Well, thank you for joining us today on this webcast. I'm Pete O'Heeron, founder and CEO of FibroBiologics. I'm joined by my Chief Scientific Officer, Hamid Khoja. We'll be having some forward-looking statements today, so here is our resident disclaimer for that. The leadership of our company has over 60+ years of experience in operations, product rollout, clinical trials. We are covered in everything with these three executives. Our board of directors have a cross-section of skill sets, from clinical trial development to financial operations, rollout of products, and business development. We really appreciate our board of directors. They are all in the game, as we say, all currently working for biopharmas. Our scientific advisory board, it's one of the treasures of the company. These are all world leaders in stem cells. They had no prior knowledge of fibroblasts, with the exception of Dr. Bhowmick, and they are now part of the team to help us with our scientific rigor and to advise us on our advancement of our clinical programs. Some of the highlights we'll be talking about today, we have a phase I/II clinical trial in diabetic foot ulcers coming up in Q1 of 2025, followed by the multiple sclerosis and degenerative disc disease. We have a strong IP platform. By strong IP, I mean we have more patents in fibroblasts than the rest of the world combined, 150 patents issued and pending. We have, again, an experienced management team, and our near-term outcomes are to develop the clinical product needed for our clinical trials. We look at the current market dynamics, and one of the things that we like about cell therapy is that as you review what's happened over the last 60 years in big pharma and chemical compounds, we've come yet to find a cure in chronic diseases using chemical compounds. We don't think it's ever going to happen. We don't know that we will ever see a time when an external man-made chemical compound will be introduced to the human body and will cure a chronic disease. We think that cure will come from cell therapy, gene therapy, or immunotherapy, and these really occupy the last three big Nobel Prizes in medicine. So when we look at cell therapy, the 2012 Nobel Prize was given to Dr. Yamanaka in Japan for the first induced pluripotent stem cell. The irony is he used a fibroblast to create that stem cell, so we like to say fibroblasts started the stem cell revolution. After that, you saw Dr. Jim Allison at MD Anderson with immunotherapy for cancer, and they set off about a 10-year run of development in immunotherapy, and most recently, it's Jennifer Doudna and Emmanuelle Charpentier for CRISPR, and you just saw a sickle cell anemia approval for them last December. So while stem cells have had a head start, and there's 30, 40 different companies with some form of ownership of stem cells, to our knowledge, FibroBiologics is the only public company working on therapeutic use of fibroblasts for chronic disease management. You'll be learning more about our pipeline today. We have our diabetic foot ulcer. You'll hear Dr. Khoja talk about it, about an 80% improvement over the existing number one product in the market. You'll hear about multiple sclerosis, our first human trial in that. We did a very small human trial, five patients for safety. What we saw in those patients, we saw in all five patients, and that was a cessation to the progression of multiple sclerosis during that trial. Degenerative disc disease, we have some really exciting data coming to you on psoriasis and then thymus regeneration. In the world of extension of human life, we can't imagine anything having a more complete impact on the extension of human life than regeneration of the thymus. The thymus is the gland that sits right under the breastplate, and it's the teaching center for the immune system. When you turn 50, 60, and by the time you're 70, the gland is almost non-functioning. If we can regenerate the function of the thymus gland, we can keep humans alive another 10 or 15 years. It's very exciting, and we are the only people working in that area. And then our cancer program will be coming together in the next couple of months. This is our pipeline in graph form. You can see where we are preclinical, phase I. Again, our product line, area disease paths are on the bottom. We like to think fibroblasts are a great alternative to current stem cells. They have significant anti-inflammatory, immune modulation capabilities. They're involved in every stage of wound healing. They have repair, maintenance, and regeneration of all tissue types, and they share many of the same characteristics of stem cells. How do we stack up with stem cells, and what are the differences? Well, fibroblasts are the most common cell in the human body. They actually outnumber stem cells 5,000 to one, and in all of our studies, they outperform stem cells. So they're much easier to source, minimally invasive. They again are the most common cell in the human body. They're easier to culture and maintain, they're easier to manufacture, and fibroblasts will always be a lower-cost alternative to stem cells. At this point, I'm going to turn it over to Hamid Khoja, our Chief Scientific Officer, and then we'll regroup back with me at the end. Hamid? Thank you very much, Pete. So I will go through our product candidate pipelines and some of the data that we've generated both in preclinical IND-enabling studies as well as clinical trials. We'll first look at the wound healing for diabetic foot ulcer, our IND-enabling studies. As many of you are probably aware, fibroblasts play a critical role in every stage, every single stage of wound healing process. So we've taken advantage of that in developing a therapeutic for diabetic foot ulcers and chronic wounds using fibroblasts. Now, our first study here compares our product, which is a spheroid-based, topically administered fibroblast, against Grafix from Smith & Nephew, which has been FDA-approved for as a therapeutic for diabetic foot ulcers. In our animal model studies, as