Can - I can give you the name after. Yeah. Oh, yeah, we're starting.
Bob and Roee. Bob Lechleider . Bob and Roee, R-O-E-E.
Good morning. Thanks for joining us for another session at the 44th J.P. Morgan Healthcare Conference. I'm Brian Cheng. I'm one of the senior biotech analysts here at the firm. On stage, we have Immunome. I will now pass the mic to their CEO, Clay Siegall, for a short presentation followed by a live audience Q&A. Clay, welcome. The stage is yours.
Thanks, Brian, for the introduction. I am delighted to be here, and thanks to J.P. Morgan for the invitation. So I'm delighted to tell you a little bit about what we're doing at Immunome. And before I get going, I'd like to mention that I will be making forward-looking statements, so please refer to our SEC filings for more information. So at Immunome, we're working very hard on targeted oncology therapy, and we're delighted with the progress we're making. We have a passion for treating patients, and you'll hear about that through the presentation. The most important thing is to deliver breakthrough and innovative novel technologies that really make a difference in patients' lives. It starts out with our program, AL102. It's an oral drug. It's once daily. It's a gamma-secretase inhibitor, and it's for a treatment of a sarcoma type of drug called a desmoid tumor.
We reported in December positive top-line data. We'll present that at a medical conference this year, and we're planning to submit for approval with the NDA in the second quarter of this year. And we're working very hard to make sure it's as fast as possible, but very accurate. This drug is positioned to be a best-in-class option, and I'll show you some data there. We have deep expertise in ADCs. I've been working in ADCs for probably 30 years. And so we'll talk a little bit about what we're doing in ADCs and how we're going to the next generation and driving differentiated molecules for our pipeline with a novel payload. The first of those ADCs in clinic targets ROR1, and we have talked a little bit about clinical data there. We've said that we've seen objective responses at multiple dose levels, so we're delighted with this.
I'll explain a little bit about the drug. I'm very pleased with the performance so far in Phase I. We've added more sites in the U.S. We've added more sites in Europe. I wouldn't be adding sites and expanding what we're doing without seeing something that I like in the clinic, but we've not reported clinical data yet, and we are positioned to have three INDs for this year and three INDs for next year, all solid tumor molecules with great targets.
We have a radioligand targeted to fibroblast activation protein for, it's been cleared by FDA, and that should start in clinic soon within the next couple of months, and we have a great leadership team I'm honored to work with, and we have a great cash position with enough money extended into 2028. We have a broad portfolio of targeted agents. We work in a specific area of targeted therapy.
It targets the cell surface or inside the cell. We are not working on cell therapy and immuno-oncology. These are great areas, but it's a different infrastructure. We're focused on targeted therapies. We have a small molecule, AL102, I'll tell you more about. Our ROR1 ADC I mentioned, our FAP radiotherapy, and then our three other ADCs, and I'll show you data on all these. So we'll start with AL102. We showed some top-line data in December, and we're very excited about it. We have met all primary and secondary endpoints. We only put out a few in the top line, but we hit every one of them with very strong data. So I'm excited to put the data out at a clinical conference and have our PI present the data from-hopefully from a podium we'll be submitting, and we're excited to look forward to that.
Our hazard ratio was 0.16. I've developed quite a few drugs in my career that are on the market around the world. My previous best hazard ratio was 0.22, so this is my all-time record, and so I'm really excited with 0.16. The objective response rate was 56%, and that's by strict FDA criteria. Our median tumor reduction was 83%, and the drug was generally well tolerated. So we're going to be submitting in the second quarter and hopefully as fast as possible. So this drug targets a type of sarcoma related to sarcoma called desmoid tumors. And you see the picture of this gal up here. She has desmoid cancer, and if you look at her neck, you can see a very large tumor on her neck. She can barely move her arm, barely move her neck, and she's in pain every day.
While desmoid tumor is not like pancreatic cancer, and you don't die rapidly from it, it is not a friendly disease. I don't want any one of you to have this disease. It's a very painful, very difficult disease to manage, and it strikes a lot of patients, more women than men. There's up to about 1,600 new patients in the U.S. each year diagnosed, about the same in the whole E.U., and so quite a lot of patients worldwide. In the U.S., there's about 10,000-11,000 patients that kind of come in and out of active management each year looking for really good therapies, which we think we have.
