The Goldman Sachs Group Q4 2023 Earnings Call Transcript

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Provided by Quartr
February 21, 2024

There are 15 speakers on the call.

Operator

Hello, and welcome to the Arcus Biosciences Full YearQ4 2023 Earnings Call. My name is Elliot, and I'll be coordinating your call I'd now like to hand over to Pia Eaves, Vice President of Investor Relations.

Speaker 1

Quarter 2023 financial results and pipeline update. I'd like to remind you that on this call, management will make forward looking statements, including statements about our cash runway and our expected clinical developments, milestones and timelines. All statements other than historical facts reflect the current beliefs and expectations of management and involve risks and uncertainties that may cause our actual results to differ from those expressed. Those risks and uncertainties are described in our annual report on Form 10 ks, which has been filed with the SEC. We strongly encourage you to review our filings.

Speaker 1

Today, you'll hear from our CEO, Terry Rosen COO, Jennifer Jarrett CMO, Dimitri Nautzen and CFO, Bob Gels. We'll also be joined by our President, Juan Haiyan, for questions after the prepared remarks. During today's call, we'll refer to slides in our corporate deck, which can be found on the Investors section of our website. With that, I'll now turn it over to Terry.

Speaker 2

Thanks very much, Pia, and thank you all for joining us today. We've really come a long way since our founding 9 years ago, and I think it's fair to say we have evolved into an integrated biopharmaceutical company. We've got 7 molecules in clinical development, a broad late stage portfolio, multiple mid stage clinical trials, a robust discovery engine and now something I think new, a line of sight to commercialization. With $1,200,000,000 in cash and equivalents and runway into 2027, we're well positioned to deliver on the promise of the late stage pipeline that we've built. We'll start 3 new registrational trials.

Speaker 2

We're going to continue to invest in our early stage programs. We also have a partnership with Gilead as well as collaborations with Taiho, Exelixis and AstraZeneca. And I think it's very fair to say without these partnerships and the resources that these companies provide, we would not be able to execute on everything that we're doing. All of our programs target markets that are massive and really are the sweet spots of large pharmaceutical companies. All comer patient populations in lung cancer, gastric cancer, pancreatic cancer and renal cell carcinoma, RCC.

Speaker 2

Our funding and partnerships enable us to not only pursue these settings, but to compete and compete effectively and aggressively. We're really doing what we're saying we're doing. We also continue to build for the long term with a broad pipeline of potential best in class and 1st in class product candidates that will continue to replenish organically with our drug discovery engine. Today, we have 3 advanced clinical stage programs. Domplazim, our Fccellin anti TIGIT, it's very differentiated molecule in our anti PD-one antibody, Quemly, our small molecule CD73 inhibitor and AB521, our HIF2 alpha inhibitor, which is as of today known by its generic name casdatervan or CAS.

Speaker 2

Domzim is in Phase 3 and we expect to initiate Phase 3 studies for both CAS and Quemly by early next year. So we have 4 molecules all with distinct mechanisms in Phase 3 in 2025. We also have some exciting data sets coming in the first half of this year for another molecule and these really are exciting. Etruma, that's our A2 receptor antagonist and it's and Gilead believe support further investment in the molecule. We made a lot of progress across all these programs in 2023, presenting 2 large datasets for damsin in 2 different cancers and another large dataset just last month for quemly and pancreatic cancer.

Speaker 2

I want to start today by reviewing these programs and data sets, then spend a few minutes on the recent Gilead partnership updates and finish with some new data for CAS, our HIF-two alpha inhibitor. So starting with our anti TIGIT program, Domazim, our primary competitors in space are Merck and Roche. We have the only Fcsilon anti tingent antibody in late stage clinical development. So with DAMA's potentially best in class profile, it's optimized dosing regimen as well as a broad development program focused on lung and gastric cancers. We're really in a very strong competitive position.

Speaker 2

Our conviction in Damsen is supported by 2 datasets that we presented in the last 12 months and are summarized on Slide 9 of our corporate deck. 1st, at ASCO last year, we presented data from our randomized Phase 2 ARK7 study showing a PFS hazard ratio of 0.67 for Domzim relative to Zim monotherapy in first line PD L1 high non small cell lung cancer. We also presented data from our Phase 2 EDGE gastric study where we evaluated Domazen plus chemo in first line upper GI cancers at the ASCO plenary session in November. These data demonstrated impressive 6 month landmark PFS rates of 93% in PD L1 high patients and 77% overall. This really compares quite favorably to the historical benchmarks for anti PD-one is focused on settings where we have the best chance to be a market leader.

Speaker 2

Today, we have 3 Phase III trials enrolling and we expect both STAR-one hundred and twenty one and STAR-two twenty one, our chemo combo trials and PD L1 all comers for first line non small cell lung cancer and upper GI cancers respectively to complete enrollment this year. In fact, we can share now today that we anticipate STAR-two twenty one will be fully enrolled by the middle of this year. Due to the extremely rapid enrollment of STAR-two twenty one and relatively short OS for the standard of care, we expect STAR-two twenty one to be the first of our Phase III trials to read out. And importantly, with no other Phase III trials ongoing with the antitigid antibodies in this setting, we expect to have a significant first to market advantage. Meanwhile, we continue to invest in the expansion of our damsin program.

Speaker 2

We and Gilead will initiate STAR-one hundred and thirty one, which will evaluate damsim plus chemo and perioperative lung cancer. This is an exciting early stage and potentially curative setting. We also expect to initiate a 4th Phase 2 study in a setting outside of lung and GI cancers. Beyond our damsin program, today we'll be sharing data from the dose escalation phase of our ARK20 Phase 1b trial of casdasepan or AB-five twenty one. The 100 milligram expansion cohort of ARP-twenty enrolled quickly and then completed enrollment ahead of schedule, November of last year.

Speaker 2

Later today, we'll touch on what we're seeing so far in these data. The competitor here is Merck with their HIF-two alpha inhibitor, dalzunafan, which was just improved for advanced clear cell RCC, but we believe that cats has a best in class profile and that's addressing a very well recognized limitation of belzutafan. What we've seen thus far in ARC-twenty has given us confidence that our molecule has a superior profile to that of belzutafan. We're advancing casts rapidly and are on track to initiate a Phase 3 study early next year. And last for Quemly, our CD73 inhibitor, we presented overall survival data in pancreatic cancer from our ARK8 study at ASCO GI last month.

