Q3 2024 Mersana Therapeutics Inc Earnings Call
Michael Schmidt, Michael Schmidt, Brian DeSchuytner,
Speaker Change: Good morning and welcome to Mirsana Therapeutics' third quarter 2024 conference call.
Currently, all participants are in listen-only mode.
Speaker Change: There will be a question and answer session at the end of this call.
Speaker Change: Should you need assistance, please signal a conference specialist by pressing star then zero on your telephone keypad. Please note this event is being recorded. I would now like to turn the conference over to Jason Fredette, Senior Vice President, Investor Relations and Corporate Communications. Please proceed.
Speaker Change: These risks and uncertainties are discussed in our quarterly report on Form 10-Q filed with the Securities and Exchange Commission on August 13, 2024, and in subsequent SEC filings.
Speaker Change: Our filings are available at sec.gov and on our website mursana.com. Except as required by law, we assume no obligation to update forward-looking statements publicly, even if new information becomes available in the future.
Speaker Change: On today's call, we have Mirsana's Chief Executive Officer, Dr. Marty Huber, our Chief Development Officer, Mohan Bala, and our Chief Operating Officer and Chief Financial Officer, Brian DeSchuytner. With that, let's turn the call over to Marty to begin our discussion.
Thank you, Jason, and good morning, everyone.
Speaker Change: I'm pleased to report that Mirsana made significant progress in the third quarter as we continue to dose escalate in our Phase 1 clinical trials of both XMT 1660 and XMT 2056.
Speaker Change: We also achieved multiple milestones in our research collaborations, and we maintained the strength of our balance sheet.
Speaker Change: These accomplishments position us well as we prepare to disclose initial XMT-1660 clinical data at a company event by the end of this year.
Speaker Change: XMT1660 is Mirsana's ADC candidate targeting B7H4 that was developed using our DolaSymptom platform with site-specific bioconjugation and a drug to antibody ratio of 6.
Speaker Change: The dose escalation portion of our Phase I clinical trial is ongoing, and we still have not established a maximum tolerated dose. We recently escalated to 115 mg per m2, or about 3.1 mg per kg.
every four weeks.
Speaker Change: This is up from the 80 mg per m2 dose we mentioned on our last conference call, and it's well beyond the highest doses we investigated with any of our prior ADCs.
Speaker Change: We believe our ability to reach this dosing level speaks both to Dola's symptoms differentiated tolerability profile and to the limited expression of B7H4 in healthy tissue.
Speaker Change: In parallel with our dose escalation work, we are continuing to investigate more frequent dosing schedules for XNT1660, and we're working to refine our biomarker strategy to prepare for expansion and later stages of development.
Speaker Change: Let me turn the call over to Mohan Bala, our Chief Development Officer, to share a little more color on our enrollment in this trial and one of the indications we are focusing on.
Mohan Bala: Thanks Marty. As a reminder, the dose escalation portion of our phase 1 trial of XMT1660 is being conducted exclusively in the U.S. and it is enrolling patients with the cancers that most commonly express B7H4.
Mohan Bala: These include heavily pre-treated patients with recurrent, triple-negative, and HR-positive breast cancers, endometrial cancer, and ovarian cancer.
Mohan Bala: We believe XMT1660 has the potential to address important unmet needs for patients with each of these tumor types.
Mohan Bala: That said, about three quarters of our enrolled patients have breast cancer.
Mohan Bala: Today in the U.S., topoisomerase-1 ADCs are being used very frequently in breast cancer.
Mohan Bala: In fact, approximately 90% of our enrolled patients with triple-negative breast cancer and about half of our HR-positive patients have been treated with at least one prior topo1 ADC, whether it be Tredelvi or NR2.
Mohan Bala: We've discussed previously the growing body of retrospective data demonstrating that patients develop resistance to TOPO1 payloads.
This has become a significant concern for physicians.
