We'll go ahead and get started a little bit early here. Anyone else who wants to trickle in can do so. It's my pleasure to introduce the Nektar team and Mary Tagliaferri.
Thanks, Jake, and thank all of you for attending today's presentation. I will be making some forward-looking statements, and our most recent filings can be found in the SEC website in our Form 10-Q. Today, Nektar is focused on immunology and inflammation, and we basically have five different pillars that we've built the foundation of our drugs on. First and foremost, we have a very deep understanding of immunology, and we decided to address specifically the imbalance and the dysfunction of the immune system by targeting regulatory T cells. All of the compounds that we have in development are novel, and our lead compound is rezpegaldesleukin, which I'll refer to as respeg, and we have a preclinical program, TNFR2 agonist antibody. Today, I'll share with you the compelling data from our phase I-B study in atopic dermatitis, which we find is highly differentiating.
And then all of the markets that we're going after are very large in immunology, and today we're very well capitalized, and we ended last year with $329 million, and we have a cash runway all the way through until the third quarter of 2026. On this slide, you can see our pipeline. At the top, under the purple banner, are our immunology assets, and respeg is our keystone immunology compound, and we are evaluating this in the two phase II-B trials, 1 in atopic dermatitis and 1 in alopecia. We also have our TNFR2 program, and we have a PEG- CSF1 program. Both of those are preclinical.
Then under the blue banner, you can see our oncology assets, NKTR-255, which is our IL-15, and we have multiple studies ongoing, as well as NKTR-288, which is in the preclinical phase. So why T regulatory cells? I think this slide demonstrates it very clearly, that rather than just target a T cell, a T helper cell, or target the cytokines that are generated by these T helper cells, we chose to go after T regulatory cells and target the expansion of these. And the reason for this is very clear, T regulatory cells can impact the aberrant cytokines produced by a Th1, a Th2, or a Th17 aberrant T cell. And so therefore, we can cast our net very wide and treat a number of different immune diseases.
Likewise, we can treat patients that have a mixed picture of a combination phenotype of a Th1 and a Th2. So how do you target regulatory T cells? Well, the main driver of T regulatory cells is the cytokine IL-2. So what Nektar has done is very cleverly taken the native protein sequence of IL-2, and we did that to avoid immunogenicity. And we have attached our polymer conjugation technology, and we used the exact same PEGylation technology that we use for Adynovate. And by doing so, we have created a highly selective IL-2 that targets T regulatory cells, that selectively binds the T regulatory cells, the CD25 receptor, and it's strongly agonistic. And with that, with our PEGylation technology, we also created a long half-life for the drug. So it has a 10- to 14-day half-life, so you can very easily inject it in patients.
And again, as the native sequence of IL-2, we don't see anti-drug antibodies produced. So today, rezpegaldesleukin has actually been studied in 600 patients. That's quite a lot and puts our drug furthest along among the armamentarium of IL-2 drugs that are currently in clinical testing, that are run by both large and small pharmaceutical companies. And you can see here that in the 600 patients, 400 of them actually had autoimmune conditions, and about 200 of them were in healthy volunteers. And whether we looked at our single ascending dose data or multiple ascending dose data, or in these autoimmune diseases, all of our pharmacology is highly predictable and highly consistent, and we've been able to expand T regulatory cells 10- to 14-fold in these studies. We also showed that there was a clear benefit in skin-related autoimmune diseases.
So in four different studies, in our MAD study with SLE patients, in our phase II study with SLE patients, in our study with patients that had psoriasis and atopic dermatitis, we have seen a clear benefit to a decrease in skin pathology. And what's also good is after treating 600 patients, our biologic agent is very well tolerated with minimal side effects. So if you're gonna remember any slides that I'm presenting today, this is the one. These are data that Dr. Jonathan Silverberg presented at EADV in 2023, in October of last year. And you can see here, shown in gray, are the placebo patients.
Shown in blue is our low dose of Respeg, and in red are the data from those patients randomized to our high dose. There are a few key takeaways that Dr. Silverberg highlighted from his perspective as both a immunologist and a dermatologist, that you can see at our highest dose, there was a very rapid onset of action. So patients with just two doses of drug derived a very, very positive clinical benefit. Second, you can see a very clear dose response. Third, even though our randomized placebo-controlled trial had an induction period of only 12 weeks, whereas for most biologics it's 16 weeks, you can see that the magnitude of benefit was very profound. In fact, there was an 83% reduction in EASI from baseline to 12 weeks, which is the highest number that we've seen for a biologic today.
