Good morning. Thank you for joining the Processa Pharmaceuticals presentation. It's my pleasure to introduce Sheila Gujrathi, Founder and Executive Chair of Vidya Therapeutics, which has recently entered into a merger agreement with Processa Pharmaceuticals. With that, I'll hand it off to Sheila. Great. Thanks, Nate. Thanks everyone for coming. I'm really thrilled to be here and present an overview of Processa and also the Vidya transaction that we just did. Can you guys see the slides here? Okay, great. We'll be going through a company overview. This is our disclaimer slide and our forward-looking statements. I will be making forward-looking statements and so this is our safe harbor slide. Actually about a month ago, Processa merged with Vidya. This was a stock-for-stock transaction. Basically, Processa acquired Vidya, and we did a non-converting preferred shares as well. At the same time, we did a $200 million pipe. The gross proceeds came in at the end of July, so it's been, again, about a month. With that gross proceeds, we have a runway well to the second half of 2029, which is very exciting. It gave us the capital to be able to advance VT-7208 very rapidly into parallel development that I'll be reviewing with you. We had an amazing group of investors that came into the syndicate, as you can see here on the slide. Just really terrific investors, many people who we've been speaking to for some period of time. So we're really thrilled to see this type of support for Processa and for the Vidya program, VT-7208. As part of that transaction, I joined the board of directors. So my name is Sheila Gujrathi. I am a board member at Processa. I am the founder and executive chair of Vidya Therapeutics. I have a significant background in clinical medicine and immunology drug development. I'm a clinician trained in internal medicine, allergy, immunology. Spent some time at McKinsey, Genentech. I ran immunology at BMS, and I've been in many small companies. I was a CMO of Receptos, a former CEO of Gossamer, and really now starting to do many startups. So really thrilled to see the outcome for this deal with Processa, and really thrilled to be working with the Processa team. So, what we're here to talk about today is giving you more of an overview about VT-7208. Now it's become the lead program for Processa. VT-7208 really has this amazing pipeline and a product opportunity and optionality from a single optimized molecule. VT-7208 has been engineered to be a next generation, potential best-in-class BTK inhibitor that was really designed to address the efficacy and safety limitations and liabilities of earlier generation programs. So again, there's a lot of intentional engineering that has gone into VT-7208 that took a number of years actually to get to this profile. Again, we're really excited about the potential low dose, once daily oral dosing for VT-7208. We spent some time thinking about the development indications. As you're going to see on the next slide, we actually have a lot of different options to go after. But through a number of very informed discussions, we came up with this parallel development strategy. We are very excited about going into food allergy and chronic spontaneous urticaria on the peripheral systemic side for immune diseases. Then for neuroinflammation, we're pursuing relapsing MS. Those are three phase II trials that we're going to be kicking off. The phase I is complete. I'll be sharing some of the data with you later in the presentation. In terms of the cadence and the execution timelines, our goal is to get food allergy and CSU initiated in the second half of this year, with data readouts for food allergy being in the second half of 2027, and for CSU the first half of 2028. Then for relapsing MS, and we have a lot of really ideal CNS penetration for this indication. We'll be initiating that trial in the first half of 2027 with the goal of reading out the MS study in the second half of 2028. So a really nice set of cadence for data milestones and value inflection milestones coming up for VT-7208, really in the next one to two years. Again, this is a very exciting opportunity at this time. BTK is a high-value target. It has been clinically validated now substantially in the immunology area. BTK inhibitors either have regulatory approval or positive proof-of-concept data in about 10 indications outside of oncology, and this list is growing. There are BTK inhibitors that are approved in CSU, ITP, GVHD, and non-relapsing secondary progressive MS. There is clinical proof of concept through robust phase II studies that have been demonstrated in other relapsing forms of MS and progressive forms of MS, food allergy, Sjogren's syndrome, HS, PMR, lupus, and the list is growing. Again, a very exciting time for BTK. Our thoughts behind pursuing food allergy and CSU as well as neuroinflammation is that again, it expands the optionality for this program. Food allergy and CSU provide near-term validation endpoints and opportunities for BTK. These are fast, capital-efficient proof-of-concept studies with endpoints at week four or week 12. So we can really rapidly enroll these trials and get quick data readouts while MS is the longer term upside with the great CNS penetration that we're seeing with our program. Of course, the phase II MS will also rapidly read out. Again, large markets CSU, 1.7 million patients are still not treated adequately with antihistamines. Food allergy, we're talking about 15 million patients who are still being treated by avoidance and emergency rescue treatment. Then all forms