CytomX Therapeutics Inc (CTMX) 2017 Q4 法說會逐字稿

Good afternoon, and welcome to the CytomX 2017 Full Year Financial Results and Operational Update. (Operator Instructions) Please be aware that today's conference call is being recorded.

I would now like to introduce the first speaker, Debanjan Ray, CytomX's Chief Financial Officer and Head of Corporate Development. You may begin.

Thank you, operator. Good afternoon, and thank you for joining us for our 2017 full year results review and operational update for CytomX Therapeutics. Here with me today is CytomX's President and Chief Executive Officer, Dr. Sean McCarthy.

Before we begin, I would like to remind you that we will be making forward-looking statements during the call, including guidance on cash utilization, the evolution of our pipeline and expectations for our collaborations. Because forward-looking statements relate to the future, they are subject to inherent uncertainties and risks that are difficult to predict and many of which are outside of our control. Important risks and uncertainties are set forth in our most recent public filings with the SEC at sec.gov, including our Form 10-K filed today on March 7, 2018. We undertake no obligation to update any forward-looking statements whether as a result of new information, future developments or otherwise.

A webcast of this call will be available on the Investor Relations page at CytomX's website at cytomx.com.

I would now like to turn the call over to Sean.

Thanks, Debanjan, and good afternoon, everyone. I'm very pleased to be here with you today to review our impressive operational achievements in 2017 and to provide a look ahead to 2018.

During 2017, we continued to advance our deep and differentiated oncology pipeline of potentially transformative Probody therapeutics by bringing 2 wholly-owned programs and 1 partner program into the clinic. In 2018, we expect to file 2 additional INDs, and therefore, by year-end, we expect to have a total of 5 clinical stage Probody programs, all of which we consider to be compelling product candidates for the treatment of cancer.

In this regard, 2017 was a pivotal year for CytomX, in which we matured into an integrated highly innovative research and development company.

Before I review our accomplishments for 2017 and anticipated milestones for 2018, I'd like to provide a brief overview of our Probody approach. Probody therapeutics are engineered therapeutic antibodies designed to exploit certain unique conditions present in the tumor microenvironment to more effectively localize antibody binding and activity, while limiting activity in healthy tissue and in circulation.

With this unique platform approach, we aim to reinvent therapeutic antibodies for the treatment of cancer. The CytomX pipeline includes potentially best-in-class cancer immunotherapies against clinically and commercially validated targets, such as PD-L1 and CTLA-4, where our goal is to drive towards differentiated safer and more effective combination therapies by reducing systemic autoimmune side effects.

We're also developing first-in-class product candidates with potential across a wide range of tumor types, including Probody drug conjugates against highly attractive targets, such as CD166 and CD71. This new class of targets has previously been considered inaccessible to conventional antibody-drug conjugates, given their presence on many normal tissues.

But the Probody platform affords us a unique opportunity to evaluate their clinical potential.

In addition to our wholly-owned pipeline, CytomX has formed strategic collaborations with several leading biopharma companies, including AbbVie, Amgen, Bristol-Myers Squibb and ImmunoGen. I'll cover updates for our collaborations later on today's call, including a discussion around the termination of our 2013 Pfizer alliance, which we announced today.

Now let's turn to our 2017 accomplishments and our 2018 anticipated milestones, starting with our most advanced drug candidate, CX-072, a Probody therapeutic that targets the clinically and commercially validated anticancer target PD-L1.

The PD-pathway is the target of several approved antibody therapies, including Merck's Keytruda, BMS's OPDIVO and Roche's TECENTRIQ and has quickly become a central intervention point for the treatment of a wide range of cancers. At CytomX, we believe the full potential of inhibiting the PD-pathway for the treatment of cancer has yet to be realized, because systemic PD-pathway blockade can result in impairment of normal immune tolerance for healthy tissues and serious and sometimes life-threatening immune-related toxicities can emerge, particularly in combination with other anti-cancer agents. CX-072, our wholly-owned PD-L1 Probody therapeutic, is designed to uncouple anticancer immunity from autoimmune toxicities by inhibiting PD-L1 more locally in the tumor microenvironment, thereby potentially creating new monotherapy and combination therapy opportunities.

In January 2017, we began enrollment of cancer patients in PROCLAIM-CX-072, an ambitious Phase I/II study, evaluating the safety, activity and translational biology of CX-072 as monotherapy and in combination with the CTLA-4 inhibitor, Yervoy or the BRAF inhibitor, Zelboraf. I'd now like to provide an update on the various arms within the study.

Let's start with our evaluation of CX-072 monotherapy, for which we have 3 arms in progress. Part A, our first clinical experience with the Probody platform is a monotherapy dose escalation arm, enrolling PD inhibitor-naive patients in tumor types that do not have an approved PD inhibitor available to them. This arm was designed to provide our first look at the safety profile of CX-072 at various doses and also to provide insight into how the Probody platform behaves in patients, whilst also allowing for the opening of subsequent study arms as dose escalation progressed.