The last point is those patients at week 12 stopped treatment, and by week 19, any patient that had an EASI 50 score or above were followed for an additional 36 weeks. 9 months, no treatment whatsoever, and these patients had durable responses. This is what we call remittive effect in the industry, and it is the first time that we've seen an agent that had this type of durable remission of the disease and really could be a disease-modifying agent. The drug is given sub-Q every 2 weeks, and in our phase II-B study, we are gonna look at a maintenance dosing that affords patients to have less frequent dosing. But before I go on to our phase II-B trial design, I wanna say that we also care about the journey of patients.
What is shown here is a DLQI, which is a patient-reported outcome and measure of the burden of disease to patients. You can see here that patients also, in a dose-response way, with a very fast onset of action, reported a very quick and positive and deep clearance of their skin. Of course, you can imagine that for the value proposition of a drug, having patients that personally experience a very fast and deep response to their disease, this could have incredible commercial value. So, Dr. Silverberg, when he was on the podium, was very impressed with these data. The reason that he is, is because he himself is an immunologist. What he said was: "We never knew if actually boosting T-regulatory cells could have the ability to suppress inflammation.
Of course, theoretically, it made sense, but we weren't sure if we actually gave an agent that boosts T-regulatory cells, if we would see a reduction in atopic dermatitis." So he was very excited that this was the very first proof of concept in immunology to demonstrate this effect. If you mechanistically can increase T-regulatory cells, you can control the inflammation and decrease the burden of the disease for patients. I think most of you probably know that atopic dermatitis is an extremely large market. There are 30 million adults in the United States with atopic dermatitis, and half of them have moderate to severe disease and would need a biologic agent. Unfortunately, only 8% of patients with moderate to severe disease are actually being treated today. With that small proportion, Dupixent actually sells over $6 billion just for atopic dermatitis.
What doctors share with us is that while Dupixent was great when it came on the market in 2017, unfortunately, half of their patients don't benefit from Dupixent. Certainly, the need to continue to do subcutaneous dosing for the rest of their lives every two weeks is very challenging. What they're seeking is a drug that could provide greater benefit to a larger proportion of patients, not just 50%, could have deeper resolution of the disease, and offer a dosing schedule that is better than every two weeks for the rest of a patient's life. One of the things I wanted to share with you about where we think this market is actually going to grow to is using psoriasis as a case study. In psoriasis, in 2004, Enbrel came on the market.
Soon after that, you had Remicade and Humira. And in 2010, those three drugs sold about $3 billion. But it wasn't until Stelara and IL-12, IL-23, followed by Otezla, a PDE4 inhibitor, followed by Cosentyx and Taltz and Skyrizi, and then a TYK2 inhibitor, that the psoriasis market grew exponentially. And today, with all those new drugs on the market with novel mechanisms of action, the market has now grown to $24 billion. Atopic dermatitis is four times the size, and we believe the same type of growth will be seen once we bring new and novel mechanisms to this indication. So currently, there are two main classes of drugs that are approved for atopic dermatitis. You have the IL-13 biologic drugs, and, you know, we've been talking a lot about, you don't see a remittive effect with these biologics.
For example, with Dupixent, if you stop taking Dupixent after four months, 80% of patients need to restart treatment. So you have a lack of dosing flexibility, a lack of remittive effect, and then there are some other, you know, highly annoying side effects that happen for patients. They can get conjunctivitis, they can get this red erythema on their face, they can have arthralgias. And so we definitely need to provide new and different alternative agents to treat more than 50% of the population that don't have the same toxicities and have a much more flexible dosing. And the JAK inhibitors have also recently been approved for atopic dermatitis. However, the FDA level label is after a patient progresses on a biologic.
Many of you probably know there are multiple black box warnings with the JAK inhibitors, serious infections, cardiovascular death, myocardial infarction, stroke, and a physician is obligated to tell the patient about these black box warnings before they prescribe the medication. But probably the biggest drawback for the doctors isn't just even having to describe all the potential serious side effects, but rather after their patients stop taking treatment, the disease very rapidly and quickly rebounds, and sometimes it's worse than before the patient even started treatment. So with the limited armamentarium of approved drugs with an adequate benefit-risk ratio, this is a great opportunity for rezpegaldesleukin.