of MS continue to experience, or patients in these different subtypes continue to experience what we call PIRA, progression independent of relapse activity. That is a huge unmet need for the MS population. I have now developed many drugs in MS, including ocrelizumab and ozanimod, ZEPOSIA and OCREVUS. I can tell you still, there is so much unmet need for progressive MS patients who continue to have irreversible neurologic disability despite having relapses and MRI lesions controlled. We are really excited to bring BTK inhibitors into this space. Why is BTK such a compelling target, and how does it work in all these disease areas? BTK is what we consider really fundamental as a central node in the immunology area, really attacking both the adaptive and innate immune pathways. BTK inhibition really affects BCR signaling and leads to the reduction of B-cell proliferation, antigen presentation, autoantibody production, and cytokine secretion. Then on the innate side, is very important in inhibiting Fc receptor signaling and disrupting IgG, Fc gamma receptor signaling, as well as IgE, Fc epsilon receptor signaling, which then leads to, again, the reduction of cytokine secretion and myeloid cell proliferation. When you think about the cell types that we are going after, it is mast cells, basophils, and microglial cells. This is important, again, for both peripheral, systemic inflammation, as well as neuroinflammation. That is how you are seeing how one molecule and one mechanism can have such pleiotropic effects and have really affecting a number of disease areas, and that has led to really substantial ability to address unmet need across therapeutic areas. As I mentioned, VT-7208, it was really intentionally and rationally designed to overcome the earlier limitations that we saw from the first and second-generation compounds that have come out from oncology into immunology, and we spent a lot of time iterating on the profile. Of course, we wanted to focus on having a very potent and selective inhibitor. That is obviously really critical. We also made the choice to use a less reactive warhead. We are incorporating butenamide versus acrylamide, and this is very important because we have much less reactive metabolite formation, which is a key factor in potential hepatic toxicity risk. While we were doing this, we were really optimizing for CNS penetration. We now have head-to-head data from both murine and cyno studies, so mouse and monkey, showing that we have the most robust CNS exposure and CNS target engagement and occupancy than any other BTK inhibitor that is being studied currently in neuroinflammatory conditions. What that profile then resulted in is on this slide is potent in vitro and in vivo with strong peripheral and CNS target engagement. Really consistent efficacy across a number of disease models, including MS disease models, as well as autoantibody-driven preclinical models. A very clean metabolic profile. We do not have any substantial reactive metabolites or active metabolites with very predictable PK, which you are going to see that also played out in the clinic. Low hepatic toxicity risk, and this is true for all the scoring algorithms and risk assessments we performed. We also have a completed chronic tox package with six and nine-month rat and dog studies completed with wide safety margins, as you see here on the slide, really substantial safety margins. All of this led to our prediction of having a low once-daily oral dose. This is our phase I design, which we actually ran. It started end of last year, and we got the data earlier this year. We actually were able to start at 20 mg because of our wide safety margins, and we had modeled that this would be a potentially efficacious dose. We escalated to 60 mg, but we saw such excellent target occupancy with our initial doses that we actually dropped down to 5 mg to explore what would be our target engagement of that dose. Our criteria to move into the MAD was we wanted to see 95% target occupancy for greater than 24 hours. We well exceeded that, which I will show you on the subsequent slides. Then we went into our MAD. This was a seven-day dosing cohort. We studied 10 mg and 20 mg. We also did CSF sampling or lumbar punctures at day one and seven to look at our CNS exposure and a food effect cohort. Importantly, in addition to looking at PK safety tolerability as we typically do in phase I trials, we did important secondary assessments looking at receptor occupancy and phospho-BTK inhibition, and of course, the CSF exposure analysis. The safety of the phase I results really demonstrated a favorable safety and tolerability profile. As you see, there are a number of zeros on this slide, which is what we like to see. We had no SAEs or Grade 3 events. We had two mild headaches that resolved without any treatment. We had one Grade 3 event of arm pain at the site of multiple blood draws, so not clinically concerning, and again, no liver safety signals or bleeding event signals that were picked up in the phase I. Here is the PK profile of VT-7208. It really demonstrates consistent, well-behaved, predictable PK. We are seeing nice dose proportional increases here, as you see on the slide, with a median half-life of about six hours, which is really ideal for a covalent irreversible inhibitor. You actually come in, you covalently bind the target, and then you have this long-lasting pharmacodynamic effect. We call this a PK/PD disconnect. This is really ideal because you have, again, enough half-life to get the strong target engagement, but then you are