Thank you so much. So welcome to this conference call, which will focus on today's interim report and the associated press release. Slide 2. So as usual, the presentation does include some forward looking statements. Let's go to Slide 3.
We announced today that Alligator will focus clinical activities to our lead programs, EIDR1017 and MIDASALAMAND. In short, the decision is based on the strong positioning and positive data for these 2 programs, while there is a need for further evaluation of data in the ADR1015 program. So our focus will be on ADR1017 and META, while further clinic development for EIT1015 is to be conducted with a partner. These are the key messages, and I will now go into this in more detail. First slide summarizing the most recent news flow, Slide 4.
So during the Q3, we have presented data from all three clinical programs as well as a novel biospecific drug of concept, Neo X Prime and the recruitment of Gail Mills as Chief Business Officer at Alligator. Let's now start with EADOR1015, Slide 5. Slide 5, the ongoing dose escalation study. It's currently evaluating repeated intravenous dosing at 750 milligram or approximately 12 mgkg. And this is a really high dose.
For reference, about 4 times higher than the highest dose used for Yervoy. As communicated earlier, we have observed infusion related reactions that are believed to be related to the development of anti drug antibodies. The reaction seems to be manageable, and we still expect completion of the ongoing study before end of the year. It does, however, call for changes to the clinical dosing and dosing regimen for future studies and for oral evaluation of clinical data, including biomarker analysis. In parallel, we have initiated discussions for conducted further clinical development with a partner.
So this allows us to focus our resources to ADER1017 and mitaxelimab and to make sure that their clinical development programs reflect their great potential. So let's rotate to 10/17, Slide 6. ADER1017, it's at the front of the 2nd generation 400 EB antibodies. Now why is that important? The 1st generation antibodies had design flaws.
The BMS product, urelimod, the left hand side, that induced strong activation of all 4 1BB receptors, leading to toxicity and a maximum tolerated dose of 8 mg, which is very low. Whereas the Pfizer compound, eutamilumab, it's overcompensated with an antibody with too low activity even at very high doses. ADER1017 is assigned for high efficacy, but with more selective activation in the tumor area, and this is to reduce systemic toxicity. So this profile is now supported also by emerging clinical data. Next slide, Slide 7.
So Slide 7. Data from the ongoing dose escalation study was reported in August, a flat dose of 40 milligram. This is 5 times higher than that of urelimod. That was cleared with few adverse events. Dose evaluation now continues at 100 milligram, and we expect to be able to report the full study within 6 months.
The individual patients are shown in the swimmer spot below, where the colors represent different doses.
So the
study allows interrupt patient dose escalation. This is to give every patient best chance of benefiting from the treatment. This has allowed to start at low doses and fast dose escalation in single patient course, while still having all patients escalating to clinically relevant dose levels. We find the data very encouraging and are now planning for bringing ADOR1017 into Phase II efficacy studies in 2021. 41BB has potential in several important solid and liquid tumor indications, including head and neck, gastric, ovarian, lymphoma, and there's a large number.
And our goal is to be able to start more than one such efficacy study with this product. With that, I will move on to Midland. This is Slide 8. We are finalizing our preparations for a clinical efficacy study in pancreatic cancer. The background is, of course, the emerging clinical validation for CD4 in this disease where current treatment options are very limited.
We plan to combine with chemotherapy, which is mitasalumab on top of modified folferonox. And to add on PD-one, once an efficacy signal has been demonstrated with midda on top of folferonox. CTA for this study will be submitted before end of the year, and we plan to record 1st improved efficacy data in Q4 2021. We also recently presented data confirming a clinical proof of mechanism for mitaxelimab as a single agent. Since there is no active clinical trial ongoing, this may sound confusing, so let me briefly explain.
Slide 9. This is based on data collected in the Phase I study run by Janssen and that was reported last year. They included a lot of advanced biomarker assessments, including RNA sequencing. And when we compile this data, a distinct pattern emerged confirming the proof of mechanism. A large number of immune genes were upregulated in the patients upon treatment with metasalumab.