The quality of life is really difficult with this disease, and so it's really important to especially impact the pain, and we really have, and our data on pain relief is really good, and you'll be seeing that in clinical presentations in the future. Now, there is one systemic therapy that was approved, I don't know, about a year and a half ago or whatever, and that's good. That was a big step in treating desmoid tumor, and we just think we are the next generation of drug, so AL102 is a gamma-secretase inhibitor, and I would say a lot of investors have said to me, "So why is this better than nirogacestat?" and I think that the easiest short answer is it has a much better pharmacokinetic profile, and so that is why, and because of that PK profile, it has a sustained exposure above the target threshold.
It's a once-a-day treatment, not twice a day, and so it's very user-friendly. Doctors like it. Patients like it. Now, the study that we did at Phase III, we called Ringside, and it's the largest study that's ever been done in desmoid tumors, and the design was very consistent with previous studies in desmoid. We did not reinvent design. It was a very standard design, AL102 versus placebo. We allowed for an open-label extension for patients on the trial. A lot of patients went in. We took no data out on that. That'll be something time in the future, and the inclusion criteria were just that patients would have to have progressed within the last 12 months, and that's the key one.
The key endpoints are PFS, which is a regulatory endpoint, and then some key secondary endpoints are objective response rate, which it always is in these tumor studies, tumor volume, and the pain intensity, which in this disease is really important. Not all cancers have the pain intensity, but this one does. Of course, we also looked at safety and tolerability, etc. This is our Kaplan-Meier plot showing AL102 versus placebo. You could see there's what I like to call a lot of white space between the different lines and the hazard ratio of 0.16, which is outstanding and with a p-value with a lot of zeros. This drug really works. There's really no question about that. I have developed a lot of drugs, and I like waterfall plots.
The reason I like waterfall plots is you can't hide things in charts and graphs that some people do that are hard to read. Waterfall plots are one patient at a time. There's nothing to hide. It's like full exposure. If you look at a waterfall plot like we have here on the left, this is the type of waterfall plot that you want to see if any of you are drug developers. This is an exciting waterfall plot. If you look at the right side, we looked at the two different arms, AL102, where we saw a median of an 83% reduction in tumor burden, and with the placebo, a growth of 11%. Very obvious data that this drug is exceptional. It has a generally well-tolerated safety profile equivalent to gamma-secretase inhibitors, that class of medicine.
The most common adverse events include diarrhea, fatigue, rash, nausea, and cough. Most of these events were grade one and two and generally well tolerated. With this class of drug, there is an ovarian toxicity that is always looked at and doctors talk about. We had 55% of premenopausal women having some level of ovarian toxicity, generally reversible rapidly. If you look at the previous entry into this gamma-secretase market, that drug had about a 75% ovarian toxicity. So we're better than that. It's still something to monitor, and doctors monitored, and there were no deaths on the study, so a relatively safe drug. So if you look at the history of treating this type of sarcoma, desmoid cancer, pre-2018, doctors relied on some therapies that generally weren't approved. You had about a 20% response rate, difficult to treat, a lot of pain with patients.
And then in 2018, sorafenib was studied, and the ORR was 33%. It was the best one seen to date. So that became standard of care in 2018. And then in 2023, nirogacestat came out, and the response rate was 41%, so better. And now with our AL102, it's 56%. So we're very proud of that. And the important part of 83% median tumor volume reduction, no patients on our trial progressed. The worst we had was stable disease. So it's really important to note that there's a lot of patient benefit with AL102. So we're very excited where we are. And we're planning to launch this drug, submit FDA and launch. So we're working very hard already with doctors. We have a commercial team. We have a medical affairs team. Treating the 10-11,000 actively managed patients is really important with GSIs.