Speaker 2

With a large pool data set, 100 to 22 patients, we showed 15.7 months median overall survival for Quemly plus chemo, both with and without ZYN. This compares to the median OS from historical GEM, NAAP, paclitaxel studies 9 to 11 months in first line pancreatic cancer. We also conducted a MAPS synthetic control analysis that showed a statistically significant improvement in OS with a hazard ratio of 0 point 63. Based on the strength of these data, we are on track to initiate a Phase 3 pancreatic cancer trial by early next year. With Gilead's equity investment in January, we had approximately $1,200,000,000 of cash on hand and we're really well capitalized to support the breadth of programs that we are pursuing.

Speaker 2

At a high level, Gilead's investment accomplishes 2 things. First, it provides us with runway into 2027 while enabling us to fund Phase 3 programs for 4 different molecules. 2nd, it enables us to fund our pre commercial activities and on the other end of the spectrum to continue supporting our robust discovery engine. I'd like to turn things over to Jen right now to spend a few minutes on the details.

Speaker 3

Thanks, Terry. Gilead invested $320,000,000 by purchasing our stock at $21 per share, which represented an effective premium of nearly 40% to our share price just before the announcement, increasing their ownership to 33%. In parallel, Gilead's Chief Commercial Officer, John Amarcier, joined our Board. For addition, increases our Board membership to 3, provides representation commensurate with their ownership and brings a very experienced commercial perspective to the Arcus Board. The investment falls for 2 dynamics: 1, the expansion of our late stage clinical development plans and 2, the extension of our cash runway into 2027 and through multiple data events.

Speaker 3

Concurrent with the investment, we made a few strategic portfolio changes related to donsim and queblyne. First, for donsim, we closed enrollment of our Phase 3 ART10 study evaluating Donsim and PD L1 high non small cell lung to focus our resources and capital on areas with the highest unmet need and greatest market opportunities. A seminal factor that drove our decision was the evolution of the lung cancer treatment paradigm toward increased use of anti PD-one plus chemo for patients with PD L1 high expressing tumors. Therefore, we believe this segment of the patient population is best addressed by our STAR-one hundred and twenty one study, our chemo combination study and PD L1 outcome or non small cell lung cancer. The clinical trial landscape for PD L1 high lung has also become increasingly crowded with several anti TIGIT and other investigational therapies and we were not expected to be first or second in the PD-one high chemo free setting.

Speaker 3

At closing our on rapidly completing enrollment for STAR-one hundred and twenty one, which is addressing a much larger market opportunity. We'll also initiate a 4th Phase 3 study for DOLMSIM, STAR-one hundred and thirty one, a potential first to market opportunity. 2nd, for Quemly, we announced that Arcus will be operationalizing and funding a Phase III study evaluating Quemly in pancreatic cancer. Gilead retains an option to the pancreatic cancer program with the opportunity to pay a premium to their share of the Phase III costs in the future. While Gilead is not co funding this study, as you might imagine, they are aware that proceeds from the investment will be used to fund the study.

Speaker 3

I'll now turn it back to Jerry.

Speaker 2

Thanks, Jim. Now I'd like to switch gears to Cas, our HIF-two alpha inhibitor. This year is essentially going to be a coming out for this program as we're planning to release a lot of new data as well as more information on our future development plans. We believe that by hitting the HIF-two alpha target harder than Merck's belzutafan, we can improve outcomes for patients. We'll discuss the pharmacokinetics and pharmacodynamics that support this thesis in more detail shortly.

Speaker 2

But I'd like to start with the potential areas for differentiation versus belzutafan. Belzutafan was recently granted approvals monotherapy in third line clear cell RCC after just a 3 month FDA review process. This really validated the mechanism and highlighted the high unmet need for new therapies in this market. In Merck's Phase 3 LightSpark 5 trial, belzutafen showed an improvement in PFS over everolimus with a statistically significant hazard ratio of 0.74 who supported its approval. While these results are absolutely encouraging, the study reveals multiple opportunities for new agent to prove upon belzutifan's profile and provide even more benefit to patients.

Speaker 2

1st, on clinical efficacy in LightSpark 5, belzutafan had a high rate of primary progression, specifically a 34% PD rate, which was actually higher than that of the Everolimus control arm at 22%. This means that over 1 third of patients on belzutifan progressed at or before their first scan. We believe that casdutafan could stabilize tumor growth faster, resulting in a lower PD rate and therefore longer PFS. 2nd, with an overall response rate of 21.9% in LightSpark O05, we believe there is room for improvement. 3rd, while LightSpark 5 showed a statistically significant PFS hazard ratio, the median PFS was only 5.6 months.

Speaker 2

CAS may result in more durable tumor stabilization or shrinkage and therefore longer medium PFS. 4th, and this is an important point, we believe there's an opportunity for a better tolerated combination regimen. Dalsudafan's TKI partner in earlier line CCRCC studies is lenvatinib, which is perceived and it's really as perceived that way to be less well tolerated relative to other TKIs such as cabo and XANZA. Last, we are being very thoughtful in our development strategy for CASK and we'll focus on settings and combinations where we believe we can be first to market or differentiated relative to belzutifan and you'll hear more about this over the course of the year. As you may know, Merck is now projecting that belzutifan has blockbuster potential.

Speaker 2

Given the opportunity, we're pushing this program as hard as possible and while our data will be more mature later this year, we want to share as much as possible today to illustrate why we're so excited about this program. I'll now turn things over to Dmitry to share new data from our ARC-twenty trial evaluating cast in cancer patients.

Speaker 4

Thanks, Terry. I'll start by turning to Slide 29 of our corporate deck, which shows design of the trial, including both the dose escalation phase and expansion cohorts. The dose escalation portion enrolled patients with any advanced solid tumor, while the dose expansion cohorts are only enrolling patients with second line or later clear cell RCC. There are 3 expansion cohorts, each of which will enroll 30 patients. The first evaluated our go forward dose of 100 milligrams per day and completed enrollment in November.

Speaker 4

Satisfy the FDA's requirement for dose optimization, we are also evaluating a 50 milligram dose cohort and another cohort at a higher dose than 100 milligram in the expansion phase. Enrollment of the 50 milligram cohort is nearing completion. Collectively, these expansion cohorts will generate a lot of valuable safety data and efficacy data in clear cell RCC patients. The dose escalation portion employed a 3 by 3 design where 3 patients received 20 milligrams followed by 3 patients who received 50 milligrams and then 3 patients who received 100 milligrams all daily dosing regimens. The safety results of our healthy volunteer trial enabled us to start in ARK20, our patient trial at a relatively high and pharmacologically relevant dose and we saw no dose limiting toxicities allowing us to complete the dose escalation phase with only 9 patients.

