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spk05: Ladies and gentlemen, thank you for standing by. Welcome to Infinity Pharmaceuticals conference call to discuss the company's operations and financial results for the third quarter 2020. My name is Kathy, and I'll be your operator for today's call. At this time, all participants are in a listen-only mode. There will be a question and answer session to follow. Please be advised that this call is being recorded at Infinity's request. Now I would like to introduce your host for today's call, Jane Kaufman. Please go ahead.
spk06: Thank you, Kathy, and good afternoon, everyone. Welcome to today's call to discuss our recent business progress and review our third quarter 2020 financial results. On the call with me today are Adeline Perkins, Chief Executive Officer, Larry Block, President, and Brian Schwartz, Consulting Chief Physician. We will open up the call for Q&A following our remarks. The press release issued this afternoon details our results and is available on our website at infi.com. Please note that during this call, we may make forward-looking statements about our future expectations and plans, including clinical development objectives, the therapeutic potential of our product candidates, our strategic plans and strategies, and financial projections. Our actual results may differ materially from what we project today. due to a number of important factors, including the considerations described in the risk factor section of our quarterly report on Form 10-Q for the third quarter of 2020, and in other filings we make with the SEC. These forward-looking statements represent our views only as of today, and we caution you that we may not update them in the future, whether as a result of new information, future events, or otherwise. Now, I would like to turn the call over to Adeline.
spk09: Thanks, Jane, and thank you to everyone for joining us today. We are reaching an exciting inflection point in InfiniDate, having progressed the development of Eganilisib toward data readouts across our clinical program in diverse treatment settings and indications, strategically designed to evaluate the potential of Eganilisib to improve outcomes for cancer patients. Over the past two years, we have focused on the execution of our Phase II clinical trials leveraging the strong scientific foundation of PI3 kinase gamma inhibition with aganalysib, and are now positioned to deliver important clinical and translational data in the coming months. On today's call, our Consultant Chief Physician, Dr. Brian Schwartz, will provide more detailed clinical updates. But before that, I'd like to review some highlights from the past quarter. Starting off with MERIA-275. our randomized control phase two study in collaboration with BMS, in which we are evaluating aganalysib in combination with Opivo in patients with advanced urothelial cancer. We previously announced that we reduced the dose of aganalysib from 40 milligrams to 30 milligrams daily to address the reversible liver enzyme elevations, which were reported at the first scheduled IDMC meeting last spring. We've continued treatment of patients still on study at 30 milligrams and have continued monitoring the safety of the 49 patients enrolled in the study to date. And we recently reviewed updated data from these patients with the IDMC. We're pleased that the IDMC concluded that the risk-benefit ratio of aganalysib and Opdivo in this patient population warrants ongoing evaluation. We will continue to follow the patients still on study through year end and evaluate data on maturing time-to-event measures, including progression-free survival and overall survival, to determine the best path forward for aganalysib plus Opdivo in second-line bladder cancer. I will now move to Mario 3, our Phase 2 study in collaboration with Roche Genentech, in which we are evaluating the combination of aganalysib with ticentric and abracadabra as a frontline treatment in patients with triple-negative breast cancer, or TNBC, and in combination with Dicentric and Avastin as a frontline treatment for patients with renal cell cancer, or RCC. Last quarter, we shared that we were on track to present data from the TNBC cohort of MERIO-3 and have been accepted to present these results at the San Antonio Breast Cancer Symposium, or SABC, next month. We were also pleased to have received fast-track designation for ganylysin in combination with a checkpoint inhibitor and chemotherapy for first-line treatment of patients with advanced TNBC. This week, at CISSE, our investigators are presenting updated data from the melanoma and squamous cell cancer of the head and neck cohorts of MERIA-1, our Phase 1, 1B study in collaboration with Krister Meyers Squibb, evaluating aganalysib in combination with Updivo in patients with advanced solid tumors. These data support the tolerability and activity of this combination and provide additional translational data supporting both the on-mechanism immune modulation of aganalysib and our clinical strategy to move aganalysib to earlier lines of treatment. And finally, in addition to these INFINITY-sponsored trials, our collaborator, Arcus Biosciences, will also be presenting data at SABC from their Phase 1b study, evaluating aganalysib in a novel checkpoint inhibitor-free regimen that includes the Trumadant, their dual receptor antagonist, the identity antagonist, also known as AB928, and Doxil in patients with relapsed refractory triple negative breast cancer, adding to our aganalysis data set in TNBC. We are pleased with our progress in the clinic, which enables us to share data over the coming months that reveal the potential of aganalysis. We're grateful for the commitment and dedication of our employees, collaborators, and partners who have enabled this progress. With that overview, I will now transition the call over to Brian to provide more detail on our trials and upcoming data presentation.
