platform is based on a very normal immune response to a very normal or common virus called Epstein-Barr virus. You might be more familiar with this. It's called mononucleosis or kissing disease. Pretty much everyone's infected by the age of 35, about 95% of the population. And what we can do is actually take this immune response. So we all have an immune response. We create T- cells, and we can basically take these T- cells and make it into a therapy. And so that's what we did for our lead product. So this is a product called Ebvallo, also known as Tab-cel or tabelecleucel. This is really taking these T- cells that recognize Epstein-Barr virus, and we take these for Epstein-Barr virus-driven disease. So most people that have normal immune responses can essentially keep Epstein-Barr virus at bay. It doesn't cause any downstream consequences past that first infection.
However, some patients have compromised immune systems for one reason or another, and that can allow these EBV-infected B cells to basically proliferate uncontrollably. So this product is actually right now commercialized in Europe through our partner. It's a French-based company called Pierre Fabre, again under the brand name Ebvallo, and we're making good headway with the FDA. We actually have a PDUFA date target action date of January 15th, 2025, so it's coming right up for a potential approval. And then we also take this platform and we're able to build on this. And so it has some unique attributes, which I'll talk about in a minute, for our CAR part of the platform. So you might be familiar with autologous CAR-T. They've been around for seven, eight years or so. They've been transformational for the hematological side, liquid disease basically.
And so we take this platform, we stick a chimeric antigen receptor in there, and that's the CAR. So we have two assets on that side of the portfolio, ATA3219, that's a CD19 CAR. We have a phase 1 study in autoimmune disease right now for lupus. So we have two cohorts, lupus nephritis, as well as one in extrarenal lupus without lymphodepletion. I'll talk about that a little bit, but that's a very unique differentiated aspect that very few other companies are pursuing that no lymphodepletion or no LD cohort. We also have an ongoing phase 1 study in non-Hodgkin lymphoma that also is a CD19 CAR with initial NHL phase 1 data expected in Q1 of 2025. So again, coming right up, and that lupus data is coming mid-2025. We have another asset a little bit further behind. It's a bispecific. It's a dual-targeted CD19, CD20 CAR.
We're anticipating an IND for the second half of next year. So just to kind of lay a little bit of a foundation here about what we do. So autologous, as I talked about, this is what's currently on the market. There's six CAR-Ts. This is basically a patient presents with some kind of malignancy, cancer. A manufacturer will essentially extract the cells, ship it off to the manufacturer. They will put the CAR in and then ship it back to the patient. So that whole process takes three, four, five, six weeks. There's a lot of limitations associated with that, as you might imagine. If you have a cancer patient that is rapidly progressing, you, of course, wouldn't want that person to have three, four, five, six weeks of waiting time. So they normally have to go on bridging therapy, which is obviously not ideal.
Lupus or autoimmune patients as well, you don't want them to get off their immunosuppressive drug regimen. There's capacity constraints, scalability constraints, especially as you move into autoimmune space. There's very severe limitations with that. So allogeneic has been something that's kind of come up over the last couple of years, maybe three or four years. That's making some headway in cancer, and it's really moved into autoimmune as of late. But what this is, is it takes cells from healthy donors. As I alluded to at the beginning, we take cells from patients that have been exposed to Epstein-Barr virus, but the concept is the same across all allogeneic companies, is that they take these cells from healthy donors, they stick the CAR in, they scale it up, and then they bank it. They put it in liquid nitrogen.
The whole concept here is that they're ready to go before a patient needs them. So a patient presents, we can ship it to them within three days, as demonstrated with our Tab-cel product, rather than having to wait three, four, five, six weeks. So that's the main difference between autologous and allogeneic. Now, a little bit more about kind of the economics and supply challenges for autologous. So right now, even the best in the business, Kite Gilead, they only have about enough slots or capacity for 6,000 starts per year. There's very obvious limitations with that, even in the cancer space, multiple myeloma. When you're looking at incidence prevalence rates of tens of thousands of patients, there's just an obvious breakdown from just a scalability perspective.