Mohan Bala: At ESMO in September, the first prospective data exhibiting the same phenomenon were presented by a competitor that's developing ETOPO-1B7H4-ABC.
Mohan Bala: The Phase I dataset included eight patients who had previously been treated with the TOPO-1 inhibitor, and notably, none achieved an objective response to the competitor's ADC.
Mohan Bala: These presentations help to reinforce the urgent need for ADCs with non-topal payloads in breast cancer.
and XMT 1660 fits this profile.
Mohan Bala: In fact, just last week at the 15th Annual World ADC in San Diego, we presented new preclinical data demonstrating 70-60-60s anti-tumor activity following TOPO-1 treatment.
Speaker Change: So, what is the standard of care today for patients with late-stage breast cancer who already have received a TOPO1ABC?
Well, it's generally single-agent chemotherapy.
Speaker Change: And the prognosis for these patients is exceedingly poor, as evidenced by data for the control arm in the afferent trial for Tredelvi in TMDC.
Speaker Change: Importantly, ASCEND may be a potential best case, as this trial enrolled patients who were naive to the treatment with TILPO1ABC.
Now back to Marty.
Marty Huber: Thanks Mohan. In multiple presentations over the course of the past year, we have shared data demonstrating the potential for dolacentin ADCs to generate anti-tumor activity and avoid many of the toxicities that have limited other ADC platforms.
Marty Huber: We believe our initial XNT1660 data will shed light on its clinical potential across tumor types, including in patients who have previously received TOPA1A DCs.
Marty Huber: We expect to present our initial clinical safety, tolerability, efficacy, and biomarker data from dose escalation and backfill cohorts at a company event by the end of this year.
Marty Huber: On the safety side, we would hope to show a profile that is differentiated from other ADCs.
Marty Huber: And on the efficacy side, we expect to characterize the relationships between anti-tumor activity and dose as well as anti-tumor activity and B7H4 expression.
Marty Huber: In addition to our expected data disclosure, we also remain on track to initiate the expansion portion of our Phase I clinical trial of XMD1660 by the end of this year.
Marty Huber: In fact, we have already determined that our first area of focus for expansion will be patients with triple negative breast cancer who have previously received at least one TOPO1 ADC.
Marty Huber: Beyond XMT 1660's potential as a monotherapy, we would hope to demonstrate a profile that may be amenable for use in combination with other agents, including combinations that we believe our competitors would not be able to pursue.
Marty Huber: As a reminder, dolosynthin ADCs are equipped with a proprietary or a statin payload that has been shown clinically to avoid dose-limiting severe neutropenia, peripheral neuropathy, and ocular toxicity.
Marty Huber: These types of adverse events are preventing many of today's ADCs from combining with certain standards of care due to the risk of overlapping toxicities.
Marty Huber: Now let's turn to XNT 2056. This is our lead candidate that was developed utilizing Immunosymptom, our innate immune stimulating ADC platform that leverages our novel and proprietary sting agonist payload.
Marty Huber: XMT 2056 targets a novel HER2 epitope which we believe offer opportunities for development both as a monotherapy and in combination with other therapies including those that target HER2.
Marty Huber: At CIDSE 2024, which took place last week, we presented new preclinical data demonstrating XMT2056's ability to activate stain signaling and inhibit tumor growth at very low doses.
Marty Huber: We continue to advance the dose escalation portion of our Phase 1 trial of this candidate.
Marty Huber: Eligible patients include those with a range of HER2-positive tumors, including breast, gastric, colorectal, and non-small cell lung cancer.
Marty Huber: And finally, business development remains a core strategic focus for Mursana, and we're making further progress in our collaborations with both Johnson & Johnson and Mark KGA.
Speaker Change: Our efforts in this area were most recently exemplified by the milestones we achieved under these collaborations in the third quarter. For a little more color on our financials, let's turn things over to Brian.