spk02: Thank you, Adeline. These are exciting times at Infinity, and we are looking forward to sharing our progress and data. Starting out with an update on Mario 3. As Adeline mentioned, we have two cohorts in this ongoing phase two study. One evaluating Eganilisib in combination with Ticentric and Abraxane as a frontline therapy for triple negative breast cancer patients for which we have received fast track designation from the FDA. And the other evaluating Eganilisib in combination with Ticentric and Avastin as a frontline therapy for patients with renal cell cancer. Last quarter, we shared that we have generated encouraging signals of clinical activity in the triple negative breast cancer cohort. Today, I am happy to share that we will be presenting these data at the San Antonio Breast Cancer Symposium in December. At this symposium, we will be presenting data from our frontline Mario3 triple negative breast cancer cohort, together with an update on enrollment, enrollment outlook for this cohort, and also, Arcus will be presenting data in the second line triple negative breast cancer setting as well. Taken together, we believe that we may have a unique opportunity with egg analysis to make an impact in triple negative breast cancer, the deadliest form of breast cancer with limited treatment options. We have also made progress in the RCC cohort of MARIO3, having completed enrollment ahead of schedule with 30 patients enrolled across approximately 25 sites. Moving next to MARIO-275, which is our controlled, randomized Phase II study evaluating iganilisib in combination with Optivo in platinum refractory IO-naive patients with advanced urothelial cancer. This is run in collaboration with Bristol-Myers Squibb. As we previously reported, we implemented a dose reduction from 40 milligrams once a day to 30 milligrams once a day to address the reversible liver function elevations identified at the first IDMC meeting. We were pleased that this dose reduction was successful, enabling the continued treatment of patients previously enrolled in the study. We have continued treating patients previously enrolled in the study and presented updated data from these patients at our latest IDMC meeting. After reviewing these data, the IDMC concluded that the risk benefit to patients supported and continued evaluation of Eganilisa plus Optivo in this patient population and supported reopening of enrollment of MARIO275. We are pleased that the 30 milligram dose is well tolerated and are confident in moving forward at this dose from an efficacy perspective with PK data that shows near complete or sustained inhibition of PR3K gamma with Eganilisa monotherapy at doses of 50 milligrams once daily and above, as well as robust PD markers of activity at the 30 milligram dose. So what is our path forward in metastatic urothelial cancer? We are continuing to evaluating the clinical benefits in patients currently enrolled in MARIA-275 across maturing time to event measures, including progression-free survival and overall survival through the end of the year to inform next steps. Our path forward may include reopening enrollment of MARIA-275 to generate additional data or leveraging the clinical and translational insights from the first 49 patients to design a follow-on study. And finally, we are presenting data this week at CITSE from Moria 1, our phase 1 slash 1B study in collaboration with Bristol-Myers Squibb. which enrolled a bunch of patients with advanced solid tumors. As a reminder, the melanoma and squamous cell cancer head and neck cohorts of Morio1 were designed to carefully isolate the clinical benefit of Eganilisib by examining its clinical activity in patients who were not expected to respond to checkpoint inhibitor monotherapy. while having progressed on checkpoint inhibitor as their immediate prior therapy. By targeting these patients not expected to respond to checkpoint inhibitor monotherapy, we put iganilisib in a difficult test to ensure that patient benefit observed can be attributed to the addition and contribution of iganilisib, making any disease control in these patients meaningful. In a poster presented by our collaborators at Memorial Sloan Kettering on the Melachnoma cohort at Tsitsi, we reported that Eganilisib in combination with nivolumab was generally well tolerated and associated with a favorable safety profile. We are pleased to see clinical activity in patients who are not expected to respond to checkpoint inhibitor monotherapy immediately prior that they progressed on, immediately prior to coming onto treatment. Most encouraging disease control was observed in more than half or 52.6% of the 19 patients who had been refractory or relapsed to checkpoint inhibitor therapy following two or fewer prior lines of therapy, with a partial response rate of 21%. Importantly, we demonstrated what we hoped to show in the study, the reversible of progressive disease in patients with immediate prior treatment with anti-PD-1 PD-L1 therapy. When we look at the translational data from the cohort, we see on-mechanism effects of eganalysib decreasing immune suppression reflected