Right now, very few of those patients are getting the first GSI. Our intention is to really make this drug available and easy and daily and work with doctors on that. We're talking to doctors about it and connecting up, and really to support and the benefits and the adherence to once a day. I think that for this journey that patients go on, which is chronic and painful and hard, making a simple-to-use medicine is critically important, and we think because there's really only in the U.S. about 85 centers for sarcoma, centers of excellence, that it's really approachable with a modest-sized sales force and not overspend on a sales force to really hit every doc, so we're excited to get out there, get this approved, and make this drug available.
So I'd like to switch now and talk about our ADC program, and I'll start with talking about IM-1021. Now, when you look at ADC and you look at history, so we look back in 2000, there was a first approved product, and it was Mylotarg. And Mylotarg is a pioneer. It's not a great product. There's a lot of things wrong with it. It was on the market, went off the market, but it was a pioneer, and it showed a lot. And so while I did not discover ADCs, they were discovered a long time before me. I led the charge for many years with all my work and founding Seagen and building it up into the modern ADCs. And I made ADCs that had stable linkers and different types of engineered antibodies and good conjugation systems.
And so the work that I did, I'm very proud of, it led to a lot of different ADCs on the market helping patients, and it really changed the field. And now there's more than 100 companies using ADCs, and so I'm proud of that, and they're making a real difference in the life of patients, which is what I'm all about. So that was 2000. By 2011, the first drug and data started coming out with Adcetris, and many of you probably know that. It's still on the market, doing well, helping a lot of patients. And we used different types of linkers and payloads. It still had a relatively narrow therapeutic window, so it was certainly an advantage. I like to call the early ADCs ADC 1.0 and what I put together ADC 2.0, if you will.
And so then you look a little later, and some of the topoisomerase inhibitor payloads started coming out, and they look like they could have improved therapeutic indexes, but they're still susceptible to resistance, to efflux pump resistance and other things, and they had limited bystander activity. So improvements, improvements, but not tons of improvements. We want to see more. We want to see better drugs for patients. So what are we doing at Immunome? 2025 and now 2026, we're making drugs and drug linkers and ADCs that are better. They have improved therapeutic index. They overcome resistance, which is a big issue, and they have bystander activity, which is also a very important issue. So IM-1021 is a potential best-in-class ROR1 ADC. I like ROR1. It's got a really nice expression profile across a lot of liquid tumors, very ubiquitously.
It's on solid tumors, but not as ubiquitously, and we've made a diagnostic tool that will be employed starting probably mid-year this year that no one's ever had a good diagnostic tool for ROR1. So I think solid tumors are going to be approachable with the diagnostic tool. For now, the main focus that we have is on the liquid tumors, and we're working really hard. We're doing a dose escalation in B lymphomas, and it's the main B lymphomas. It's follicular, it's mantle cell, it's diffuse large B. So those are the ones you'd expect. Those are what are in our trial. Like I mentioned, we have been doing dose escalation. We're doing expansion. We've seen multiple objective responses. I don't want to claim victory yet.
I'm very cautious with that, but I am quietly optimistic that this is a real drug, and as we expand it and we do work on it, this could really help patients be our second drug that we're going to submit for approval someday. So we're working hard on that. Now, preclinically in lymphoma, we have outstanding data, and that's on the left in a mantle cell lymphoma model. On the right, we have a non-small cell model. And like I said, I think it's critically important, and historically, ROR1s were developed and looked at in solid tumors, but without a diagnostic tool. And in a sense, you're looking, you're blind. You don't know what's going on with the tumor. And with tumors that are not ubiquitously expressed like the lymphomas are, you need a diagnostic tool, and that's why we developed one.
We're working with a diagnostic company to make sure it's validated, and that'll happen by mid-year. And our clinical development plan is pretty straightforward. It's a dose escalation to look at proof of concept. We have the lymphomas that we're all treating, and then they'll be separate with the solid tumors that we're going to use our diagnostic tool. And then with anything that looks good, you expand. And I've developed molecules for lymphoma. Adcetris was for lymphoma. And when I started developing Adcetris, I heard a lot of, "Well, you're going to come up with another drug at 20% response rate, and we already have 10 of those. We don't need that." And Adcetris, single agent with 73% response rate in Hodgkin lymphoma, 87% response rate in T-cell lymphoma. That's differentiated. We got Phase II approval, single agent, go into frontline combination. It became a multi-billion dollar drug.