Brian DeSchuytner: Thank you, Marty. Let's begin with our balance sheet. We ended the third quarter with $155.2 million in cash equivalents and marketable securities. We continue to expect our capital resources will support our current operating plan commitment into 2026.
Brian DeSchuytner: Please note that our Cash Runway Guidance does not assume any future milestone payments that we may earn from our current collaborations or proceeds that we may realize from future collaborations.
Brian DeSchuytner: Net cash used in operating activities for the third quarter of 2024 was $8.6 million, which included the benefit of an $8 million milestone payment and a $3.5 million payment for manufacturing activities from J&J.
Brian DeSchuytner: Net cash used in Q3 was significantly lower than the $46.1 million net cash used in operating activities during the year-ago quarter.
Brian DeSchuytner: The decrease primarily reflects our portfolio reprioritization efforts, including the OPEX reductions we implemented in the second half of 2023 as part of our restructuring, as well as the payments from J&J.
Brian DeSchuytner: Turning to our income statement, collaboration revenue for the third quarter of 2024 was $12.6 million, compared to $7.7 million for the same period in 2023. The year-over-year change was primarily related to the increases in revenue recognized.
under our J&J and Merck KGA collaboration agreements.
Brian DeSchuytner: Research and development expenses for the third quarter of 2024 declined significantly to 14.8 million dollars compared to 30.5 million dollars for the same period in 2023. For the most recent quarter approximately 2.3 million dollars of this spending was related to non-cash stock-based compensation.
Brian DeSchuytner: The year-over-year decline in R&D expenses was primarily related to reduced costs associated with manufacturing and clinical development activities for our discontinued ADC upgrade and reduced employee compensation expense following the restructuring we substantially completed in 2023.
Brian DeSchuytner: General and administrative expenses for the third quarter of 2024 declined to 9.9 million dollars compared to 12.9 million dollars during the same period in 2023. Approximately 1.7 million dollars in non-cash stock-based compensation expenses were included in GNA for the most recent quarter.
Brian DeSchuytner: The year-over-year decline in G&A was primarily related to reduced consulting and professional services fees and reduced employee compensation expenses following our restructuring.
Brian DeSchuytner: And finally, Masada's net loss for the third quarter of 2024 was $11.5 million, compared to a net loss of $41.7 million for the same period in 2023.
Speaker Change: That concludes our business update. Operator, would you please open the call to questions from the audience?
Speaker Change: We will now begin the question and answer session. To ask a question, you may press star then 1 on your telephone keypad. If you are using a speakerphone, please pick up your handset before pressing the keys. If at any time your question has been addressed and you would like to withdraw your question, please press star then 2. At this time, we will pause momentarily to assemble our roster.
Speaker Change: The first question comes from Tara Bancroft of TD Cowan. Please go ahead.
Tara Bancroft: Hi, good morning. So thanks for disclosing the nature of the patients a little bit more. It's really helpful to see. So I guess what I'm curious about is...
Tara Bancroft: Since most patients are post-TOBO here that you've enrolled, do you have any updated thoughts on how we should benchmark this versus what we've seen from other B7, H4, ADCs, which are not, I mean, besides Astra, which of course was not effective there. Thanks so much.
Thank you.
Morning Tara. We're not providing any specific guidance on ORR.
We do recognize that there are...
Tara Bancroft: excuse me, other benchmarks out there. I mean Pfizer has shared their data.
with a 20% response rate at their...
Tara Bancroft: doses, which we're still trying to understand exactly which doses of those patients or the doses they'll take forward.
Tara Bancroft: We've seen the HANSO data, which as you recall was China data, so we doubt there was a heavily pre-TOPO treatment in those patients.
Tara Bancroft: And then the most recent AZ data, they actually, while they did show three out of 12 patients with breast cancer, none of those patients had seen a prior topo. So I think it's, those are the benchmarks that are out there, but we think there's...
Tara Bancroft: non-trivial differences between the populations. So for us to try to get into predicting exactly which one's the right benchmark for us is a little difficult at this point in time.
