Syndax Pharmaceuticals Inc (SNDX) 2018 Q2 法說會逐字稿

Good day, ladies and gentlemen, and welcome to the Syndax Second Quarter 2018 Conference Call. (Operator Instructions) It is now my pleasure to turn the conference over to Melissa Forst, with Argot Partners. Please go ahead.

Thank you, operator. Welcome, and thank you to those of you joining us on the line and the webcast this afternoon for a review of Syndax's second quarter financial and operating results.

I'm Melissa Forst, with Argot Partners. And with me this afternoon to discuss the results and provide an update on the company's progress are Dr. Briggs Morrison, Chief Executive Officer; and Rick Shea, Chief Financial Officer. Also joining us on the call today for a question-and-answer session is Michael Metzger, President and Chief Operating Officer; and Dr. Peter Ordentlich, Chief Scientific Officer.

This call is being accompanied by a slide deck that has been posted on the company's website. So I would ask you to please turn to our forward-looking statements on Slide 2.

Before we begin, I would like to remind you that any statement made during this call that is not historical is considered to be a forward-looking statement within the meaning of the Private Securities Litigations Reform Act of 1995. Actual results may differ materially from those indicated by these statements as a result of various important factors, including those discussed in the Risk Factors section in the company's most recent quarterly report on Form 10-Q as well as other reports filed with the SEC.

Any forward-looking statements represent our views as of today, August 7, 2018, only. And a replay of the call will be available on the company's website, at syndax.com, following the call.

And with that, please turn to Slide 3, and I'm pleased to turn the call over to Dr. Briggs Morrison, Chief Executive Officer.

Thank you very much, Melissa, and thanks to everyone for joining us on today's call and webcast.

This afternoon, I will share the progress we've made during the second quarter as we continue to execute on our corporate strategy in support of our primary mission: to realize a future in which people with cancer live longer and better than ever before.

Slide 3 provides a summary of the investment highlights for Syndax. During this call, I will discuss both the progress we are making with our lead program entinostat, as well as provide some commentary on the clinical development strategy for SNDX-6352, our anti-CSF-1R antibody.

I'll review the plans for the upcoming progression-free survival, or PFS, readout from our Phase III entinostat hormone receptor positive breast cancer trial for which we received a breakthrough therapy designation from the FDA, and I will review the upcoming milestones related to our exciting ENCORE clinical trial program, which combines entinostat with PD-1 antagonists.

Slide 4 provides a summary of the milestones that we communicated on our last call, back in May of 2018. As you can see, we have a lot of definitive clinical data reading out over the next period, a potentially transformative time for our company.

Let me now turn to Slide 5 and give you an update on our Phase III trial of entinostat in hormone receptor positive HER2- breast cancer. Slide 5 summarizes the trial design and the endpoints of the trial. We've also summarized the key upcoming milestones.

As we have communicated previously, in the fourth quarter of last year the ECOG Data Safety Monitoring Committee completed the final progression-free survival analysis and the first interim overall survival analysis of this trial. And these analyses are held confidentially by the ECOG-ACRIN study statistician and the Date Safety Monitoring Committee.

No communication regarding this analysis will be released until the completion of enrollment. The trial is now 98% enrolled as of the end of July, and we anticipate enrollment completing sometime in the next 2 months, by the end of this quarter.

Once final enrollment is achieved, we will learn of the results of the final PFS analysis, and, if positive, we are poised to file an NDA within about 4 to 6 months of receiving the data from ECOG-ACRIN.

We received many questions about what exactly will be communicated at the time of the completion of enrollment. So to clarify, if the PFS analysis is statistically significantly positive, Syndax will communicate top line results and full data will be presented at an appropriate medical meeting. If the PFS analysis is not met, Syndax will not receive any data from the trial and will simply communicate that PFS was not met and indicate when the next interim OS analysis will be conducted. We will not communicate completion of enrollment. We will communicate the result of the PFS analysis.

I'd also like to remind you that the Data Safety Monitoring Committee will examine updated overall survival every 6 months, generally in May and November. The next interim analysis for overall survival is scheduled for November of this year. Should any of the interim analyses of overall survival show a statistically significant benefit, the trial will end and all data will be released to both ECOG and Syndax. In that scenario, we would communicate top line overall survival results, and again full trial results would be presented at an appropriate medical meeting.

We remain confident in the potential outcome of E2112, as it's based upon strong Phase II data which led to FDA breakthrough therapy designation.