That's how you do it. My goal here with ROR1 is not to come and bring you another 20%-25% response rate drug, single agent. If we're doing that, my next sentence is going to be that we're closing the program. That's not of interest to me. We need something that's differentiated here. What I see so far in Phase II makes me very excited. We have a potential differentiated drug. I don't want to call it victory yet, but we're excited and we're expanding. And I wouldn't be expanding it if I wasn't excited about the drug. So I'd like to tell you a little bit about our ADC platform and what we've done that's different. We call it our HC74 platform. So we are able to, we have a payload on here that's not sensitive to the standard efflux pumps, the multi-drug resistance pumps.
You could see on the left side, you see HC74 in a tumor cell line, and then the next line in the middle is a tumor cell line with a certain type of resistance mechanism, and the third one is another resistance mechanism. HC74 works identically, whether it has two different of the most important and most common resistance mechanisms. You look at DXd on the right, okay? That's the drug used by the Daiichi molecules. If you look at all ADCs in the world, the most payload, what they're using, the most drug linker payloads are either the Seagen-Pfizer system with that system or tweaks of it, or the Daiichi system with tweaks of it. Those are the two most heavily used systems. Here with DXd, you could see with either of the resistance pathways, you have less activity. Now, this is important.
If you look at bystander activity, that's another important thing. I've been putting tumors on the back of mice for decades. We use cell lines. These are homogeneous cell lines. In humans, tumors are heterogeneous. They're not homogeneous. They're not like a cell line. And so it's important to get a drug into a tumor and have it not released in the circulation. That's not bystander activity. That's instability. Bystander is when it hits a few cells around it in the local tumor microenvironment. We've developed a payload that has a good amount of permeability, and we've measured it in multiple models, and it has really good bystander activity. It's also four-fold more potent than DXd with topoisomerase inhibition activity. And so we have looked a lot at the efflux pump because this is probably the most critical thing that most companies aren't looking at with ADCs.
They're making ADCs. They're taking drugs. They're taking linkers, antibodies. They're super gluing together, but they're not thinking, "What is the issue? What is the problem? How do we solve it?" and so if you look on the right side, you could see this is data using Enhertu, and you could see using Enhertu that there's, and on the bottom chart, there's a 47.1% ORR if you don't have P-glycoprotein, but if you have P-glycoprotein, it's a 17% ORR. It doesn't take a rocket scientist to see that. That's a big difference, and that's something that we could do a lot better than, so we are working very hard on that, so we've looked at HC74 in CRC models, colorectal cancer, and looked at different sensitivities, and we've seen that with HC74, we can evade the resistance that's in certain models, much different than a DXd situation.
So we're excited about that. And we have done a lot of work in bystander activity models. And so we create models looking at bystander activity, looking at tumors that have the target and tumors that don't have the target in the same tumor microenvironment, and we have very potent bystander activity. So this is all good. We've done a lot of work to show that we have great ADC technology in preclinical models, but we have to bring it to clinic, and you have to show that it works in clinic and not just in preclinical models. And that's where we are with our ROR1 ADC. We're in clinic. We're seeing efficacy. We're excited, and we're expanding it with this technology. So the other thing is we need to really expand what we're doing with ADCs. Now, there's 10 targets out in the world.
Many of them I've made drugs for. I know these targets well. There's 10 targets that amount for half of all ADCs being developed. To me, this is not appropriate. There's 25 or more ADCs in development for HER2 and Nectin-4 and all these things. It's too many that are not necessarily better than the other ones. And so one of the things we've done is we've prioritized targets with really compelling tumor biology and no approved ADCs and focused on treating it with our technology and trying to get better and do better by patients. So one of them I'd like to tell you about is called IM-1617. Now, I'm going to tell you about six different ADCs. I am not going to tell you the targets, and I apologize for that. There's a lot of competition across the globe.
