Good morning, and welcome to the ALX Oncology Conference Call. Today's call is being recorded.
Hello, and thank you all for dialing in to today's conference call. I'm Pete Garcia, Chief Financial Officer of ALX Oncology. Today's call will focus on the clinical data of ALX-one hundred and 48, a CD47 myeloid checkpoint inhibitor and specifically our Phase 1b study in gastric cancer combining ALX-one hundred and 48 with trastuzumab, ramasirumab and paclitaxel that was presented at the recently completed European Society of Medical Oncology World Congress on Gastrointestinal Cancer, also known as ESMO GI. A slide deck for this webcast is available on our website in the Investors Events section. Doctor.
Jammal Pond, our President and CEO, will provide a brief overview of ALX-one hundred and 48 and Doctor. Sofia Randolph, our Chief Medical Officer, will then discuss the updated Phase 1b gastric cancer combination study. At the end of our prepared remarks, we will open the line up for questions. Before we begin, as reflected in Slide number 2, we would like to remind you that today's presentation will include forward looking statements based upon our current expectations and beliefs. Such statements represent our judgment as of today and involve substantial risks and uncertainties that may cause actual results to differ materially from the results discussed in the forward looking statements.
Please refer to our filings with the SEC on our website. With that, I'd like to turn the call over to Doctor. Ajamal Panz. Ajamal?
Let's move to Slide number 3. ALS Oncology is an immuno oncology company focused on the CD47 pathway. The CD47 pathway is a checkpoint that bridges the innate and adaptive immune system. Our lead candidate, ALI-one hundred and 48, is a CD47 blocker that is designed to be used in combination. In the clinic, the molecule has shown a very good tolerability profile that has enabled high dosing, and this higher dosing has enabled us in the clinic to achieve better efficacy.
We already have clinical proof of principle in both hematological and solid tumors. Our initial focus is on MDS, AML and solid tumors. Slide number 4. CD47 is a highly expressed on tumor cells, but also normal cells. In the left panel, you have C47 in RNA expression in tumor cells in red and in adjusted normal tissue black.
So if we want to use CA47 as a tumor associated antigen and directly kill CA47 positive cells, we would also kill normal cells and the therapeutic window will be narrow. What makes CD47 an interesting target to me is its function as a neolod checkpoint shown in the right panel. CD47 interacts with receptor alpha that is expressed on macrophages and other neoloid cells. This interaction is a inhibitor interaction that we call a do not in missing node. Many anti cancer agents like anti cancer antibodies or chemotherapy provide if missingals that can target cancer cells for destruction.
For example, anticancer antibodies by antigens on cancer cells and through the introduction of the C of antibody with Epsilon receptor for macrophages provide an immune signal and macrophages would hit cancer cells. In that situation, cancer cells are privileged CA47 to provide a broad immune signal, preventing the productivity of many anticancer agents. What's important here is that in absence of an absence of positive signal, C437 blockade is not enough to activate macrophages. In Slide 5, we see that if we try to use antibodies with an active Fc that directly kill CD47 positive cancer cells, will also, at the same time, will be targeting normal cells for destruction, for example, red blood cells and platelets. In the clinic, CA-forty 7 antibodies with active Fc have been associated with anemia, thrombocytopenia and neutropenia.
This toxicity limits dosing, and in the combination setting, they cannot be dosed high enough to totally block CYP-forty 7, and they cannot maximize the activity of the combination of the combination drug that specifically target cancer cells. To solve this problem, we decided to create a molecule that potentially blocks C57, but is not able to provide the positive signal in Slide number 6. Despite the bonsameral cells, it does not destroy them. But in the combination setting, we can safely dose very high, totally block C47 fetal heart interaction and maximize the PPP of the combination drug that provides the required positive signal in a cancer specific manner, for example, an anti cancer antibody. In Slide number 7, you can see that our molecule, ILX-one hundred and 48, comprises what we call a high affinity cell alpha.