When you start talking about autoimmune with tens of thousands, hundreds of thousands, millions of patients where CAR-Ts are moving into now, there's no business case for autologous, so the field is really moving into allogeneic and in vivo, which is, I think, a little bit further removed from reality yet, and I won't be talking too much about that today, but that's really where the field is going. You'll see a lot of these big companies looking at allogeneic platforms because of that, but the proof of principle is really in the autologous. The other aspect of this is just cost. It's very expensive. We're looking at COGS in the high five-digit, low six-digit number range for autologous, where it goes down to very low, as you can see for allogeneic, which again allows for the scalability aspect.
One donor can actually scale to hundreds and thousands of doses versus a one-for-one, which is current for autologous. Now, this brings us to Atara. What we do is, as I talked about, we take healthy donor cells. We have healthy donors from across the United States. We have very specific criteria that we look for, and we essentially extract out and enrich for those T- cells that recognize Epstein-Barr virus. We do that for a couple of reasons, but the main reason is that every allogeneic company has to solve for two things, every single one. How do you get a foreign cell into a patient without it causing an issue? Like graft-versus-host disease, for example. How do you get the cells into a foreign host without that host or patient rejecting the cells?
Because again, it's a foreign cell at the end of the day. Most companies, if not all companies, there's only about one or two that don't gene edit out the T-cell receptor and the MHC, or the major histocompatibility complex. There's limitations with that, just with gene editing, generally speaking, that introduces double-stranded breaks that can cause genomic instability. It's a very inefficient process. At best, it's about a 60% efficient process. So if you're looking at two, three, four edits, it's obviously 0.6 times 0.6 times 0.6, et cetera. So you're going to a very low efficiency process when you're looking at manufacturing. What we do is we keep the Epstein-Barr virus T-cell receptor. And I like to kind of use the analogy as like putting blinders on a horse. If you do that, horse can't look left, can't look right, can only look straight.
It's what these T- cells do. On the normal manufacturing and scale-up process, you'll have T- cells that are what are called polyclonal. So they have T cell receptors that can recognize all sorts of things. You put that into a body, it's going to cause graft-versus-host disease. You put a T cell that can only recognize Epstein-Barr virus, it only recognizes Epstein-Barr virus. And if it does, that's great. That's fine. We can obviously eliminate Epstein-Barr virus. It's not a desirable virus to have in the body. And then the other part of this is actually kind of just basic transplant biology. You can't just stick any old organ right into a patient and expect it to graft and stay there. It's going to get rejected. You have to have a certain level of matching. So we do the same thing.
It's just not the same level of stringency. So we do two out of ten allelic matches. And basically, and very simplistically, it's just making our cells look similar enough to the host that it doesn't get rejected outright. Of course, these cells are going to get rejected eventually. If they didn't, we would all die of autoimmune disease. So we want some level of rejection eventually, but we want these cells to stick around long enough. And so that's the basis of our platform is that we have these Epstein-Barr virus T- cells. Again, we can use them in its native form. That's the basis of Tab-cel. Or we can use this platform, stick chimeric antigen receptors and redirect them towards different protein targets for different diseases. Now, for Tab-cel, like I said, that's our product that's already approved in Europe.
We're tracking towards a PDUFA target action date of January 15th of 2025, so great headway. This is a very unique product. It's a very ultra-rare lymphoma. It's ultra-rare indication. It's only a few hundred patients per year. We have orphan drug designation, breakthrough therapy designation. There's actually no approved therapeutics on the market for this indication. There's no competition really, even in the pipeline whatsoever. I think there's one academic study that's looking at a phase one, and this entire product now is actually we made a corporate decision a few years ago to partner this completely out with that company that's commercializing this in Europe, Pierre Fabre, and so what that looks like is we have $640 million in potential consideration total.