For now, until we have to say targets, it's important to protect your targets and protect them with intellectual property on the composition of matter, on the conjugation, on how you manufacture, how you test it, how you combine it. We're putting a picket fence together on our intellectual property, and we're not yet talking about the targets. Quite frankly, if I told you some of the target names, you would say, "Never heard of them." We'll just show you some data. IM-1617 targets solid tumors. It's expressed in very high density on lung, pancreatic, colon, ovarian. I mean, this is a great target and very, very limited normal tissue activity. This is a really exciting target, and we've made ADCs, and you could see ADCs where we have tested it in animal models with tumors, and the data is spectacular.
So this drug, the short story is this drug will be submitted for an IND in the not too distant future, hopefully within the next few months. We've manufactured the IND tox, done all the work, and so we're going to get this submitted. We intend to submit this year early in the year, mid-year, and late year, three INDs and three solid tumor ADCs. So this chart shows you six different ADCs, starting with 1617, which I already explained, but here are six different ones. We've not defined the target, and I apologize once again, but it's very appropriate in 2026 not to do that. I used to stand in front of here 15 years ago, and my second slide was, "Here are my targets I'm going after." I can't do that anymore. It's just not appropriate to do that anymore. But we have spectacular data.
These are all six solid tumors. They're going to be one after another after another in clinical trials with our state-of-the-art ADC technology, so I'd like to talk about the last of our programs, and this is a radioligand that targets fibroblast activation protein or FAP. I have liked FAP for a long time. FAP is one of the best targets I could ever imagine in the world. It binds to 75% of all solid tumors. I mean, I don't know another target that binds to that much. It's really spectacular. The problem with FAP is I can't make an ADC to it, okay, and if anyone can make an ADC, that would be me, but this binds to a stromal target, so it's not binding to the receptor and getting internalized normally. It's to stroma.
If you're binding to stroma, and there's a ligand for it, I don't like antibody radioligands because they have long half-lives. There's some tox problems, but I like ligand radioligands, and ligand would link with radioisotope like Pluvicto, which is a ligand, and that's a great drug in helping a lot of patients. FAP is something that other companies have looked at. Clearly, Novartis put one in clinic 10 years ago. Clovis put one in clinic. Novartis had no responses. Clovis had two responses out of something. They got a little bit better. We know those molecules. We've studied them. The issue with radioligands is you need to get enough gray that's the measure of radioactive exposure into the tumor without walloping the kidney. You're developing an ADC.
You're looking at heme tox and lung tox, but kidney tox is the issue with radionuclides, and you need to get a good amount of exposure of the radiation to make it work. And that's why Pluvicto works. It's got a good profile. And so what we did in our labs is we took apart these types of molecules, and we made about 50 of them, and we changed every piece and part. It reminded me of some of the work we did with ADCs. We did science with ADCs, deep science, and took apart everything and rebuilt it and said, "How can we make it better?" So with the radioligand, we took apart everything and looked at all the component pieces and made a really good molecule. And when you look at this, there are a lot of FAP binding proteins.
I think there's 15 or more out there of FAP binding proteins. And I had talked to people developing FAP in the past, and I said, "Which binding protein did you use and why?" And they'd say, "We used FAP." It's not an answer. And so we've studied binding proteins. We've studied different linkers, different albumin binders, different ways of doing it. And so we've come up with, after looking at dozens of different molecules, we've selected one, one that has fantastic properties. We submit it to FDA. We're cleared, and as soon as we get our tracer radiation from the manufacturer, which is soon, we'll start the trial. And it's very active, and it's really exciting with this new generation that we're making of radioligands. So lastly, I am very honored to work with such great people. I've worked with some of them in the past at Seagen.
We've hired a lot of ex-Seagen people. I don't want to hire all ex-Seagen people. I think it's healthy to bring in people from other companies as well and have good dialogue. But I'm delighted some of my key colleagues are here today, and I don't take for granted that I was able to put together such great executives and also great investors and have gone out to raise dollars. And I'm really honored with the investor group that we have that has given me a lot of money at Seagen to build a company and continues to provide me money to build another company. And so then my last slide, just in summary, on left, these are the new three INDs we're going to do this year, and they're all solid tumor ADCs, big market opportunities.
