Jounce Therapeutics, Inc.

Good morning, ladies and gentlemen, and welcome to the Jones Therapeutics First Quarter 2022 Earnings Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session, and instructions will follow at that time. As a reminder, this conference is being recorded at the company's request. I will now turn the call over to your host, Eric Laub, with Jones Therapeutics. Please go ahead.

Thank you, Operator. This is Eric Laub, Vice President of Investor Relations at Jounce Therapeutics. Good morning and welcome to the Jounce Therapeutics First Quarter 2022 Financial Results Conference Call. This morning, we issued a press release which outlines the topics that we plan to discuss today. The release is available in the Investors and Media section of our website at www.jouncetx.com. Speaking on today's call will be our CEO and President, Dr. Richard Murray, who will review our pipeline progress and key milestones, followed by our CMO, Dr. Beth Trehu, who will provide an update on our clinical activities. And lastly, our CFO, Kim Trapkin, will review our first quarter financial results. We will then open the call for your questions. Before we begin, I would like to remind everyone that today's discussion will will include statements about our future expectations, plans, and prospects that constitute forward-looking statements for the purposes of the Safe Harbor provisions under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including the risk factors discussed in our SEC filings. In addition, any forward-looking statements represent our views only as of today, May 5, 2022, and should not be relied upon as representing our views as of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so even if our views change. With that, I'll now turn the call over to Rich.

Thanks, Eric. Good morning, and thank you for joining today. Before I turn to our pipeline and quarterly accomplishments, let me take a moment to recognize the entire Jounce team on their continued commitment to excellence and dedication to improving patients' lives, which they bring to work every day. We were pleased to announce this morning in our press release that we met the initial pre-specified response criteria to continue expansion of two of the innate study cohorts to 29 patients. We are encouraged by this progress and continue to execute across all cohorts. Beth will provide more detail on the innate study in a few moments. While the use of PD-1 inhibitors continues to grow and expand into earlier lives of therapy, including non-metastatic settings, the size and scope of PD-1 inhibitor resistant markets continues to grow. as there are more patients who are resistant to the therapy than benefit from it. Unfortunately, there are few alternatives for these patients in many tumor settings. We see this resistance as a fundamental scientific and medical problem that stands in the way of the broader and more durable impact IO could have for cancer patients. As scientific evidence continues to point to the myeloid immune cell lineage as being causal to at least some aspects of IO resistance, we undertook a comprehensive target discovery interrogation of the myeloid cells from human tumors. Our discovery work prioritized the low RB or ILT family of receptors as being key mechanisms that could mediate such immunosuppression leading to IO resistance. These mechanisms could occur in certain patients independent of any T-cell focused immunosuppression, such as PD-1 or CKLA-4. There are five LLRB inhibitory receptors and six LLRA activating receptors. From this work, we prioritize LLRB2, or ILT4, as our lead, LLRB4, or ILT3, now in IND enablement studies, and LLRB1, or ILT2, in discovery. Each of these programs has common as well as unique features of biology and the mechanisms by which they may lead to therapeutic benefit. Our highest priority program, CTX8064, blocks the function of LIL-RB2 on tumor-associated macrophages and other myeloid cells. It aims to convert immunosuppressive activities of these cells to an immune-active state. First, by inhibiting ligand binding to LIL-RB2, the immunosuppressive macrophages can be reprogrammed which we believe favors an immune response in the tumor. Second, we believe the mechanism also allows for more effective antigen presentation leading to T cell activation, thus creating a bridge between the innate and adaptive immune systems. This is something T cell checkpoint inhibitors cannot do alone. And the preclinical data tells us it may result in the potential to reverse PD-1 inhibitor resistance. We're extremely pleased with the progress of the innate study as we try to bring benefit to the patients that historically have not benefited from or become resistant to PD-1 inhibitors. I'll now turn to SELECT, our randomized phase two proof of concept trial of vopratilumab, or VOCA, in combination with our PD-1 inhibitor, PIMI, and non-small cell lung cancer. We've completed the test VOCA biomarker screening and expect to complete enrollment this month, as we reiterate our guidance of expecting to share full clinical trial data at a medical meeting in the second half of this year. Our next potential clinical program, JTX1484, is an anti-LowRD4, or IL-3, program currently in IND-enabling studies. LowRD4 is expressed on immune-suppressive myeloid cells in the tumor microenvironment, with both overlapping and distinct cell types in biology compared to LIL-RB2. We look forward to advancing this program to the clinic. Led by the LIL-RB family, as well as additional myeloid target mechanisms, our discovery teams are actively building rationally designed bispecific antibodies, where our goal is to identify development candidates that have activities superior to that of the combinations of individual antibodies. We're excited for what lies ahead at Jones as we work toward our key data readouts this year. Our strong financial position enables our continued growth and execution beyond the proof of concept inflection points of innate and select, while continuing our robust novel discovery efforts, identifying and progressing new mechanisms to benefit cancer patients, particularly in the settings where patients have few therapeutic options. With that, I'll turn the call over to Beth to discuss our clinical pipeline in science in more detail.

