to be asthma in the target patient populations. So kind of the summary here, you know, again, mast cells depletion can be driven by c-Kit antibodies. That can start in a matter of days to weeks. You can see very durable, again, very durable depletion of mast cells. It takes mast cells a significant amount of time, which gives you a nice therapeutic window. And again, there already is clinical validation for this mechanism. Celldex has presented very good data in both CIndU and CSU, as well as PN. So, that's where we're headed. So, speaking specifically to chronic urticaria, this is our lead program right now, the BEACON trial. It's a phase 1b/2a study in patients with CSU. We began enrolling it earlier this year. Our most recent update, this is the study schema, our most recent update was as of our year, our Q1 earnings release, which was a few weeks back. We were enrolling in the 80 mg Q8 weekly cohort, so the third cohort. And we had actually already enrolled enough patients in that cohort that we had been through the safety review and had been cleared from a safety perspective to proceed with the 120 mg cohort once we completed enrolling in the 80 mg. So we're making good progress on this. Right now, as you'll see, we're actually exploring really two different dosing timelines, multiple doses. It's your typical dose-ascending study to really identify both the safety and efficacy around ascending doses. But, you know, we're also exploring two different timelines from a dosing perspective. We have a Q8 weekly timeline, which we're exploring at 80 mgs and 120 mgs, and then we're going to explore a Q12 weekly dosing regimen at 120 mgs and 180 mgs. And so I think the... Right now, we've guided to presenting initial data and interim data look on the first four cohorts, so that's the 10 mg, the 40 mg, the 80 mg at Q8 weekly, and the 120 mg at Q8 weekly, in the third quarter of this year, and we continue to be on track to meet that timeline. The subsequent cohorts, the 120 mg Q12 weekly and the 180 mg Q12 weekly, will come later in the year, as well as the 240 mg, which is a cohort we added that's a single dose, a very high dose, intending to drive deep mast cell depletion and then allow us to follow those patients to really be in a position to kind of create our own data around the timeline for the replenishment of the mast cells. So the second study that we started this year is in CIndU, chronic inducible urticaria. Similar to the CSU study, you know, really is a multi-dose ascending dose study intended to basically suss out both safety and efficacy in this patient population. You know, I think the—for those of you that aren't familiar with CIndU, there's multiple different varieties of it. We're looking basically at two, symptomatic dermographism and cold urticaria. So that's symptomatic dermographism, graphism is when patients respond and develop rash and wheals as a result of pressure being put on their skin, and cold urticaria is exactly what it sounds like, similar symptoms as a result of being exposed to cold. These are effectively both challenge studies, so they will be dosed with the drug and then basically exposed to the insult that typically drives that after having been benchmarked in the initial visit. We are exploring two doses here, 40 mg, and again, I would say the 40 mg dose in this indication, as well as the 10 mg and 40 mg doses in the CSU indication, are really below kind of the levels at which we saw efficacy in the healthy volunteer study. But we wanna make sure as part of these programs, we're also complying with FDA guidelines around exploring minimum efficacious doses as well. So I think while at 10 mg and 40 mg, we're not necessarily expecting robust efficacy, we wanna have stepped through that process as part of this initial study. Here, we're moving to then a 120 mg dose, or sorry, a 120 mg dose. And again, this is a single-dose study and looking for reaction to the stimuli on the other side of that. This study is well underway, and we've guided to data on this study in the second half of this year as well. So the second half of this year, we'll be showing both CSU as well as CIndU data. So moving to asthma. So we only recently announced about two weeks ago that we had selected asthma as our third mast cell-driven indication. We did a nice KOL event with Dr. Josh Boyce. That KOL event, the webcast of that is actually up on our website. For those of you who didn't have a chance to tune into that, I encourage you to look at it. Dr. Boyce was excellent, and a lot of the scientific rationale behind our selection of asthma is laid out there. So asthma is an indication where mast cells are a key driver. They are not only contribute in early asthma through degranulation to the inflammatory reaction, they also play a role in recruiting additional inflammatory cells in later phases of asthma. So they are a key player in the inflammation associated with asthma. And so, again, with our antibody, the ability to deplete those cells and take them out of the equation, we believe will show-- could, could potentially show significant benefit for patients. We have some preclinical data that was generated here. Amgen did some work, when they initially explored this antibody in IPF years past, in African green monkeys, lung cell counts in African green monkeys, and as you can see, showed basically significant reductions in mast cells and dose-dependent reductions in mast cells. And then we did work with our own proprietary Jasper c-Kit mouse, which has the human c-Kit binding region, so that we can actually do preclinical work with the human antibody. And as you can see here, we saw significant reduction in the impact of allergens on pulmonary function in the mice by basically depleting mast cells via briquilimab. So these were two pieces of... and again, a challenge study there as well, so response to a specific stimuli. These are two pieces of preclinical data that weighed heavily in our decision to select asthma among a myriad of indications we were evaluating. The other kind of factor was we felt like there was actually good clinical validation out there for an anti-c-Kit mechanism in asthma. Both imatinib had phase II data in a challenge model that showed good patient response, and masitinib actually showed, if memory serves, in the neighborhood of 30%+ reduction in exacerbations in their phase III data. Now, masitinib obviously had some toxicity issues, which is why it ultimately wasn't advanced, their off-target toxicity. But again, from our perspective, good clinical