Then toward the middle is the FAP RLT, already cleared by FDA for trials. We'll start soon. A little further to the right is the ROR1 ADC. Our intention is to put clinical data out this year. People have said, "Is it ASCO? Is it ASH? Whatever." I don't have an answer for you. I mean, for a lymphoma data set, ASH is a good place for that. That's where a lot of the doctors are, so I wouldn't be against that. And AL102, it's something, a drug that's great. We're submitting it. We're going to put it at a clinical conference. I think an ASCO could be a good type of conference for a real coming out party of all the data and on this very exciting state-of-the-art gamma secretase inhibitor.
With that, I will turn over to Brian, and I'll ask two of my colleagues, my Chief Medical Officer, Bob Lechleider , and chief or head of commercial, Roee Shaviv, to come up and join me and address whatever questions.
Let's start the Q&A. For those of you who are in the audience, if you have any questions, feel free to raise your hands. For those joining us virtually, you can also submit questions on the portal. As we think about the approval path for AL102, can you talk about your preparation today and what is really the gating factor before filing for AL102 in the near term?
Okay. I think Bob's team, Bob's Chief Medical Officer, his team is doing a lion's share of it. We do have manufacturing people and other people. The head of manufacturing for Immunome, I worked with for 18 years at Seagen, and he manufactured everything there, so we have a star there. But Bob, can you talk a little bit about that? You might need to lean into the mic.
Sure. Thanks for the question, Brian. There's really nothing gating except doing the work. So we just had top-line data released in December, and what we're doing now is going through the data, making sure we understand the full efficacy and safety profile and being able to prepare the documentation for the FDA. So it's just a question of getting the work done.
Look, a lot of big companies take six months from their data to submit. We're going to do it faster. I'd like to do it in five months. I'd like to do it better in four months. So we're working hard to get this submitted.
Just one of the key questions of the data, I think I get a lot of questions of, how do you know that it's better than nirogacestat? What are you hearing from doctors? And ultimately, as you think about commercial, do you expect that patients that are on nirogacestat, they will switch right away to AL102? What is that switching dynamic going to look like?
So first of all, any patient on any cancer drug, and I'm a cancer specialist, and I care about cancer patients, any patient on a cancer drug that they're responding should never come off for a different drug. So that is not our intention to go to a patient that's responding to nirogacestat saying, "You should switch." It's the wrong thing to do for cancer therapy. Now, if you're not responding to nirogacestat, or if you're a new patient, or if you're a prevalent patient, absolutely. And so that's what we'll focus on. Now, keep in mind, their drug is twice a day and has difficult pharmacokinetics. We hear from doctors over and over that even if we had the same data, which we didn't, our data is far superior.
They said, "Even if you have the same data in your once a day, we would use it because compliance has been really bad." And so what they see, and we've interviewed patients, and it's true. And so what we've seen is that they have 41% objective response rate in a trial where they're forcing you to take it twice a day. Out in the real world, there's a lot of people taking it once a day. I don't know what the response rate is. It's certainly not 41%. And what happens is these patients have a lot of pain. And if the pain isn't getting relieved from their big tumor nodules, they're going to use a different drug. And ours has an 83% median tumor volume reduction and a better pain reduction index. Bob, do you want to comment on this?
Yeah, no, I think it's important to remember that the two studies are very similar, the DeFi study and Ringside. The patient populations are nearly identical. The study design is very similar. So I think doing a comparison across the two studies is always something we try not to do, but the results speak for themselves. We met our primary endpoint. We met all of our key secondary endpoints. It had a lot of alpha left over, so there are really significant differences.
Any questions from the audience? Yeah, we have seven minutes left, so I want to really touch on your ROR1. So one of your slides, you said that it really caught my interest. So one of your slides, we know that there is activity at multiple doses. So just the first question is, how do you define activity? Is that activity dependent on RECIST response? And then secondly is there's a bullet that says the starting dose, I believe it's 2.5 mg/kg, is similar to the recommended Phase II dose that Merck had used. Can you also comment on the therapeutic window? Do you expect that the higher dose should be able to deliver more efficacy based on, obviously, preclinical data?
Right. So your first question was about.
Criteria, the criteria, at least I can answer that very well.
How do you define activity?
Oh, yeah. How do you define activity? All right. We use strict FDA criteria.