Speaker 4

We subsequently backfilled 50 milligram dose cohort with 3 additional patients, resulting in 12 patient data set for this portion of the study. Of the 12 patients, 4 patients have clear cell RCC. Slide 30 is important and shows data for CAS and BELLs on EPO. Reductions, the peripheral or normal tissue biomarker for HIF2 alpha inhibition. On the left hand side, the dotted line shows the EPO reductions reported for the 120 milligram or the approved dose of belzutafen in clear cell RCC patients.

Speaker 4

In contrast, CAS achieved the same level of EPOSuppression at just 20 milligrams showing here with the purple line and that is 1 5th of our go forward dose of 100 milligrams. This means that 20 milligrams is roughly equivalent from a PD perspective to the approved dose of belsutafen and therefore 100 milligrams of CAS has the potential to achieve a meaningfully greater

Speaker 5

HIF2 alpha inhibition. On the

Speaker 4

right hand of the slide, you can see that CAS has a linear almost perfect dose proportional pharmacokinetic profile. In addition, CAS has a half life of approximately 21 hours and this enables daily dosing. Slide 31 emphasizes the ideal PK of CAS relative to that of balsutafen and it explains why balsutafen cannot simply be dosed higher to achieve greater HIF2 alpha inhibition. On the right, for CAS, we show that we increased the dose from 20 to 100 milligrams at steady state and we observed roughly 5 times increase in exposure. By comparison, as you can see on the left, when Bell's dose was increased from 120 to 240 milligrams, the drug exposure only increased by about 30% at study state.

Speaker 4

A 30% increase in exposure is less than the typical patient to patient variability at any given dose and therefore is not a clinically meaningful increase. This illustrates why doses higher than 120 milligrams of dalsutifen are unlikely to result in meaningfully better clinical activity. And in fact, this was demonstrated by Merck in the LIGHTSPARQ 13 trial comparing the efficacies of 120 milligrams and 200 milligrams of dalsudafen. In summary, these data show exactly what we have been predicting that CAS has a best in class PKPD profile, which should result in hitting the target harder and potentially in greater clinical activity relative to balsutafan. Turning now to safety.

Speaker 4

On Slide 32, we show the reductions in hemoglobin levels at various doses of CAS relative to that to the approved dose of dalsitaphan. Hemoglobin reductions appear to plateau at doses above 50 milligrams for CAS, likely due to compensatory mechanisms. And you can see that 100 milligrams daily of CAS resulted in similar reductions of hemoglobin as balsutafen despite the fact that we are achieving higher doses much higher doses of potency corrected drug exposure for CASK. For this reason, we expect CASK's safety profile to be manageable and not meaningfully different than belsutifen. On the next slide, Slide 33, we show the AE profile so far in the dose escalation phase of the study.

Speaker 4

Anemia and hypoxia are expected on target toxicities related to HIF2alpha inhibition, while we are watching very closely with a median follow-up across all those levels of the escalation of about 8.8 months so far, these rates do not appear to be higher than the rates seen with dalsutifen in historical clinical trials. These data demonstrates that while we believe that we are hitting the target harder, CAS appears to have a similar safety profile to that of dalsutifan. So let me tie this together. We are effectively able to deliver an exposure to CAS that is 5 fold greater than that which achieves the same level of inhibition of the peripheral biomarker for HIF-two alpha blockade associated with the approved dose of dasudefan with no apparent differences in safety profile. While efficacy was not the objective of the dose escalation phase, particularly given the advanced stage of patients and the different doses evaluated and the different tumor types included.

Speaker 4

On Slide 34, we do summarize what we observed in RCC patients, specifically clear cell RCC patients. As I mentioned earlier, there are 4 patients spread across the 3 different dose levels we evaluated 20 milligrams, 50 milligrams and 100 milligrams. These are all late line patients with a variety of prior treatment regimens, including at least 1 anti VEGF treatment and 1 anti PD-one treatment. 3 out of 4 patients are actually 4th line or later. And for these 4 RCC patients, 2 had meaningful tumor reductions just short of 30% and a third patient did not experience any tumor growth for over 14 months and still remains on treatment.

Speaker 4

The time on treatment is impressive for these patients in very late line setting ranging from 8.5 to 14.5 months and 2 of the 4 patients still remain on treatment. This indicates the potential of very durable effects of CAS even with monotherapy in a very advanced patient population. We are also seeing signs of CASA's ability to bring even aggressive tumor growth under control. For example, one of the 4 patients I mentioned was very heavily pretreated, had received 3 prior VEGF TKIs and an anti PD-one treatment. And this patient had stable disease early on with slight increase in tumor volume, not meeting formal progression per resist.

Speaker 4

And after about 18 months, the tumor volume started to come down. And now after about 10 months and still ongoing on treatment, the patient is nearing a response. I would like to emphasize that while the primary goal of an all comer dose escalation study is to establish the safety profile and assess the pharmacokinetics and pharmacodynamics. We have already seen clear signs of antitumor activity in patients with advanced clear cell RCC and we believe that tumor shrinkage and the duration beyond 1 year for patients who have exhausted all available treatment options are very clinically meaningful. The ongoing extension portion of the phase is designed to give us a better read on efficacy and this is already providing clear support for the initial observations in the dose escalation phase.

Speaker 4

And I would like to make a few comments on the early data of the expansion portion of the study. The 100 milligram cohort has completed enrollment in November. So we have a mature and rich data set in hand for 30 clear cell patients treated at 100 milligrams of CAS. While these data are still early, we are already seeing glimpses of CAS' potential for differentiation over belzutafan. We'll share the full data set at a medical conference later this year, but we did feel it was important to share some highlights of the data today.

Speaker 4

First, the majority of patients in the expansion cohort have only had 1 or 2 scans and we scan patients approximately every 6 weeks. So it's about 1.5 to 3 months of follow-up. Nonetheless, even with this very short duration of follow-up, the response rate we are seeing, which includes unconfirmed responses given how limited the follow-up time is, it's already in line with the response rate seen for balsutafan in light SPARC005. We also have a substantial number of patients early on their treatment who have experienced tumor shrinkage, but have not yet crossed the formal threshold of 30% to meet a response, but this obviously can happen with longer duration of treatment on future scans. Secondly, we are seeing a relatively low primary progression rate and this is the percentage of patients whose best overall response is progressive disease.