Thanks, Rich. We are making great progress on our two proof-of-concept studies, and I'm very pleased to be able to provide some updates on both studies for you this morning. Let's start with the innate trial of JTX8064 our LIL-RB2 inhibitor. Last year, we completed the Phase 1 dose escalation for both monotherapy and combination with PIMI, selected 700 milligrams as the recommended Phase 2 dose, and initiated the Phase 2 expansion cohorts for both monotherapy and combination treatment in seven different indications. Enrollment is going very well, and as Rich mentioned, we are delighted to report that two combination cohorts have met the response criteria to expand to 29 patients and are actively enrolling. For competitive reasons, we are not disclosing which indications have expanded at this time. Both JTX8064 alone and in combination with PIMI continue to be well tolerated. As a reminder, each of the expansion cohorts is a Simon's two-stage design. For the combination cohorts, the first stage consists of 10 patients per cohort. Each cohort must meet pre-specified criteria based on radiographic response before resuming enrollment of the additional 19 patients for a total of 29 per combination cohort. Our goal is to demonstrate proof of concept in the full set of 29 patients, which requires that the response rate of JTX8064 in combination with a PD-1 inhibitor is greater than what would be expected with a PD-1 inhibitor alone. The response rates for PD-1 inhibitor monotherapy are different for each innate indication and are all quite low, generally in the single digits. This reflects the high unmet need in patients who have failed a PD-1 inhibitor therapy or have tumor types where PD-1 inhibitors alone have minimal impact. True to our focus on the interrogation of the tumor microenvironment, the tumor types being investigated in innate were chosen because they are expected to have a high percentage of immunosuppressive macrophages, have a high unmet need, and provide opportunities across three major groups of patients. As we have previously stated, we are studying three distinct patient populations across the seven indications in the innate study. PD-1 inhibitor naive patients who have tumors for which there are approved PD-1 or PD-L1 inhibitors, PD-1 inhibitor naive patients who have tumors for which there are no PD-1 or PD-L1 inhibitors approved, and patients who have failed a PD-1 inhibitor therapy and whose tumors are PD-1 inhibitor resistant. We have included all three groups of patients in our expansion cohorts to determine the best opportunities for JTX8064 to make a difference for patients with cancer. An important aspect of the trial is evaluation of the correlation of pharmacodynamic and predictive biomarkers with efficacy, which will be done later this year. We are very pleased with the pace of enrollment in INATE and we expect to present data on all 31 Phase I dose escalation patients, nine of whom were in combination, and at least 60 Phase II patients from innate at a medical meeting in the second half of 2022. This data will include complete Phase I monotherapy and combination dose escalation data, including the respective safety, PK, PD, biomarker, and preliminary efficacy data. Phase 2 data will include safety, preliminary efficacy based on at least two response assessments per patient, pharmacodynamics, and potential predictive biomarker correlation with efficacy. We believe that this predictive biomarker analysis will be useful in interpretation of the clinical data later this year. there is a growing body of evidence that biomarkers expressed by immunosuppressive macrophages are a negative prognostic factor in many cancers, regardless of treatment, and that high levels of LIL-RB2 relative to interferon gamma are a negative predictor of response to PB1 inhibitors. If we observe an association of improved clinical outcomes with biomarkers typically linked to worse outcomes, particularly in the combination cohorts, we will have greater confidence in the contribution of JTX8064 to clinical efficacy. Now, on to our other Phase II program, Vopratelemab and the SELECT trial, our randomized Phase II proof-of-concept trial of Vopra, our icosagonist. SELECT had a target enrollment of 75 patients to achieve 60 evaluable patients. We stopped patient screening when we met our goal of 60 evaluable patients and expect to complete enrollment in the next few weeks. Therefore, we are on track to present the complete study data in the second half of 2022 at a medical meeting. In Select, studying two doses of Vopra in combination with PIMI compared to PIMI alone in biomarker-selected patients with metastatic non-small cell lung cancer who are PD-1 inhibitor naive and have progressed on a platinum-based chemotherapy regimen. This trial seeks to address two important questions. One, will Vopra plus a PD-1 inhibitor in biomarker selected patients result in greater activity than a PD-1 inhibitor alone? And two, which dose of Vopra should we choose for further development? The predictive biomarker selection of patients utilizes TIS-VOPRA, an RNA-based 18-gene signature that includes genes relevant to both PD-1 and ICOS biology. Only patients with a value above the biomarker threshold are enrolled, and the trial is designed to show the statistical superiority of VOPRA plus our PD-1 inhibitor, PIMI, versus PIMI alone. The primary endpoint is the mean change from baseline in tumor size, averaged over 9 and 18 weeks. And the secondary endpoints are overall resist response rate, progression-free survival, overall survival, and duration of response, which represent all of the standard regulatory endpoints. We will assess the data and determine next steps by analyzing both the primary and the more familiar secondary endpoints. The doses we are exploring, 0.1 mg per kg and 0.03 mg per kg, were selected based on differentiated patterns of pulsatile target engagement demonstrated in prior studies and based on a hypothesis that the sustained target engagement required for antagonist antibodies is not ideal for an agonist molecule like Vopra. We expect to choose a dose for further clinical development of Vopra based on the results of SELECT, and a positive result in SELECT may lead to biomarker-directed development in multiple potential tumor types. Lastly, I'd like to discuss our SELECT study patients in Ukraine. Thanks to the incredible efforts of our team and the inspirational fortitude of the Ukrainian patients and study site personnel, I am very happy to report that all of the ongoing Ukrainian patients are continuing to receive study treatments and assessments. Every site in Ukraine has enough study drug to last through the end of this year, and some patients have moved to study sites in other countries. Our thoughts are with the patients, their families, and those who provide their care as they continue to navigate this tragic situation. We will continue to monitor the situation very closely. In conclusion, I would like to take a moment to thank our valued investigators and, most importantly, the patients who put their trust in our medicines to make a difference in their lives. I would also like to thank our team at Jounce and their dedication to advancing these critical programs. We look forward to reporting on our continued progress this year. I will now turn the call over to Kim.