For lymphoma, it's Lugano criteria. The responses that we see, we would not talk about a response unless it met the criteria for a response based on RECIST for solid tumors or Lugano for lymphoma.
When we say we've seen responses, we are talking about the kind of responses that are real objective responses, not just, "Hey, we see 2% reduction in tumor burden." This is a real Lugano criteria response. So that's important. And then the second part was.
Around the dosing and the comparison to Merck.
Right. So ROR1, there's a drug out there that was developed in ADC, developed by VelosBio, and then acquired by Merck. And so that's out there, so we know a lot about it. I know that antibody well. That antibody was developed by a small little company that doesn't exist anymore. It was not screened and made for an antibody that internalizes well like ours is. It was not done well, but it was a long time ago, and it existed. And we are using a modern ADC tool, a drug linker on here that's improved. So we have a better antibody and a better ADC technology on it. We've gone into clinic. We have objective responses at multiple doses. If you look at Merck's single agent activity, they had, and just let's focus on lymphoma, they had about a 20% response rate that's at a safe dose.
They went to a higher dose. There was a lot of heme tox. They had about a 40% response rate, but it was a non-usable dose. So they have a single agent response rate. I don't want to, it could be 20%, it could be 25%. I don't know exactly, but something like that. That's not what we're looking for. We're looking for something differentiated that we could go forward on that potentially we could get registered with a single arm Phase II study. So I don't know exactly what we're looking for. There's not a number the FDA puts out there or doctors put out, but it's going to be 50%, 60%, 70%, 80% response rate. Something big will capture the attention of doctors, will capture the attention of ADCs, much like Adcetris did, and will be differentiated.
And then we'll go forward and look at single agent approval and then combination approvals in earlier line. So that's what we want to do. So far, we're very excited with what we see, but you have to determine a lot of data. And if you're a real drug developer, you have to look at a lot of different factors. And we're doing that. We're expanding our sites, treating more patients. We're investing more in it because what we see so far, we're pretty excited with.
Just based on the responses that you see across multiple doses in liquid tumors, does that give you more comfort in the probability in solid tumors today?
You're asking a really good question. When I think about ROR1 ADC, I think about this is a liquid tumor ADC for B-cell lymphoma, and the solid tumor aspect to me is on top of it. I can't tell you, I don't want to hype it and say, "Oh my God, preclinically, we could shrink solid tumors and everything looks good." Our data preclinically in solid tumors is great, but we needed a diagnostic tool, or else we would be blind. We wouldn't know. In solid tumors, you have limited expression in different tumors. Some tumor types have almost none. Other tumor types have some. I think it's critically important to do that, and no one has made a robust diagnostic tool till now.
So I think that starting mid-year, we can approach solid tumors and say, "Is this a possibility?" So what I would leave you with is we have a full pipeline of solid tumor ADCs. ROR1 is a fan. So far, we're very excited with the data in liquid tumors. And there's a big upside in solid tumors that I don't want to hype too much. Our preclinical data is good, but I want to see more data.
Great. Well, just before we wrap up, we have about two minutes left. So if we have the same conversation today in December of this year, where do you think investor conversation will be? Where do you think that number one key focus will be if we have the same discussion in December?
Well, I'm hoping that we get approved in AL102 this year. I'm hoping we submit fast. I'm hoping the FDA gives us priority review. It's up to them, not me. And I'd love to get approval this year, this calendar year. And I don't know what that means, October, November, December. It's not going to be early in the year because we haven't even submitted yet. But that would be great. And investors will see that we got approval and we're on the market. I think by the end of the year, we'll have a substantial amount of data on the ROR1 ADC, IM-1021 as we call it. And they'll see real data and understand the power of this ADC. I think we'll have, by the end of the year, three solid tumor ADCs, INDs, and treating patients with at least the first two of them.
And we'll be treating patients with our radioligand to FAP, which is a very big market opportunity with very high science. So I think by the end of the year, we could have seven drugs in clinical development, a drug on the market, a lot of data being presented. It's going to be an important and exciting year for us.
Great. Well, that's all the time we have, and thank you so much for your time today.