This is the extracellular domain of cell alpha, the receptor for C47 that has been affinity mature to bind C47 with picomolar affinity. Natural human cerepulsa binds ce47 with an affinity of 500 nanomolar to 1 micromolar. So we have thousands of poll higher affinity for ce47 than the natural cell alpha. We have used that high affinity cell alpha to a completely inactivated hep C of an antibody that is not able to interact with Fc gamma receptors and is therefore not able to activate macrophages. However, BSFC does provide the same half life of antibody.
So we have 30 days half life at the steady state at 10 mg per kg and 15 mg per kg. The molecular weight of ELIS-forty 8 is half of the antibody. So we have twice the number of molecules per gram of protein. So 10 mgs per kg of ELIS-forty 8 is the equivalent of 20 mgs per kg of antibody intensive binding sites. Also, the smaller sites may provide better tumor penetration, enabling activity inside tumors.
The manufacturing of ELIZON-forty 8 is completely antibody standard with very high yields of more than 4 grams to liter at 2, 000 liters biogram for scale. And we already have 3 years of stability of 4 degrees as a liquid formulation. Is truly a very well behaved molecule. Now I want to introduce Doctor. Sofia Randolf, a Lex Oncology Chief Medical Officer that will describe the clinical data that we disclosed last Saturday at Desmos Genes.
Thanks, Jama. Good morning. Today, I am going to present updated Phase 1 data summarizing ALX-one hundred and 48 in patients with second line or greater advanced HER2 positive gastric and gastroesophageal cancer. As represented on Slide 8, ALX-one hundred and 48 is designed to safely maximize trastuzumab's antibody dependent cellular phagocytosis of cancer cells by targeting CD47 as a myeloid checkpoint inhibitor. On Slide 9, I'm pleased to present the initial Phase I data from ASPEN-one summarizing ALX-one hundred and 40 eight's activity in patients with advanced HER2 positive gastric cancer who have progressed on prior anti HER2 targeted therapies.
This data was presented recently at the virtual ESMO GI 2021 meeting on July 3, 2021. On Slide 10, in the ASPEN-one gastric portion of the Phase 1 study, ALX-one hundred and 48 was administered in combination with trastuzumab with and without standard ramisirumab plus paclitaxel in patients with second line or greater disease. The primary endpoint of the study is the determination of the maximum tolerated dose of ALX-one hundred and 48 in combination with objective response rate PK and PD as key secondary endpoints. These data cutoff date was May 3, 2021. The baseline characteristics of patients enrolled to the study are seen on Slide 11.
Patients were enrolled from the United States and South Korea predominantly Asian subjects enrolled into all cohorts. The majority of patients had an ECOG score of 1. 38 patients were enrolled across the 2 cohorts of patients with All but 1 patient in each group had tumors that progressed upon prior anti HER2 therapy and slightly less than half in the ALX-one hundred and 48 plus trastuzumab cohort had tumors that had progressed upon 2 or more prior anti HER2 agents as well as prior checkpoint inhibitor therapies. In the ALX plus TRASRAM PAC cohort, 3 patients received ALX-one hundred and 48 at 10 mgs per kgqweek plus the standard escalation cohort receiving ALX-one hundred and 48 at 15 mgs per kg plus trasrampack. In the ALX plus trastuzumab cohort, all patients received ALX at 10 mgs per kgq week in combination with standard trastuzumab.
All groups had significant burden of disease as measured by percentage of visceral metastases. Slide 12 shows that ALX-one hundred and 48 was well tolerated in combination with trastuzumab and ramasirumab plus paclitaxel. The safety of ALX plus On Slide 13, we can see that there were minimal Grade 3 and above ALX-one hundred and 48 associated adverse events. There were no dose limiting toxicities. There were no on study deaths or ALX-one hundred and 48 associated serious adverse events.