Thank you, Beth. As we reported in this morning's press release, cash, cash equivalents and investments as of March 31st, 2022 were $186.4 million compared to $220.2 million as of December 31st, 2021. The decrease was due to cash burn from operating expenses incurred during the period. Turning to the P&L, no revenue was recognized during the first quarter of 2022. compared to 1.5 million of revenue recognized during the first quarter of 2021. The 2021 revenue was comprised solely of non-cash revenue related to the performance of research and transition services under the Gilead License Agreement. During the first quarter of 2022, we incurred 30.1 million in research and development expenses compared to 20.5 million for the same period in 2021. The increase in R&D expenses was due to increased manufacturing activities performed and increased clinical and regulatory expenses for innate and increased payroll and stock-based compensation expense. General and administrative expenses were $7.3 million for the first quarter of 2022 compared to $7.6 million for the same period in 2021. The decrease in G&A expenses was primarily a result of decreased external consulting and stock-based compensation expense. Net loss for the first quarter of 2022 was $37.4 million, resulting in a basic and diluted net loss per share of 72 cents, as compared to a net loss of $26.5 million for the same period in 2021, resulting in a basic and diluted net loss per share of 58 cents. The increase in net loss is attributable to increased operating expenses incurred during the first quarter of 2022. Based on our current operating and development plans, we are reiterating our gross cash burn guidance for the full year 2022 to be approximately $115 to $130 million. Given the strength of our balance sheet, we continue to expect our existing cash, cash equivalents, and investments to be sufficient to fund our operating expenses and capital expenditure requirements through the third quarter of 2023. I'll now hand it back to Rich for some final words.