Okay, I understand. Thanks so much.
Speaker Change: The next question comes from Jonathan Chang with Lyrinc Partners. Please go ahead.
Speaker Change: Hi, this is Yander Li on for Jonathan Chang. Thanks for taking my questions.
Speaker Change: So, my first question on XMT 1660, so how many patients at efficacy-evaluable dose are we expecting to see for the initial data update, and what is the percentage of them would you consider as bellmark or positive? Thank you.
Yeah, well, good questions there.
Speaker Change: But actually, we just haven't provided that information to date. That will be shared along with the data later on this year. So, we gave the specifics today on the types of patients we've enrolled, some prior treatment, but we haven't gotten into specifics on patient numbers.
Speaker Change: for B7H4 Expression. As I think you know, we're enrolling all comers.
Speaker Change: and looking at the B7H4 data retrospectively and we do tend to get that information in batches.
Speaker Change: So even when we share the data, there may be some patients where we don't have complete B7H4 expression data on, but we'll share what we do have.
Speaker Change: Got it. Oh, thank you. And another follow-up question I have is that
Speaker Change: You've previously mentioned that you are evaluating a dose schedule that is more frequently than every four weeks.
Speaker Change: So, could you provide more insight into how the more frequent dosing cohort is performing relatively to the every four-week cohort? And yeah, are you continuing to escalate this more frequent dose as well? Thank you.
Thank you.
Speaker Change: Thank you, Jonathan. We're not getting into the details of the doses schedule. What we do, what I think we have shared is there is the kind of the core schedule that we're on now of every four weeks, and that's the one we're up to 115 milligrams per meter squared that we're dosing now. What we're doing on, we're looking at more frequent doses where we split this dose at different intervals in between.
Speaker Change: Today, we're not sharing any data on the relative performance of those two. We will have, but as we noted during the script, we are going to be sharing
Speaker Change: some data on is there a dose correlation with activity etc. or not but that will be part of what we describe when we show the data set.
Understood. Thanks for taking my question.
Thank you.
Speaker Change: The next question comes from Charles Zhu with Lifesci Capital. Please go ahead.
Speaker Change: Good morning, everyone. Thanks for providing this update and congrats on the progress.
My first question...
Speaker Change: Looking at some of the recent Phase 1 clinical readouts for B7H4ADCs, we've seen median prior lines of therapy ranging from 3 for Pfizer up to 5 for Astra. Can you provide any additional color on what you'd expect your Phase 1 patients
Speaker Change: to see with respect to prior treatment history and number lines beyond, you know, the topo-ADC experience.
Speaker Change: has a similar question as well. Looks like you also have a handful of breast cancer patients who are topo-naive, almost like an inverse to what AstraZeneca read out at the recent ESMO 2024 conference.
Speaker Change: Can you make any high-level commentary regarding what you're seeing in between the topo experience versus your naive patients?
Speaker Change: Well, I'll start with the lines of therapy. We're not providing the detailed information, but as Mohan outlined, this is a heavily pre-treated population and we will describe that.
Speaker Change: I think one of the things that will be important, and we'll give some kudos to AZ, they actually did call out, specifically,
flyer topo exposure in their data set.
Speaker Change: The others haven't even shown that. So I think it's not only number of lines, it's what are those treatments that becomes very important.
Speaker Change: For example, if a patient was started out hormone receptor positive and got four lines of hormonal therapy, how relevant that is to them now that you're using a cytotoxic in a late line. So I think it is important to understand kind of the nature of the treatment as well, really specifically have these patients seen ADCs.
Speaker Change: The second part is an interesting observation. Why aren't we seeing more topo naives? And I think one of the things we've heard from investigators, from KOLs and ...
Speaker Change: you know, as we were wandering around the halls of ESMO saying, how is it that AZ had nobody with SOFO, prior SOFO and breast, and...
