Hello, everybody. I'm Dr. Bob Hariri. I'm the founder, chairman, and Chief Executive Officer here at Celularity, and I want to take this moment to thank everybody for joining us, both in person, live here at our headquarters in Florham Park, New Jersey, as well as online. It means a tremendous amount to me personally and to my entire team here at Celularity. So today, we're going to be sharing with you an important update on the research, development, and commercial progress here at our company. Celularity is a very unique company because for the last 25 years, we have literally been turning the miracle of nature into important medical breakthroughs, and that's the theme for our presentation today.
So for the past 2.5 decades, Celularity has been at the forefront of cellular and regenerative medicine, dedicated to transforming living cells and tissues into medical solutions for a myriad of acute and chronic illnesses that afflict humanity. Our journey at Celularity has been driven by a fundamental mission: to harness the unique biological power of the human placenta to create these medical breakthroughs. Now, over 25 years ago, I had the epiphany that this organ, typically discarded as waste after the completion of a full-term, healthy pregnancy, held enormous potential as a rich, ethical, and renewable natural resource that could be highly proprietary and a powerful supply chain for cells and biological materials for the emerging industry of cellular and regenerative medicine.
In those early days, this mission demanded a very innovative approach to the procurement of these organs, following the completion of a healthy, full-term pregnancy, and a deep investment in research to fully understand the powerful biology that was resident in the cells and tissues which could be recovered. Cell therapy at the time was in its infancy. There was no roadmap on how to take these products from the bench to the clinic, ultimately, to regulatory approval and then to commercialization. Yet through relentless research and development, we've made substantial progress in understanding the fundamental biology of placental-derived cells, particularly their role in combating complex diseases like cancer, autoimmune disease, and the whole spectrum of degenerative processes associated with aging.
We've been able to engineer the systems and processes that enable us to manufacture at scale, quality, and compliance with the critically important and rigorous regulatory standards that are prescribed by the FDA and other global regulatory agencies. This is going to allow us to impact healthcare in a broad way. For those of you who are not familiar with the appropriate legal disclaimers that we were required to provide, these will be available in hard copy if anyone requests them. Among our foundational discoveries was the realization that the placenta acts as nature's professional universal donor tissue. This source material, as I mentioned, is abundant. There's 150 million placentas incinerated annually in the world, and it can be procured ethically, with no risks to the donor, and extremely attractive economics.
With stringent quality controls and unique and a unique bifurcated business model, we not only isolate cells that can be developed into for therapeutic purposes, but we also are able to isolate a range of biological materials and unlock many applications in areas like wound care, orthopedics, aesthetics, treating burns, and beyond. The future is very, very bright for this field. Excuse me. You will learn from my colleagues, who will be joining me today, that we're on track to file three 510(k) submissions to the FDA from 2025 to 2026, unlocking multi-billion-dollar market opportunities in orthopedics, wound healing, and aesthetics. Our progress with the FDA and our robust product pipeline present various opportunities in this advanced biomaterials space and cellular medicine.
This innovative approach transitions us from the traditional HCT/P regulatory environment to the device regulatory environment, allowing us to potentially capitalize on significant market opportunities. We have demonstrated a significant revenue growth rate over the last 12 months, with a 280% Q1 year-over-year increase in revenue. Let me repeat that. Our Q1 year-over-year revenues rose 280%. Now, that's a profound, profound testimonial to the value of these products in the different indications they're used. And it also means that other innovative products we'll be introducing have a tremendous head start and, and we believe will be very successful, in their own applications. We also have created first-in-class and best-in-class therapeutics that, that take advantage of the sophisticated GMP manufacturing infrastructure that we've built here at Celularity.
For those of you who are not familiar, the regulatory community has prescribed a very, very rigid set of standards for the manufacturing of products to ensure quality, consistency, and reliability. Those GMP manufacturing requirements in our business, where we're turning living cells into medicines, requires investment in tremendous operating infrastructure in the form of clean rooms for manufacturing, support laboratories for analytics, et cetera. Our state-of-the-art research and development system, combined with this world-class GMP manufacturing, underpins our opportunity to be highly successful. And, not to, not to belabor this, but Celularity, often thought of as a developmental stage company bringing assets through the regulatory process, is actually a commercial stage company as well. Our company has generated over $110 million in cumulative revenue since 2018. We have biobanked over 45,000 newborn donor cell samples.
We've delivered over 100 stem cell units for transplantation from our LifeBank business unit. Additionally, we have treated over 250,000 patients with our biomaterial products and built a robust patent portfolio with over 1,000 issued patents. So this testimonial to the value resident in the company should be apparent to everyone. Our expertise around the management, production, and deployment of cellular products for therapeutics, and our ability to innovate and create novel and innovative technologies using biomaterials, we believe can be heavily levered going forward in the next several years for our company. Our company evolved from the private corporation, Anthrogenesis, which I founded late in 1998, on my belief that cellular and regenerative medicine could transform healthcare.
Upon the discovery of stem cells in the leftover blood of the umbilical cord, reported by other scientists and other clinical teams, I was convinced that this meant that the origin of these cells, these very valuable stem cells, was hidden deep within the placenta itself. So why not look there? Initially focused on offering the service of biobanking newborn stem cells, which provided us access to these donated or discarded organs under full informed consent, ethically procured, with the understanding that we would be efforting to turn these into useful clinical products, we laid a scientific foundation through extensive research, which identified opportunities to monetize our technology through creating products from these biomaterials. Now, in the world of biotechnology, it's not often that companies rapidly transit to generating revenues.
The traditional path often takes a decade or longer before you've actually reduced something to a practical therapeutic tool. However, we, we had the ability to use our work with human stem cells to devise tools to support drug discovery work and actually came into the view of this emerging biotechnology giant, Celgene Corporation, and this exciting company merged us in at the end of 2002, allowing us to leverage their oncology expertise to drive many of our cell therapy development efforts. Now, one of the fundamental common denominator themes here at Celularity is to understand the fundamental biology that distinguishes cells from newborns versus cells that are available from adults or older patients. And so along the way, our work with newborn-derived cells showed there were stark differences to adult-derived cells.
We realized that these differences reflect the impact of aging on cells, and that the biology of aging is both a common denominator and a risk factor in many diseases. As evident here on the left side of the slide, the rising incidence of virtually all diseases with age speaks to the importance of common mechanisms that are responsible for this increased incidence. This has led to our approach targeting the senescent phenotype, where cells no longer divide and secrete inflammatory factors, which contribute to diseases such as dementia, cancer, and other aging-related illnesses. But it also signals that we learn as we go. Our first efforts in taking natural killer cells into cancer provided the foundation upon which we recognized that, that same mechanism, that natural killer cells from the placenta hunt and destroy cancer cells, also allows them to hunt and destroy senescent cells.
This understanding has created vast opportunities for our technology to impact a range of conditions. If you think about Celularity as having an umbrella of opportunities that range from cancer, degenerative diseases, immunologic disorders like autoimmune diseases such as Crohn's or multiple sclerosis, neurodegenerative disorders, they all have a common relationship to the process of senescence. Fortunately, we believe that we are the only company that has a range of cellular and biomaterial products that are already potentially targeting age-related and senescence-related conditions.
Now, we're fortunate because as a company that has focused on being the world's leader in the procurement of this raw material, and then derivation of that material to create biomaterials, cellular medicines, and simultaneously allowing us to provide services around biobanking, it allows us to create a range of products and a diversified stream of revenues that enable our continued investment in our core mission. So grounded in 25 years' experience in newborn cell banking, I'm very happy to say that we just initiated launching an adult stem cell banking service, this second quarter of 2024, which you'll be hearing more about throughout the second half of the year. And it's an opportunity we have to complement our revenues, provide us access to, again, a broad range of cell types to use in our research activities.
And in addition to our cell therapy candidates, we've established a significant strategic relationship with a number of companies developing products in both of these areas. If you look at the opportunity for us to leverage our success in our biomaterials business today, and I mentioned before that we're on track for filing three 510(k)s in areas such as orthopedics and wound care and aesthetics. This speaks to a very, very, we believe, a very modern approach to interacting with the regulatory community, the FDA, in order to advance these products to being treated as devices, which affords us greater flexibility in interacting with consumers, with physicians, and with the scientific community. And our pipeline features a range of promising candidates at a variety of stages of development.