Thanks, Kim. The combination of our clinical execution, innovative science, and financial resources puts us in a strong position to move beyond our next set of inflection points. We're extremely pleased to be able to update you on the progress we've made in the innate and select trials keeping us on track to report data later this year. We are working hard to build an I.O. pipeline which looks to address the growing unmet need faced by cancer patients. We're privileged to be working on this mission together with such a talented group of individuals at Chounce and fortunate to have such dedicated collaborators and clinical investigators. This is an exciting time at Chounce, and we look forward to updating you on programs as the year progresses. With that, we'd now like to open the call for your questions. Operator?

Thank you. And as a reminder, to ask a question, please press star, then 1 on your telephone keypad. To withdraw the question, press the pound or hash key. Again, that is star, 1 to get in the queue. First question comes from Boris Beaker with Cowan. Please go ahead.

Good morning, and congratulations on the progress. Can you guys hear me?

Yes, thanks, Boris.

Yeah, thanks, Boris.

Fantastic. My first question on 8064. I guess for the five combo cohorts in an aid that we haven't received an update on, how close are they to enrolling and follow-up on the initial 10 patients? Just trying to gauge the timeline of when other cohorts may be expanded.

Hi, Boris. Thanks for the question. This is Beth. Yeah, so... Some cohorts are still enrolling and some cohorts have completed enrollment and we're still waiting for data. So I think, you know, our plan is on every earnings call we'll give you an update on how the study is going. But I am really excited about the fact that even at this point in time we're going to have data on over 60 Phase II patients later this year.

Got it. And just to follow up on AD64, based on its mechanisms of action, I'm curious if you're assessing the HLA of the enrolled patients, and can different HLA have a material impact on activity? And also, I guess, do you have any clinical assessment of finding different human HLAs for the drug?

Sure. So HLA molecules, particularly the ones that are ligands for LIL-RB2, will be included. We presented data at a poster I think in 2020 showing some of the work from our human histoculture data showing that some of the HLA molecules could potentially be predictive biomarkers. So those are things that we're looking at. Those are probably lower priority than things like LIL-RB2, CD163, things that we've talked about as clearly negative prognostic factors for cancer or for prediction of response to PD-1 inhibitors that we think could be, you know, promising predictive biomarkers for JTX8064.

Great. Thank you very much for taking my questions.

You're welcome. Thank you. Your next question comes from Steve Seedhouse with Raymond James. Please go ahead.

Hey, good morning. Thanks for taking the question, and nice to hear about the progress, specifically in NA, but also across the board. I just wanted to ask if you could sort of rehash how you determined what the actual response rate criteria were in each of the cohorts. And if you could reference, I mean, you have some tables in your presentation slides, your corporate deck. It sort of lists historical PD or PD-L1 response rates in the different tumor types. Should we look at that as like a sort of a benchmark or a general guide for how you determine the response rates, or is that a bit off-base?

Yes. yeah thanks steve that's a great question yes i would say the the response rates that we've shared in our corporate deck which are you know these are drawn from small studies i would say the strongest one of them is the 19 response rate for pembro in frontline pdl1 positive head and neck cancer right so that's in the product label that's the the data on which pembro was approved um the others are um numbers that we've gotten from small studies that as closely as possible match the eligibility criteria for the patients in our study. They're generally below 10%. So our goal ultimately is to demonstrate proof of concept in the full 29 patient cohorts. And so that will have to show that our combination looks like it's producing better efficacy than you would see with a PD-1 inhibitor alone based on those benchmarks.

Very helpful. Thanks. And then the other two questions I just want to ask is, one, is there anything you can say about the monotherapy data that's accrued, just if you're seeing any encouraging signals there? And also, I think you mentioned that you'd be updating every earnings call, the progress of the trial. So I just wanted to confirm, like, as if you were to meet the response rate criteria in a cohort at some point between now and the next earnings fall, that wouldn't be something that you would update us on until earnings. Thanks for taking the questions.

Sure. So I think, you know, we're not reporting on any individual cohort at this time. As we've said, we're actually, I'm really proud of the fact that we enrolled the first patient in January 2021 in phase one, and we're going to have clinical data. on over 60 Phase II patients in the second half of this year. So monotherapy patients will be included in that data, and we'll be reporting at that time. And right now, yeah, our intention is to update on the progress of the study quarterly at our earnings calls.

Great. Thanks so much.

And your next question comes from Ted Tenthoff with Piper Sandler. Please go ahead.