in reduced MDMC levels and increased immune activation via T-cell invigoration and upregulation of interferon gamma responsive factors. The data from squamous cell carcinoma of the head and neck cohort which were presented in an oral presentation from our collaborators at UCSD at CIPSE, were similar to what we observed in the melanoma cohort. As in the meneloma cohort, the combination of treatment with the Ganalysib and the Volumab was generally well tolerated and had a favorable safety profile. In addition, we see clinical activity in patients not expected to benefit from checkpoint inhibitor monotherapy due to immediate prior progression on a checkpoint inhibitor. Disease control was observed here in 45% or nine of the 20 valuable patients with partial responses in 10% or two out of 20 valuable patients who had been refractory to or relapsed on immediate checkpoint inhibitor therapy. Just as seen in the melanoma cohort, Patients with two or fewer prior lines of therapy had a greater clinical benefit, with 20% or two of the 10 evaluable patients achieving a partial response. These results are meaningful for a few reasons. First and foremost, we see an excellent safety profile. Second, we see an on-mechanism activity with immune modulation as intended with treatment. Thirdly, as we just mentioned, we saw clinical activity with a considerable disease control rate in patients who progressed on or immediately prior to checkpoint inhibitor therapy. Having deliberately set a very high bar for activity in this setting, we are pleased with the contribution of the analysis in improving outcomes of these patients. And finally, in both cohorts, we see the greatest clinical benefit in patients that receive two or fewer prior lines of therapy. This is important validation of our overall clinical strategy in which we have moved Eganilisib to earlier lines of therapy in our ongoing studies. In second line, urothelial cancer in MARIO275, and in the frontline setting in triple negative breast cancer and renal cell cancer in MARIO3. In summary, the data from Morio-1 suggests that Eganilisib can potentially be safe and well-tolerated immunotherapy capable of improving meaningful clinical benefits in multiple cancer types and treatment regimens. Overall, we are encouraged with our progress across our clinical program, and despite the challenges associated with COVID-19, we have been able to continue the treatment of patients with limited disruptions. In the coming months, we look forward to sharing the data across our programs, which will highlight the potential of Eganilisib as a unique macrophage-targeted treatment to expand the benefit of immunotherapy to diverse patients across indications and settings. Before I transition the call over to Larry, I would like to thank our patients, investigator, collaborators at BMS, Roche Genentech, and Arcus, whose continued dedication has enabled our clinical progress. With that, I will turn it over to Larry.
spk03: Thank you, Brian. Turning to our third quarter financial results, at September 30th, 2020, Infinity had total cash cash equivalents and available for sale securities of $41.3 million, as compared to $42.7 million at June 30, 2020. R&D expenses for the third quarter of 2020 were $6.1 million compared to $7.1 million for the same period in 2019. And this decrease is primarily related to a combination of drug purchase during the third quarter of 2019. G&A expense was $2.9 million for the third quarter of 2020, and this compared to $3.6 million for the same period in 2019. And this decrease is primarily related to reduction in professional services as well as consulting expenses. And net loss in the third quarter of 2020 was $9.5 million, or a basic and diluted loss per common share of $0.16, compared to a net loss of $11.4 million, or a basic and diluted loss per common share of $0.20 for the same period in 2019. We expect to end 2020 with a cash investment balance ranging from $25 to $35 million, and based on our current operating plans, which exclude additional funding or business development activities, we anticipate that our existing cash, cash equivalents, and available for sale securities will be adequate to satisfy our capital needs through 2021. If any financial guidance does not include potential additional funding or business development activities, a potential $5 million milestone payment from BVF based on Pellifarm's ongoing Phase III clinical trial of pedigree of topical gel engorlut syndrome, or any milestones from or the sale of the company's equity interest in Pellifarm. We're very appreciative of your continued support as we move forward with development of the GANALYSIB and look forward to providing our next update on GANALYSIB development at the San Antonio Breast Cancer Symposium next month. At this time, we can open the call for questions. Operator?
spk05: At this time, in order to ask a question, you will need to press star 1 on your telephone. To withdraw your question, press the pound key. We'll pause for just a moment to compile the Q&A roster. And your first question is from Anutan Rama from J.P. Morgan.