We're advancing multiple programs through clinical trials, each with the potential to transform treatment paradigms in their respective fields. Some of the highlights that are illustrated on this pipeline slide include that our biomaterial pipeline, developed, as I said before, under the 510(k) regulations of the FDA, will hopefully open new markets to us, new market opportunities that are much greater than currently covered under the HCT/P regulations. Our CAR T and NK cell therapies are showing promising early results in early-stage studies in senescence and solid tumors, and you're gonna be hearing more about this from my colleagues, Doctors Brigido, Gosiewska, and Kilcoyne, in the subsequent slides. Now, doing all this requires us to have the right environment to do a number of things. We need to attract and retain talent.
We need to have an environment that coalesces expertise in research as well as in technical operations, regulatory, commercial operations, and in order to do that, we found our home here in Florham Park, New Jersey. What hopefully you'll see today is that our state-of-the-art research and development capabilities are a cornerstone of the company and are equipped with cutting-edge technologies, staffed by leading cellular and tissue engineering scientists. It's robust. It's an in-house system. It allows us to accelerate the discovery, innovation, and development of novel therapies. Complementing our R&D capabilities is the world-class GMP manufacturing center. This facility ensures that all of our products are produced to the highest quality standards prescribed by the FDA.
Our GMP facility is capable of scaling production to meet the demands of clinical trials, clinical research programs, as well as all the way to commercial production, and this is all under our control without the dependence on third parties. For those of you who follow the industry, you'll recognize that many companies choose to operate with manufacturing partners. Those relationships have, in my opinion, limitations in the ability to innovate, but more importantly, it creates a clear dependence on the third party that ultimately you might not be able to control when you're moving towards commercialization. So we firmly believe that these are success factors, and you're gonna be hearing more about our technical capabilities from our Chief Technology Officer, Dr. Ramji Krishnan. So with that, I'm gonna turn the presentation over to my colleague, Dr.
Stephen Brigido, who will talk about our degenerative disease business.
Thank you. Thank you, Bob. Again, my name is Steve Brigido, and I'm the President of the Degenerative Disease Division here at Celularity, and we're gonna talk to you a little bit about our biomaterials program and some of the exciting opportunities that have been brought to us. You know, one of the great opportunities that a building of this nature, and as you tour this facility here in a few hours, one of the great things that you're gonna see about this facility is it allows us to take our source material, the full, healthy, full-term placenta, and utilize 100% of that biomaterial, that cell and cell by-product and structure, to allow us to create different therapeutics.
One of the core visions that Bob had back in the late 1990s, you know, was utilizing the scaffolding of that placenta to create therapeutics, to create... You know, to help disease states, whether it's a full-thickness wound in a diabetic patient, whether it's utilized in a homologous state for augmenting soft tissue or structural anatomy deviations. And what we've found is over the last 12-18 months, our commercial opportunity has become fantastic. And, you know, Bob mentioned earlier a slide about 280% growth, Q1 year-over-year, 2023- 2024.
When you look at our financials, utilizing they're preliminary, but utilizing GAAP net accounting, we were doing in 2023, first quarter of that year, about $3.9 million of revenue, with the overwhelming majority of that revenue being biomaterials and a consistent portion of the biobanking revenue coming in at about $1.5 million a month. When you look at this, the 2024 Q1, our revenue has skyrocketed to $14.8 million, and that's a 280% increase year over year, Q1. This is due to the fact that we've been able to take that healthy, full-term placenta, utilize this purpose-built facility, and find a way to create therapeutics that we've been able to monetize and deliver to patients and create access.
And when we think about, you know, when we think about what's driving this growth, it really is about access. We have to identify the patients that need our therapeutics and find ways to deliver them. The star of the show in the last six months or so has been a product that we're gonna talk about in a second called Biovance 3L. And one of the reasons that's been a star of the show is because it's, because of the way it's being regulated and because of the way CMS identified its reimbursement schedule, we've been able to provide more access to patients in need. But at the end of the day, we've also had to take an internal approach to how we want to build our commercial organization....
One of the ways we've done that is internally, we've identified independent sales force of about 40+ reps that focus on wound care and general surgery across the country. We have a partner in ophthalmology for ocular surface disease, in Verséa Ophthalmics, based out of Tampa, Florida, which has over 100 reps that are distributing our products to patients in need across the country. And then finally, in orthopedics and sports medicine, our partner, Arthrex Incorporated, has well over 1,000 sales reps that are representing our brands and identifying those patients that are in need. So for us, it's about taking our core source material, identifying gaps in patient care where we can find ways to help those individuals, creating it all within this building, and then ultimately delivering to the patient.
So, you know, oftentimes, Celularity is thought about or the fantastic R&D that we're doing. I'm gonna talk a little bit about, before Anna gets on stage, we're gonna talk a little bit about the biomaterials-driven R&D that we're gonna do. But at the end of the day, this is a commercial entity that is showing tremendous amount of growth, and as you can see here, it's got a tremendous amount of access and access potential that we're only gonna continue to build, going forward through the remaining of 2024 and beyond. So, you know, just a brief overview of our biomaterials, and I don't want to belabor this, but at the end of the day, all of our biomaterials, and we've got five commercial products that are available today for patients that need them, and they're all based on the same core principle.
That principle is they're decellularized, they're dehydrated, they have a shelf life that is best-in-class, meaning they don't have to be stored in any unique, material freezers or anything like that. They can be stored in ambient room temperature. Most of our biomaterials have a 10-year shelf life, but the idea behind that is that they're regulated under what's called an HCT/P 361 pathway, which means they're minimally manipulated and they're homologous use, in short. Minimally manipulated means that we're able to take, in this case, Biovance, the amniotic membrane from the placenta, and we're able to eradicate some of the things that make you and I different, some of the things that if I were to put my tissue in your body, would make you get an inflammatory response or things of that nature.
But ultimately, when we eradicate that, when it's used in a homologous setting, cells will essentially become attracted to that scaffold and help repopulate that tissue. Biovance was the first product that we've released, and we've basically built on our platform since then. Interfyl is a product where Biovance comes in a sheet. Oftentimes, people think of it, it looks like a layer of Saran Wrap or tissue paper. Interfyl is a product that comes in the form of a powder or flowable. It's derived from the chorionic plate of the placenta, and it can be injected or placed with forceps into, you know, a clinical setting. A lot of the work you'll see, and I'll show you a slide in a second, we think of wounds that are tunneling.
When somebody's perhaps in a nursing home and gets a sacral decubitus wound, and it sends little fistulas or little pathways into the tissue, Interfyl is a wonderful product that can help situations of that nature. As I mentioned to you before, Biovance 3L, which is our tri-layer, decellularized, dehydrated human membrane, is our workhorse. This is our product that's probably has the most fanfare. This past weekend at the symposium for Advanced Wound Care in Orlando, Florida, this product generated a lot of buzz. We're very fortunate. We're helping a lot of patients with a lot of different complicated situations, mostly related to the diabetic full-thickness wound.
But this is the product that has been, for us, a significant boost in, first and foremost, helping patients get better from their condition, and then, as a by-product of that, it's helped our revenue stream and has allowed us to see the kind of shift in revenue that we've noticed from Q1 of last year to Q1 of this year. Biovance 3L Ocular is our scaffold that's utilized to treat ocular surface disease. It looks like a little contact lens. It's placed on the surface of the eye, things like corneal abrasions, et cetera. And then finally, CentaFlex, which is a decellularized umbilical cord product, which is primarily utilized in the operating room setting, traditionally in orthopedic surgery. It helps to augment or cover periarticular tendon damage and things of that nature.
So here's our pipeline, and, you know, these are the products that have been on the market today. As Bob mentioned earlier, we've been fortunate enough over the course of the life of our company, you know, these products have generated over about $110 million of revenue, and we've helped approximately 250,000 patients with our technologies. So it's something that the, you know, the manufacturing team, our research and development team, and certainly the commercial team have everything to be proud of because the amount of growth that we've seen here has been fantastic.
And the patient testimonials that we see, when people reach out to us and tell us how they've been touched and affected in a positive way by our therapeutics, has been, nothing short of outstanding. Here's a case study, and I'm not gonna belabor this because I know not everybody likes to see these types of pictures. But at the end of the day, this is one of the most dramatic scenarios that I think demonstrates the power of what we utilize with our decellularized dehydrated scaffolds. Biovance was used in this particular setting. This is a patient with a second-degree burn on their lower extremity. Basically, everything below their knee was burned, and because of the massive size of the burns, the investigator here decided to utilize this patient as a control.