Great. Thank you very much. I'm excited to hear about the progress with an A2. Since everyone's been asking about that, I'll ask you about some of the other little RB programs. And when it comes to sort of the profile that you see emerging here, is this something where, you know, potentially multiple little RB2s, sorry, little RBs might be used together, or do they have different profiles that such that they may have different applications. Thanks so much for explaining.

Hey, Ted. This is Dimitri . Thanks for the question. You know, we're clearly excited about building a pipeline of highly potent and specific antibodies that block the function of LRB2, LRB4, and LRB1. These are the most well-studied LRB family members with clearly clearly demonstrated inhibitory function in immune cells. You know, I think the function of different LLRB family members may be distinct in different cancer contexts, and this is what we are studying, and this is how we're approaching our clinical development using this translational angle. I mean, I think there may be some redundancy among LLRBs, but we also see clear evidence of non-overlapping activities. And I think having the pipeline of these three highly potent and specific blockers of the Larbi family members gives us an opportunity for rapid combination in the clinic. And finally, what I would say is that, you know, one of the core pillars of our strategy in discovery right now at Jones is building a bispecific molecules that would combine different specificities and would allow for more complete coverage of LRB family members. And that's a really exciting new development for us.

Yeah, absolutely. Awesome. Thank you for sharing that with me.

And your next question comes from Corey Kasimov with J.P. Morgan. Please go ahead.

Hey, good morning, guys. Thanks for taking the questions. Two of them for you, both regarding innate. As you think about the data update later this year, how do you think about success, given that you're going to have a variety of different arms and indications with both monotherapy and combination data? Is this about finding one or two lead indications or more about the breadth of activity across them? And then as a follow-up, how important is monotherapy activity in your view when evaluating a cancer compound, even when it's primarily designed to be used in combination?

Sure. So thanks, Corey. So for your first question, I think the answer is possibly both, right? So we obviously will, you know, be looking for signals that enable us to move forward as quickly as possible on a registration path. in one or more indications. But also when we're looking at data across the indications, that's where this year we actually, I think, will have enough data to really be starting to evaluate those biomarkers. And in smaller patient sets, which is, you know, what we're still having this year, that's where I think that fact that some of the biomarkers that we're studying are are known to be negative prognostic factors. And so if we see a correlation between response and some of these biomarkers, that's kind of the holy grail, right? Because you can take something that really predicts the worst outcomes, and you can turn it into something that predicts better outcomes for patients. So I think that's going to be really powerful. And as I've said before, I think that's one of the strengths of the studies that we have a whole panel of predictive biomarkers. Now, they may be more needed in some cancers than others. That's some of the data we'll be starting to get later this year. So we are planning sort of internally. We have clinical development plans with registration paths mapped out for every cohort. the study and you know as the data matures we'll start prioritizing which ones we're focusing on for further development and then your second question remind me sorry I just yeah just the importance of monotherapy activity for yeah I can answer product yes sure so I guess I would turn to examples from things like lag 3 you know which is doing great and showing a benefit on top of PD-1 inhibitors in PD-1 inhibitor-naive patients. So we feel clearly immunotherapy is going the path of cancer therapy since the beginning in terms of combination. And so whether or not a drug has to show monotherapy activity I think is a question. What's important is that you design your study in a way that you're able to demonstrate that your drug is actually adding to the PD-1 inhibitor if it's in combination. And that's what we've tried to do in the PD-1 experienced cohorts in Select, where we're requiring their most recent prior therapy to be a PD-1 inhibitor. So people who have just progressed on a PD-1 inhibitor are now coming on to the combination therapy. And then also giving those benchmarks to show, you know, what you would expect from a PD-1 inhibitor alone. Most of the indications we're studying, you wouldn't expect much from a CD1 inhibitor.

Okay. Thank you, Beth. That's helpful.

You're welcome. Your next question comes from David Adai with SMBC. Please go ahead.

Hi. Thanks for taking my questions. So for JTX8064, especially on the two expanding indications, Could you comment on whether you have performed any biomarker analysis to support the expansion to enroll the additional 29 patients each?

No, no biomarker analysis is involved in that decision. That's based purely on responses, clinical responses. We'll be doing the biomarker analyses later this year and reporting them when we report on the full body of data. Okay.

Got it, that's helpful. And then for GTX 1484, you decided to move forward with the IoT 3.0 target, whereas other companies are pursuing IoT 2.0 as the lead target. Could you just help us understand the rationale part of the IoT 3.0 versus the IoT 2.0 based on your personal data? What are the advantages of targeting IoT 3.0 pathways?