A maximum tolerated dose was not reached and the maximum administered dose in combination was 15 mgs per kgq week. This initial data suggests that ALX-one hundred and 48 may be safely administered with trastuzumab, ramasurumab and paclitaxel and is consistent with ALX-one hundred and 40 eight's molecular design and the absence of exposure cytopenia and the absence of an exposure cytopenia relationship that has also previously been reported. On Slide 14, we see the PK profile of ALX-one hundred and 48 following combination therapies with trastuzumab is comparable with and without chemotherapy. On Slide 15, we see confirmed objective responses, including 1 confirmed CR in patients receiving ALX plus trastuzumab and ramasirumab paclitaxel. In addition, PRs have been reported in patients receiving ALX plus trastuzumab.
Slide 16 shows the waterfall plot in patients receiving ALX plus trasram pack. All patients with partial responses had confirmed responses and of course that patient with the complete response was confirmed after data cutoff. 9 of the responding patients, including the patient with the confirmed response remain on study. Objective response was seen at both dose levels as indicated by the asterisk. In the spider plot, anticancer activity was observed with the initial disease assessment at 8 weeks with continued shrinkage of the measurable tumor lesions and that appears to deepen over time.
Here on Slide 17, we summarize initial anticancer activity of ALX-one hundred and 48 in combination with trastuzumab and ramasirumab paclitaxel in the predominantly South Korean population enrolled into the Aspen Gastric Cancer population. We've compared that with other second line or greater study populations. The Aspen objective response rate was 72.2%, which compares favorably to the 52% objective response rate seen in the South Korean study with TRP or trasrampak from Ra et al. At this year. It also compares well with the 41% objective response rate seen from the INHER2 DESTINY-1 study in Japanese and Korean patients and with the 34% objective response rate seen with the current global regulatory comparator ramasir map paclitaxel from the RAINBOW study, specifically the Asia Region 3 subgroup.
Although the sample size of patients treated with ALX-one hundred and 48 in combination at this time is small, the initial data is very promising. Consistent with immune oncology therapy experience, we may also be seeing a potential clinical benefit evident in the later survival based endpoints where the ALX TRASRAMPAC estimated overall survival rate at 12 months is 75 point 8% with a 10.5 month median follow-up. Updated clinical activity data with the doublet ALX-one hundred and 48 plus trastuzumab, this is a chemo free regimen, is summarized after a median follow-up of 27 months. Objective response rate was 21.1 percent and median overall survival was 8.1 months with an estimated 12 month overall of 38%. As ALX-one hundred and 48 is not designed to have monotherapy activity and based on the randomized TACT or Tx study, trastuzumab added minimal activity to paclitaxel in the similar population.
The enhanced ADCP activity seen here with ALX traz doublet supports the rationale for adding it to the current global standard care ramicirumab paclitaxel. On Slide 18, you can see in the swimmer plot that 9 of the 13 responders remain ongoing on the study. On Slide 19, near complete CD47 target occupancy is maintained throughout the ALX-one hundred and 48 dosing interval in combination with chemotherapy containing regimens. And on Slide 20, in an exploratory evaluation, we see a numeric increase in the percent of baseline tumor infiltrating immune cells in the ON study clinical responders compared with that of trastuzumab with and without chemotherapy in patients with 2nd line or greater gastric cancer. Preliminary data suggests that ALX-one hundred and 48 can be safely combined with no maximum tolerated dose reached and a maximum administered dose of 15 mgs per kgq week in combination with standard trastuzumab plus ramisirumab and paclitaxel.
ALX-one hundred and 48 demonstrates a promising 72.2 percent objective response rate in patients with second line or greater disease in combination with TRASRAMPAC and this compares well with the historical data and supports our plans to evaluate this combination in an upcoming randomized Phase twothree study in patients that have progressed upon prior HER2 targeted therapy, where the Phase II portion will confirm ALX's activity on top of Traz, ramasirumab and paclitaxel. To our knowledge, this is the only CD47 targeted agent in the clinic to date that has shown this type of activity in the solid tumor setting. So on Slide 22, we look forward to updating you on the trial design and the beginning of our Phase II trial in gastric cancer in the second half of this year. And this program has received We will now take questions. Operator, could you open up the line for questions?