I must say that it's a truly riveting time to be at Syndax. Completing any clinical trial is always extremely gratifying, but finishing a Phase III trial for what could potentially be the next breakthrough therapy for women with hormone breast cancer is simply thrilling.

I'd like to take a moment to thank the many people who have made this trial a reality: our colleagues here at Syndax, our colleagues at ECOG and at the many clinical research sites involved in the trial. Perhaps most importantly, I want to thank the hundreds of women and their families who took part in the trial. We look forward to sharing the results of this landmark clinical trial with the medical and investment community.

Slide 6 emphasizes the potential for the entinostat-exemestane regimen to be the preferred agent after a CDK4/6 therapy for HR+, HER2- breast cancer. We know that CDK4/6 therapies, most notably Ibrance, are being used increasingly as first-line agents, but there's a clear desire to understand what therapies will be effective in a patient who has stopped responding to a CDK4/6 inhibitor.

Our current estimate is that somewhere between 30% and 50% of patients in E2112 will have received a CDK4/6 inhibitor prior to entering the trial, and, thus, we will have a highly relevant data set in this population. This population of patients is relatively large, with an estimated 34,000 patients who go on to receive hormone therapy after failing first-line therapy and could, therefore, potentially be eligible to receive entinostat.

Let me now turn to Slide 7, which summarizes our ENCORE clinical trial program in which we are testing entinostat in combination with PD-1 pathway antagonists, either PD-1 antibodies or PD-L1 antibodies. We are now exploring entinostat in combination with a PD-1 antagonist in 6 different tumor types: melanoma, non-small cell lung cancer, microsatellite stable colorectal cancer, triple negative breast cancer, ovarian cancer and hormone receptor positive breast cancer.

This broad clinical trial program is supported by an extensive [corollary] science program that is designed to identify biomarkers that could predict which patients will experience a clinical benefit from our combination therapy, an effort that, as we have previously communicated, is starting to yield exciting preliminary results.

We are extremely encouraged by the results we are seeing across this clinical trial program. As we complete our initial clinical trials in each tumor type, we will prioritize which indications to advance to registration trials based upon unmet medical need, the competitive landscape and our ability to generate an attractive return on our investment.

I'm pleased to report that during the first half of this year we've completed enrollment in 2 of the 3 cohorts of ENCORE 601, as well as having completed enrollment in both ENCORE 602 and 603. As I noted previously, we have a lot of definitive data reading out from this program in the coming months.

Slide 8 is a brief summary of where we are with the 3 cohorts of ENCORE 601. At ASCO this year, we presented data on the first 57 patients who were treated with the combination of entinostat and pembrolizumab for their non-small cell lung cancer that had progressed on a prior PD-1 antagonist.

There will be an oral presentation at the World Conference on Lung Cancer in September of this year on the full 76 patients enrolled in this cohort. That presentation will also provide updated data on the utility of peripheral blood classical monocytes to enrich for patients who derive clinical benefit.

As a brief reminder, in the data we presented at ASCO we saw a 28% overall response rate and a 5.4-month median PFS in the approximately 30% of patients with high peripheral blood classical monocytes at baseline. We expect to communicate our development plans for entinostat in this indication in the fourth quarter.

Also at ASCO this year, we presented data on the first 34 patients who were treated with the combination of entinostat and pembrolizumab for their metastatic melanoma who had progressed on a prior PD-1 antagonist or both a PD-1 and CTLA-4 antagonist. Updated data from the full 55 patients in this cohort is anticipated by the end of this year.

And as we have previously communicated, we will also be examining the utility of the peripheral blood classical monocytes to enrich for patients who derive clinical benefit in this cohort and anticipate making a decision on our registration plans by the end of the year.

Coming out of ASCO, we have not seen any agent that provides a level of efficacy we have seen with the combination of entinostat and pembrolizumab in patients who have progressed on both a PD-1 and a CTLA-4 antagonist.

Finally, we also presented data at ASCO this year on 16 patients who were treated with a combination of entinostat and pembrolizumab for their metastatic microsatellite stable colorectal cancer, another area of clear unmet medical need. We expect to complete enrollment of a total of 37 patients in this cohort by the end of this quarter and anticipate making a decision whether to enroll additional patients in the first half of 2019.

Slide 9 summarizes ENCORE 602 and 603, our Phase II trials in triple negative breast cancer and ovarian cancer. I'm pleased to report that both trials have now completed enrollment, and we anticipate top line results from both ENCORE 602 and 603 in the first half of 2019.