So the first half, everything above the versus sign on the leg was treated, what was considered to be standard of care at that time, a silver dressing, and everything below that was treated with our product, Biovance. You can see here, after we get to about three months post-repair, the tissue where the Biovance was treated doesn't have hyperpigmentation. When you grab and touch the skin, the texture and turgor of the skin has been restored. There's no adhesions, there's really no remnant that the burn even happened. But the area above that, where the silver dressing was utilized, you have hyperpigmentation, you have some stiffening of the tissue.
And then when you look at the cell-based histology, you can see that the tissue, because of this unique biomaterial that's been placed in the area, the tissue has allowed itself to reorganize and become much more structurally intact. And this is an example that we see many, many, many times, and you're gonna see it on this slide as well. This is a little bit more of a detailed slide. This is a patient that has a diabetic foot, full-thickness wound, and had just resolved an infection.... This is a very complicated condition to treat. This is the number one most common cause of admission for a diabetic patient in the United States. This is about a $1 billion stress on the healthcare economic system.
You can see after three Interfyl treatments, the patient's skin, the texture and the turgor of the skin, the color of the skin has been restored. The subdermal tissue has been restored, and the patient's able to ambulate without complication. Here's our last similar scenario. Again, this is a diabetic patient with some necrotic tissue on the dorsal aspect of the foot. Was treated with a single application of Biovance 3L, and you can see again, the tissue has been restored and the patient's back to wearing normal shoe gear and ambulating appropriately.
So these are all ways where, you know, we can, we can basically take our technologies and deliver them to patients that are suffering from some of the most devastating conditions, that, in the case of diabetes, you know, 50% of, of the patients that end up with a diabetic foot infection will end up with an amputation, and 50% of those patients will end up dead in five years. So the statistics for this are very significant, and, you know, one of the things that I think is very important and that sets Celularity apart from our peers, is that we have invested so much, in the facility.
And the facility allows us to invest so much in our research and development and also making sure that we take an onus on utilizing the peer review process, the publication process, to ensure that we're putting out the highest quality product we possibly can. Our products today are manufactured with the same therapeutic standards that our cell therapy products are manufactured, and I think that's an important distinction that we really, you know, when we talk about Celularity, it's something that we should all be proud of. So when we think about... "Steve, that's great. You've got, you've got five commercial biomaterials, you've got growth. You know, where are we going to go tomorrow?
How are we gonna maintain that growth, and how are we gonna maintain access to patient care?" Well, you know, for those of us that are following the marketplace and how... You can have the best therapeutic in the world, but if you don't have access and you don't have coverage, you don't have a therapeutic. And one of the ways that we think that we're gonna be able to approach this in the future is that we've been able to. We really feel like we've predicted some of the shifts in how the government, both at the Medicare level and also at the level of the FDA, are gonna look at evaluating these products down the road.
And we've decided as a group that we're gonna basically take our assets, which is we wanna find differentiated, you know, approaches to both scientific, clinical, and regulatory. We're gonna utilize that robust patent portfolio of over 1,000, 1,000 issued patents, and we wanna look at who our partners are and how what they do best, and what we can do to leverage those relationships so that we get a greater commercial penetration at a quicker rate when we bring these products to market. And the way we've, as Bob had mentioned when he started the presentation, the way that we're really gonna tackle this is we're gonna tackle this by utilizing the device designation pathway. And we've been able to work with the government through something called a Q-Sub.
What a Q-Sub meaning, it's a non-binding meaning, but it allows us to come to an agreement with the specific regulatory body at the FDA that says, "We want to bring this product to market. This is how we're going to do it." And they give us an unofficial yay or nay. These products have been given the unofficial yay, which is a great thing for us. We really feel that... The next slide I show you is gonna really kind of bring this home, but we really feel that each of these, the Celularity Tendon Wrap, which is gonna be utilized in periarticular tendon augmentation, think of rotator cuff, quad tendon, Achilles tendon. We're thinking of our FUSE Bone Void Filler, which will be the first human placental bone void filler to come to market.
And then finally, this Celularity Placental Matrix that has an opportunity to help patients not only in wound care but also in things like subdermal fillers, the cosmetic aesthetic market. We really feel that all of these products first meet what we think is keystone to having a successful product launch is, it's identifying an unmet need. Number two, we feel like with our Q-Sub submissions, we've been able to minimize the risk associated with bringing these products to market. It doesn't guarantee anything, but we can certainly de-risk it as best as we can. And then we're, again, we're gonna utilize this wonderful purpose-built facility to make sure that we can bring all of these products to market and deliver them to patients that need them. So when we look at the markets, these markets are what I consider our first opportunity outside of wound.
These are our first opportunity to get into what we call blockbuster markets. These are multi-billion-dollar markets that when you look at them globally, the ability to penetrate this marketplace with the technology that needs it is gonna be disruptive. It's going to be a situation where by utilizing the device designation, we're gonna be able to talk about an indication for use. We're gonna be able to educate with an indication for use. And when you can talk about your indications and you can educate around it, you're gonna be able to grab some of that market.
We feel really, really strong about the fact that we've got, you know, a $2.2 billion global tendon market that's growing at a 7%-8%, you know, compounding annual growth rate, all the way looking at that from the global filler market, which is $5 billion and change, to going up to 15 by the time we get to 2031. So with that being said, I'm gonna bring Dr. Anna Gosiewska up. She's gonna—she runs our. She's the Vice President of Research and Development and manager of our biomaterials platform, and, she's gonna talk to you a little bit about how we're gonna bring these products to the market and the timeframe that we're gonna do it. So thank you.
Thank you, Steve. Let me bring your attention to our first product in development, Celularity Tendon Wrap, or CTW. This product is indicated for effective management and protection of tendon injuries. This is our farthest along and most de-risked product in our portfolio. We have achieved a significant de-risking, as Steve mentioned, via our framework. The majority of our critical milestones, including alignment with FDA on our development strategy, has been achieved, and we are on target to submit 510(k) first half 2025. We believe that CTW is well-differentiated product. It was designed to address clinical challenges as well as drawbacks associated with current products on the market. We all realize that tendon healing is very ineffective and slow, especially for those of us who have experienced tendon injury.
There is higher recurrence rate, up to 40%. And the current products on the market, which include cadaveric allografts, xenogeneic, bovine, or porcine-derived materials, as well as polymeric-based products, all have some drawbacks, which we believe we can address with our innovation. So we are very pleased with our CTW performance in animal studies, where we saw effective tendon healing. And as you can see on the middle actual image, that our Celularity tendon wrap can be wrapped around the tendon and suture through arthroscopic procedure. We saw in our animal studies, there was effective tendon healing with minimal inflammatory response at six weeks. We will be sharing our science at the upcoming ORS Tendon Conference hosted at the Mayo Clinic at the end of May.
So that will be the opportunity for us to share our research with both clinical as well as scientific community. So moving on to our second development product, which is FUSE Bone Void Filler. This product is indicated for filling defects in skeletal system, extremities, spine, and pelvis. We also envision that this product will be applicable to dental applications as well. Fuse is also significantly de-risked. We are leveraging the same development framework as we shown before, and we are on target to submit 510(k) second half of 2025.
We are very excited about FUSE product, as we believe it will be well-differentiated and also capable of addressing clinical challenges and unmet needs associated with the current, products, including ineffective integration of the current implants with the bone, migration of the mineral from the defect when mineral is used alone, or mismatch rates of implant degradation. So what is our FUSE product difference? FUSE is a composite, is composed of 100% decellularized human placental matrix and combined with a mineral with excellent bone-forming abilities, or we call this osteoconductive ability. We are very excited and pleased with the animal results, as we saw new bone formation as early as three weeks, as shown by the darker line of the professional bone-forming cells forming new bone within the implant.
Also, as shown here by the series of micro-computed tomography images, you could see the new bone ingrowth within FUSE, as you can see by the arrows, both yellow, showing the mineral, and then the gray zone, this is the new bone infiltration into FUSE. You can compare in contrast what is happening in the control, which is practically minimal or no bone ingrowth. So moving on to our third product, which is Celularity Placental Matrix or CPM. This product will allow us to enter the wound management market, and this product is indicated for a chronic, acute burns, full thickness, partial thickness, a wide variety of different wounds, including surgical wounds, which also allows us to enter the aesthetics markets with post-laser and post-grafting procedures.
This device leverages the same development framework, as well as all the technological advances, as we described for the placental extracellular matrix when discussing a FUSE product, except the mineral, of course, and is substantially de-risked using our framework, with 510(k) submission projected second half of 2026. We believe that Celularity Placental Matrix will be able to address significant clinical unmet needs and also challenges currently associated with wound management overall, but mostly also with chronic wounds, as there is lack of effective therapies for chronic wounds, as Steve mentioned earlier. Also, the current standard of care is ineffective and has been unchanged for over decades. It's just basically moist gauze.