Thank Our first question comes from the line of Michael Yee with Jefferies. Your line is now open.
Hey, guys. Good morning and congrats on the data. I have 2 questions. 1 was, I guess, given the higher response rates and potentially higher signals of survival, is the plan to move to a Phase 2b type of pivotal against a ramu based regimen. Is that the thought?
So maybe just talk about the next steps. And then the second question is, I guess, taking the learnings from this and head and neck, can you just describe your thoughts around the MDS study that is ongoing, the progress there and how to think about what you would show there versus other CD47s that have shown data in MDS? Thank you.
Sure. This is Sofia. So I'll take that. So thank you for your question. For the first question, in terms of what is our next steps for the gastric study.
So certainly we are looking at a Phase really a Phase twothree type study design, the Phase 2 portion. What we'd like to be able to definitively show, especially given the raw data presented recently at ASCO, is that ALX is providing added benefit onto that backbone of the And there we'll be looking for not only improved delta between the 2 arms, but also looking at the magnitude of ATRP versus historical controls for RP. So certainly, those are the goals, the main goals of the Phase 2 portion of the study. Now as you know, TRP is not a regulatory comparator at this point in time. So beyond the Phase II, we do intend to do the Phase III where we will be combining ATRP excuse me, comparing ATRP versus RP in the Phase III portion of the study.
For the second question, as you were alluding to, in our head and neck data, which will be updated at a conference later on this year. We'll also be looking at a fully accrued cohort, looking both at overall response rate as well as some of these later time points, survival based time points. And then in terms of how that is impacting our MDS study or what our MDS study is doing right now, for the MDS study where we have our Phase I portion looking at ALX-one hundred and 48 in combination with azacitidine, there we anticipate being able to read out that Phase I portion of the study at a conference towards the end of this year and then seamlessly moving into the Phase II portion of the study, which will be randomized, looking at ALX plus azacitidine versus regulatory comparator of azacitidine alone.
I guess the question was given what we've seen in totality that you've presented, do you have more confidence in MDS and what others have seen? Do you expect that to be similar, better? How do you think about that given all the data that we've seen now? That was kind of the question.
So yes, I mean, I think that I think clearly we've shown that this even with this early data is an active drug. And so our hopes that are in the MDS study, where we can also capitalize off of principle that other CD47 targeted agents have shown in that space, that our drug, ALX-one hundred and 48, in combination with then certainly, the signals of activity that we're seeing really across these different tumor histologies in different combinations suggest that ALX is truly providing added benefit via its myeloid checkpoint inhibition.
Thank you.
Thank you. Our next question comes from the line of Collin Bristol with UBS. Your line is now open.
Hey, good morning. Thanks for taking the questions and congrats on the data. Just any other details you can give us on the Phase II design, anticipated timing of enrollment readout? I was just curious, are you going to explore a higher dose? You didn't hit any DLT.
I'm just curious if that you have any appetite for that. And then just 1 final question on the head and neck program. Can you remind us when we should expect to get the next update on this data set and what that will consist of? Thanks.
Sure. So for the ASPEN, we're calling ASPEN 6, so for the Phase IIIII study of ALX in the gastric cancer population. Here, as we just discussed, we will be looking at ATRP versus TRP. We anticipate that we'll be opening in the second half of this year. As a typical and is anticipated to be approximately 100 patients.
And as a typical Phase II, we would anticipate about 2 years or so to complete enrollment and be able to have some idea of study readout. I think this will be a global study and given the footprint of gastric cancer, it will certainly be enriched for sites in the Asia Pac region, but it will be a global study. In terms of the head and neck cancer studies, the Phase Ib cohort that enrolled head and neck cancer in our ASPEN-one first in human study. We anticipate having that an update of that towards the end of this year at a conference, hopefully SITC, but obviously, we haven't submitted the abstract yet.