Enrollment to Part A is now complete, and we expect to present a comprehensive summary of data from this arm in mid-2018. Part A2, our second CX-072 monotherapy arm is an expansion of several doses in the middle of the dose escalation range of Part A, in the same patient population with the additional requirements the patients must be positive for PD-L1 and tumor biopsies are mandatory.

We expect to report initial results for Part A2 in the second half of 2018.

The third CX-072 monotherapy arm is Part D, an initial expansion at a single dose level in a cancer type that has demonstrated sensitivity to other PD-pathway inhibitors. We initiated enrollment into this arm in late 2017. Given the competitive nature of PD inhibitor clinical trials, we're not disclosing the specific indication at this time. But right now, we do believe this cancer type could have registrational potential if we further expand this arm at a future time

So in summary, for the CX-072 monotherapy arms, the study is progressing well from an executional perspective, and we expect to be in a position to share data starting with Part A and beginning mid-year.

The combination arms of PROCLAIM-CX-072 were initiated in the second half of 2017 and continue to enroll patients. Part B is assessing CX-072 in combination with Yervoy. Now in contrast to current -- certain current clinical trials where dose levels and schedules of Yervoy are being significantly reduced, we're combining various doses of CX-072 with the full approved label dose of Yervoy of 3 milligrams per kilogram every 3 weeks in this Part B. This protocol also allows for the escalation of the Yervoy dose to 10 milligrams per kilogram, and we expect to present initial findings from Part B in mid-2018.

Part C of PROCLAIM-CX-072 is assessing CX-072 in combination with Zelboraf, the BRAF inhibitor, in PD naive V600E mutated BRAF myeloma patients. In this arm, we're combining CX-072, with -- again, with the label dose of Zelboraf at 960 milligrams twice daily.

Since standard of care for patients with V600E mutated melanoma in the U.S. has evolved to a BRAF inhibitor in combination with a MEK inhibitor, we're enrolling this study outside of the U.S. and primarily in Eastern Europe.

We expect to present initial findings from Part C in 2019.

Now turning to our second wholly-owned program in the clinic, CX-2009. A Probody drug conjugate targeting CD166, an antigen that's broadly and highly expressed in many types of cancer.

CD166 illustrates our approach to the selection of novel first-in-class drug conjugate targets. To avoid unacceptable toxicity, traditional antibody-drug conjugates are limited to targeting those few proteins that are expressed highly in tumors, but that are absent or poorly expressed in normal tissues. Very few cancer-associated proteins have this profile of high expression on the tumor and low expression on normal tissues. Because Probody therapeutics are designed to minimize binding of drugs to normal tissues, we have the opportunity to pursue an entirely new class of targets with attractive features that were previously unsuitable because of expression on normal tissues.

CD166 is an example of this kind of target, and CX-2009 is a Probody therapeutic directed against CD166 and conjugated to the cytotoxic agent, DM4 under license from ImmunoGen.

Enrollment began in 2017 -- in June 2017 in Part A of the PROCLAIM-CX-2009 Phase I/II trial, evaluating the safety in pharmacokinetics of CX-2009 in multiple solid tumor types, that are known to highly express CD166, including non-small cell lung cancer, prostate cancer, cholangiocarcinoma and ovarian cancer.

Enrollment is ongoing, and we also recently began enrolling patients in a second monotherapy arm that we called Part A2 at several doses from the higher-end of the dose escalation range and in the same subset of cancer patients, now selected for the highest levels of CD166 expression.

We're also requiring mandatory biopsies in this arm to inform our translational program, and we plan to present initial data from PROCLAIM-CX-2009 in the second half of 2018.

Our third wholly-owned program advancing towards the clinic is CX-188, a PD-1 targeting Probody therapeutic. As with anti-PD-L1 therapies, PD-1 monotherapy and combinations have been associated with significant toxicities. Our preclinical studies have shown that CX-188 has the potential for an improved safety profile relative to PD-1 antibodies. And given the size of the market and the potential opportunity for differentiated PD-pathway inhibitors, we're progressing development of CX-188 in addition to CX-072.

CX-188 is currently in IND-enabling studies, and we expect to file an IND during the second half of this year.

Now I'd like to turn attention to our Pharma partnerships. Today, we announced that on March 6, 2018, CytomX received notification of Pfizer's intent to terminate our research collaboration option and license agreement. The Pfizer collaboration entered into in 2013, included the selection of up to 4 PDC targets for the treatment of cancer. And this was our first Pharma partnership formed at a time when our platform was very early in its development. The initial target selected was EGFR, which Pfizer had previously discontinued with certain rights reverting to CytomX. The second and third targets were terminated during the first quarter of 2018, and Pfizer had previously declined its option to select a fourth target.

Although we believe that our approach improves the properties of each of the PDCs generated during this collaboration, these PDCs did not meet Pfizer's internal criteria with respect to projected clinical and/or commercial potential to warrant further advancement in the Pfizer pipeline. Pfizer has been very supportive of CytomX over the past 4 years, including leading our Series C financing and investing in our IPO, and we learned a great deal in this collaboration.

We're obviously disappointed that we were not able to advance any of our Pfizer collaboration programs to the clinic, but we do continue to make excellent progress in our other alliances, and I'll now turn to our foundational alliance with BMS.