The deal kinetics is that we received $27 million upfront, $40 million from regulatory milestones that we've achieved so far, $60 million contingent upon that BLA approval in January. Then what happens after that is this product essentially is off of our books. We're left with significant double-digit tiered royalties, sales and commercial milestones moving forward, and then a step down and basically spend because we're not spending any money on Tab-cel. At that point, we become a smaller, very focused allogeneic CAR-T company, again using this EBV-T cell platform, but for CAR-T therapies. What we've done so far is, and really unique, is that we have over 600 patients that we've treated across Tab-cel and another asset I'm not going to talk about. We can talk about it later after the talk if you'd like, that we did in multiple sclerosis.
But we have over 600 patients that we've treated far more than any other company in the allogeneic space, which is very interesting. And really what we're trying to do is move away from this kind of onerous, complicated, expensive autologous CAR-T patient journey to what we did with Tab-cel and 188, which is it's off the shelf. Patients don't have to undergo apheresis, which is a significant benefit to patients. They don't require lymphodepletion. So we've never used lymphodepletion, which is a standard for all CAR-T therapies to date. Five- to ten-minute outpatient infusion, one- to two-hour monitoring, which is very different than that one- to two-week inpatient stay that's required right now for patient monitoring. So that's kind of this we're not there yet. This is aspirational. This is kind of our vision for our CAR-T platform.
Now, as I alluded to, allogeneic really does require a different approach to overcome some key challenges. One of these, again, is this graft-versus-host disease. If you just stick in a whole pool of T- cells into a body, it will cause graft-versus-host disease. You will get allo rejection because that host will essentially reject it. So you have to solve for that. These cells also kind of first, second generation CAR-T, you can essentially have too much activation too quickly. It's kind of like to give it, again, the analogy of giving a kid too much sugar. They get really excited and they're kind of tired. T- cells do the same thing. They get really activated and they kind of get tired over time and lose their effectiveness. So you have to solve for that.
An inflammatory response, which basically goes to what I just said, is that if you have too much activation, you have too much cytokine release. That's how T- cells work to kill their target cells. If you have too much of that, you get cytokine release syndrome, neurotoxicity. These are very known side effects from a CAR-T, hence the one- to two-week inpatient stay that you have to have to monitor CAR-T. Our platform, as I talked about, 3219, it's a CD19 CAR, CD19, CD20, dual-targeting CAR for 3431. How we solve for those, as I talked a little bit about now, is that we have that Epstein-Barr virus T cell platform. This really solves for the graft-versus-host disease as well, as well as the allo rejection component of it.
We also engineered a couple of other key features that we talk about here. 1XX signaling domain is one of them. So I talked about with a chimeric antigen receptor, you can essentially get too much activation all at once. So what you can do is kind of slow down that activation. And you get the same overall activation, but you just kind of attenuate that initial curve. So it's a little bit softer. So you have less cytokine release. And what that literally does for you is reduce the cytokine release syndrome side effect that you might have downstream. What it also does for you is it drastically increases potency and helps mitigate exhaustion. So these T- cells basically just work better, stay around longer. And the other part of this is the less differentiated phenotype.
This is basically T- cells and all cells can kind of take different states, right? So you have kind of more of the stem cell state, more of the differentiated state. Stem cell state being able to make more of itself in the differentiated state are kind of more of like the soldiers. Those are the ones that go out and are able to kill the target cells. So we and many others, Novartis, Takeda, have demonstrated that this more memory phenotype, so it's kind of right in the middle, it allows more in vivo. So when you get into the patient expansion rather than having the expansion ex vivo, so outside of the body in the lab, such that when you put it in, it doesn't have that strong activation. It's a little bit softer, but you still have that full activation, but again, potentially less cytokine release.
Now, what's the unmet need here? So I presented this in two different ways here for oncology on the left, lupus, and kind of autoimmune on the right. But for oncology, as I said, autologous CAR-T has been on the market for a number of years. However, there's access challenges. So there's room to compete here from two perspectives here or two angles. One is accessibility, one is efficacy. The accessibility is for reasons, as I said, logistical, manufacturing challenges, scalability challenges. Really, only tier one academic centers have the capability and infrastructure to treat these CAR-T patients. 80+% of the U.S. population is treated in the community setting, and CAR-Ts just haven't penetrated there. So allogeneic potentially can kind of solve for that, but only 20%-40% of eligible patients right now are even receiving CAR-T in the first place.