In surgery, especially, in aesthetics, tissue ablation post-laser surgery is requiring innovative and highly effective wound management to facilitate and then to speed up the, recovery post, treatment. So moving on, Our innovation and development efforts, do not, end here. We are also moving forward to develop a placental dermal filler, addressing significant unmet needs, in today's, as, dermal fillers related to aesthetics. We are capitalizing on the uniqueness and properties of placental 100% decellularized matrix to utilize, for dermal filler applications. Ultimately, we believe that we are the only company that will be able to combine our placental extracellular matrix, as we discussed, with our cellular, placental cellular technologies, which we believe is the future of regenerative medicine. I would like to now transition to Dr.
Adrian Kilcoyne, to share our ongoing innovation and exciting development in cellular therapeutics. Thank you.
Thank you, Anna. Thank you, Bob and Steve. Thank you all for coming here today. I'm going to take you through a whistle-stop tour, really, of our cell therapy platform. Why are we doing this? Well, Bob has already introduced this to us, and I think it's really we want to just remind you of our approach. We fundamentally believe that the aging cell is really the reason why we develop multiple different illnesses. So this umbrella term of aging-related diseases is not necessarily what your mind will immediately jump to. So that's why we wanted to focus, 'cause some people may forget that cancer is an aging-related diseases. Yeah, it, it is.
and the fundamental biology that Bob talked about is actually, and I hope I convince you of this in the next 30 minutes or so, is absolutely fundamental to developing not only of cancer, but multiple age-related diseases, including fibrosis, autoimmune disease, the degenerative diseases that we're already addressing. But I just want to remind you of our overall pipeline that Bob has shared up front. What we've shared thus far is our near-term growth drivers. From our current biomaterials program, which has five commercialized products, to the three very large market potential 510(k)s that are going to be submitted between now and 2026. That's going to be a tremendous opportunity for us over that period of time.
But what I want to spend the next 30 minutes or so introducing you to is the tremendous value that we believe is resident in our cell therapy programs. It is broad. We have a richness here in Celularity, in that we can investigate multiple cell types. We have our MLPs, we have our NK cells, we have our T cells. We have them unmodified, we have them modified, and we can all do it here in this, in the Florham Park facility. And during the tour, which I hope you enjoy, you'll see our labs. You'll see the amount of expertise that is resident here in this facility, which is representative of the huge investment that Bob made when he moved here. I'm gonna give you a whistle stop through a lot of different areas.
Now, I am mindful that many of you may feel that cell therapy, incredibly difficult, incredibly scientific, but hopefully, I'll convince you of our approach, that it is rational, it's reasonable, and actually, that the academic community, based on what we've presented thus far this year, is happy, is quite open to how we're approaching this. So let's talk, go back to the placenta. Bob talked passionately about why he was attracted to the placenta, but I'm gonna take a little step back and talk about cell therapies in general. When we develop a cell therapy, what are we trying to develop? What are the key characteristics of the ideal cell therapy? And we know there's no such thing. It's always deciding where are we willing to compromise, where are we not? The one thing we can never compromise on is efficacy.
These are to treat patients who are very unwell, and for most cases, have run out of options. This is their last chance, so efficacy remains the king. However, there is a lot of other things we want to build into a cell therapy. We want them to proliferate. When they go back into your body, we want them to expand. We want them to do that, but ideally, we want them also to be relatively naive. What do we mean by naive and stemness? Stemness is really the ability to self-renew. Naive phenotype means they're still fairly young. Now, it may not surprise you that if you use cells that are derived from a placenta, they might be young cells. This is really important because young cells are more likely to give you better outcomes and more durable responses. Seems to make sense, right?
The other bit is persistence. For those of you who've had any family members with cancer or any other age-related diseases, they come back. So we want our cell therapies to persist, and if they come--if the cancer does come back, we want your cell therapy to still be there to address it if needed. And for that, we need to make sure when you give a CAR T therapy, they...essentially, it's an activated cell, and it works hard, and it never switches off. So they become exhausted, and if they become exhausted, they don't work. So even if you have your cells present, they're probably not gonna do very much. So we will also want our cells not to become exhausted, okay? Then it's resistance.
For those of you, again, who have any family members who've had a cancer that has relapsed, that is kind of a devastating piece of news for these patients, and it's devastating for the physicians, too, and especially for these patients, 'cause as I said, last chance saloon for these, what do we do if they relapse? So we need to make sure that we are having, our cells do not start developing what we call checkpoint inhibitors. These are the kind of things that cancer cells, allows cancer cells to bypass our own immune system, and your cell therapy doesn't work. And finally, tolerability. For those of you who have followed anything in the cell therapy space, one of the big challenges we've had throughout this time is cytokine release syndrome and immune effector cell-associated neurotoxicity. It's important in a number of ways.
One, it makes the patient sick, but two, it adds tremendously to the cost of the therapy. So we know that cell therapy generally is what? Between $375,000-$500,000. When you add in the management of these patients on top of this, for many, the numbers differ. Some say it's $1 million, some say more, some say less, but it's significant. So if we had an ideal cell therapy, it would probably tick all of these boxes. But there was interesting. A few years ago, you know, there was a questionnaire asking physicians why they didn't adopt cell therapy, because when you look at the total number of patients who've been treated, it's not as many as you might think. The number one driver of uptake was actually concerns around tolerability.
So that's key that we address that. So why am I sharing all this with you? Well, it's because when we look at our starting material, we assess each and every one of those criteria. And I'm gonna take you through each of these in as simple a way as possible so that you can kind of understand why we think this starting material is better. The first is efficacy. So if we're looking at this, and these are all preclinical data, but the first thing we want to do is take an autologous product, and on the graph there, you'll see it as a PBMC, versus ours and using our own CAR, our own Chimeric Antigen Receptor. And the first thing we look at is cytotoxicity. How well does it kill cells?
Hopefully, you can see that our cells kill just as well as the autologous cells. That is good because efficacy is important. No matter what we do, we cannot compromise that. The second is proliferation, and I told you earlier that we want to have naive young cells, and we measure that by looking at the TSCMs, TN or TSCMs. It's the, on the middle graph, the left-hand side, you can see the tall bar charts. Our cells retain a lot of naivety and therefore stemness, so we expect to have tremendous proliferative potential. There's another little thing here is we want a really good cell therapy. We want your CD4 and your CD8. Why are CD4 and CD8? CD4, your helper cells, CD8 is your cytotoxic cells. We want them to balance 50/50 as much as possible.
That helps you with your toxicity, it helps you with your efficacy. We can see, hopefully, you can see that our cells are really skewed to the left. Lots of young, naive cells that are ready to proliferate, okay? Then there's persistence. We've talked about the importance of persistence, but there's a few other things in here. We measure a thing called CD57. You don't need to remember that, but I can tell you what it is. What it is, senescent exhausted cells exhibit CD57. If you're exhibiting that on your cells, they're starting to reach the end of their life. What you can see there on the right-hand side is very clearly that the autologous cells are starting to express that far more frequently than our cells, probably as a result of the lack of exhaustion that you're seeing with these very young, naive cells.
But equally important, I added in something there about telomere length. For those people who don't know what we mean by telomere length, when your cells divide, you have a telomere. Now, I've seen people describe it, and the best I could describe it is that little plastic thing at the end of your shoelace. That's your telomere. Every time your cell divides, it gets a tiny, tiny, tiny bit shorter. But it's the reason it's there is to protect your DNA and your repair mechanisms. When that telomere gets to a certain level, it switches off cell division. That's your senescent cell. That's why the fundamental biology is all really related to cancer. But once you get that telomere shorter, you stop functioning. So we measure telomeres.
They're really important, and it shouldn't surprise you that our telomeres are longer, a sign of a younger cells ready to proliferate and ready to stay longer. The next is resistance. So we measure things on the surface of cells that allow them to bypass the immune system. The important ones here are LAG-3 and TIGIT. On that first, the second two bar graphs is looking at LAG-3 and TIGIT. They're a sign of resistance, 'cause again, you don't want your cancer to gain resistance because it'll come back. So this is really encouraging. Now, many of you who are familiar with the PD-1 space will say, "But you've got high levels of PD-1." In this context, that's what we call an activation marker. It's too early to decide if it's an issue, but it almost certainly isn't.