And this included key signals such as PD L1 shown to the right. Overall, we've got strong confirmation that we activate both dendritic cells and MACD failures in these patients, which are the key target cells for mirasalumab. So Slide 10. We've also reported on our progress within discovery by launching a novel concept for more specific cancer immunotherapy called Neo X Prime. Neo X Prime, this is our bi specific built on a bi specific platform, Ruby.
And I will try to explain why it's so novel and why it has such great potential. The new X prime antibodies, we bring tumor parts to the antigen presenting cells, which allows them to selectively guide the immune system towards the tumors. If you look in the lower left corner, I would try to explain. The new ex prime antibody catches tumor exosomes in the circulation or otherwise in the body and brings them to antigen presenting cells. Now move to the cell in the middle.
This is where the new X prime activates the antigen presenting cells and promotes uptake of these exosomes and the tumor neoantigens that are inside the exosomes. And finally, on the right hand side, this allows the antigen presenting cells to selectively initiate a tumor specific immune response through cross presentation and priming of T cells and hence the cool name Neo X Prime. One particular beauty of the Neo X Prime concept is that the tumor exosomes, they carry all the mutated material of the tumor, which is specific for each patient. In other words, the neoantigens of the tumor. So instead of guessing what the immune system should be attacking, like you do with, for example, a cancer vaccine, our new ex prime antibody solves this problem by picking up the patient's own tumor exosomes, Very promising from a theoretical perspective, but the reason we are so very enthusiastic about this is that there seems to be that this is what makes all the difference.
Let's look at Slide 11. Nerex Prime, in short, outperforms every immunotherapy antibody we have tested previously in our model, and this is illustrated in one example in this slide. Our plan is to move forward and build a platform of several drug compounds by initiating X Prime concept. And this is one of the key objectives of our BD efforts, which are now led by our new CBO, Chief Business Officer, Gael Mills. Next slide.
Slide 12. Gail joined Alligator a month ago and is now part of the executive management team. She has a very long experience within oncology, within antibodies and immune oncology and with several major deals on CV. Gail is based in California, and she has a very strong network work in the U. S.
And she will lead our partnering activities going forward for discovery, but of course, most importantly, for our clinical programs. So finally, let's move to Slide 13, the financials. And the important number in this slide is money in the bank, SEK137,000,000. This will take us another 12 months and allow us to progress 8 or 10, 2017 and amidazolamab into efficacy studies. So next slide, Slide 14.
Now with this slide illustrating our focus for 2021 and our potential to have 2 major assets starting up clinically figure studies in 2021. I would be happy to open up for questions. Thank you so much.
Thank you.
And we have a couple of questions coming through so far. The first is from the line of Sameer Devani of Rx Securities.
It's just on 10:15. I guess I'm a little bit surprised on the back of last month's announcement where you guided that the 600 mg was you haven't seen any significant adverse events, and that's obviously a clinically relevant dose. So I'm just trying to perhaps if you can elaborate on what further data you've seen that has meant that you're sort of deprioritizing that asset? Thanks very
much. Yes. Thank you, Samir, for the question. And you're quite right. 600 milligram was a manageable dose.
And we still did see infusion related reactions at this dose. We have seen it at lower doses. And we've seen it at 750. We did have 1 grade 3 event at 750. But in essence, we are convinced that we could manage the toxicity, for example, by pre medication.
One complicated factor here is that it's associated with development of anti drug antibodies, and that makes it more difficult for dose further dose escalation and also for more longer term repeated dosing. So we are now looking into the data. We are starting to analyze biomarkers. And what we are looking for now is to form a sound basis for a study with a modified design. And the first, of course, impact of this is that once you modify the design, we need to redesign the protocol and we need to start all over with a regulatory submission.
So that will lead to a major delay in the program plans. And that is also why, 1, as we have very promising data for 10, 2017 and for mirasalumab, especially since they are extremely well positioned in their respective fields, we think it's wise now to focus our investments on these two programs. So at the same time, we are looking for a partner for clinical development of 10/15, but it's not our priority right now because of these challenges.
That's very helpful. And can I just maybe just one follow-up, just on the antidrug antibodies, is the rate that you're seeing there significantly higher than, say, for Yervoy?