I want to emphasize that both of these trials are randomized, blinded, placebo-controlled trials that will provide robust evidence on the utility of entinostat in these populations. Positive results from either trial could prove transformational for Syndax and could directly inform the design of potential registration trials in these indications. Again, we're very pleased with the breadth of our ENCORE clinical program and the excitement that has been expressed by physicians who are conducting these important clinical trials.

Let me now turn to Slide 10 and SNDX-6352, our potential best-in-class monoclonal antibody therapy targeting the CSF-1 receptor. We presented the Phase I healthy volunteer data at SITC in November of 2017, and the multiple ascending dose study in cancer patients is now ongoing. In January of this year, we were very pleased to announce our collaboration with AstraZeneca to study the combination of 6352 with IMFINZI, and that combination trial is now underway.

We had previously indicated that we would provide an update on our clinical development program for SNDX-6352 around mid-year. Given the many competitors who are working on this target, we've chosen to outline aspects of our clinical development program at the time of initiation of a specific trial. Today we are announcing that we have filed a separate IND to study SNDX-6352 for the treatment of chronic graft versus host disease, a well described frequent complication of hematopoietic stem cell transplantation. This Phase I trial is anticipated to start this year.

Slide 11 provides a brief summary of the rationale for developing SNDX-6352 for chronic graft versus host disease, a disease in which the proinflammatory activity of donor-derived macrophage contributes to the initiation and development of fibrosis and manifestation of many of these advanced disease symptoms.

Testing in preclinical models of chronic graft versus host disease has demonstrated that that blockade of the CSF-1, CSF-1R axis with anti-CSF-1R antibodies results in depletion of the proinflammatory profibrotic donor macrophages, thereby preventing and reducing chronic graft versus host disease.

Based on these data and significant unmet need, we believe that chronic graft versus host disease provides an attractive opportunity for testing the safety and efficacy of single agent SNDX-6352, and our trial is the first to test an anti-CSF-1R inhibitor for this indication. This trial represents an extremely modest investment which we believe, if positive, could unlock significant value for SNDX-6352. It's estimated that upwards of 12,000 patients per year globally suffer from this disease.

Last, but certainly not least, on Slide 12, we summarize our Menin-MLLr program, which spans a broad range of genetically defined leukemias and potentially other indications as shown on the slide. We remain on track pending successful completion of our IND-enabling studies to file an IND in the first half of 2019. Exciting positive data was presented at this year's AACR, demonstrating efficacy against both MLL-r PDX models as well as NPM1 mutant PDX models, and those presentations can be found on our website.

I want to emphasize that we see a rapid and straightforward clinical development path for our Menin-MLLr inhibitor. The molecule is anticipated to have single-agent activity, and we will of course target patients who have an MLL rearrangement. It's quite possible that we could observe clinical activity very early in the clinical development path, again unlocking significant value for Syndax. So, really, stay tuned on this program.

And with that, I'll turn it over to Rick for the financial update.

Thank you, Briggs. Turning to Slide 13, for the 3 months ended June 30, 2018, Syndax reported a net loss attributable to common stock holders of $18.4 million, or $0.74 per share, compared to $13.6 million, or $0.70 per share, for the prior year quarter.

Second quarter research and development expenses increased to $14.9 million, from $9.9 million for the prior year. The increases were primarily due to increased activities in CMC manufacturing for SNDX-6352, increased development activities for the Menin program and increased clinical costs for the entinostat ENCORE 602 program, partly offset by completion of entinostat pharmacology trials and lower program costs for E2112. Employee compensation also increased, due to increased headcount.

G&A expenses totaled $4.5 million for the second quarter of 2018, compared to $4.3 million for the prior year. The increase was primarily due to increased entinostat precommercialization activities and increased patent-related legal expenses.

As of June 30, 2018, there were 22.7 million common shares issued and outstanding, a 2 million share reduction from the 24.7 million shares outstanding at the end of Q1. In June 2018, the company signed an exchange agreement with Biotechnology Value Fund, under which BVF exchanged 2 million shares of common stock for 2 million warrants to purchase common shares. This was not a sale of common stock by BVF, but an exchange of stock for warrants.

On a fully diluted basis, we had 24.8 million shares outstanding at June 30, including 22.7 million common shares, the 2 million warrants held by BVF and 45,000 shares from in-the-money stock options, using the Treasury method. For purposes of calculating the company's earnings per share, the warrants are included in the weighted average number of shares used to compute the net loss per share. So the warrants will not impact the calculation of EPS, going forward.