You guys seem to have a lot.
Speaker Change: they had already, based on the retrospective and anecdotal data and their own patient experience, decided that they don't want a topo payload after the patient has seen a topo.
Speaker Change: So one of the things we hear from our investigators and others is they are continuously looking for non-TOPO payloads or novel payloads that they could try in this population. So I think it's not an accident that we're ending up with this patient population.
Speaker Change: The investigator is telling us we need something different than a topo payment.
Speaker Change: Got it, great. And also, as you continue to push the dose up to and potentially beyond 115 mg per mL squared,
Speaker Change: Is there a scenario where you'd continue dose escalating even as you initiate dose expansions? And can you also talk about, you know, potential reasons why you may be able to push the dose so high, maybe specifically around things like payload retention while in circulation?
for free payload versus intact AADCs. Thank you.
Speaker Change: Well, I mean I'm gonna do the second one first and I'll come back is I mean our core hypothesis when we design this molecule was to avoid neuropathy, avoid neutropenia, avoid ocular tox.
Speaker Change: And as you've seen from our previous data with UPRI and 1592, we weren't limited by those toxicities. And so in some ways, the reason we're able to continue to escalate is...
Speaker Change: kind of validates our hypothesis, you know, and Tim, our chief tech officer, you know,
Speaker Change: He was right that if you the molecule was designed to avoid those DLTs and it's doing that now That doesn't mean there's not anything and we'll that'll be part of the nature of the data is what do we have and we'll share That with the upcoming safety thing
Speaker Change: with regards, could we go beyond 115? That will be driven by the data at this point in time.
Speaker Change: Does that Prevent us from initiating expansion? No, we have the way the protocol is designed is we can take, in fact, we're probably gonna take at least two doses into expansion. That's important in the current era of project Optimist that you kind of get.
Speaker Change: It would be very easy for us to start with one dose and then come with a second dose later on.
Speaker Change: The direct answer is if the data allows us to escalate, we would escalate, but that's a data-dependent decision and yes we can initiate expansion even if we do continue to escalate.
Great, thank you for taking our questions and congrats again.
Thank you.
Speaker Change: Again, if you have a question, please press star then 1.
Speaker Change: The next question comes from Ashik Mubarak with Citi. Please go ahead.
Ashik Mubarak: All right guys, thanks very much for taking my questions. I appreciate all the updates here.
Ashik Mubarak: I just wanted to ask if you have any thoughts as to whether we should expect any differences in effect of XMT-1660 depending on which TOPO-1 ADC was used in the prior line.
Ashik Mubarak: I know triple negative breast is kind of a moving target in between Yusuf and Hertu versus Trudelvy.
Ashik Mubarak: But is it fair to assume that the majority of patients got at least in her two in the prior line?
Ashik Mubarak: And then last question for me, how are you thinking about development in gynecological tumors? Is that still part of the long-term plan or are you planning to leave that to competitors not focused on TOPO1 and prior ones? Thanks.
Bye.
Speaker Change: I'm going to give a quick answer and then I'm going to turn it over to Mohan to talk about the you know, the different types of topo ADCs patients are receiving in the gynecological development. But the kind of the short answer is our hypothesis, this is not an antigen difference. So in HER2 versus Tredelve, even though they're targeting different, ultimately they inhibit topoisomerase 1.
Speaker Change: and there are two known mechanisms, there's probably more, of resistance. One of those, they switch from TOPO1 to TOPO2. But that's for both of them, so we would not imagine a difference.
Speaker Change: The other potential mechanism of resistance is PGP pumps, where basically you get efflux of the payload. As a reminder, our payload is not a substrate for PGP. So, no matter which of the mechanisms of resistance, which both those molecules are kind of...
Speaker Change: most commonly expected to occur, we should be able to overcome both of those. And I'm going to turn it over to Mohand to address the rest of your question on you know the population and the guide on development.