And then potentially higher dose?
Yes, sorry. So for the gastric cancer study, ASPEN 6, there and then it's just 1 of the benefits of our drug given its safety profile, we'll be dosing ALX at 30 mgs per kg every other week. And the idea there is we'll be using an every other week dosing strategy for trastuzumab and then ramasirumab and paclitaxel are also being dosed on a standard 28 day regimen. So it puts everything onto a 28 day cycle. So it's more convenient for patients and for the treating physicians.
So the ALX-one hundred and 48 will be dosed at 30 mgs per kg every other week. That's a dose that we have already shown to be safe in our Phase I study. The exposure levels, steady state exposure levels, we've also shown to be similar to 15 mgs per kgq week, and that added Cmax of going 15 to 30 has been safe.
That's great. Thank you.
Thank you. Our next question comes from the line of Chris Raymond with Piper Sandler. Your line is now open.
Hey, thanks. Just a couple of questions. Just on the inclusion criteria, I just want to just clarify, in terms of prior platinum exposure, just kind of curious on your wording that patients in this cohort had to have progressed on prior trastuzumab and florapiridine or platinum chemo. I just want to clarify, did they all see platinum chemo or if not, can you sort of clarify the percentage of patients that did that were platinum naive? And then the second question, oh, yes, go ahead.
No, no, no.
That's okay. Go ahead, please.
Okay. Yes. So second question is on just on the 1 patient that had the CR. I know this was confirmed after the data cut off, but just can you clarify, is the waterfall plot in your deck representative pre or post data cut
So good question. I'll just do the latter 1 first. So the waterfall plot is pre the patient was, as you just said, had the confirmed response after the data cut off. So their response did deepened. And then the other piece about the prior therapies.
So in yes, it's just the way it's worded because there are sometimes different first line regimens that are used whether patients are in clinical studies or not. But in this study, everybody had progressed upon a regimen that contained both, afluoropyrimidine and aplatin. And the eligibility stated they had to have progressed on prior trastuzumab. We did have 1 patient who only received the 5 SU based and then the platinum and did not have the trastuzumab, but everybody else had progressed upon that doublet plus trustuzumab.
Awesome. Thank you very much.
Thank you. Our next question comes from the line of Alethia Young with Cantor. Your line is now open.
Congrats on the data. I guess a little bit more on the CR. I just wanted to get like was there anything notable, notably particular about that patient that drove CR? And then when you look at like Slide 17 where you have the comparables, can you talk about where and if CRs we're seeing there and comparable populations? And then I guess as far as for CD47 target occupancy, do you think this is something that in like all tumor types, the occupancy levels need to be about for the same duration?
And so 1 can make kind of a read across to some of the other indications you have going on as well. Thanks.
Yes, thanks. So for the patient with the CR, beyond that particular patient did have, well, 1 notable thing is that they were HER2 their HER2 scoring was 2 plus as opposed to 3 plus. And I think that, that is significant. We haven't actually in this study, we haven't looked at FISH status or looked at amplification. So for eligibility purposes, HER2 scoring is done locally at the site.
However, the HER2 scoring that's presented on the waterfall plot is an exploratory analysis where we've taken archival samples and then central assessments to look for HER2 score. And in that analysis, that complete responder did have a scoring of 2 plus. So that was actually significant for us. Other than that though, the patient had sort of typical standard first line therapy. And again, consistent with some of the other responders in this population, their response has appeared to deepen over time.
In terms of the second question, looking at CR rates in other studies, In all of these studies, there is about, I'd say, about a 5% or so CR rate, maybe a little bit less. So I think you would expect to see some hopefully some CRs. And I think in the smaller data set, where we're seeing the 1 CR, it kind of puts it at about 6%. I think the TAVR impact data coming out of ASCO a couple of weeks ago had a 2% CR rate, but our numbers are pretty small. So I think the presence of the CR is significant and in this smaller data set, and then we'll see what happens as we get into the Phase II setting.