rapidly cleared, so you do not have any systemic accumulation, which is, again, very favorable from a safety perspective. We think this is a really ideal PK profile for this type of a molecule that we have. Also, we had CSF exposure showing really nice CNS exposure as well. Based on that, we modeled that we would have excellent target engagement in the brain. This is the data slide that we got very excited about. This is actually looking at BTK target occupancy in the blood. As you see, we really saw near complete target occupancies. This is 99%-100% target occupancy at all doses studied, so 5 mg, 20 mg, and 60 mg. Really excellent data. As you can see, we were looking at 95% target occupancy for the first 24 hours, we had that for 48 hours. At 48 hours, the 5-mg dose group drops down to 95 target occupancy, and then it drops down to 90% at 72 hours. This type of durable, sustained inhibition and the complete inhibition we are seeing across dose levels in the first 24 hours, we think is very differentiated and distinct from what other BTK inhibitors have shown to date. It also gave us confidence in that QD once-daily profile, and that if patients miss a dose or two, they will not be affected. That again is a very important profile when you think about the indications that we are pursuing. Then, as you can see in the MAD cohort, really this flat line of BTK inhibition over time. In addition to looking at target occupancy, we also want to look at what we call functional inhibition. So we looked at the ability to block the downstream phosphorylation of BTK. So this is looking at phospho-BTK inhibition. As you can see, again, near complete phospho-BTK inhibition that lasts about three days after cessation of dosing. So really, again, long-lasting, durable effects. This is exactly the type of profile you want to see with this type of low-dose once-daily administration. We were really thrilled to see this data, and that gave us the confidence to then move rapidly into multiple phase II trials. So our phase I is complete, and we are in the process of initiating, again, these three phase II studies in parallel. We are just thrilled to be in this position where I think we are going after a very important target in the immunology disease areas. The translation that we have seen from preclinical to clinical has really borne out nicely. The clinical data is, I think, very compelling. The indications we are pursuing are really well-validated and with excellent regulatory pathways, so we know how to run these studies. They are also, again, very capital efficient. From a corporate strategic perspective, it enables us to do parallel development, which we are pursuing at this time with the timelines I mentioned to you. Really looking forward to getting these studies off the ground and being able to come back to you, hopefully, with very compelling clinical differentiated data. With that, I think I am open to taking some questions if you have any. Yes. Can you share some, can you work with more? Yes, sure. Remibrutinib, a very exciting drug, also known as Rhapsido, as you know, got approved in CSU last year and read out positive food allergy data earlier this year. They released that at the AAAAI, and recently also read out positive two studies in relapsing MS. So now that they have about 4,500 worth of patient data, which is compelling. Some of the main safety issues with the remibrutinib is around bleeding risk. Actually, they picked up these Grade 1 bleeding events in phase I within their 10-day MAD cohorts. They picked up that signal quite early. In contrast, we have not seen anything of concern around bleeding for our program. Also, of course, that continued to play out in phase II and phase III. I think that is one of their main concerns. They have been clean on liver, which is great because we want to make sure that this was not mechanism related. So we are actually really excited to see their clean liver data. They said in their MS programs they had no Hy's Law cases or evidence of significant DILI. We have not seen the complete data set, but I think that was very encouraging. We are significantly less reactive than remibrutinib and on obviously much lower dose. So we are pretty excited that we think we can differentiate, continue to have a clean liver safety profile, and hopefully avoid the bleeding risk. That's what we are focused on because we do hear from CSU patients, many of them have a lot of bruising and petechiae and can be kind of concerning from that perspective. That is a big issue when you think about the pediatric and adolescent populations for food allergy. Again, really looking to improve upon that safety profile. We have also been hearing in terms of just talking a little bit more on the efficacy side, that if patients miss a dose of remibrutinib, they can get a pretty rapid return of symptoms. We see this pretty fast drop off on some of the PD markers with remi. It really is a BID drug and needs to be taken BID. If they do miss a dose, they actually have recurrence of symptoms pretty quickly, which is problematic for CSU because of the pruritus and it can be really a miserable quality of life for patients who are not treated well. Obviously, that would be a big issue for food allergy as well as MS, because you really want to make sure you are not getting disability events. Those are some of the thoughts on differentiation for remibrutinib. Thank you very much. Any other questions I can address? I am happy to stay after the presentation to speak as well. All right, great. Well, thank you very much.