Syndax ended the second quarter with a cash balance of $98.4 million, which we believe is sufficient to fund development for at least 12 months, enabling us to reach key development milestones.

Subsequent to June 30, in the third quarter of 2018 through August 6, pursuant to our ATM financing facility, the company has sold 633,000 shares of common stock, with net proceeds of $4.4 million. Additional financial details will be available in our 10-Q, which we intend to file this week.

Looking ahead, we expect R&D expenses to be $14 million to $16 million for the third quarter and $59 million to $62 million for the full year 2018. Total operating expenses are expected to be $18 million to $20 million for Q3 and $77 million to $81 million for 2018. And those total operating expense numbers include approximately $1.5 million of noncash stock compensation costs per quarter. The cash burn in the third quarter of 2018 will be offset by the $4.4 million in net proceeds from stock sales using the ATM facility.

I'll now turn the call back over to Briggs.

Great. Thanks a lot, Rick. So looking ahead, we anticipate several key upcoming milestones, summarized on Slide 14. As I've noted, we anticipate definitive clinical data readouts and investment decisions on 6 indications in the coming months; the readout of the PFS results from our Phase III trial in hormone receptor positive HER2- breast cancer in the E2112 trial; as well as the next overall survival analysis in November of this year; as well as data from our ENCORE program in non-small cell lung cancer, melanoma, colorectal cancer, triple negative breast cancer and ovarian cancer.

As I said earlier, it's an absolutely thrilling time to be at Syndax. I think it's almost unprecedented for a company of our size to have so much data coming out over such a short period: a phase III trial and 5 Phase II trials over a matter of months. It will be an extremely busy next few months for us here at Syndax.

As always, I'd like to thank the team here at Syndax, our collaborators and, most importantly, the patients, the trial sites and the investigators involved with our clinical programs.

With that, I'd like to open the call for questions.

(Operator Instructions) Our first question comes from the line of Chris Shibutani of Cowen.

Just maybe for Rick, the operating expense guidance for the balance of this year, some reduced levels of operating expenditure, as well as R&D. Can you give us a sense for where you're perhaps borrowing from? And does this represent a delay or push-out into 2019? Or how should we think about following into 2019 now that we also have sort of data readouts that you're talking about in the first half of next year?

Our earlier guidance anticipated that we would be commencing at least one follow-on clinical study to our ENCORE 601 program. And we weren't exactly sure which indication, but we felt that sometime in the second half of 2018 we would be starting a follow-on study. Since we're continuing to evaluate that data and letting it mature, it's unlikely that we'll be starting one of those studies prior to year-end. So that's pushing any of those costs out into 2019.

Great. And then the new news. As far as your pipeline development, you mentioned an efficient way to explore looking at CSF-1R in chronic graft versus host. When we think about, broadly speaking, antibodies to CSF-1R, sort of some of the on-target as well as perhaps off-target related AEs, the issue that that approach has had, particularly looking at either benign tumors in the orthopedic area or in cancer, have included things such as periorbital edema, liver function test issues.

Can you comment about what it is that you perhaps learned from preclinical work or pre-IND work about dosing that you think might make it amenable to probably the relatively complicated environment of patients in the setting that they would be vulnerable to graft versus host?

I'll have Michael Meyers, our Chief Medical Officer, take that question.

So Chris, great question. So what we've seen is that the periborbital edema and, specifically, the liver function abnormalities don't become an issue until what would be considered to be higher, more frequent dosing. And we believe that the GvHD indication may allow us to see efficacy at significantly lower doses than would need to be achieved to treat solid tumors.

Our next question comes from Konstantinos Aprilakis of JMP Securities.

A follow-up to Chris' if I may. So your thoughts on the competitive landscape in GvHD and sort of how did that inform your decision to pursue this as a potential indication? You've got a number of assets in active clinical development, late-stage trials. IMBRUVICA was recently approved. Where do you see 6352 potentially fitting in?

Right. So I'll have Mike Metzger take that question.

So really good question. I think there's a lot of opportunity second and third line in chronic GvHD. I think you're probably aware of the BTK IMBRUVICA has been approved as the first second-line agent after steroid use in the first line. So that being the only one that's sort of approved, other agents are used. They've been tested, but small patient numbers and nothing has really distinguished itself in the second or third line necessarily, other than the BTK inhibitor.