Speaker 4

So these patients have tumor progression on the first scan. This may indicate that CASA's ability sorry, that CASK can stabilize tumor growth early on during treatment and this will be an important parameter to monitor in the future as it represents an opportunity to or proof upon something that was reported for belsutifan. In summary, we are very encouraged by these early dose escalation and expansion cohort data, which while early have provided an encouraging signal that Kessler's PK PD profile could translate into greater efficacy in the clinic. By mid year, we will have a minimum of 7 months of follow-up for all 30 patients in the 100 milligram expansion cohort, which should provide a mature look at the overall response rate and we expect to present these data at a medical conference in the second half of the year. As I mentioned earlier, ARC20 includes 2 additional expansion cohorts and we expect this to also be presented over the next 12 to 18 months.

Speaker 4

We also expect data from STELLAR-nine, our study evaluating CASK together with censalitamib, sorry, also referred to as CENSAR sometime in 2025. We are full speed ahead to our Phase III study and we expect to disclose more on our development plan in the coming months. Terry will outline our other catalysts for 2024. But first, I will turn things over to Bob to discuss our Q4 and full year financials.

Speaker 6

Thanks, Dimitry. As Terry outlined earlier, Arcus continues to be in a very strong financial position. Our cash as of December 31, 2023 was $866,000,000 an increase to $1,200,000,000 after Gilead's January equity investment. Importantly, our partnership with Gilead is very capital efficient because we share the majority of costs for option programs fifty-fifty, including multiple Phase 3 studies for domzim. Gilead has also committed to pay the $100,000,000 option continuation payment due in July under the collaboration agreement.

Speaker 6

So we expect our cash balance at the end of 2024 to be between $870,000,000 $920,000,000 and now expect our cash to fund operations into 2027. This guidance excludes other potential opt in payments and approval milestones from our partners. Turning to our P and L, we recognized GAAP revenue for the Q4 of $31,000,000 which compares to $32,000,000 for the Q3 of 2023. Our revenue is primarily driven by our collaboration with Gilead, and we are evaluating the impact of the recent amendment on our revenue for 2024 and beyond. In addition to our partnership with Gilead, we have a partnership with Taiho for Dom in Japan.

Speaker 6

In the 4th quarter, we received Tay Ho related to their participation in our STAR-two twenty one pivotal study and will receive another $30,000,000 in the Q1 of 2024 related to their participation in our STAR-two twenty one and STAR-one hundred and twenty one pivotal studies. We are also eligible for additional milestone payments of $10,000,000 in the Q1 of 2025 from Tayo related to STAR-one hundred and twenty one.

Speaker 5

Our R

Speaker 6

and D expenses for the Q4 are stated net of reimbursement from Gilead and were $93,000,000 as compared to $82,000,000 in the Q3 of 2023. In the 4th quarter, non cash stock compensation represented $9,000,000 of our R and D expenses. The increase in the 4th quarter was related to standard of care purchases for our clinical trials. We continue to expect modest increases in R and D expenses as our Phase III studies mature and spend will fluctuate primarily based on the timing of clinical manufacturing activities and the purchase of standard of care therapeutics for our clinical trials. G and A expenses were $29,000,000 for the Q4 of 2020 3 compared to $30,000,000 in the Q3 of 2023.

Speaker 6

Non cash stock compensation represented $9,000,000 of our G and A expenses for the Q4, and we expect G and A to remain stable for 2024. For more details regarding our financial results, please refer to our earnings press release from earlier today and our 10 ks. I'll now turn it back to Terry for concluding remarks.

Speaker 2

Thanks very much, Bob. Before we open the floor to questions, I'd like to briefly touch on upcoming catalysts for 2024 beyond the ARC-twenty datasets that Dmitry highlighted. There's a lot. This will be another data rich year for Arcus. For the anti TIGIT program, we'll be presenting updated data from EDGE Gastric, our Phase 2 study evaluating Domzyn plus chemo in upper GI cancers at ASCO this year.

Speaker 2

We expect this data set to include updated ORR and PFS data. We also look forward to announcing the completion of enrollment for STAR-one hundred and twenty one and STAR-two twenty one, which will obviously start the clock for potential regulatory filings. We also may share data and insights from our 10 at a future medical conference. As I mentioned earlier, we presented impressive overall survival data from our Phase 1b ARC8 trial that was evaluating Quemly in first line pancreatic cancer. Also related to the adenosine pathway, we have 2 randomized data sets that we expect to share in the first half of the year for etruma, our A2 receptor antagonist.

Speaker 2

And we believe these confirm our findings in ARC8 that adenosine modulation confer profound improvement on overall survival. So first off, Roche will be presenting data from Morpheus PDAC. This is a randomized study operationalized by Roche that evaluated etruma in combination with chemotherapy and atezol, their anti PD L1 antibody versus chemo in pancreatic cancer. So a randomized study that involves etruma. 2nd, we submitted data from the 3rd line cohort of ARK9 presentation at a medical conference.

Speaker 2

This cohort enrolled 105 patients and evaluated etruma plus ZYN plus bev and fofox versus rego, the current standard of care in 3rd line colorectal cancer. The presentation will include mature PFS and importantly OS data, which we believe are also very supportive of the potential for adenosine modulation when combined with immunogenic chemotherapy to robustly, we mean robustly prolong PFS and OS. So in conclusion, we've covered a lot today, not immaterial. But if there's one thing to take away from today's call, it's that Arctis is now fully enabled to execute on its diverse late stage portfolio with funding into 2027 and that excludes potential future opt in payments. Our portfolio includes 6 ongoing and planned Phase 3 trials, multiple Phase 1 and 2 studies and a discovery engine that's just capable of generating at least one IND per year.

Speaker 2

Our trials are focused on huge markets by any standard, lung and GI cancer, pancreatic cancer and RCC where we're extremely well positioned to compete with potential first to market or best in class therapies. We have a lot going on adding a lot more to come this year. Thanks for your interest and support for Arcus as we continue to broaden our portfolio of innovative combination cancer therapies and we're working to bring these treatments to patients as soon as possible. We'll now open the floor to questions.

Operator

Thank First question comes from Terence Flynn with Morgan Stanley. Your line is open. Please go ahead.

Speaker 7

Hi. Thanks for taking the question. 2 part one for me. Just wondering on CAST, the HIF-two alpha program, Slide 24, the dose expansion data. Can you just confirm what the ORR was and how many of those were actually confirmed versus unconfirmed?

Speaker 7

And then the second part of the question relates to a potential Gilead opt in on this program. Maybe, Terry, you could just remind us the mechanics of how that type of a decision would work in terms of how little or how much data you would provide to Gilead and then how long they have to make a decision? Thank you.