Then of those 20%-40%, only 30%-40% are actually having a long-term durable response at six months. Again, efficacy isn't great. There's a lot of room to compete there. Now, on the lupus side, this has really been just a revolutionary switch over the last two years. This is from an academic lab from Dr. Schett in Germany. He basically said, "Look, B-cell-driven disease, CAR-Ts work extraordinarily well in the hematological setting. Why not do this in autoimmune? That's still malignant B cells and autoreactive B cells." So that's what he did. The study came out about a year and a half ago now, and the data are amazing. These are now gone through lupus, myositis, rheumatoid arthritis, scleroderma, myasthenia gravis, multiple sclerosis.
These patients have seen in the lupus setting in particular two, three years now of long-term drug-free remission. These are quite literally patients that have been on daily, weekly, monthly immunosuppressive therapies that have completely been removed from any therapies and had essentially full recovery. As you might imagine, there's been a huge influx of companies either doing full-scale pivots into the autoimmune space or using their CAR-Ts like we have ourselves moved into the autoimmune just because the opportunity there is ginormous. Like I said, there's millions of patients, up to eight million patients or so across the autoimmune conditions. Now, preclinically, like I said, we're just doing first-in-human studies right now. I have preclinical data to share today.
But what really gets us excited for the oncology side is for 3219, with all those different features and set up in kind of the profile of the platform that I talked about and a NALM-6 tumor model. It's a relatively rigorous tumor model in mice that we're able to see long-term persistence and much better efficacy than autologous counterpart. And how we do this is with the cells that we start with. We basically just make autologous cells and we make our cells so we can compare apples to apples. So this is exactly the same starting material. We just have different kind of differentiation pathways and development pathways, manufacturing pathways. And you can appreciate much better efficacy than the autologous counterpart. So this provides us a lot of confidence in moving into the oncology side. And autoimmune, this is also pretty interesting.
So what we were able to show here on the top left is that we had the same cell-killing capabilities as autologous, but with a much better on the bottom here, inflammatory cytokine release profile. So what this means and what this translates to is, like I said before, one of the major issues in CAR-T is cytokine release syndrome, ICANS, or neurotoxicity. So if you can get to a profile that has less of these inflammatory cytokines, interferon gamma, interferon alpha, IL-6, you might potentially have a better clinical profile, less toxicity, better safety. So again, we have to prove it. This is just preclinical data. But again, so far, we're able to see the same potency and efficacy preclinically and a better inflammatory cytokine release profile. Now, for 3431, I just wanted to kind of close on. This is our dual-targeted CD19, CD20 CAR-T program.
This is a really exciting one. One of the major issues with relapse in the oncology space is essentially just downregulation of one of the antigens. It's called CD19. This is due to selective pressure. If you have a CD19-targeted therapeutic, tumors, not that they can think, but they kind of just evolve to downregulate CD19, and therefore then your therapeutic doesn't work anymore. So by targeting both, you are basically guaranteed to have incrementally better efficacy. It's what we've seen already from companies that are before us in the autologous space. So ImmPact Bio, which actually just got bought out this week or last week, I'll say this week, and then AbelZeta, which is a Chinese company, they also have a CD19, CD20, and they sold their CD19, CD20 to J&J last year for $245 million upfront.
The efficacy that they've showed both are about 90%, low 90s in the objective response rate and mid 70s for complete response. This was at ASH last year. So the efficacy is outstanding, as you would imagine. So we're really excited to move this one forward, both potentially in oncology and autoimmune. It's early days in autoimmune, but there is some support that's come out that targeting both antigens could be beneficial in certain autoimmune indications as well. And again, for preclinical, this is a very challenging model. It's called a Raji model. So this is a CD19 low expressing model. And what again you can kind of appreciate here is much better anti-tumor efficacy compared to the autologous benchmark. This is actually very rare to show past day 30, day 40. You almost never see companies present this because most mice will just die at day 30, day 40.