Mohand: Yeah, so I'm maybe going to start with not talking specifically about our trial, but what's happening in the breast cancer kind of treatment landscape.
Mohand: So, I think, you know, you can see this from the Gilead earnings call as well. Prodelvie is probably the standard of care in chemo pre-treated patients in triple negatives.
They have the bigger market share.
Mohand: and, you know, some of those patients are also then subsequently treated with nHER2.
Speaker Change: But as Marty said, the increasing preference is for physicians to seek alternate payloads and alternate targets.
Speaker Change: In hormone positive it's a bit a bit more kind of split between you know and I'm talking about what the general kind of treatment pattern is.
Speaker Change: and sorry can what was the opportunity and guide yeah so clearly kind of I would start with endometrial
Speaker Change: The endometrial kind of second slash third line space is completely open right now because the standard of care is shifting to treatment with both checkpoint inhibitor and chemotherapy in front line.
Speaker Change: and if you don't get kind of checkpoint inhibitor frontline in say an MSS population they get it second line. But I think in the future most patients will get both in frontline and once you get those treatments there there's really no good treatment option subsequent to that.
Speaker Change: So the opportunity in endometrial cancer is quite big, the unmet need is high, and we clearly hear this.
Speaker Change: In ovarian cancer, clearly there are a lot of treatments in development in platinum-resistant.
Speaker Change: But where there's actually kind of an increasing unmet need is in platinum sensitive.
Speaker Change: for either therapies that can combine with platinum and then continue treatment beyond the completion of that platinum therapy.
Speaker Change: So, even though there's kind of a lot of treatments competing in the platinum resistance space, there are not that many novel treatments that are being developed in the platinum sensitive space.
Thank you for all the coverage.
Speaker Change: The next question comes from Michael Schmidt with Guggenheim Securities. Please go ahead.
Speaker Change: Hey, good morning. This is Ige Alfermaiko. Thanks for taking our questions and thanks for the update.
Speaker Change: Two questions from us. The first one looks like you will first focus on triple negative in the expansion cohort relative to HR positive. Wondering, is it based on preclinical rationale such as a B7H4 expression or was any clinical observation also part of the consideration?
And I have a follow-up.
The primary reason we're going there is
Speaker Change: to be perfectly candid, it's just unmet medical need. This is where we have the most patients coming into our trial. It's an area where we believe, once again we haven't talked to the agency or anything, that the regulatory hurdle will be quite low because essentially, as Mohan alluded to, once they've seen a topo payload ADC,
Speaker Change: There is nothing. I mean, the response rate with chemotherapy is 5%. And that's in the control arm of Ascent, which was not post-trudelavy. That was the same patients getting trudelavy. If you think about post-trudelavy, it's certainly no reason to expect that response rate would be higher than 5%.
Speaker Change: So, I think, you know, overall this is a place for us that we see we could go very fast. We do see hormone receptor positive as an important population, and one thing that's kind of interesting is if you look at the late-line hormone receptor positive breast cancer patients,
Speaker Change: especially when they get to kind of the HER2 ultra lows, they're starting to look a lot more like TNVC. You know, once they've seen that in HER2, there's nothing left for them. So we think those are both opportunities, but TNVC is the cleanest, easiest, fastest.
Speaker Change: Got it. That's very helpful. And then second question. There was a poster at last year's ASCO discussing optimal sequencing of SN38 and DXD-ADC in breast cancer patients. I'm just wondering, is there any preclinical rationale or even clinical observations suggesting, you know, optimal sequencing of DOLLAR-SN10 and TOP1-ADC?
Speaker Change: I think there's well we're not really focused on the is there an optimal we're kind of what we've been focused on is the reality of the clinical situation is we're going to be post-topo for the initial indications so what the focus on data we showed this year at World ADC was showing that we have
Jason Huber, Jason Fredette, Brian DeSchuytner
Speaker Change: So, we're not, you know, I think that's an interesting long-term question. Should we be in front of the topo? But to be perfectly frank, right now, today, given that the topos are so well established in the marketplace, our point of entry is going to be post-topo.