Speaker 2

Thanks, Terrence. So on the first question, we didn't share a specific ORR intentionally. Actually 70% of the patients have only had 1 or 2 scans. So we will wait till the second half of the year to give that number, but we're seeing a number of responses. And in fact, then there's double digit patients that are stable disease with tumor reduction that may convert to response.

Speaker 2

The second part with respect to Gilead often, we have defined very specific criteria together with them. We haven't shared those exactly, but if you look at what we've described in general for the relationship, that opt in occurs when we've generated proof of concept data. So you can draw your own conclusions as what's coming later this year. And our belief is that they're very excited about the molecule in the program, but we'll see what they actually decide. I'll make one last final point.

Speaker 2

That is a program that we obviously wouldn't mind taking forward ourselves and we also have had plenty of inbound interest from other companies that might see a strategic fit with the rest of their portfolio.

Operator

We now turn to Peter Lawson with Barclays. Your line is open. Please go ahead.

Speaker 8

Great. Thanks for the update. Thanks for all the information. On cash, is that able to reduce the number of fast progresses you were talking about? And are you seeing any complexity in recruiting patients for, say, HIF-two alpha plus SAMHSA, both 2 non approved drugs, if that in any way you think affects the patients you get to see?

Speaker 2

So, we actually have had a number of discussions on that topic. We do not see that we're going to be, while we'll define for the rest of the world the future development strategy, we're going into settings that we think makes sense, including with Zanza. And we also, in parallel, will be exploring combination with Cabo. So we'll have both of those under our belt. But we feel very good about our ability to enroll.

Speaker 2

And keep in mind, we're not planning, obviously, in the context of this question, to be going after monotherapy at this point. And so, we'll be going against the standard of care that doesn't involve belazutafan and we feel like very well positioned to execute on those trials. And in fact, a huge degree of excitement. We've already had a first ad board meeting and the enthusiasm for both HIF-two as a general mechanism from what investigators have seen with Bells, as well as their anecdotal experience, which is now starting to get to be substantial with CAS, makes the field very exciting. So we actually expect very rapid enrollment as we've seen already for this molecule.

Speaker 8

Got you. And then just on the kind of the rapid progresses, are you kind of seeing that or a reduction in that run?

Speaker 3

Yes. So if you look at VITESPAR-five, which is a Phase 3 study for belzutifan and you can look at what the primary progression rate was in that study and were lower than that. We talked to investigators about 5, the primary progression rate, which was relatively high, was sort of a thing that stuck out for them. The results overall were very encouraging, but I think that's one thing that they would love to see improved upon was the primary progression range is the number of patients that kind of blew right through belzutifan treatment. So like I said, we're seeing a lower number than that.

Speaker 3

We think it's another opportunity to improve upon belzutafan and there'll be more to come on that later in the year.

Speaker 8

Perfect. Thank you so much.

Operator

We now turn to Kaveri Pullman with BTIG. Your line is open. Please go ahead.

Speaker 9

Good evening. Congrats on the progress and thanks for taking my questions. For 521, dose expansion data, the ORR that you provided, can you tell us or provide any color on how pre treated these patients were compared to the LIGHT PARP005 trial? And the trial, I believe, excludes patients with prior HIF-two alpha treatment. But do you think higher exposure could make these patients respond to 521?

Speaker 2

So Dmitry, why don't you talk a little bit about the pretreatment of those patients in the expansion study?

Speaker 4

Sure. Yes, thanks for the question. So regarding the prior treatments, the inclusion criteria for the expansion cohort allow for patients in a slightly earlier setting than in the dose escalation phase. So in the dose escalation phase, we required people to have exhausted all reasonable treatment options, and therefore, 3rd to 4th line was what we expect. In the expansion cohort, we are still seeing a fairly similar profile of pretreatment and that's something we think is, let's say, what we are expecting.

Speaker 4

It also puts our early efficacy observations in a positive daylight. Many patients in the expansion cohort also had 2 or 3 prior FEGF TKIs and they all are required to have PD-one. So if I summarize it, we do allow slightly earlier stage patients, 2nd line and beyond, where in the escalation phase, it would have been 3rd line and beyond. But overall so far the prior treatments are very, very similar. As to the belsutifan question, it is an interesting question.

Speaker 4

It is something I think worthwhile thinking about. However, including patients now with balsutafen prior treatment, I think will make it really hard to interpret the data because one reason could be that patients did not response because the target wasn't hit hard enough. There could be complete, let's say, resistance for HIF-two targeting. I think that looking at the balsutafen data, if you look at the primary progression rate, a number of those patients presumably would have been hard to get under control. Those might benefit, but patients there could definitely be patients who have resistance to HIF-two alpha targeting.

Speaker 4

So I know it's not a simple answer. I think for a clean efficacy signal right now, that's why we are excluding prior HIF2 treatment because it's too complicated and one patient who progresses on balsutefan would not be the other patients. So that would have to be explored in a more detailed setting where you really capture the detail of prior treatment.

Speaker 3

I think it's a little more granular prior lines of treatment and that expansion cohort, I can give you the exact numbers, so it hasn't in front of me. So 4 of the 30 were second line, so it was a minority of the patients in that arm. 9 were 3rd line and then the remainder, so that's 19 were 4th line or later.

Speaker 2

I don't have all those numbers As a reminder

Speaker 3

Yes. One other reminder, on LYZYBARC, 5, again, the Phase III study for VELV, the inclusion criteria was 1, 2, 3 prior lines. So patients with more than 3 prior lines were excluded from that study.

Speaker 2

Go ahead, Kirbar. Did you have a follow-up?

Speaker 9

I just have if I can ask another question. For Morpheus PDAC study, can you tell us what you're expecting in terms of efficacy, especially OS? And whether you expect AKTRUMA to perform better or worse than Quemly and if outcomes from this trial could change anything for your plans to initiate a Phase 3 trial for Quemly?

Speaker 2

So, Kibari, it doesn't change anything. And what you'll see is the OS data, I'll just say, they're going to be similar to what you saw for Arcade. Now there's two interesting components. There's actually they have a gemabraxane control arm in the study. So it's randomized.

Speaker 2

Our study, as you know, we conducted a synthetic control analysis, which gave us great data. The thing about ARC8 is that, it's a larger end, but on the other hand, the Morpheus study had the randomized arm and they both point to the same answer. So to me that's the big takeaway is you have 2 studies that affect adenosine in 2 different ways, but bottom line are removing the effects of adenosine. They're both producing what we would say are pretty profound effects on overall survival, which is to us very important. And so far as the Trumo versus Quemly, we've had that question in mind for some time.