you look at the data with multiple administration, at day 19, when the wound closed, we had 83.8% of the wound closure with our product, as compared to 60% for Grafix and 51% for control. As you look at the data with an n, a number of 10 for each cohort, you'll notice that fibroblasts as compared to spheroids, the data is significantly different, which is the same for control, so our results are statistically significant. Well, again, it's not just being able to heal the wound quickly. As we know, with diabetic foot ulcers, about 70% of them reoccur within 2 years. So it's important to be able to generate healed wounds that not only heal rapidly, but also heal at a high quality of wound healing. So what we've done is in our animal model studies, we've compared against Grafix using IHC, using seven different metrics, and all these metrics, we've been able to show that our product, CYWC628, which is a fibroblast spheroid, performs statistically significantly better than Grafix in all of these metrics, and I will quickly go through them. Fibroblast spheroids can promote re-epithelialization significantly better than Grafix. They also have significantly improved granulation of skin during the healing process as compared to Grafix. We also noticed significantly improved cell proliferation and healing of the skin, which is visually, if you look at these slides, you can actually see the difference between Grafix, control, and spheroids, and you can see the significant improvement at every stage. We also noticed a significant improvement in neovascularization with our product as compared to Grafix at the remodeling phase of wound healing. We're also noticing significantly improved fibroblast recruitment and proliferation in the chronic wounds, and also keratinocyte migration, which is significantly important. And here in these slides, you can actually see the vast difference between what Grafix can do and what our product does to wound healing. And wound healing in terms of quality, you see significantly higher keratinocyte migration, which is one of the last phases of wound healing during the remodeling phase. We're also noticing significantly improved epithelial-mesenchymal transition, which is, again, another quality metric that's used in terms of quality of wound that has healed. And you see the significant difference between Grafix and our product. Now, here's a view of our product. So basically, it's topically administered spheroids. As you can see on the left panel, the spheroids were added to the surface of the wound, and they actually adhere and begin migrating. On the right-hand panel, you can see 6 hours, the spheroids have migrated, the fibroblasts have migrated from the spheroids to cover the wound area. And on the bottom, you just see the graphical representation of what happens when a spheroid is administered topically on the surface of a chronic wound. In terms of the conclusion, we see a significant increase in wound healing rate as compared to an FDA-approved product, which has gone through a very similar IND-enabling animal model studies, and we see an improved healed wound quality metrics as compared to this FDA-approved product. We find FDA spheroids are a promising candidate for a cell-based therapeutic for treatment of chronic wounds such as diabetic foot ulcers, and it's also a potential therapeutic for treatment of burn wounds as well as surgical wounds. Our next product candidate pipeline is multiple sclerosis. In some of the preclinical data, In rats in which we have induced experimental autoimmune encephalomyelitis, as you can see, with a single administration, we were able to resolve EAE that was durable up to beyond 60 days. So these were just intravenously injected 30- 150 micron spheroids. So they were able to accommodate an inhibition of EAE, and it, it was practically resolved in all these animals within a week with no relapse. We've also been able to show in our as well in vitro and in vivo studies, in vitro being on the left and in vivo on the right, we've been able to show a significant stimulation of T-regulatory cells in vivo as well as in vitro as compared to stem cells that were tested. We also see a significant suppression of reactive T cells, which are a major component of the autoimmune disorder for multiple sclerosis, and we see that as compared to adipose and mesenchymal and bone marrow-derived stem cells. So this takes advantage of the immune modulatory effect of fibroblasts that has been very well described in publications. One additional thing that we are noticing is we're noticing significant increase in myelin detection. That's one thing that we have not seen in other publications for other therapeutics that have gone through FDA approval. Myelin remyelination has not been seen, but we see that specifically in both in these animal models, we see remyelination occurring in the cerebral cortex as well as in the spinal cord. And again, that's just one form of looking at remyelination, but we've also been able to see a quantitative measurement of the dividing oligodendrocytes, which generate the myelin sheath. And as you can see, with both of those methodologies, we see a significant increase in oligodendrocyte expansion in the cerebral cortex. We also see a significant reduction in microglia expansion in fibroblast-treated EAE rat brain. So this is, microglia are the resident immune cells in the brain, and as you can see with the control and adipose-derived stem cell cohort, you still see, you see a significant increase in microglia expansion and, and presence, whereas with the spheroid-treated cohort, you don't see any microglia expansion. So we are not only able to control systemic inflammation by controlling the T-regulatory cells and significantly suppressing reactive T cells, we're also being able to see significant suppression of microglia activation. But also, at the same time, we're seeing significant increase in myelin expression in these areas of the brain that were impacted by multiple sclerosis. So I'll