It's the LAG-3 and TIGIT that we're really interested here. Finally, is tolerability. We want cytokines because cytokines kill cancer, but we don't want so much that it makes you sick. So that's the balance we always have to come up with. So this is where we look at our TNF-alpha and interferon gamma. What we can see is that we have much lower levels of cytokines. What does that mean? I want to bring you back to the efficacy. We're able to kill it, but without making you as sick. So all of that, when you pull it together, we believe we fulfill many of the criteria for the ideal cell therapy. But there's the so what? Does that actually reflect into our in vivo data? So I'm gonna very quickly bring you through this to say, does it hold true? So this is mouse data.
So you can see and under the efficacy, you can see people who've been given the autologous product versus our product. Hopefully, everyone can see that with our starting material, with these CAR T, which is our CAR, our own in-house CAR T, we can see that these mice not only survive much better response, but they also survive longer. There's another part to this, which is on the other side of it, where we reintroduce the tumor, and once you reintroduce the tumor, your cells still respond to allow you to live right out to 215 days. That's really strong data. And in between there, we're able to measure the stem cells and show they're still present. So taken all together, we get really good efficacy, we get really good durability, and we can get effect when we challenged.
So this leads us to believe this is a great platform on which to build a cell therapy program. So I'm going to introduce another topic, you know, concept around CD16. Now, I'm not going to talk in huge detail about what CD16 is, but what you can see on the graphic there is an antibody. It's the one that's the Y-shaped thing, and that has two portions. It's the Fab, which is the. Sorry, Fc, which is at the bottom of the Y, and the Fab, which is the dual one on top. That's important. Why? Because CD16, which is present on many cells, like NK cells, et cetera, they bind to the Fc portion, the bottom of the Y.
The top of the Y binds to your tumor, your virus, et cetera, and therefore, that activates what we call an effector cell, and it eliminates the tumor, the virus, whatever. Now, we can take that biological mechanism and use it. Why? Because lots of commercially available monoclonal antibodies attach to that Fc portion to the CD16, so they have the Fc portion. Not all monoclonal antibodies have that Fc portion. The majority do.
So it means that if we were to take our T cell and have CD16 on the outside and combine it with a monoclonal antibody like trastuzumab, and I'll show you the data, it means what you can do is the trastuzumab will bind, and it will traffic your cell therapy to the tumor, and then it will be activated. So this is a really important concept 'cause that's what gives us our universal engager phenomenon. And I'll show you the data. Now, as I said earlier, we're lucky in that we can test T cells, NK cells. And the first graph you see there is us looking at CD16 on the surface of our NK cells and on the surface of our T cells, combining it with trastuzumab and say: Do you kill cells?
The answer is yes for both, but much better for T cells. So we know that in this, it looks like T cells are better, but it's better with an important distinction when you look at the middle one. What we know about NK cells is they're broadly very well tolerated. Within our phase 1 study in acute myeloid leukemia, we were able to treat patients with very large numbers of cells, around 1.8 billion cells over multiple doses, without eliciting any real cytokine release syndrome, et cetera. So they're very well tolerated. So when we look at the cytokine levels here on NK cells versus the T cells, it's surprising that despite the better efficacy, you appear to have a better tolerability profile. This is really important. The third one is showing we're only hitting disease cells.
Your normal cells in the background are not affected. So that is very encouraging for us as we develop our data. And this, again, is taking this into the in vivo setting. So we have a number of lines here. It's very busy, but essentially the vehicle is you do nothing. You just have your tumor, mouse with a tumor, you follow it, measure tumor burden, then we test Trastuzumab, CD16, pT-CD16, and so on, pT-CD16+ trastuzumab, and we thought it was worthwhile adding in the current standard of care in this clinical setting, which is Enhertu.
Now, for those of you who aren't aware, Enhertu is an antibody-drug conjugate built on trastuzumab with a chemotherapy payload, so the trastuzumab goes to the site of the tumor, which expresses on this instance, Enhertu, and then once it binds, it releases its chemotherapy payload, and it's very effective. That's why when we look at this, it appears that we have superior in vivo tumor activity than Enhertu, which is really, really encouraging for us. If we look at the next graphic, the bottom one shows the proportion of these animals that actually got a complete response. It's really quite impressive. We're very reassured that this will translate well. I wanted to show you because it's one thing seeing the data.
It's really nice to see these things live in action because we are able to look at this. So there's a on the right-hand side, you can see a really nice schematic of what happens when a cell goes through the process of apoptosis. It breaks down. So what we have here on the left-hand side, the bright orange with the yellow is your cancer cell. The green is your T cell that has been brought to the tumor by the trastuzumab, so trastuzumab is in here. And I just want you to see when we run this video, that you can see that these bright cells are called viable. They're living, they're healthy, and as they go through it, you'll notice them getting dark in color, you'll notice to get...
See them getting irregular, and then you'll see that those apoptotic bodies as they disappear. So we'll just run this. It only takes a couple of seconds. You're starting to see the color decreasing now, and then you'll see the apoptotic bodies coming on the outside of it. Can you see it? And that's your cancer cell gone. That, that's it in action. That's what it does. So it's really nice to see that. You're going to see a few more of these in relation to many of our cells. So why CD16? We talked about exhaustion, we talked about a number of things. The real beauty about it is, it won't work unless you give an antibody. So if someone is having a toxicity, don't give the antibody. If somebody is suddenly become resistant, give a different antibody, it'll still work.
So it overcomes many of the issues we see with cell therapy in terms of antigen escape. But there's also another piece in that this works incredibly well in vivo, but we need to translate this now into patients. And for that, the history has told us the cell therapy space has had a very difficult time over the last couple of years because the results haven't been entirely what we wanted them to be. While they've been good, maybe not good enough. But I think now we understand the importance of editing these cells, editing them to improve functionality, to address the tumor microenvironment, really important, really get better at our tumor targeting.
Make sure that you retain that stealth so they're not seen by your immune system, really important, and avoid any graft versus host disease, which we think is incredibly unlikely with our material. But nonetheless, this is important that we do that, and, and we do have a gene editing partner, which we're not currently allowed to disclose. But this is setting us up to be certainly a first-in-class, best-in-class approach to multiple tumors. Now, you'll notice an antibody, hopefully, in the middle of the schematic there. The reason it's there is that there's multiple antibodies. Now, the trastuzumab data that I shared with you has just been presented at the AACR, sorry, which is prestigious conference, which my colleague Katy presented over there.
All the data on the other antibodies, that I cannot share it with you 'cause it's embargoed, because it's gonna be presented at ASCO in just a week and a half's time. So, for those of you who are interested, you can watch out for that. All the data I presented on the placental difference, that was recently published in the J, the JITC, a prestigious manuscript. We have copies if anyone is interested, but while it's a very technical, it's a really interesting read, and I think this is the first time we've really been able to take all our research over the years and bring it together as one to show this is why this starting material may be better. But I don't want us to forget our NK cells.
I still think they have a fundamentally important role in managing disease. For us, right now, in our approach with HER2 positive tumors, T cells likely to be better. But that's not to say they're not effective. This is looking at our NK cells. This is called 101. 101 is the, our NK cell with our CD16, so the universal engager, adding in trastuzumab, and this is against gastric cancer. Now, you can see when you add the SYNK- 101 with trastuzumab, you get a synergistic effect, much better tumor shrinkage. Really important. Now, I'm gonna show you another video so you can see it. Now, I want you to look at a couple of things. You'll see one cell out on its own that's getting ganged up on by our NK cells. Great.
But then I want you to see what's happening in the clump of cells. That's a big lump of tumor. 'Cause what we want to see is the NK cells going inside into that and actually working within the tumor, infiltrating this tumor. So we can look at this again. Hopefully, you can see that, poor tumor cell being surrounded. You'll start to see it getting dark. You'll see it starting to break up, and you can see an NK cell inside in the clump. Can you see that? It's gone in, gone right inside into the tumor. And you can see that lovely picture of that apoptosis scene right in front of you. There you go. It's just gone.
So for anybody who doubts the power of cell therapy, they should watch these because, yes, it's going through a hard time, but these are amazing, amazing therapeutics that once we get it right, they're going to have completely revolutionized the care of these patients. The reason I wanted to show you cells, but I'm not taking it in cancer, but we've already touched on it. Cancer cells and senescent cells look remarkably alike, and we can target them, and I'm gonna show you some of the data on that, too. And you, you'll get to see yet another video. Don't worry. Senescence. Now, Bob has covered this very well, but I want to take you through why senescence is important. We talked about telomeres. Telomeres, they get shrunk to a certain level, after which they stop dividing.