Speaker 2

At this point, we'll still say other than in some very specific settings where there may be known non CD73 mechanisms for adenosine formation from adenosine triphosphate, we would say we'll hold judgment as to which might be better. You can make rationale for both. De novo, if you forced me to pick 1, I would still go with CD73 inhibition with the idea being that if you could block the formation of something versus have to reverse the actions of something that tends to be better, but that will play out over time. But I think by the time the big take home message is by the time you see these 3 data sets combined, think it's going to read very positively on adenosine modulation as a mechanism that has a meaningful role, particularly in the context of immunogenic chemotherapy as a standard of care where there's headroom for improvement.

Speaker 9

That's very helpful. Thank you.

Speaker 2

Thank you.

Operator

Our next question comes from Jonathan Miller with Evercore ISI. Your line is open. Please go ahead.

Speaker 6

Hi, guys. Thanks for taking the question. I would love to ask about HIF-two time to response and maybe some context about how ORR could evolve from here. Obviously, you're talking about already reaching a similar level to LightSpark and hinting that you would expect ORR to be mature by mid year. But what's the to your expectation, what's the evolution from here to there?

Speaker 6

How much more ORR would you expect to see in later scans? And then relatedly, given linear PK up to 100 milligrams in the escalation cohort so far, do you expect that 50 milligrams could also show differentiation versus Merck? Could you put a little bit of that dose optimization in context for me as well?

Speaker 2

Jonathan, great questions. So let me start with the first one that gets a little bit to your kinetics. So that's all anecdotal, to date, but let's first put a line in the sand. LightSpark 5 is roughly 3.8 months median time to response. The way things are looking, if you played around with the numbers, it looks like at least at the outset that we're doing perhaps better than that and we'll see how that plays out.

Speaker 2

And obviously, that leads to the opportunity for deeper response, longer PFS. Those are as you know, those really aren't independent variables. So hitting the target harder at the outset, maybe driving kinetics that are known to be not particularly fast. Although we have seen a couple of later patients having dramatic tumor reduction after multiple scans. On your second question, even though we didn't say anything about it in the script and it's even earlier, What I'll tell you is the 50 milligram cohort, it's almost fully enrolled.

Speaker 2

So that's going to be another 30 patients. And honestly, if you just took a look and not even all the patients have had a single scan yet, but it actually looks pretty good. And the kinetics, that's where I would tell you on the first group of patients that have had scans. And so I don't want to get as you know, I could get ahead of the skis because I tend to be pretty transparent with what we've seen. But the first group of patients are seeing some pretty significant reductions.

Speaker 2

And so feeling optimistic both about the kinetics and we're looking hard at 50 is clearly more than pharmacologically relevant. And it does look like on the early, early efficacy readouts that's playing out. As we stated, 20 milligrams was essentially giving the same effect as the approved dose of belzutafan on the PD marker. In the 50 milligram dose, certainly, if you didn't know any different and it was labeled 100 from what we've seen, you would say it fits right in. But that's way too early to say that's how it's going to play out.

Speaker 6

Makes sense. And then one more also on the escalation side of things. Obviously, only a very few of those patients were RCC patients. Could you tell us about some of the other indications in that escalation set where you might have seen clinical activity?

Speaker 3

Yes. So there it was a mix of tumor types. So I would say there really wasn't anything I'd say in the other tumor types and they're all patients that have seen multiple prior lines of therapy. We did have 2 patients with RCCs and not clear cell, but non clear cell RCC. And interestingly, one of those patients had a nice response and is still on treatment.

Speaker 3

So not a 30% tumor reduction, but they've been on treatment for many, many months and continues to be on treatment. So it seems to indicate that the drug has activity in non clear cell RCC as well.

Speaker 5

Okay, makes sense. Thank you.

Speaker 2

Thanks, Jonathan.

Operator

We now turn to Yigal Nochomovitz with Citigroup. Your line is open. Please go ahead.

Speaker 5

Hi, Terry and team. Did you say what the doses were for the 2 RCC patients that showed the tumor reductions just short of 30%. And then I have another question on Phase 3.

Speaker 2

Why don't you go ahead and Yes.

Speaker 3

I believe one was the 100 mg dose and the other I think was the 20 mg, if I remember correctly.

Speaker 2

Yes, it's funny because out of the 4 patients you had all covered by I think Jane got that right. Definitely one was 100 and definitely the other one either 20 or 50. They're probably looking while we speak.

Speaker 5

And then the

Speaker 3

so

Speaker 5

Okay. And then at this point, as far as what you would do for the Phase 3 dose, I mean, you finished the dose expansion for 100 milligram first, but doesn't mean that that's going to be the base case for Phase 3, right? I mean, you could go with 50. You also said you have you're evaluating a higher dose up to 200, although I don't know what that is. But what's the base case for Phase 3, that's still TBD?

Speaker 2

The base case is 100. We again, it really comes down to Yigal. Unless we see something dramatic from any of the either of the other arms, which obviously are being done to support the that we've got the optimal dose from a ultimately a regulatory standpoint. We felt that if you look at the Merck data and you look at what they've achieved and you look at their waterfalls and you look at their kinetics that once we've established that 5 fold increase over matching the peripheral PD marker that we felt like you should be maximizing the response in the tumor. So it's a practical call.

Speaker 2

As you know, oftentimes when you and it's unusual, more unusual in cancer, but when you have a very safe drug, at some point you say, this from a practice standpoint makes sense. But if we see something in these other expansion cohorts that would cause you to feel like there was something different, we would consider doing something alternatively. But right now, we're on a trajectory to that 100 milligram dose. The other thing that's nice about safety profile is appearing very clean.

Speaker 3

And Yale, sorry, just to clarify close to responses, one was the 100 meg and one was 50 meg.

Speaker 5

Okay. Got it. And then you mentioned LightSpark 5 a bunch of times. So obviously that was versus Everolimus. So for Phase 3, I'm assuming you'd want to go up against belzutafan, but I don't know.

Speaker 5

Is that the right assumption?

Speaker 2

Yes. So the thing we're and once we describe exactly what we're doing, so we're not going to be going into that same monotherapy setting. So we'll actually be going in a setting where belzutifan wouldn't be the standard of care and we will go against the standard of care. And we'll say a little bit more about that as the year goes along, but that was part of the strategy when we considered what would be the best places to go first.