In terms of receptor occupancy, so this is a very interesting area where what we've shown, I think, over the course of ASPEN-one is that having full receptor occupancy in the periphery is important. But even more than that, being able to push that dose past full receptor occupancy in the periphery, the hope is that it drives that drug into the tumor microenvironment, where in the solid tumor setting, drug exposure may be limited. So going back to previous presentations of this data set in our non Hodgkin lymphoma cohort, certainly there we found an exposure response relationship where even after having full receptor occupancy in the periphery, as we increased exposure that led to increased responses in that population. And so for that reason, in these other solid tumor indications, we've moved towards an exposure level that is equivalent to 15 mgs per kgq week. So here in our gastric population, you'll notice we have increased the dose to 15 mgs per kgq week, and it's that exposure that we'll be bringing into the Phase II setting at the 30 mgs per kg every other week.
Similarly for our MDS study, there we are dosing up to 60 mgs per kg q month. But again, that's a building block. It will have the same exposure as 15 mgs per kgq week. So we're doing that program
wide. Great. Thank you very much.
Thank you. Our next question comes from the line of Swayampakula Ramakanth with H. C. Wainwright. Your line is now open.
Thank you. Good morning folks. Most of my questions have been answered, but I just want to have an understanding of the patient profile or the patient baseline characteristics in those studies that you were trying to compare on the Slide 17 of your presentation. Any commentary on how universally similar they were in terms of the baseline characteristics? And I know Aspen stacks better than the rest of them, but I'm just trying to understand how similar are the baseline characteristics as well?
Sure. Well, I think as we just sort of go down the line, as you look at the raw et al data from ASCO, 2021, there, overall, the patients, the demography was fairly similar. I think 1 key difference is they had a much higher percentage of IHC3 plus patients. In their reports, they had 78% of their patients were again, all of these are done with archival. In this particular slide on 17, these other study populations have been defined based off of archival blocks.
And we'll talk about DESTINY in a second. So for the Raa et al, there they had I think about a 78% reported IHC3 plus population as compared to us where in terms of our known 3 plus made up about 22% of our population and then about 28% of our population a third of the patients who we did not have sufficient archival biopsies to be able to adequately characterize her HER2 score. So in terms of known IHC3 plus, our population had less. So that actually, I think, is significant given that even with that, we're seeing a 72% objective response rate across the board in our cohort. So that's 1 thing.
1 would anticipate that with the higher IHC3 plus status and certainly the DESTINY-one data that was presented at ESMO GI as well where they did the characterize the patients with regards to IHC as well as ctDNA exploratory analysis there. They do see that with a higher amplification or with a higher CT score, that does seem to correlate with increased response. In terms of DESTINY-one, I think the key difference there is that in that population, all patients enrolled were 3rd line or greater. They had failed 1 prior trastuzumab, but had failed 2 prior regimens. In our study, we are a second true second line study, where all of the patients in this particular cohort had failed 1 prior regimen.
I think we had 1 patient who had failed 2 priors. So very much a standard second line population, but all patients, with the exception of 1, had failed prior trastuzumab. In terms the IHC status there, I have to go back and look. I actually don't know off the top of my head the percentage of IH3 versus 2 plus in that study. But certainly, they saw the correlation that with increased IH3 plus or amplification, there was greater response.
And then in terms of Rainbow Asia or Rainbow overall, there this is also a second line or greater population. The study was done, obviously in time was done earlier in time compared to the more recent DESTINY-1 randomized data. So their standards of care, they would have also received trastuzumab and presumably 5F use and a platinum in the first line setting. So there, I think, it's probably most similar to our population. I think overall, about half the patients in the RAINBOW overall study were Asia, about half were ex Asia.