That'd be great if they just died or disappeared in some way, but they don't. They become as close to immortal as can be. But what do they do when they're doing that? Well, they produce cytokines and cause inflammation. So what does that mean for all of you sitting in the room? Well, if you get. There's a thing called inflammaging. This inflammation in your muscles causes sarcopenia, reduced muscle amount of muscle. You see that. It's you know, you can see muscle loss in these patients. You can also... We don't call them patients, they're just people. This is normal. But also, it's in lots of other types of disease. Senescent cells are important, though, as long as they're transient. We have to have mechanisms by which we can remove them.
They're generally your NK cells, but as you get older, your NK cells and your surveillance mechanisms are not quite as good, and therefore, they're allowed to continue. So when you look, we've got a graphic there on transient and persistent. In the transient, they're really important. They actually prevent tumors, and actually, for the developing embryo, really important that we have some senescent cells 'cause it dampens down immune systems and everything else. It's when they become persistent, they're a problem. And there's one piece that for those of you who have any relatives, who are aging, we talk about the phenomenon of slow then fast. There's the sudden decline. Why is that? It's because these senescent cells become self-perpetuating, they drive further senescence. So it gets to a point where you suddenly decompensate, and things get an awful lot worse.
This is the same thing with senescent cells, all that inflammation, your NK cells, your immune system has dampened as well. They're not able to surveil, you're not able to get rid of the mutations, you're at high risk of cancer, you're at high risk of multiple age-related diseases and fibrosis. So we think targeting this is incredibly important. Bob showed this earlier, and it's just to show you that those senescent cells, once they start building up, you're at high risk of mutations, you're at high risk of cancer incidence increase with age. Yes, young people get cancer, but a lot more older people get cancer. That is for sure. So it's really important that we think about that, because if we can address the issue of senescence, we don't have to treat cancer, we can hopefully prevent cancer.
I think that's a much more desirable outcome for everyone. So the one thing we can do, if you stress a cell, you can, you can make them senescent, right? And an easy way of doing it is give them some chemotherapy. So this is, this top graphic, there is no zooming. These three images are the same magnification, but what it's doing is we've taken some normal cells, treated them with some chemotherapy, made them senescent. And what you can see, the cells, they lose their structure, they get bigger, they get flabbier. They're clearly morphologically different. The one thing they do is they express something called beta-gal, so we can spot them, generally speaking. So we've been able to measure the beta-gal across these, and so you can see we're able to induce senescent cells. The next thing is, can we kill them?
Can we preferentially target senescent cells? The answer, of course, is yes, and you can see it in the end graph there, cytotoxicity. What you can see is the top two graphs. Now, just a reason why you'll see some killing in the normal cells, 'cause these are based on tumor models, so you're going to get some background killing. But it's the delta you're seeing, that's the senescent cells, preferentially targeting the senescent cells, and we can see that in action on the next one. So I'll probably get you to look at the left-hand side. These are fibroblasts. What you can see, much bigger, not that attractive-looking cells. But what you can see is these are NK cells. The only thing different about these cells, they're senescent, and we can see it targeting them, we can see it killing them.
This is really important, 'cause if we can translate this into humans, we are. I think it could be revolutionary in terms of what we could do for patients. So I don't know, hopefully, I've convinced you that cell therapy is tremendous. It's exciting, and I would say despite the hundreds of companies that are working in cell therapy with sometimes negative results, I don't think the cell therapies have failed. We just haven't cracked the code quite yet, but I think we're really close. So I want to then now move on to our neurodegenerative disease. Guess, you know, for those of you who have relatives, you will be aware dementia is front of mind for many of us, elderly parents start to struggle. But again, it's an age-related disease.
I remember when I was in medical school, somebody told me, "If you live long enough, you're guaranteed to have dementia." And I think with our aging population, you're going to see far more people doing it. But now at least we're starting to understand why, and once we can start to understand the why, there might be something we can do about it, and that's where our MLASCs come in. We've got extensive clinical experience with our MLASCs. We have had great results in Crohn's disease. We've had diabetic foot ulcer trials, which showed almost 40% complete wound closure. Steve showed a lovely image earlier on that I'm sure we all loved, but those kind of wounds, we can get complete closure with this therapy as well. So it's really interesting. But why do our MLASCs work?
Now, these types of therapy have been routinely investigated in Crohn's disease and currently marketed, but there's a lot of probably near misses with these therapies. But that's because we probably didn't understand the fundamental biology of how they work, and I think now we do. I think if I was to explain how they work, I would say in two ways: immunomodulatory and regeneration. We've seen many of our products are associated with regeneration. So the immunomodulatory macrophages, for those of you who aren't aware, macrophages are the kind of ones that phagocytose, they get rid of viruses, et cetera. But there's two types, M1 and M2. M1 is the inflammation. They cause lots and lots of inflammation, they stop cell division. Not good.
The other is M2, which is very much reduced inflammation, pro-wound healing, and we can see that if we treat with our MLASCs, you get a switch from the M1 to M2. Very good for wound healing. Really important. Dendritic cells, they're an interesting one because we have two parts to our immune system. There's the innate and the adaptive. The innate is your first line, but then when the first line doesn't work, there has to be a signal to tell your immune system to kick in, and that's where dendritic cells come in. So they, if they're overactive, you can get a lot of inflammation. And again, our MLASCs dampened that down, became more of what we call tolerogenic. Really important aspect. And the T cells, really important, produce lots of these cytokines we talked about. Hugely important in autoimmune disease.
We talked about cancer, we've talked about aging, but immune disease is really important, specifically two types, Th1 and Th17. They drive the production of things like IL-23, IL-17. Really, as targets on their own, we're able to actually diminish those quite significantly. So from an immunomodulatory perspective, they're really powerful. But then, when you say about the regenerative, we hinted on the wound healing. They are regenerative. And when we look, there's three pictures down the bottom, which, first is stroke. And what you can see is it's not a big image, but you can see new blood vessels there. Really important. And that's probably one of the reasons why we have such good effect in diabetic foot ulcer. You're actually getting blood flow back. Really important.
The middle one is kind of a teaser to the next slide I'm about to show you, which is related to Parkinson's disease. We have TH neurons in our, in our brain. TH neurons are the ones that produce dopamine. We know that dopamine is really important, and it's a deficit of dopamine that causes Parkinson's disease. We'll go into that in a bit more details. Hopefully, you can see that the staining is your TH neurons, lots more. And the third one is really showing the reversing of limb ischemia, which is, you know, put together, they're a powerful treatment, but what's the best place to use them? And we have a few ideas. And I'll take you through that.
We've talked about Parkinson's disease, but what people don't realize is Parkinson's disease is really one of a multitude of diseases that are on a spectrum. It's all about Lewy bodies. Parkinson's disease on one end, and the other end of the spectrum is actually Lewy body dementia. For those of you who haven't heard of Lewy body dementia, Robin Williams had Lewy body dementia, so it's something that affects about 15% of patients with dementia, so a very significant problem. And it all depends on where you get your deposition of proteins. It's either in the substantia nigra, which is for Parkinson's, or the cortical region for dementia. But because it's progressive disease, they ultimately meet in the middle, and you're gonna get Parkinson's disease and dementia. So, you know, this, there's no upside for these patients. This is a rather devastating disease.
But I'm gonna take you through a bit of data. Now, the first thing to, if we look at the two slides, we're looking at two things. We're looking at TH neurons. These are the ones that produce dopamine. Because Parkinson's disease is deficit of dopamine, really important that we can try and protect those. And the second is alpha-synuclein. We know in Alzheimer's disease that it's deposition of beta-amyloid. This is not different, it's just a different protein deposition that's causing it. It's called alpha-synuclein, so it's, it's predominantly alpha-synuclein. We're looking, 'cause back in 1982, there was a number, seven young adults got Parkinson's. Very unusual. It's just, in the same area. And they realized they had taken a synthetic heroin, which had given them Parkinson's. It happened to be something called MPTP, a synthetic heroin.
But it was that that allowed people to understand what the pathogenesis of Parkinson's disease was. And that allows us now to treat animals with MPTP, induce Parkinson's, and see, can you stop the ill effects of that in two ways: looking at the TH neurons and the alpha-synuclein. What you can see from this, without going into details, if you give someone our MLASCs and treat them with MPTP, you protect them from development of Parkinson's disease, and you protect them from the deposition of that alpha-synuclein. That is hugely important to us. Why? Because we have now completed all the preclinical studies. We are working towards our IND, and that's going to be over the next period of time. That is probably an area we are going to be very active in. We believe this has got huge unmet need and a huge commercial opportunity to us.