Speaker 5

Okay. All right. Understood. Thank you.

Operator

We now take Salveen Richter with Goldman Sachs. Your line is open. Please go ahead.

Speaker 10

Hey, thanks. This is Matt on for Salveen. Maybe just following up on that last question. Could you share any additional details at this point on the Phase 3 design forecast? And then secondly, you cited the changing treatment paradigm in first line PDL and high lung cancer away from KEYTRUDA mono as the reason for for discontinuing ARK10 and shifting to 121.

Speaker 10

I was just curious if you could share any details on what data this shifting trend is based on and why you believe this is happening now? Thank you.

Speaker 2

Thanks for the two questions. It's Scott. Now I'm going to walk and chew gum at the same time since those are 2 different programs. So what I'll comment is, you can think about RCC. It's from a standpoint of both development, the need, ultimately commercialization, it's there's multiple lines where you can think of going.

Speaker 2

And so we would probably move up a bit from where that third line population was. And you could think about patients that have received anti PD-one and or TKI. So, you wouldn't have Bell's standard of care. We feel like that's a great place to go. And so far as your question about Arc 10 and the strategy there, So clearly, let me give a couple of points on that.

Speaker 2

So clearly, like with many therapies and particularly in cancer, it's one of those places where obviously there's a Goldilocks spot, but physicians do and patients tend to be more focused on efficacy than safety within reasonable bounds. And I think as time goes along and physicians become both more comfortable with the liabilities of a therapy, how to administer it as well as a conviction about the real efficacy. That's what's happened in a very continuous way in this high PD L1 population. Going from anti PD-one alone and increasingly to anti PD-one plus chemo, particularly in a more healthy patient population or with a patient with a bulkier, more rapidly progressing tumor. We think that's only going to be more enhanced, particularly with a molecule like DAAAM, which we're already seeing from a study, for example, like EDGE Gastric that essentially doesn't bring any additional side effect liability on top of anti PD-one plus chemo.

Speaker 2

So we think that that's going to further cannibalize that particular approach to treating that population. So we do feel that STAR-1 hundred and twenty one best addresses that population with the best opportunity to become the standard of care for all comers. What I'll also say from a biological standpoint, I think one of the important things is you move like down the spectrum from toxic agents, beta tubulin inhibitors to things that are you very much understand the biology, what you really want to start thinking about is less the organ that you're treating than the biology that you're treating. And we do feel and the biology that supports anti TIGIT is a couple of things. At the highest level, CD155 is a bad thing.

Speaker 2

If you've got CD155, what CD155 is doing is it's keeping you from getting all of the mileage that you might otherwise out of anti PD-one because anti PD-one relies on CD226 to get its full efficacy. And so when you have CD155 engaging that CD226, you're losing part of what you might otherwise gain. And that's the whole rationale and now what's being borne out clinically behind anti TIGIT and why we feel like the best place to go for anti TIGIT is where you already know that anti PD-one works and that PD L1 all comer population with chemo is absolutely right down the middle of the fairway for where you want to go with a molecule like Dom.

Speaker 5

Helpful. Thank you.

Operator

We'll now turn to Robin Konarkas with Truist. Your line is open. Please go ahead.

Speaker 11

Hi, team. All right. Several questions. Thinking about the 200 milligrams of CASK, do you think there'll be a diminishing limit of return if you actually do you think you could push the efficacy up higher? What are your thoughts in 200 milligrams?

Speaker 11

Second question is about 801.

Speaker 5

How is

Speaker 11

it different from XANZZA? And 3rd might be, do you think you could leapfrog, how you cut ARC-ten and you did a different trial leapfrog into frontline with 521? Is there a strategy there? And like how do you incorporate your own 801 into that process? There's a lot going on there, but maybe you can take those at once.

Speaker 2

So the second question, what was the advance question? What was 801?

Speaker 12

Yes, compound.

Speaker 11

So 801, how is it differentiated from this? It was Axle only. And could you incorporate that into your clinical trials going forward, right? So you're doing all these XANSA clinical trials. The second question would be 200 milligrams of CAS, like what do you think is going to happen there?

Speaker 11

Are you pushing Omid already? Do you think you'd get greater And third would be, could you leapfrog ahead giving your Phase IIIb trial and go into first line RCC? Because you've done brilliant things in the past by cutting things off and like skipping ahead of other people, given the knowledge you have to get like first line indication versus refractory indication? Thanks.

Speaker 2

Great. So I'll start with the 200 milligram and I'll be brief on that. We do think that's probably overdosing, but we want to see it because we'll also give us some additional safety data if we do go higher, does it do anything else on the other physiological roles of HIF2 alpha. But we do think that the 100 milligram dose is really hitting the target hard enough, but we'll see what we learn from 150 or 200 milligrams. Juan, you want to take the 801 question?

Speaker 12

Yes, sure. Zanza as well as cabo is primarily a VEGF TKI. It incubates XL with both molecules with decreased potency, but the clinical activity and it's really generally accepted to be the result of VEGF inhibition. So the 801, we believe, is going to be a more surgically effective inhibitor of XL, but probably not the first thing you would reach for in the context of RCC, where the rationale we primarily to go after VEGF TKI. So the place where

Speaker 2

we see XL going are things like STK11 mutant non small cell lung cancer. And by the way, on 801, since you asked about it, I might as well call out a bit. We have completed the healthy volunteer dosing. PK profile and safety profile look really good. So this is in our minds the first molecule that has the selectivity to really test the actual hypothesis.

Speaker 2

So we're very excited about that molecule. Jen, do you want to comment or Dmitry on the 521 leapfrogging into a frontline setting?

Speaker 4

So we are considering all options and we could leapfrog into the first line, we could leapfrog into the adjuvant setting, but we really want to make sure we select the setting for the 1st registrational trial that is a mix of different factors. It has to have the data, let's say safety and early efficacy data to support it. It has to be a sweet spot when it comes to competitive time lines to Merck. There's other considerations about timelines to readout. A first line trial is an interesting market opportunity.

Speaker 4

But for example, the bar in first line is higher than in second line. The time to readout is longer, of course, in first line than in second line. So we are considering all these different options and we'll make a decision and communicate that in the near term future what our first opportunity would be that we pursue, but it's a factor of multiple factors.

Speaker 2

Great. And Robin, I would like to just give you Since you asked about that, I would like to emphasize the point of your question conceptually though is really good one. HIF-two alpha is going to end up being really important. I think that's why Merck has started to call it out as blockbuster. AB-five twenty one barring some weird unforeseen thing, it's a drug.