give you a summary of our phase I clinical trial, which was a safety-first outcome. And we saw no adverse events noted during the intravenous injection of pyrogenic these allogeneic fibroblasts in five patients. It was a safety profile, safety outcome first. Five patients, we saw no long-term impact in blood count both for CBC and WBC in the 16-week monitoring period, and we saw no short-term or long-term impact noted in electrocardiogram results in the 16-week monitoring period. The reason why we did the electrocardiogram is because quite a few of the new biologics that monoclonal antibodies that have been approved for use in MS have a cardiovascular adverse effect that has been noted with a few with black box warnings. In terms of efficacy, we noted general improvements in two of the neurological tests, such as Paced Auditory Serial Addition and Nine-Hole Peg Test, but we didn't see any general improvement or deterioration in the 25-foot walk test, or EDSS. None of the patients exhibited any further deterioration, or any MS episodes during the course of the study, which was very interesting for us. We do also have some early-stage research that is currently going through IND-enabling, and that is with the first one being psoriasis. And just to show you some animal model results, this is looking at a moderate psoriasis PASI score. PASI score is basically grading that is done in both humans and animal models to show how the impact or the severity of psoriasis, looking at thickness, erythema, and scaling, and at the bottom, you can see the average score. We were able to, with a single dose, resolve a moderate psoriasis. And the same with multiple administration, when we look at severe psoriasis, with psoriasis, we were able to significantly reduce the severity with three administrations over a 15-day period in these animal models, which typically in humans would every administration would be about every two to three weeks in humans as compared to animals. We've also, being that some of the best, products out there that have been FDA approved for use, for treatment of, psoriasis is, monoclonal antibodies against interleukin-23. We also included that in our studies and as comparator, and we can see that even our product, with a single administration, does better than a multiple administration of, of IL-23 monoclonal antibody, as well as a single administration of the monoclonal antibody. So if you can see on the significance, the p-values are very low, and it's significant when we compare them to the control and compare them with the interleukin-23, anti-interleukin-23, cohorts. So, this is, incredibly good in that we are looking forward to continuing and doing more studies, to further show some of the, immune response. That experiment is ongoing, and we should have those results within the next few months. If you look at epidermal thickening, you can actually see that as compared to a negative control, we reduced the epidermal thickening, and significantly as compared to control, which is imiquimod control and as well as negative control. We're also seeing reduced immune cell infiltration in these psoriatic lesions and both as compared to negative control and imiquimod control. Imiquimod is basically, it's the, it's the chemical or that is used to induce psoriasis-like symptoms in mice. You can see the results are quite significant as compared to those controls. We're also seeing reduced cell proliferation when we look at IHC, and it's significantly improved or reduced as compared to an imiquimod control and negative. So we're having a strong impact, not only locally, but we're also seeing a strong impact systemically in terms of the immune modulation that occurs in systemic inflammation. We do see an advantageous characteristics of these spheroids that not only improves viability and reduced cell size, but it's a potentially more efficient redistribution when administered intravenously. We do see a therapeutic potential for these spheroids in mitigating the severity of psoriatic skin lesions and suppressing the immune activation or inflammation that is associated both systemically and locally with psoriasis. HDF spheroids are certainly based on our results to date, a very promising candidate for cell therapy in the treatment of psoriasis and potentially other immune-related skin disorders. We do have two additional products in our early-stage pipeline, CYTR915, which is the extension of life that Pete alluded to. Basically, what we are trying to do is to reverse the involution process of the thymus, and by the time we reach our sixties, we've lost 95% of the capability of the thymus gland, which makes elderly individuals more prone to autoimmune disorders, cancers, infections, and a reduced response to vaccination. We have, as you probably noticed in one of our press releases recently, we've been able to show that we can generate a fibroblast-based artificial thymic organoid, that we have been able to show that it not only hides from the immune system, but it can teach the T cells. So that's a very promising results that we have to date, and we have experiments that are ongoing to further elucidate what we are seeing. This, by the end of the summer, we will also begin our studies for cancer, which is at really early stages at this point. I'm going to hand it out to Pete for the next slide. Thank you, Hamid. Thank you. Just in summary, we are a clinical stage pipeline of candidates for clinical trials. This is a platform technology, and in some cases specific to wound care, it's a platform within a platform. Again, we have an experienced management team. We have some near-term outcomes coming up on our clinical trials. We'll be doing interim analysis on some of those as well. I wanna thank you for joining us. If you're looking for any other information, or you'd like to keep track of what is going on at FibroBiologics, please go to our website. You can register, and we are—you can keep up with our news and events there, and thank you for joining us. Thank you.