This data is pretty compelling. You will have seen from the pipeline slide that our nearest term asset is actually in something called facioscapulohumeral muscular dystrophy, FSHD. I'm going to use FSHD from now on. Now, it's an interesting disease, and it's not that uncommon. It's about one in twenty thousand. Right now, it's 17,500 cases just in the USA. What is it? It's a genetic mutation of the DUX4 gene gets activated. When it gets activated, you get disruption of normal cellular function, which cause muscle damage and inflammation, stress, inflammation. It's the inflammation that gives you that progressive, progressive muscle weakness and atrophy. Really important. Why is this important to us? Well, we've touched on the importance of muscle loss, sarcopenia.
We know that if we can show a benefit in FSHD, we're likely to have an effect broadly on muscle and preventing further muscle loss in age-related frailty, sarcopenia, and other muscular dystrophies. So we think there's a compelling reason why this should work here. But while it's not that uncommon, still about 25% of patients over 50 require a wheelchair. This is a huge burden to society. Now, where are we with this? We have our IND cleared, and we were rather hoping by today we'd have had our orphan drug designation decision. It's hopefully imminent, but this is probably our nearest term clinical program. That's not to say we're you know, this has been a busy, busy 2024. We've had multiple abstracts and publications presented at the most prestigious conference.
We're going to be at ASCO two weeks' time. We've just come back from the ASGCT, the American Society of Gene and Cell Therapy. We've presented at AACR, really well received the data, and the Journal of Immunotherapy of Cancer, there's a few copies of the manuscript there, if you really want to take it home. But also, you can see from Steve and Anna, a lot happening in that space, too. You saw Steve's slide where it showed how much data dissemination there is. When these products come to market, there's a lot of awareness out there. So with that, I'm gonna stop, and I'm gonna hand over to Dr. Ramji Krishnan, our head of technical operations.
Good afternoon, everyone. Thanks, Adrian. How do we go about doing all of this? Fantastic science, fantastic commercial capabilities that we can leverage on. As Bob commented earlier on, our technical teams operate in a commercial-ready facility to support all manufacturing requirements for Steve and his commercial team for advanced biomaterials, and at the same time, to advance our cell therapy portfolio. Our technical teams operate in a fully integrated fashion across process development, analytical development, clinical product supply, and commercial product supply to allow us and ensure complete operations in a manner that's commercially and clinically successful. We're not reliant on any third-party manufacturers, and we have sufficient bandwidth to support our partners for development and commercialization.
This state-of-the-art facility that some of you are going to get to be able to tour is well equipped to support the complexity of manufacturing for both allogeneic and autologous platforms, in addition to supporting the needs of advanced biomaterials. It is a purpose-built facility with multiple Class 10,000 suites for manufacturing of cell therapy products. The clean rooms are equipped to be flexible across the platform. It maintains unidirectional flow of material and personnel with appropriate controls through the classified corridors and airlocks. The manufacturing suite is also home to other Grade D labs for the quality control activities, media preparation, and other support functions. At the same time, we have identical at-scale equipment in all of our process and analytical development labs. This allows us to manufacture at scale in our PD labs. Why is that important?
It facilitates for a rapid transfer of processes and methods to the manufacturing team and ensures manufacturing success, and allows us to troubleshoot as appropriate in the process development labs. Our commercial-ready team and facility have supported successful outcomes during inspections by the FDA and audits through various other accreditation agencies. The FDA has reviewed our operations to satisfaction across all of our documents and records, supplier oversight, change controls, and training. We are built to be scalable, flexible as needed, and commercially ready. We can manufacture up to nine cell therapy products and/or up to 18 tissue-based advanced biomaterials as needed. All unit operations for autologous and allogeneic operations are well supported through a robust quality oversight for chain of custody and chain of identity, from the initial starting material receipt to shipment back to the treatment center as needed.
As a result of our combined technical strength and our superior state-of-the-art facility, other leading biopharma drug developers have engaged our expertise to support the needs for technical development with their next-gen cell therapy services. With that, I'm going to hand it back to Bob.
Thank you. Thank you, Ramji. So I appreciate everybody's attention. I know this has been a pretty in-depth discussion. I think everybody can see that there's a lot going on here. As a company that spans regenerative medicine and cellular therapy, you can appreciate that the skill sets required to perform in these areas is quite diverse, and fortunately, we've been able to take full advantage of the internal talent, and through these strategic relationships, amplify our capabilities by working with talent in other companies and academic institutions and so on. So our success can be amplified through strategic partnerships and collaborations with these leading academic institutions, biotechnology companies, industry experts.
These partnerships enhance our internal capabilities while exposing our capabilities to third parties that may, in fact, wind up becoming much more closely involved with our programs. It also opens up opportunities to broaden our commercial activities. They present business development opportunities that we think are incredibly important to our future, because a company that has the infrastructure we have is a... like I said earlier in the presentation, is really a potential partner of choice for these different players. What if— Let me see if I can go to work. So our vision for the future, looking ahead, is to continue pioneering advancements in cellular and regenerative medicine. We aim to further diversify and grow our revenue streams.
You've seen our strategy to take advantage of a new regulatory approach, which has many benefits compared to the current HCT/P regulations. We want to enter new therapeutic areas and bring these innovations to patients worldwide. There's an entire globalization opportunity in front of us, and we're looking to create a sustainable, diversified, and growing move towards profitability as quickly as possible. In conclusion, Celularity addresses aging-related diseases through innovative approaches, as mentioned, our growing diversified revenue and our development of new regulatory approaches to get new products, ever-increasing innovative products into the marketplace, will allow us to capitalize on potentially multi-billion dollar market opportunities. Our investment in the state-of-the-art infrastructure we've got, we believe, is going to pay dividends going forward.
There's no, there's no doubt that in the last three years, our industry, biotech in general, as an industry and cell therapy, specifically as a sector, has really faced unprecedented challenges. We believe our business model, which is unique, creates both a pathway to profitability as well as long-term value creation that's very differentiated from other companies in the field.... We appreciate all your attention, appreciate your support, and look forward to continuing to report on developments in the coming months, and we believe that 2024, 2025 will be a pivotal time in our company's history. Thank you very much. So it, it, we do have an audience online, and we've got a couple of questions that have been asked.
I'm gonna ask my colleagues to join me up here, so you can address some of the questions that we have. And then if we have time, I'll see if there are any questions in the audience here. Steve, if you can address the first two questions right here.
Sure.
If you wouldn't mind reading them as well.
Yep. So question number one is: can you give us a sense of the reimbursement landscape in tissue repair? It's been a moving target in the past. Is it attractive in the United States? It's a great question. You know, as I alluded to during our discussion, you know, the market, I think we've anticipated these changes in the landscape for quite some time. And, you know, we, we're not quite sure where it's going to go, although we feel like we've got an opportunity to understand it. But what I do know is that, you know, we showed, both Adrian and I showed you both slides of the importance of how we stress our peer-reviewed literature and evidence-based medicine to support what we're doing.
And I do believe the market is shifting in that way, where that's gonna be reinforced. And today, you know, three of our products have, you know, national coverage. Three of our products have, you know, excellent commercial coverage across the country, which leads to access. You know, when we look at the patients that are in the markets that we serve, you know, that is an important way of reaching those people. And so, you know, I think from a current landscape, I do believe that we're in a position of strength.
I do believe that we're evolving with those changes that are coming that will keep us in a position of strength, and I'm very bullish on how we can find ways to help, to continue to help patients. The second question that we have is: Does your bone growth approach work faster than current approaches based on reduced bone resorption? And would the approaches need to be staged if used together? Another great question. Thank you. So when you look at Project Fuse, you know, healing of any type is based off of three main principles: cell, signal, scaffold, okay? And those signals can come in a variance of order, depending on what you're trying to achieve.
In the setting of bone growth, ideally, what we have to have is a signal tied to a scaffold that becomes an attractant to cells to continue to build. If we're building a skyscraper in New York City, we start at the base, and we want to build up. It's no different with bone repair. And what, Anna and her team have been able to create is a placental-derived scaffold that basically acts as a very attractant signal to a bone cell so that it continue to migrate across the scaffold. The bone cell itself then will release the important growth factors that will allow a signal to occur for more recruitment of bone cells, and ultimately, what you don't see is resorption. What you see is addition.