validation of the c-Kit mechanism in asthma of anti-c-Kit antibody or anti-c-Kit targeting in asthma. So this was another aspect of the data that really led us to asthma as our next indication. So as a result of that, we announced we're gonna be starting a phase 1b/2a asthma challenge study this year. We will start that by year-end; we expect to dose the first patient. That will be a challenge study, so the patient will be exposed to an allergen. Their response will be measured and recorded. They will receive a dose of briquilimab. Some time will pass for the mast cells to deplete, and then they'll come in and be rechallenged with the same allergen. We expect to be in a position to report data in that study in the second half of next year. And then from there, we'll move on to additional studies as warranted. So again, in asthma, you know, it's not like CSU, where in CSU, the mast cell is the primary driver. If anything, the mast cell is part of a, you know, milieu of things affecting asthma patients, but it is a major player because not only, again, does the degranulation associated with mast cells being triggered lead to that inflammation, but they do play a role recruiting other inflammatory cells as well. So we do feel there's a strong scientific basis for moving into asthma here. So the broader market opportunity in mast cell-driven diseases, so this slide is specific to CSU. Again, you know, these are a little bit dated, but they're kind of the best data we have. Approximately 3.5 million is the overall size of the estimated chronic urticaria market. That's inclusive of CSU and CIndU. And right now, you know, it's very underserved from a biologics perspective. As you can see, only about 150,000 patients in CSU, for example, are receiving Xolair based on, again, the data at the time this slide was prepared. But, you know, there's, you know, over 1.3-1.4 million patients that are moderate to severe and inadequately controlled with their antihistamines. And for a lot of these patients, they are taking 3x-4 x the kind of approved dose of these antihistamines in order for it to be effective and have an impact, and that very much takes a toll on them from a lifestyle perspective, a quality of life perspective. So we feel the urticarias, there's a tremendous unmet need there for therapeutics that can be efficacious but safe and not dramatically impact quality of life. And again, here, as you can see, you know, there's a number of different companies, as per my earlier slide, taking a number of different approaches to try and address, address the urticarias. You know, I think, again, most of these, with the exception of c-Kit, you'll notice it's either inhibiting cytokines or signal inhibition, effectively inhibiting the mast cell's function, but not actually addressing the mast cell, which raises the obvious issue if patients aren't compliant, if they go off drug, if they forget to take their medication, those mast cells are still there, and they can very quickly start to see symptoms again, and their disease can crop back up. Whereas depletion is the only mechanism that can presumably really take the symptoms off the table, assuming you can do it in a safe and efficacious way. So again, briquilimab, you know, is one of two c-Kit antibodies for depletion and development right now. Celldex's Barzo is the other. You know, for us, relatively speaking, we, the relative differentiators is a question we often get. We directly bind the ligand for stem cell factor on c-Kit, so we actually prevent stem cell factor from binding. You know, other antibodies in development really take more of a dimerization approach. We do have a shorter half-life, which we think also plays well with our optimal biologic approach, the curve that I showed earlier around dosing and then letting the drug clear so that the patient can have a drug-free interval, where they're less likely to have on-target side effects and then redose only once the mast cells return. And again, I think, you know, we believe that the, the, the makeup of the drug allows for that optimized dosing profile, and so that's what we're exploring in, in the current studies. More broadly, mast cells, again, here's a list of diseases in both derm, respiratory, gastrointestinal, where mast cells are either the primary driver or play a key role in mast cell-mediated diseases. We looked at north of 20 of these diseases, did preclinical work in them, and again, ultimately, decided on asthma as our next indication. But there are, you know, a number of other indications. There's clinical proof of concept in prurigo nodularis right now out there, in EoE. Again, another company is exploring atopic dermatitis, so I think there are a number of indications, you know, for depletion, where depletion of mast cell can be impactful. So we like to refer, it's a little bit cliché, and I'll apologize in advance, but we do like to refer to this as a bit of a portfolio and a product, right? There are a number of indications we can pursue beyond even what we're doing right now. I mentioned earlier our c-Kit mouse. Again, it's a proprietary mouse, where we actually have the human extracellular domain in there so that we can actually use it to drive actual preclinical data using the human antibody briquilimab. It's a great tool for us. We can use it in a number of different disease models, and it's been a real benefit, and again, contributed heavily to the preclinical data that we presented at EAACI, which I showed a panel from earlier, not that long ago, and which really helped drive our decision to advance into asthma. So, I've already shown you the portfolio. I won't reiterate that again. Again, key milestones, so CSU, initial data from that program in the third quarter of this year on those first four cohorts. CIndU, we're currently guiding to data in the second half of this year. That study got started a little later, so we're still early in enrollment in that, so we haven't tightened up guidance beyond second half of this year. And then again, asthma, we would expect to dose first patient in before the end of the year, and that should put us on a timeline to have data, back half of next year as well. Sorry. Financial overview, we currently have about, as of 3/31, we had $118.5 million in cash on hand, and current guidance is that gives us cash runway into the fourth quarter of 2025 or through the third quarter of 2025. So that's, that's Jasper in a nutshell. I have, I have 1 minute and 38 seconds if anybody has a question. Great. Thank you for your time.