To give you some numbers to actually line up the profile of rezpegaldesleukin versus the available drugs, this chart shows you the efficacy comparison of the phase II final results for the approved drugs in purple, Dupixent and Adbry, and then in blue are the drugs that are in the most advanced clinical trials. You can see certainly here from the EASI mean % reduction from baseline, which is the primary efficacy endpoint most of these trials use for phase II, you can see that we really have a superior efficacy profile. So just taking a step back and summarizing what I was talking about in atopic dermatitis, we see highly consistent effects, whether or not we're looking at the physician-assessed endpoints or the patient-assessed endpoints. We see a very clear, rapid onset of action.
There's a very notable dose dependency among our high dose versus our low dose. Again, I just showed you that the efficacy is superior to what we've seen with the other biologics. Probably the most important to patients and to physicians alike is the durability that we've seen. Nine months, no treatment, patients can continue to see the durability of their response, and we don't see any serious side effects or adverse. We don't see any increased risk for infection either. With all that, we've moved forward into our phase II-B clinical trial. This is a relatively large phase II study, and this is giving us the opportunity to look at a maintenance period.
Probably the most important for you to take away from understanding the design is that our phase I-B, our phase II-B, and our phase III trials all include the same patients. These patients are biologic-naïve, and the eligibility criteria for the severity of their disease is the same. So we're gonna look at three different dose regimens of Respeg. We'll certainly carry forward the high dose from our phase I-B and look at two other regimens versus placebo. Another change that we've made is looking at a longer induction period. Whereas our induction period in the phase I-A, where we saw this 83% reduction in EASI, we now are gonna dose for another four weeks, and our induction period is now 16 weeks, which is standard for a biologic.
We'll have data from the induction period in the first half of 2025, and then we will also re-randomize people on the specific dose they're originally re-randomized to, to a maintenance of once a month or a maintenance dose subcutaneous every three months. And you can imagine this is highly differentiating, and when we you know speak to the medical community, this is specifically what patients want, an ability to completely suppress their atopic dermatitis, but have a maintenance dosing where they can very infrequently dose themselves at home. So now I wanna turn to our second program with rezpegaldesleukin. As I mentioned to you, we saw benefits in skin disease in patients with cutaneous lupus, in patients with atopic dermatitis, and patients with psoriasis.
So when we brought Dr. Silverberg and Dr. David Rosmarin, and Dr. Raj Chovatiya together and others, we asked them, "Knowing what we know about Respeg, where would you go as a second indication?" What 100% of them said is, "You should advance to alopecia." And why? They said alopecia is also a disorder of the skin, and you have the hair follicle. In a normal human being, if you have an immune attack of the hair follicle, you will eventually lead to the hair strand disconnecting from the hair follicle. You'll, you know, first have patchy hair loss, and then, that will move into baldness. Seeing the effect in all these other different indications in the skin, they believe there's a high probability for success in alopecia areata. Just mentioning, alopecia areata is, you know, a very large indication, like, atopic dermatitis.
And, what's very difficult is that 80% of the patients who have alopecia are younger than age 40. And, the only drugs approved for alopecia are the JAK inhibitors. And of course, you have the same issue with the black box warnings for this indication as you do for a- atopic dermatitis. But probably, what is most disconcerting to the doctors is patients can take a JAK inhibitor for 6 months, 12 months. Their hair does grow back, but when they stop taking the JAK inhibitor, they immediately lose their hair. And you can imagine that this is very psychologically damning, damaging for patients, and heartbreaking, actually. And so the physicians, you know, have shared with us, if there is a remittive therapy, this would certainly be, the most desirable for patients. So what happens in the hair follicle?
If you look on the right-hand side of this slide, what you can see here is there are several immune cells that attack the hair follicle. And normally, hair follicles benefit from immune privilege or a state where there's very limited immune cells, and it's a evolutionary adaptation to protect certain tissues in the body, like the hair, like the eyes, like the placenta, like the testes. And what Dr. Ralf Paus has published repeatedly is the way to restore this immune privilege is by balancing the immune cells, and certainly doing that through T regulatory cells to suppress the CD8 positive immune response, is one of the smartest ways to do so.