So I think what distinguishes or potentially distinguishes us is a safety profile that hasn't been seen with the other competitive agents that are being developed. Naturally, you have to achieve an efficacy bar that's not insignificant, but if you can show a safety profile and a tolerability profile that's advantageous, I think you have a shot at a good market share in second and third line.

And just for the sake of clarification, you're not deprioritizing the oncology indications. This is just an add-on to that.

That's actually correct. So as you know, we have the combo work going on with durvalumab. We -- as I said in my prepared remarks, I think because of the competitive nature, the other things that we want to do we'll talk about as they're about to start, rather than too far ahead.

So this is not in any way deprioritizing other work we would do in solid tumors or in combination with cell therapy or other things that we have thought about. It's really we think a potentially fast-to-market way to get good safety and efficacy data from single-agent antibody.

Our next question comes from Christopher Marai of Nomura Instinet.

Congrats on the progress. Another one on the CSF-1R. I was just wondering, thinking about chronic GvHD and some of the manifestations, obviously skin is one of them. Is that an opportunity perhaps to get a quick read on the efficacy of this drug? And then how do you look at sort of endpoint and taking it forward? Will you look at specific manifestations, lung, skin, specifically, just because macrophages tend to be maybe more involved in that aspect of the disease? Or will you look at more of a traditional approach to development in GvHD? And then I have a follow-up.

So I'll let Michael Meyers take that one.

So Chris, we will be looking at the specific pan-chronic GvHD scoring system to determine symptom improvement. We will also be looking obviously for biologic correlatives in specifically accessible areas such as skin.

So I think the key is that we'll be looking at something that clearly is evidence of clinical benefit, which we expect that we should be able to see at the doses that we can achieve without significant toxicity. And we'll also be looking at multiple biologic correlatives to determine a relationship between PD and clinical benefit; PD being pharmacodynamic benefit.

Got it. And then just with respect to your collaboration with AZ and to perhaps the opportunity to go into other autoimmune diseases or rarer indications with this asset. Maybe remind us of the collaboration and then how you look at, I suppose, driving this forward. Is this going to be, purely speaking, an oncology asset in your eyes? Or do you look to develop it more broadly? Obviously, you currently have an oncology focus. So would love to sort of understand that. And that's it.

Chris, it's Michael. I'll take the question. So in terms of our partnership with AZ, so I think I'll remind you that it's a clinical collaboration that we've signed with AZ, and it's nonexclusive. And we obviously have global rights from UCB.

I think the idea here is that we can develop the compound in addition to what we're doing with AZ, and that means in any indication, whether it's oncology or nononcology. And so we've chosen this indication carefully for the reasons Briggs outlined in his remarks. But it does not preclude us from going into other oncology indications, which we plan to do potentially with AZ and with others.

We have some ideas and things that we'll hopefully put in place in the future. So I think we have fortunately put the type of partnership in place that gives us great flexibility, avails us to PD-1 antagonists and allows us to do that combination in cancer, but doesn't tie us down to one particular option as we develop in multiple indications.

Chris, the only thing I guess would add is we are not precluded from developing the drug in other nononcologic indications should we decide that those provide attractive opportunities. To Konstantinos' earlier question, it doesn't in any way detract from what we're doing in oncology, but it maybe add to it.

Our next question comes from Robert Hazlett of BTIG.

Regarding 601 and the non-small cell lung cancer effort, could you describe your level of confidence with the biomarker approach you're employing there and maybe actually across indications, as well? The data has matured, and I'd love to get a sense of how your confidence is evolving one way or another.

As I said, there will be an updated presentation at World Lung. I think it's in Toronto the end of September. Looking at the data that's going to be presented there, I think it's generally consistent with what we presented at ASCO. So it seems to be maturing in a consistent way. So I don't think our confidence has changed anything from when we presented data at ASCO.

Terrific. And then secondly, could you remind us with 602 and 603, now that they're fully enrolled, is there an ability for an accelerated pathway using the results of those studies, assuming they're positive?

That's a very good question. It's -- I'd say we don't know the answer to that. We'd rather wait and see what the data shows and then potentially have discussions. As you can imagine, neither one of the partner antibodies is yet approved for the indication in which we're studying it. So you'd have the case of having 2 unapproved agents.

You would clearly have, if the trials are positive, evidence that entinostat adds to the comparator agent. So there could be a conversation with regulators, but I think we tend to think of it more as a path to a subsequent registration trial.

Our next question comes from Madhu Kumar of B. Riley FBR.