spk00: Hey, guys. Thanks for taking the question. This is Matt Bannon on for ONIPOM. So I thought it was really interesting in the MERIO-1 data set presented at CITC just how starkly responses are bifurcated between patients with two or fewer prior lines of therapy versus those with three or more. And within the responding patients, besides one blip in the chart for patient A with stage 3 melanoma, I'm referring to the time series of objective responses, there seemed to be a consistent trend in the size of target lesions from baselines in that they almost exponentially shrink before plateauing and eventually coming back in size. So two questions on this. The first is, were any bobsies taken in these responders as their tumors were increasing in size that might shed light on the specific resistance mechanisms that these tumors are using to overcome therapy? And secondly, are these the response dynamics that you would expect in other tumor types? We're just trying to think about the read-through here. Thanks so much.
spk09: Sure, I'll start and then I'll turn it over to Brian. Thanks for your question, Matt. First, your point is well taken in terms of the patients in MARIA-1 in both our melanoma and our head and neck were really challenging patients for two reasons. First is that they had all progressed on a checkpoint as their immediate prior, and then the second was that they were really late stage. So the melanoma poster, as you saw, 50% of the patients had four or more prior therapies. So this is a really sick, really late-stage patient population. So it's not surprising that we saw the better responses in the patients who have two or fewer, and even that's pretty remarkable given that they had, as you can see from the little patient vignettes, it's a real reversal of progression on a checkpoint inhibitor to a reduction. So that's not completely surprising, and it's very consistent with our strategy, as Brian mentioned in his remarks, of moving into the second line in bladder cancer and in the front line in TMBC. So we would expect that. Brian, maybe you can speak to any further insights on resistance mechanisms.
spk02: So unfortunately, there are not many paid biopsies to highlight the potential resistance mechanisms that could potentially develop over time. But I think important, as you highlighted, for patients who were progressing or had received immunotherapy as their last therapy and just had the addition of agamelisib, one wouldn't have expected an additional response to occur. And that was the interesting and exciting phenomenon that we observed in this trial. But you're correct, in the other trials, we hopefully will try and get more biopsies on progression and better learn the changes in different key immune-related cells and responses that could better inform us as to why the patient's tumors start regrowing.
spk00: Got it. That was super helpful. Thanks, guys.
spk05: The next question is from Jim Bertineau of Wells Fargo.
spk04: Good afternoon. It's Nick on for Jim's afternoon. Congratulations on the data update. First question, and it's probably passing words in a way you don't want them passed, but in terms of the IDMC saying risk benefits supports continuation of the study, Does that suggest that there was an assessment of benefit? Does that connote a futility analysis?
spk09: So, Nick, it definitely – go ahead, Brian.
spk01: No, it's okay. Go ahead. It's fine. I'll come in later.
spk09: Yeah, I was just going to say it definitely does denote an efficacy analysis. We didn't have a pre-established futility, but we were looking at, is there evidence? One of the beauties, of course, of a controlled trial is that you see the differences both in any AE signals, which was the reason that we did the pause in May, but you also can see a benefit on the treatment arm versus the control arm. And so we did see both, that at 30 milligrams, It was better tolerated, and we have evidence of a benefit of the combination of, again, ELISA and Opdivo versus the control arm of Opdivo and placebo.
spk04: Thank you for the clarification. And then, Adeline, as you think about next steps here, you suggested we could either reopen this study Or we could, you know, take what we've learned from this study and the other studies and, you know, initiate a new trial. So, I mean, where you're sitting today, which of those two options do you prefer and why?
spk09: Nick, as you know, it's going to be completely data dependent. So we're encouraged by the data that we've got to date. We're going to continue to look at that because it's progressing on both, you know, two really important metrics of PFS and OS. And when we look at that data, that will inform our next step of which is preferable. So it's just premature in the absence of having that data over the next couple of months to know which is preferable.
spk04: Thank you. And then going back to the melanoma poster, just very quickly, can you comment on baseline MDSC in these patients and whether there was any correlation between elevated levels and activity? And then we have two patients respond really quite quickly, and then two patients achieve a PR after at least six months of treatment. So what are your thoughts underlying the biology of what's going on here?