Yeah, thanks for the question, David. This is Dimitri Veroshine again. As you know, we have advanced JTX1484, our potent and specific ILT3 allyl RB4 blocker into IND enabling studies. We continue to be excited about this program. ILT4, ILT3 is expressed on distinct subsets of immunosuppressive myeloid cells in the tumor microenvironment. But as you probably know, we also have a discovery program on ILT2 or LLRB1, which is also progressing quite well, and we hope to bring it to development candidate stage in the near future. There are clearly non-overlapping biology among ILT3 and ILT2. For example, ILT2 in addition to myeloid cells, is also expressed on a subset of natural killer cells as well as CD8 T cells. So it really brings an exciting new angle to the LRB activity. So we're actually equally excited about all of our monospecific potent blockers of the LRB family members, LRB2 in the clinic already, LRB4 not far behind, and LRB1 advancing quite well through discovery. Thanks for the question.

Thank you so much, Dimitri and Beth.

Your next question comes from Arthur He with HC Wainwright. Please go ahead.

Hey, good morning, everyone. This is Arthur in for RK, and congratulations on the progress this quarter. I just want to follow up on the response criteria for the 8064 program. Besides the overall response rate, do you guys also look at the PFS, or are you purely focused on the ORR to make the decision to move it forward?

Great. Thanks for the question. So for the expansion from 10 patients to 29 patients, that's based solely on response. When we look at the data from all 29 patients, we'll be looking at the totality of data, including response rates, biomarkers, PFS, OS, all of that to help guide further development. But the initial expansion is just based on response.

Got it. And I'm just curious, regarding those two cohorts you decided to move forward, what's the highest dose level has been tested for patients? Did you guys test any dose level beyond 700 milligrams?

Yes, we did. In dose escalation, we went as high as 1,200 milligrams. But I will remind everyone, we first saw complete target engagement throughout the entire three-week dosing cycle at 300 milligrams every three weeks. And we chose a dose of 700 milligrams for our recommended phase two dose because we wanted to really optimize target engagement both in the peripheral blood and also in the tumor. And the excellent safety profile and safety up, you know, at 1,200 milligrams was our highest intended dose, and it was well tolerated. So we were very fortunate to be able to choose a dose that really optimizes our target engagement. And that's the dose that is used for all of the Phase II patients.

Got you. Thanks very much. And thank you for taking my question.

You're welcome. Thank you. And our last question is from Nick Abbott with Wells Fargo. Please go ahead.

Oh, good morning, and thanks for having my questions. And first off, Beth, thank you for updating us on those poor patients in Ukraine. It's bad enough having cancer, let alone having cancer while there's a war going on. So my first question is for Innate. Can I just confirm that no cohorts have not met the GO criteria? And then... Do you expect or are you seeing pseudo-progression? And if so, how are you advising the investigators?

So, yes, you're correct. All of the cohorts are either continuing to enroll up to the 10 patients or have completed and are waiting for data to make the decision about expansion. And in terms of pseudoprogression, so all of our investigators are quite experienced with IO therapy. We do allow continued treatment beyond progression in the study, but we don't have any particular guidance regarding pseudoprogression for the investigators. We just follow resist for our response criteria, and we do allow treatment beyond progression if patients are doing well clinically.

Okay. Thank you. And then, you know, just in terms of this go-no-go here for the 10 patients, do they have to be a resist response if you see just really outstanding, you know, long-term stable disease that would also be unexpected? Is that something that could allow you to move ahead, or would that sort of be something that you look at perhaps later on?

Yeah, for the expansion, it requires a response, a true response.

Okay, great. And then last one. So do you have data on TISVOPRIN? I'm sure you do. It's been a long time. But data on TISVOPRIN, chemo-naive versus experienced patients that would give you confidence you could move from this second-line setting to a front-line setting?

I mean, the data that we've collected is clearly in the studies that we're doing. But there is data across the literature on TIS that leads us to believe that, yes, we could certainly take this into a frontline setting or potentially into other tumor types.

Great. Thank you very much.

You're welcome. Thanks for the questions.

And thank you, ladies and gentlemen. This concludes our Q&A and program for today. Thank you for participating, and you may now disconnect.

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