Speaker 2

And so the real question is how do you fully exploit that? And if you ask me about our portfolio, it's definitely something that, as we aggressively move towards this first study, we want to look at very hard, how do you expand the footprint of the HIF-two alpha program. That's a really huge opportunity. And we actually think because it's so hard to get a good molecule, you're not going to have anyone come in with a better molecule than us. So feel we're going to end up better than Bell's and it's there's not going to be commodity here.

Speaker 11

And I'd like to thank Dmitry for making me feel not so bad pronouncing all these names. So Zanza works for me, Cas works for me. Thank you very much, Dmitry. Appreciate it.

Speaker 5

My pleasure. Absolutely. I'm told

Speaker 2

that Cass is Cass, not Kaz too. That's what I've been told. So we'll see.

Speaker 11

I'll work on that, Gary. I'll work on that.

Operator

If I can't tell the difference. We now turn to Diana Graybosch with Leerink Partners. Your line is open. Please go ahead.

Speaker 13

Hi, guys. Thanks for the questions. I have 3 on task getting into the PKPD data. First on Page 31 where you show the area under the curve, I recall initially talking about the value proposition for CASK that you expected a much higher absolute area to the curve. But what I see here with the 100 milligrams is pretty similar in range to the 120 and 240 milligrams for belbutafan.

Speaker 13

So I wonder if you can talk to that, that you're ending up in the same range. And then on pharmacodynamics, you have 2 different pharmacodynamic readouts here. First is the percent EPO change on Page 30 and then the percent hemoglobin or the absolute change in mean hemoglobin on Page 32. Which of these PD readouts do you believe is more correlated to what you expect in efficacy? And if I look at the hemoglobin, you're sort of in range of belbutafan and you're modestly higher or it looks to be modestly higher in percent EPO.

Speaker 13

So my final question is, how much better efficacy do you expect to drive with these similar to modest increases in pharmacodynamic markers versus dolutefant?

Speaker 3

Thanks.

Speaker 2

Thanks, Dana. So I'm going to tie it together. So I think the key point, I'm going to define what's better PK and what's better PD. So PD, as you know, encompasses everything, tissue penetration, potency differences, pharmacokinetic differences. So the PD readout, what we're saying and we think this is the value proposition, no question, is that in 20 milligrams of AB521, you're getting the same horsepower and let's use EPO as the marker that you get out of the approved and used dose of belzutafan.

Speaker 2

Now the PK advantage has nothing to do with an AUC relative to belzutafan. The PK advantage is that when we go to 5 fold higher doses than the dose that gives you that equivalent activity on the PD marker, we get 5 fold higher exposures. So if there's more water to be squeezed out of the activity stone, we're hitting that with 5 fold the equivalent PD dose of belzutifan. So that's the value proposition. The PK advantage is that you can go higher from that maximal effect.

Speaker 2

With respect to hemoglobin or EPO, we don't look at either of those per se as something that's predictive of more or less predictive of the activity in the tumor setting.

Speaker 13

Can I state it back? So you're hitting it 5 fold more dose than what gets you to the pharmacodynamic marker and you believe that will give you much better efficacy even though neither of these pharmacodynamic markers with 5 fold greater dose really had that much more effect than belzoutinib, is there?

Speaker 2

That is correct, but not only is it correct, that's what's predicted and that's the difference between the physiological maximal HIF-two as you know, HIF-two is a transcription factor. So it regulates a 100 things. It's a fact on EPO has nothing to do with what's going on in the tumor. So we know going in that basically you're going to max out HIF2 in the or EPO inhibition. And so that just becomes a marker for how hard are you hitting this thing.

Speaker 2

And then the fact that we can go 5x, what you can get out of the Merck molecule is what makes us feel good about hitting the tumor harder.

Speaker 13

That's very helpful. Thank you.

Speaker 2

Thanks, Damon.

Operator

We now turn to Leigh Watsack with Cantor Fitzgerald. Your line is open. Please go ahead.

Speaker 14

Hi there. This is Rosemary on for me. Thank you so much for taking our questions. So to start with casadatifan, do you happen to see any dose response when it comes to toxicity to safety profile? And do you have concerns for greater side effects when you go above 100 milligrams?

Speaker 14

And then one question on your TIGIT programs.

Speaker 13

Sorry, go ahead.

Speaker 2

No, go ahead. You finish your

Speaker 4

questions.

Speaker 14

So the question for TIGIT. So you said you plan to show some data from the ARC-ten trial, which was discontinued. So you have any color on when this could be and what kind of data we would expect? And would it potentially impact any thinking around the trials that you still have going on? Thank you.

Speaker 2

Thanks. So, the dose response, to be clear, the 20 milligram dose that we used is our lowest dose is already pharmacologically relevant. As we noted, you're seeing essentially a maximal effect on EPOS suppression at that point. So I would just say with 3 patients on each of the doses with 6 on the 50, we wouldn't say that we see any meaningful differences nor do we expect that. And similarly, because of what we know this was gets back to how I was answering Dana's question, there's either feedback mechanisms or other non HIP II mediated ways that EPO is produced.

Speaker 2

And so you hit this maximal effect on that endpoint, which to date has been the primary side effect and is very manageable. So that is the anemia that's a correlate of that EPOS suppression and basically that's been very manageable. So at this point, we don't have any expectations that going higher will induce any more of a liability. And we certainly haven't seen it at the 100 milligram dose. The other place where we're keeping a close eye is in fact on hypoxia.

Speaker 2

That has to do with HIF inhibition in the lung. Again, that may also be something that's maxed out. It's normal physiology. It's something that we're paying attention to. Some of these things may also be dependent on individual patients, particularly when you think about EPO, if there are patients that have compromised kidney function.

Speaker 2

But to date, we haven't seen anything of concern and we'll just see what happens when we go to a higher dose. And certainly on those initial 30 patients, nothing that we've seen to date has caused us concern. And to make the point, we have not yet seen a DLT. On the anti digit, Arc 10 data, that's just something we're considering. We haven't made a decision on that, But if we did do that, the idea would be that we would do a cut of the data and a cleaning of the data when we would extrapolate that we would have mature PFS minimally.

Speaker 2

And at this point, with the data that we have in hand from our other studies, it wouldn't affect any of the studies that were it would not be decision making data.

Operator

Ladies and gentlemen, this concludes our Q and A and today's conference call. We'd like to thank you for your participation. You may now disconnect your lines.

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Earnings Conference Call
The Goldman Sachs Group Q4 2023
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