spk09: I'll take a first crack, and then Brian, I'm sure you can elaborate more. What we did see in terms of the underlying mechanism, and on the poster it's really captured in some of the graphs that are right below the patient vignettes, where we did see, in the vast majority of patients that are treated, a reduction in MDSCs, which is what we'd expect, and we've seen that consistently throughout all of our data to date. We see that leading, and that happened in just the first month, we see that leading to a pretty significant increase in the proliferation of previously exhausted T cells. So we see this activation of T cells And then we see all the markers of an immune response. So we've got the data there, CXCL9, CXCL10. And then on the poster underneath the cartoon of the mechanism of action, there's a table. And what we've seen and presented is one of the most upregulated genes is CD274, which is reflective of PD-L1. So we see that with the upregulation of immune response, that there's an upregulation of PD-L1 to try to blunt that T cell response. In some ways, we see that's kind of priming for the checkpoint inhibitor by upregulating. There's data, as you know, across lots of different tumor types that patients do better on a checkpoint inhibitor the higher their PD-L1 expression. So that's a concept that, regardless of whether the patient started with high or low PD-L1, if we upregulate that, that's going to, we believe, is part of the reason for increased activity of the checkpoint inhibitor. So what we've been encouraged by in both the MARIO1 data that we're presenting at CITSE this week and some of the data that we'll be presenting in the coming months is that the activity that we're seeing is completely consistent with our understanding of the biology of PI3 kinase gamma and what inhibiting it should do in terms of activating an immune response.
spk02: I think the other important thing, yeah. I think the other important thing to remember is we have two sets of biomarkers. We have the circulating biomarkers as shown in the poster, the circulating MDSCs, and then we have the different markers of T-cell reinvigoration, And then we have what's going on in the tumor. So what we've really tried to do in Mario 3 and in Mario 275 is trying to understand better what's going on in the tumor as well. And maybe that will become a better correlation as we move forward. But, you know, we have an idea what's going on in the peripheral blood, but we really don't have a very good idea in terms of the biomarker in terms of what's going on in the tumor. And that's what we're trying to get And we have some additional studies where we're really going to try and elucidate what happens in a tumor microenvironment.
spk04: Terrific. Thank you very much and look forward to the next update.
spk05: Thanks, Nick. Your next question is from Andrew De Silva of B. Rowley.
spk07: Hi. Good afternoon. This is Noreen Kibria on for Andy. So forgive me if you've actually mentioned this before, but I was just wondering with regard to MARIA-1, were there any other tumor types where hepatotoxicity has been seen? You know, now looking back, seeing what you've seen with MARIA-275, did you observe any of that or have you observed long-term any liver enzyme elevations? Yes.
spk02: I can take that. In terms of liver enzyme elevations, we all know there's around 10-ish percent increase in transaminases autoimmune-based with immunotherapy. And with single agent, we have a little bit of data at 40 and 60 suggesting that the drug itself could cause an increase in transaminases. Across the different cohorts, and we have multiple different cohorts in the phase one trial, for example, you'll see in the melanoma cohort, we had an incidence of AST, ALT increase and then in the squamous cell head and neck cohort, there was very, very little. So I think it varied amongst tumor type. What made it much clearer was in a randomized setting where you took immunotherapy versus immunotherapy plus iganalysib, where you could really tease out the difference. Numbers were still small, but it became really apparent there was a difference when one looked in that randomized setting.
spk07: Right. That's really helpful. Thank you. And then in terms of the MARIO3 trial in triple negative breast cancer, can you remind us what the benchmark is in terms of the response rates and maybe share what internal bar you might have looking at those response rates?
spk02: So if you look at MARIO3, MARIO3 in the triple negative breast cancer will have two cohorts. It will have a cohort with PD-L1 high and a cohort with PD-L1 low. So PD-L1 low is easy. The bar is relatively low, and even though there is a response rate of around 40-ish percent with the Braxane, the approval is only for the PD-L1 high. So I think we're looking at, for the PD-L1 low, a PFS to beat the PFS, it's five months for the PD-L1 low with a response rate of about 40, and for the PD-L1 group, just over 50% response rate with a PFS of about 7.8 months. So I think we're trying to look at the totality of the data, both the, well, I call it the depth of the responses and the duration of the responses, and the totality of the data that we're looking at in the triple negative breast cancer cohort.
spk07: Great. And just one last one. So in the same study in the triple negative breast cancer, at FAB-C, what kind of data actually will you be presenting? Can you provide some guidance on that, like patient number, et cetera? Sure.