Speaker Change: Or, the really cool thing we can think about is, assuming we demonstrate the safety profile that we've shown to date with the doses, and you just go with a topo, and not even bother about the sequencing, do them together.
Speaker Change: you know, two different targets with two different payloads could be a pretty cool thing that others can't do because of either neuropathy, neutropenia, oncotox or myelosuppression.
That is very helpful, thank you.
Speaker Change: Again, if you have a question, please press star then 1.
Speaker Change: The next question comes from Justin Zeeland with BTIG. Please go ahead.
Speaker Change: Thanks for taking our question. I wanted to hear your thoughts on what a meaningful Delta would be on safety events to differentiate 1660 from the class based on your mechanism of action and and how do you think the differentiated safety profile may enable potential for combination therapy in the future?
Speaker Change: I'm going to start it out and then I'm going to let Mohan kind of talk a little bit about some of the data we've generated already in combination with CARBO with our previous molecules. One of the things that was a key focus for us is
Speaker Change: Harbo has challenges for myelopathy, basically there's myelosuppression, but more importantly, when you think about ovarian cancer patients as the best example of this, they've gotten taxanes, they've gotten platinum, they all have neuropathy.
Speaker Change: and clearly when you were trying to go into platinum-resistant ovarian cancer.
if you had a drug that caused more neuropathy.
That was very much a limitation.
Speaker Change: If you think about the neutropenia also associated with any type of chemotherapy, so we were very focused on the neuropathy neutropenia.
Speaker Change: And we were very pleased, if you look at the 600 patients with UPREAP, which is the same payload, different scapel linker.
Speaker Change: or with dolacentin, our first molecule, 1592, which was NAPI-2B, we really didn't see meaningful neuropathy or neutropenia. So we think the bar is you really...
Speaker Change: Based on that experience with the payload, we think those should be quite low.
Speaker Change: The other challenge that you see with the Topo payloads is the Milo suppression.
Speaker Change: where you see just kind of pancytopenia type effects, we really, if you go back to upper E. adolescentin, that really wasn't a challenge for us with those molecules. And we think, you know, if you think about it, you can't be getting cytotoxic chemotherapy if your ADC is causing severe myelodyspression.
Speaker Change: People have tried to do these DAD studies where they combine them and you end up significantly compromising the dose of both ADCs.
Speaker Change: So, for us, kind of the holy grail is can you give a full dose or near full dose of the ADC in combination with either another ADC or with another cytotoxic chemotherapy.
Speaker Change: While we haven't done it with this molecule, I'm going to turn it over to Mohan to talk a little bit. We did present some data recently at IGSC where we did combine with CARBO. Mohan?
Mohan Bala: Yes, so we, with UpGrade, which was our previous ADC targeting API2B on the Dolar Fluxon platform, but using the same payload, we did a study called UpGrade, where we combined
Mohan Bala: upread with carboplatin for six cycles and then continued treatment with upread.
Mohan Bala: We presented data from the study at IDCS recently, and the study really established the ability to combine an ADC with this particular payload that we are using also for 1660 with carboplatin.
So
Mohan Bala: We did not see any exacerbation of utopenia or neuropathy. There was no increased alopecia. So generally a well-tolerated profile, which was able to be dosed for that full six cycle and then actually beyond the completion of the platinum regimen.
Mohan Bala: In addition to kind of the safety, we also see some meaningful activity with a 70 plus percent response rate. So that study really, we see as a proof of concept for the potential ability to combine ABCs on this, with this particular payload with chemotherapy.
Speaker Change: It all makes sense to me. Thanks for taking my question.
This concludes our question and answer.
Speaker Change: This concludes our question and answer session. I would like to turn the conference back over to CEO Martin Huber for any closing remarks.
Speaker Change: The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.