So with that, we're running our phase II-B study in alopecia, and our key inclusion criteria is the same inclusion criteria that the JAK inhibitors have used for their studies, looking at patients with the SALT score greater than or equal to 50, and we'll randomize patients to 2 different doses of rezpegaldesleukin versus placebo. And again, we'll carry forward that high dose from our atopic derm phase II-B study into this trial. We will have an induction period of 36 weeks, and then to look at that remittive effect, we'll also follow patients for 24 weeks off treatment. We've started this trial, and we expect data soon after the atopic dermatitis data in the first half of 2025. So that concludes the discussion about rezpegaldesleukin, and now I'll move to our TNFR2 agonist antibody.
Moving, you know, a little bit to the biology, as I mentioned to you, the most potent cytokine to expand T regulatory cells is IL-2. But as these central Tregs move out of the blood and deep into the tissue, their dependency on IL-2 wanes, and they have a greater need for an NF-kappa B signaling. So TNFR2 is part of the TNF super family. It's one of the proteins, and it is abundantly expressed on T regulatory cells. And so our team has come up with a TNFR2 antibody agonist that potently is selective to the TNFR2 receptor and significantly increases the proliferation, the function, and even the phenotypic stability of these T regulatory cells. What's unique about the antibody that the team created is it actually works as a monomer.
They have created a bivalent antibody, but given that it can work as a monomer, we could actually create a TNFR1 antagonist along with a TNFR2 agonist and have a very potent immunotherapy. This drug could be used in the CNS, and we could treat diseases such as MS and Alzheimer's and Parkinson's. We have created a very stable cell line that has been manufactured to produce very high yields, and it's currently in IND-enabling studies, ready to go into the clinic next year. And finally, just before we talk about the milestones and go into any Q&A, I wanted to touch on our oncology asset, NKTR-255, and this is an IL-15 receptor agonist. And we are using this in various different combinations and checkpoint inhibitor studies and also in cellular therapy, as well as with TILs.
Starting from the top, we have 2 different studies going on in combination with CD19 CAR T cells for large B-cell lymphoma. Both Kite and those people who developed Breyanzi have shown very clearly that IL-15 levels increase the Cmax and increase the area under the curve and drive responses. And so unfortunately, people who you know receive CAR T cells for large B-cell lymphoma have a CR rate at 6 months that's just 40%, and when they go on to subsequent therapies, have a very poor prognosis. So our aim is to give NKTR-255 2 weeks after the CAR T cell and every 3 weeks thereafter for 6 months to drive the CR rate at a half a year. In addition, we're combining NKTR-255 with TILs.
You know, Dr. Scott Antonia, before Iovance went on clinical hold, did publish data in Nature to show how difficult it is to actually use high-dose IL-2 to boost TILs because of the toxicity. So there's great desire by AbelZeta, our partner, who's combining their TIL with Nektar 255 in a trial that they're sponsoring for patients with metastatic non-small cell lung cancer. Then, we've combined Nektar 255 in a randomized clinical control study that Merck KGaA is running, looking at Nektar 255 in combination with Bavencio as a maintenance therapy for bladder cancer, and we'll have data from the study in the second half of this year in their interim progression-free survival analysis. Finally, we're combining Nektar 255 with Imfinzi, and this is to rescue the absolute lymphocyte count in patients with stage 3 unresectable non-small cell lung cancer.
Many patients, when they go through chemoradiation for stage 3 lung cancer, actually experience lymphopenia, and those patients have a worse prognosis, and it's been well established in multiple studies. Finally, these are key upcoming milestones. We today announced starting the phase II-B study in alopecia. The interim results, as I was mentioning from the NKTR-255 study and our collaboration trial with Merck KGaA, will be available in the second half of this year, and that is a PFS endpoint comparing avelumab as maintenance therapy versus avelumab plus NKTR-255. Then, we will also have our IND enabling studies for our TNFR2 agonist antibody completed by the end of this year. We'll also show our NKTR-255 plus CAR T-cell data at a medical conference later this year.
And then, in terms of our top-line data for the phase II-B trials in atopic dermatitis and alopecia, we'll have those in the first half of 2025, and we are fully financed all the way through all those milestones with cash runway into the third quarter of 2026. So I thank you for your patience for this presentation, and happy to take any questions.