This is [Dylan Dupree], sitting in for Madhu. 2 quick questions. First, has there been any change in the rate of recruitment for E2112? Or has it continued at the previous pace? And then second, a little more involved, can you please walk through the preclinical and mechanistic rationale for CSF-1R inhibition in chronic graft versus host disease?

So I'll let Michael take the question, Michael Meyers, on the enrollment, and then I'll have Peter Ordentlich talk about the preclinical rationale.

So actually over the past 3 months, enrollment in 2112 has increased by about 40% relative to what the enrollment rate was for the prior 3- to 6-month period. And therefore, we are very confident that we will complete enrollment this quarter.

And Peter, do you want to make a few comments on the preclinical rationale for CSF-1R?

So basically, preclinical models of chronic graft versus host disease, both ones that looked at skin involvement as well as lung involvement, were used to determine the role of the donor-derived macrophage in generation of the sort of fibrotic effects of GvHD. And in those experiments, it was shown that those macrophage are both donor-derived and CSF-1-dependent for their growth and proliferation and infiltration into both those disease sites.

And so CSF-1R antibody was very effective in blocking both the inhibition and prevention of the symptoms of chronic graft versus host disease in both of those models. So that's really the main preclinical data that we based our moving ahead with the clinical trial on.

Our next question comes from David Lebowitz of Morgan Stanley.

Could you just give us a refresher for the hormone receptor positive trial of what type of PFS would be expected in the control population and, similarly, what type of OS might be considered, given that there's another analysis coming up?

I'll let Michael Meyers summarize the design characteristics and what the assumptions were.

So we were looking for about a 3-month increase in PFS between the treatment arm and the control arm, which equated to a hazard ratio of about 0.58. The minimal hazard ratio, or the maximal hazard ratio required for statistical significance would be a hazard ratio of 0.67, which would equate to about a 2-month improvement. We believe that somewhere between a 2- to 3-month improvement, specifically with a trend to overall survival benefit, would be considered to be clinically meaningful in this specific patient population.

And for OS, what type of assumptions, also? Would they be similar?

The assumptions for PFS were actually a bit more aggressive than the assumptions for OS. So the hazard ratio that we're trying to achieve for OS was a hazard ratio of 0.73, with a hazard ratio of about 0.8 being required for statistical significance, and that equates to about a 5-month improvement in overall survival, from approximately 22 months for the control arm to about 27 months for the treatment arm. And as you recall, the overall survival delta in the 301 study was actually in excess of 8 months.

And one more question. On the ENCORE 601 for melanoma, could you just run us through the biomarker analyses that are currently underway? And I guess when the go/no-go decision is made later this year, where you expect you'll be placing your focus?

Right. So maybe, Peter, can you go through sort of the full portfolio of things that you're looking at and then maybe comment on the classical monocytes?

For the melanoma cohort, specifically, we're looking at various immune cell subsets based on our hypothesis of entinostat regulating certain myeloid cell populations.

We have NanoString as well as RNA-seq gene expression data available actually for the majority of patients pretreatment and a fairly large number, I think up to 16 paired, on-treatment biopsies that will inform us around mechanism of action, both in responders and nonresponders, as well as PD-L1 expression conducted by Merck and tumor mutation burden through whole-exome sequencing.

So I think we'll be in a really nice position to look at responders, nonresponders, both in terms of blood-based as well as tumor-specific biomarkers over the next couple of months.

And just a comment on the classical monocytes?

So as we presented the classical monocytes data at ASCO for both lung cancer and the melanoma cohorts, we saw quite a strong trend relative to the response rates. And we're -- for the lung that we presented, both the clinical benefit in terms of PFS was also quite significant.

And I think as we indicated for melanoma, we are waiting to see how the full cohort matures before we can comment on whether or not the trends in response rates also transfer over to the sort of clinical benefit for that cohort. But from a response rate perspective, the trends appear to be the same across melanoma and lung, and so far at least we have the lung clinical benefit also matching the high monocytes. We're not quite sure yet for the melanoma.

Ladies and gentlemen, this concludes today's question-and-answer session. I would like to turn the call back to Dr. Morrison for any closing remarks.

Great. Thanks very much, everybody, for joining the call. I hope you're all staying cool and well hydrated if you're on the East Coast, and we look forward to further communications over the next period.

Ladies and gentlemen, thank you for participating in today's conference. This concludes today's program, and you may now disconnect. Everyone, have a great day.