I have not made that comparison. We will present SITC coming up here in a few weeks, and there will be a full data presentation from the study there. So there seems to be an associating with these infusion reactions, and that is part of what's complicating the picture for us.
Okay. That's very helpful. Thanks very much, Per.
Thank you. And we currently have one more question in the queue. So just a reminder to participants, if you do wish to ask a question, please dial 1. The next question is from the line of Ingrid Gafonio of Kempen. Please go ahead.
Your line is open.
Hi, good afternoon, everyone. I hope you can hear me well. I have a couple of questions, if I may. So maybe I wanted to ask start asking about the anti drug antibodies that you observed. I'll be waiting to see the data at SITC, but I was hoping if you can let us know if it was something dose dependent or something that you always started observing at higher dose?
I from as far as I understand now, there seems to be the stronger reactions at higher doses, but this is far from clear. And we do have infusion reactions also at lower doses. So there seems to be a connection there. But it's not as usually in biology, it's nothing that is 100%. And we are looking at this data right now to understand it better.
But it's quite clear that the induction of anti drug antibodies over time and it depends how fast and how much might depend on the dose, but I don't quite have that picture right now. But that complicates the initial ambition to run high doses with repeating doses over a long time. So now that is the design we have to rethink. And we think there are interesting ways forward, but that has to be modified, designed to the program.
Okay. Now that's clear. And just a follow-up on 10/15. We saw the title indeed coming up for Citi in a couple of weeks, but EdTech are not out. So I was hoping you can give us a high level idea on what we can expect for that presentation.
Yes. So for Siti, we will present the full data. We haven't started looking at some of the important biomarkers like tumor histology and so on. That would be extremely interesting. But I do not think that would be ready in time.
I don't think that has started yet. But otherwise, there will be a full presentation of the data we have so far. And that means all the patients, all the safety and the biomarkers that are analyzed to date. So essentially, a Phase 1 presentation.
All right. Got it. I have a couple more questions, but I will go back into the queue just in case there is someone else ready.
Okay. Thank you. Thank you, Ingrid. I'll just check. Once again, if there are any further questions, please dial 1 on your telephone keypad now.
No, that doesn't seem to be anyone else coming through. So I'll reopen your line, Ingrid. And please go ahead.
All right. Thank you very much. I also pretty much heard that you cannot comment a lot on their partnering efforts at this stage. But can you just share some high level information about incoming interest both for A31015 but for your Neo ex prime, what kind of interest you see coming in? Which kind of companies?
And yes, just curious a little bit to understand how we should be looking at it.
I think I mean, when it comes to 10.15%, given that we have some challenges right now and are redesigning, what we are expecting is more co development partnerships. So we do not look for a major out licensing deal at this moment. We think it's up to us to demonstrate with a partner to demonstrate an efficacy signal. And that is the plan. When it comes to the EX Prime, again, it's early concept.
We do have the drug candidates generated. And but again, with our focus on 10/17 and Midtown, we really need partner to join in, in the development of the ex prime to make it a very strong and efficient development. We are looking forward to bring several compounds forward and that in our current capacity, we cannot do ourselves. So we're talking about joint ventures here for Nueve X Prime.
Okay. All right. So that's really clear. And if I may, there was one last question on the 10/15 more about anti drug antibodies. Maybe from your data or other data of longer oncology antibodies as well.
What is actually do you think to try the antidrug antibodies towards the towards the candidate?
So I'm see if I understood the question right, if you ask what you think is a driver for the anti drug antibodies? Yes. Yes. Well, I can only speculate. I mean, if you go start with an endogenous antibody, that is sort of a perfect format that has been refined over 1000000 of years of evolution.
And then we add entity to the antibody, which we do with a bispecific like 10 15. And that always runs the risk of annoying the immune system with sort of surprising it with a new performance. But apart from that, we can only speculate. It's that is it's quite common with bispecific antibodies. So as such, it doesn't have to be a major issue, but it complicates the plans forward.
So it leads to rethinking and redesign.
Okay. That's very clear. Thank you very much for taking the questions.
Yes. Thanks so much, Ingrid. Thank you. Okay. There are no further questions coming through at this time.
So I'll hand back to our speakers for the closing comments. Okay. Thank you so much, and thank you for joining this webcast.