spk09: So, Nora, we haven't provided the patient numbers, although obviously we will be updating those at staff state. And what we'll be presenting is all the data that we have on the patients that are enrolled to date up through the data cutoff that we needed to. So it will include time on study and response rate as well as the safety update for all those patients who are on study and have had a first scan at this point.
spk07: Okay, that's helpful. Thank you. That's all from me.
spk09: I'll also just remind you, Brian, that the reason that Brian shared those benchmarks of the concentric and abraxane in the PD-L1 positive setting for which they have accelerated approval, we did design Mario 3 to mirror that approval study in Passion 130 as closely as possible. So we have all the same inclusion-exclusion criteria. So it's not a randomized study. It's a pretty good benchmark for us.
spk07: Sure. Got it. Thank you.
spk05: Your next question is from Sumit Roy of Jones Trading.
spk01: Hi, everyone. Thank you for taking the question. Congratulations on the very promising data. Looking at the SITC poster at the MDSC levels, could you give us a little color on how the trend looked like in the MDSC levels past cycle two, if you're collecting those data because historically? Prior trials we have done it very nicely correlates with the partial response. And the responders, could you tell us the PD-L1 status on these patients? Were they high or low in the melanoma trial? Thank you.
spk02: So two things. One is unfortunately we don't have the PD-L1 status on a lot of the patients from Mario 1. So we're basically in the melanoma trial with all the available pertinent data we have put in the poster. So unfortunately we just don't have all that data. The second part about MDSCs over time, in the newer studies we're collecting it, but it is quite variable, and we'd like to sort of summarize, a much bigger cohort of patients before we make any conclusions about long-term changes in MDSC levels, the circulating ones. Once again, I'll reiterate what I said a little bit earlier on. Really interested to see what happens in the tumor to see how the different markers change there.
spk01: Okay. And could you remind us the Mario 3 and... The dosage you're using is continuing to be 40 or 30 going forward?
spk02: So we've expanded it at 30 for Moria 3. Looking at the totality of the data and all the different parameters that we assess, we feel comfortable, as we've stated before, that the sufficient drug is a sufficient PD effect So feel comfortable at 30 milligrams moving forward. And we do know that as we increase the dose, there is a higher incidence of transaminases. So that has been a really well-tolerated dose, the 30. Some of the ARCIS data will be presented at 40 milligrams at San Antonio Breast, but they did a cohort of 30 and 40 milligrams.
spk01: Thank you so much. I'm glad you talked about it.
spk05: Your next question is from Kevin DeJeter of Oppenheimer.
spk08: Hi, this is Susan Ahn for Kevin. Thanks for taking our questions. I wanted to follow up on getting any details on the potential follow-on study for MARIO275. I know that you want to look at the data before you decide to enroll, but what would be the study objective and, I guess, patient population
spk09: So, Susan, we understand your question. It really is going to be a function of the data itself. What we would try to do is mirror, take the learning from Mario 275 in terms of the patients that have benefited most significantly and build a trial that leverages that data. So that's the focus. And the objective of the study will be a function of what the data are and what path that those data pave for us in the next steps.
spk08: Okay, great. That makes sense. And my second question is on the Mario 3 enrollment. You mentioned in your press release that you had implemented a number of initiatives. Can you give us color on what those initiatives are and if you plan to disclose any metrics on enrollment?
spk09: So we certainly will be providing at San Antonio an update on what current enrollment is as well as our outlook on enrollment. We're working very closely with our CRO and our site. We've done a number of things that include a social media campaign so that patients will have access if they search for our trial. We've done a number of, you know, calls and educational sessions with our site. Brian, is there anything else that you would highlight that we've done?
spk02: I think that's it. I think it's a very competitive area, but I think accrual will give you some more color, but it does seem to be a problem at the moment.
spk09: And we think ultimately, to your question, Susan, we think what will facilitate enrollment the most is good data. And so as our data mature, getting that data out, we think will be the most impactful driver of enrollment.
spk08: Okay, great. Thank you.
spk09: Thank you.
spk05: Thank you. At this time, I'm showing no further questions. I'd like to turn the call back over to Adeline for closing remarks. Thank you.
spk09: We're really excited to have reached this important new phase of development at Infinity, and we look forward to sharing data and updates in the coming months. We thank you for your continued support and for joining today's call and to updating you later this year. Thank you. Have a nice night.
spk05: Ladies and gentlemen, this concludes today's conference call. You may now disconnect.
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