And what's presented on Slide 17 is really just the Asia Region 3. Certainly, just to be complete, DESTINY-one, all Asian study with enrolled by subjects coming from Japan and South Korea. And then the raw data at ASCO 2021 was, although single arm was also predominantly single institution coming out of South Korea as well.
Great. Thank you very much. I was just trying to understand how what's the impact of biology on the doublet, the ALX-one hundred and 48 plus SaaS, that you could only achieve 4 PRs at this point. How should we think about that data? Or is that because some of them were TRAS failures or non responders that, that was the reason why you could not see any better data than what you have at this point?
I think for the doublet, I would look at it through a slightly different lens. I think for the doublet, the significant thing here is that this is also a chemo free regimen. So anytime you put chemotherapy in the mix, you're going to have a higher response rate. And I think you can see that in all of the other studies that we've presented, including our chemo combination. However, in the doublet data, here now we are in a chemo free regimen.
And so here with ALX, as we stated earlier, based on the molecular design, no anticipated monotherapy activity. When you look at the trastuzumab component, to our knowledge, there isn't a second line, TRAS only, published data set out there. So the closest that we can do is to look at, TRAS's contribution to a chemotherapy backbone. So in the randomized study, TACT, you guys are familiar with, trastuzumab, patients who had failed prior trans containing regimens in the first line went on to be randomized to receive paclitaxel alone or trastuzumab plus paclitaxel, so TRAS after TRAS. There, the data between the 2 arms was very similar.
There was about a 33% objective response Again, chemotherapy is in the mix. However, when you look at the delta between those 2 arms, it was, I think, on the order trastuzumab did not seem to be adding any additional activity in that second line setting to the chemotherapy backbone. So in our data set, when we look at the doublet to see an objective response rate of 21% in the absence of chemotherapy, we think is pretty significant. When you go on to look at the other survival based endpoints, so for example, I think in Slide 18, I have it compared to probably a more recent chemo readout, which would be the control arm for DESTINY-one, where patients received either irinotecone or paclitaxel. Here you can see the median overall survivals of Aspen 1 of 8.1 months and Destiny control arm, 8.4 months and then the sort of intriguing 12 month OS rates a little bit now later in time, you're seeing a 38% OS rate at 12 months from the Aspen of the doublet versus 29% from the DESTINY control arm.
So again, in a chemo free setting, we think this is significant, and I think it's really representative of the enhanced ADCP activity of trastuzumab. So we're no longer relying on inhibition of ErbB2 signaling by trastuzumab, but rather exploiting this ADCP activity. And that's the rationale for adding this doublet onto the current global standard of care of the Ram
Thank you. Our last question comes from the line of Adam Edwards with LifeSci Capital.
Your line is now open.
Thank you. Good morning. Just curious if we can get a better understanding of where the new responses came from versus SITC? How many of the 4 new responses came from the newly enrolled patients versus sort of delayed responses from the patients we saw at SITC with stable disease?
Let's see. So if we go up to roughly to Slide 16, The new I can say certainly the complete response that was a newly enrolled 1 of those 4 newly enrolled patients that confirmed CR. The other 3, I think they all had PRs. I'd have to get back, but I think the stable diseases were I'd have to go back and look. I think the stable diseases may have been from the earlier group.
But of those 4, there were definitely 1 CR and there would have been some of the PRs in that mix as well.
And Sofia, do you know if the 2 unconfirmed responses from SITC confirmed?
1 of them confirmed, 1 of them the patient actually came off due to let me see, 1 of them the patient came out for a reason. So this is 1 of the So it's a little bit of a mix. 1 was disease progression, 1 was patient's decision.
Okay, great. Thank you.
Thank you. There are no further questions at this time. I would now like to turn the call back over to Doctor. Jean Mapon for closing remarks.
Good morning. I just want to thank you for your attention this morning to our call. And with that, we can call the conference.
Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.