You see a cumulative effect of a recruitment of bone cells that build a scaffolding effect to allow for repair to occur. And again, that's really a guiding principle, not only of our advanced biomaterials that you're going to see downstream, but also what happens today in that homologous, minimally manipulated effect. The scaffolds purely serve as an attractant for those cells, and the body does its work. It's able to facilitate the body's endogenous physiology to allow the body to get out of its kind of revolving door of the inability to heal. And that's really how the bone project works, as well as our commercial materials today.
Great. Thanks, Steve. I've done my mic?
Oh, sorry.
We have one more question related to our natural killer cell technology, which Adrian and I can handle. The question is: Can natural killer cells target senescent hematopoietic stem cells from older bone marrow? Now, that's a great question. Here's the bottom line: all cells which undergo the process of senescence that are truly senescent in their phenotype upregulate expression of what are called stress ligands. These are molecules on the surface of the cell, which act like red flags to signal that they need to be cleared. This is a highly conserved biological mechanism, which is part of the process of everything from embryogenesis and fetogenesis, all the way through to how our body renews itself and renovates itself during our lifetime.
So as long as senescent hematopoietic stem cells express those stress ligands, our natural killer cells would, in fact, target and kill them the same way. Do you want to add anything?
Yeah. In many ways, it's almost even easier for us with this one because we've had many head-scratching moments, Bob, where we're saying: "Where have they gone?" We talked about the persistence of our cells because they disappear, and then they come back a while later. So where did they come from? We thought they were gone. They're not. They've gone to the bone marrow. So all our NK cells actually preferentially go to the bone marrow initially. So actually, the bone marrow would be probably an easier one for us. To your point, you get the clear senescent markers, and they're going exactly to where that's gonna be. So yeah, it's a resounding yes for that one.
Right. And that just highlights one important thing. We've talked about the changing landscape in cellular medicine. Regenerative medicine is making its way, and believe it or not, what we're doing in the biomaterial space is really the first reduction to practice on these tools. But in terms of what's hot in the industry, in the biotech industry, I'm sure you're all hearing all the news about the future of longevity therapeutics. Many of you probably have seen people like Bryan Johnson, the tech billionaire who's investing all of his wealth at reversing his aging... And by the way, I know Bryan for 15, 20 years, he's actually doing it. He's 55 years old. His biological age, calculated using different markers, is now in his twenties.
He's done so principally by very, very rigorous diet control, exercise, supplements. But one of the other things that he's done is he actually has been transfusing himself with young blood. What does young blood have? Young blood has natural killer cells, it has other immune-enhancing cells, and so he's combating a process called immunosenescence by replacing old cells with new cells. Well, doesn't that mean that a company that's in control of newborn cells has a significant technical advantage? That's one of the reasons why we believe that our first approach, leveraging what we learned with our NK cells in cancer, paves the way for us to be an important player in the longevity space. Okay, so I think we have a few more minutes. Any other questions from the audience?
So, Bob, you've been in the space for 25 years. When you started, there was no such thing as CAR T cells. Then it became really hot in liquid tumors and solid tumors, not as hot, and then 3 years ago, there was no discussion of CAR T in autoimmune disease. Now it's white hot. If you look out 5 years, where do you see cell therapy going next? You had the liquid tumors, which have done very well. We've now had autoimmune disease, which is now really surging. Again, if you put on your crystal ball, looking out five or 10 years, where do you see cell therapy having its next big impact?
That's a great question, Mark. Everything we have been working on and have learned over the last seven years, six, seven years, since we spun out of Celgene Corporation, is that the tools to engineer characteristics in cells are becoming increasingly sophisticated. They're becoming increasingly accessible, and as long as you have a cellular platform that is that is amenable to being engineered, you can potentially surgically precise in a precise way, use an engineered phenotype to seek and destroy anything that you want to eliminate from a tissue. Obviously, CAR T, the first target was malignancies, cancer, but you've already pointed out that eliminating certain aberrant immune cells may be, may be one of the most powerful ways to control autoimmune disease.
So I think that in the next 5-10 years, with the advent of greater and greater clinical experience with engineered cell types, with the increasing data set around the safety, tolerability, and effectiveness in more common disorders like autoimmune disease, you're soon gonna see that these same editing tools put into the ideal cellular platform will be used to augment defective or deficient tissue systems and cell systems or reprogram those systems. And so one of the areas we are very, very optimistic about is as the biotech market begins to, we believe, take another uptick, you'll see an increasing number of collaborations between the editing companies, the companies with the tools, the platform companies, and the companies that control the most important part of this in our mind, which is the technical operations.
Having the capability and the know-how, the expertise to produce cellular products to a clinical grade is a clearly, clearly differentiator in the industry.
Bob, first, thanks for the review of the business. It's outstanding. Thank you. What's the current utilization of your facility today? You have a state-of-the-art facility, very impressive. What % utilization do you have?
Another great question. So, we spun out of Celgene Corporation at the end of 2017. While at Celgene, while operating as the cellular therapy division of Celgene, we occupied a range of locations in the Celgene empire, real estate empire. One of my big objectives as a newly minted private company was to raise enough capital to build a world-class facility because we knew that we had clinical and commercial stage biomaterial products, and we were very optimistic about taking our cell therapies in cancer aggressively forward. As the market conditions changed, in some ways, as a consequence of the pandemic and also simply change in market sentiment, like every company in our industry, we scaled back considerably.
So today, we use probably 25%-30% of our operating infrastructure, but that actually means that we become very appealing and very attractive to companies in need of that technical expertise. As you know, we mentioned in the, I think we have a slide I can show you. In this slide, you can see that one of our development partners is a major biopharmaceutical company that has tremendous resources but didn't have the internal expertise around the engineering, manufacturing, production, and editing of cells. And so we were, at that point, an obvious potential partner, and we're very fortunate to be working with them. I actually envision in the future, we're gonna see many companies, you know of many of them, some of them are local here in New Jersey, many are domestic.
They will be well thought to come and work with a company like ours for two reasons: one, we have that capacity, we have that expertise, and number two, many of the existing contract manufacturing partners that are offshore or international companies such as WuXi are currently a source of concern because of the migration of data, both human clinical data as well as intellectual property, out of our country. And so there's a threat, there's a fundamental business threat to working with companies that aren't U.S.-based and established.
Well, I think needless to say, it's a rare asset with a rare set of skills there. My next question is: when do you anticipate profitability?
Great question. We obviously are aggressively developing our revenue-generating part of our business. I mentioned in the presentation that in addition to the biomaterial revenues, we're leveraging our 25-year experience in biobanking to launch a program in adult cell banking, which I think is going to be accretive to our business. I can't give you any specific forecast. However, it's my personal mission to help drive this company to profitability in the next 12-18 months. Now, that is going to have a great, great impact on where we deploy resources. We're gonna have to be very, very vigilant about investing where we have high probability of success. But when you look at the opportunities with the 510(k) products, some of those markets are tremendous.
Again, can't promise anything, but it is my hope that in the very foreseeable future, this company will go from cash-consumptive to cash flow neutral to cash flow positive.
Thank you.
Thanks.
Bob, we had a question about our ability to expand-
Yes
-online.
So another great question: What about the global opportunities? Well, one thing which is for certain is that, our business is visible to companies and to investors that wanna bring technologies in traditional cellular medicine, like cancer and autoimmune disease. But more recently, there's tremendous attention and interest in bringing our technologies into medical tourism environments in Asia, in the Middle East, in Eastern Europe, in Latin America, because the demand for cellular products in those countries is a growth industry. What we're doing is we're in a very cautious and well-thought-out manner, we're opening relationships with parties.
And by the way, one of the companies on the screen now, Genting Berhad, our largest investor, is an international conglomerate based in Asia, that is already working to develop this medical tourism capability, in parts of Southeast Asia and potentially even, even China. What I can, what I can say is that we're open to any opportunity which meets all the requirements, the regulatory requirements, allows us to participate and collaborate with scientists and clinicians in, in those communities, and allows us a pathway to whatever regulatory hurdles we have to meet in order to be operating there.
Bob, one second. I have a question.
24 for you.
It's on? Hi, I have a question. Has the company provided any guidance for revenue for 2024?
That was just the question asked over here as well. So, early in the year, we indicated that we currently anticipate total revenues for 2024 to be in the $50-$56 million range. So, we hope to shortly be able to reiterate that guidance and update based upon our audited Q1 results. But I'm very optimistic. And, if we can meet some of the other revenue-generating opportunities, such as in our banking business, we may be able to actually exceed those numbers. All right. Well, I again wanna thank everybody for taking the time and giving us your attention.
I think we'll give everybody a brief break, and then we're gonna start providing all of you an opportunity to tour the facility and see how we, how we operate here. Okay? So thank you very, very much.