So the fact that we are seeing day 60, day 70 survival is actually quite significant. So we're very excited, like I said, to move this forward. We're looking at IND of second half of next year. So where that puts us today is that we have two ongoing studies for 3219. So like I said, this is our CD19 CAR-T. We're expecting data from our non-Hodgkin's lymphoma study in Q1 of 2025, so coming right up here. For our lupus study, we have two cohorts. We have one in lupus nephritis and one in extrarenal lupus without lymphodepletion. I didn't cover this too deeply, but there's only about two other companies in the space that's pursuing a cohort without lymphodepletion. As I talked about, this is somewhat unique to Atara is that we have 600 patients that we've never used lymphodepletion in.
We do have pretty strong conviction on why we can do this without lymphodepletion just because we have in our platform never used it so far. We've seen, of course, really good efficacy from Tab-cel with a 50% lifetime objective response rate. We're anticipating data for mid 2025 for both of these cohorts. We'll be able to see these essentially side by side next year and be able to make some kind of strategic decisions about moving forward and potentially autoimmune indication expansion once we get that dosing down. ATA3431, like I said, we're expecting an IND. We're doing pre-IND work right now. We're expecting IND in the second half of 2025. Tab-cel, this is the asset that we have partnered out with Pierre Fabre. They're moving this forward. They'll be fully responsible for commercialization.
So again, we're expecting a $60 million regulatory milestone upon approval. We'll have that OpEx kind of burn decrease next year. And then we're fully focusing on the allogeneic CAR-T opportunity moving forward. So with that, really thank you for your time and happy to answer any questions.
Please. Can you just address your financials and your cash needs?
Sure. Yeah. So we have cash into 2027 right now. And that factors in a few things. So that does factor in the $60 million payment from Pierre Fabre that would, like I said, is anticipated Q1 of next year, as well as that royalty stream, as I talked about. We also will be selling intermediates and inventory to Pierre Fabre in January of next year upon approval because they're obviously going to be moving that forward. But yeah, so from a cash perspective, we're actually quite comfortable.
We just did an RDO about a month ago with our three largest investors as well as a strategic. So this is a large publicly traded biotechnology company that is choosing to remain anonymous at this point, but that was at a 15% premium as well. So between that and everything I just talked about, yeah, we have cash into 2025. And that also gets us through all the milestones that I just talked about as well. Obviously, if the data read out really positively, the needs could be different if we readily move into different indications, autoimmune indications, for example, we would probably be expanding, but we'll have to look at that.
That's a good way to get there.
Yeah. But of course, I mean, right now we have to get the dosing down, of course, because this will be first in humans.
So once we get that dosing down, we have proof of concept. PK, PD looks good. We have B cell depletion. Of course, we're going to start looking at the other indications that have had proof of principle with, like I said, myositis, scleroderma, multiple sclerosis. Perhaps that would be a logical choice for us to go back into that. So those are on the table and we're doing work internally on that. But right now, the cash runway doesn't factor that in. It's just the endpoints or the milestones that I discussed today.
The stock price earlier this year did at $39 and now you're about $9.
We did a reverse split. So that's probably what, not probably, that is what that is factoring into.
We were 75% off the back. Yeah.
Yeah. I mean, obviously, the stock isn't where we want it to be.
And it's not reflective of if you just do basic DCF of the Tab-cel, deal kinetics and cash inflows that we have. We should be trading at least $4-$6 higher than what we're at right now. So it's just not reflective of that. I think Tab-cel was an interesting one. We can talk about it later, but we were first in class. And so the FDA had just never seen this before. So we had a long kind of back and forth with them for understanding kind of intrinsic variability and comparability between different process versions, etc. That just took a lot longer. I mean, we obviously got approved in Europe before we got approved in the U.S. So I think a little bit of this is somewhat of a show me story as well, just get this across the finish line.
Obviously, the BLA has been filed and accepted. We're now, as of right now, in priority review, which is great, and we're tracking right along to January 15th, which, of course, isn't too far from now, so we're hoping that we'll see some kind of reflection of that in January. Any other questions? Okay. I'm around all day, so come find me if anything else comes up. Appreciate your time. Thank you.