In the fourth quarter of 2017, BMS initiated a Phase I/II study of a Probody therapeutic version of Yervoy, BMS-986249 as monotherapy and in combination with OPDIVO in advanced metastatic solid tumors.

BMS-986249 is the first program to advance into the clinic under the company's strategic collaboration formed in May 2014. The initiation of this clinical study by BMS reflects the strength of the pre-clinical data package generated by the collaboration teams to date, and IND clearance resulted in a $10 million milestone payment to CytomX, and we're very excited to have this program in the clinic.

Based on early successes in this alliance, during the second quarter of 2017, CytomX and BMS agreed to a major expansion of the collaboration for which BMS paid CytomX a $200 million upfront payment for access to up to 6 additional oncology targets and 2 non-oncology targets.

This broad alliance now encompasses up to 12 targets and up to $4.8 billion in potential milestones and royalties, that are payable to CytomX as and when programs advance through development and towards commercialization.

Turning now to our collaboration with AbbVie, first formed in 2016. The lead program in this collaboration is CX-2029, a CD71-directed PDC. CD71 also known as transferrin receptor 1 is highly expressed in a number of solid and hematologic cancers and has attracted molecular properties for efficient delivery of cytotoxic payloads to tumor cells.

As with CD166, CD71 is a highly attractive target, but to date has been considered inaccessible, and thus, undruggable by conventional antibody-drug conjugates, given its expression and function in many normal tissues.

CytomX is leading the preclinical and early clinical development of CX-2029 and is responsible for filing the IND for the program and generating initial clinical data. AbbVie will lead later development and commercialization with global late-stage development costs shared between the 2 companies.

We and AbbVie continue to make excellent progress with this program. And during the third quarter of 2017, CytomX received a $15 million milestone payment from AbbVie in conjunction with meeting certain criteria, allowing the initiation of GLP toxicology studies for the program.

We expect to file an IND application for CX-2029 in the first half of this year, and to initiate a clinical study shortly thereafter. And lastly, on the partnership front and consistent with our ongoing focus of forming new strategic partnerships, we entered into an important new immuno-oncology alliance in 2017 with Amgen, in the field of Probody T-cell engaging bispecific antibodies or Pro-TCBs. The leading edge of this new alliance is the co-development of a Pro-TCB against EGFR, with CytomX again as in the AbbVie collaboration, leading early development. Amgen will lead later development and commercialization, with global late-stage development costs shared between the 2 companies.

Amgen made an upfront payment of $40 million to CytomX and purchased $20 million of CytomX common stock in association with this new alliance. Further details of the collaboration can be found in our 10-K, and we are very excited about this new alliance and we look forward very much to advancing this novel modality towards clinical studies.

Before turning the call back over to Debanjan, I'd just like to reiterate the impressive continued clinical and operational execution at CytomX. We are now an integrated research and development company with very strong capabilities in the development of novel biologics with 2 wholly-owned programs and 1 partner program now in the clinic. We expect initial data readouts for our first 2 wholly-owned programs this year. We plan to file an IND for CX-188, our PD-1 targeting Probody therapeutic, during the second half of 2018. Through our partnered program with AbbVie, we plan to file an IND for CX-2029 during the first half of this year. In total, by year-end, we expect to have 5 clinical stage Probody programs investigating compelling and potentially differentiated product candidates for the treatment of cancer patients and we are well positioned to continue our momentum and expect that our existing capital resources will be sufficient to fund operations into 2020.

So now I would like to turn the call back over to Debanjan to give a summary of our 2017 results.

Thank you, Sean. Prior to turning the call over for questions, I would like to review selected financial highlights for the year. We ended the year with cash, cash equivalents and investments totaling $374.1 million compared to $181.9 million as of December 31, 2016.

The increase reflects cash provided by operations resulting primarily from the $200 million upfront payment received from BMS for alliance expansion, the $40 million upfront payment and the $20 million of proceeds from stock sold as part of the Amgen agreement, and the $15 million milestone received from AbbVie. These cash receipts were partially offset by cash used to fund operations. As Sean mentioned, our strong balance sheet allows us to fund operations into 2020, assuming no new collaborations or financings.

Research and development expenses were $92.3 million for the year compared to $54.8 million in 2016. The increase in research and development expenses was primarily attributable to additional costs related to our maturing pipeline, along with a noncash charge of $10.7 million of in-process research and development expense recognized related to an asset that we received as part of our Amgen collaboration. And a $10 million onetime sublicense payment made to UCSB, which was triggered by the $200 million upfront payment made by BMS in connection with our expanded collaboration.

With that, operator, we would now like to turn the call over for questions.

(Operator Instructions) Our first question comes from the line of Mohit Bansal with Citigroup.

Maybe if I could ask a couple of questions there. First of all, you mentioned that you will now have data from the Part B of your CX-072 program as well. Could you help us understand that -- so in middle of [now] '18, so could you help us -- and you are looking for -- are you looking for the same venue where you'd present Part A1 data? If you can confirm that?

Yes, Mohit. Good question. You're right. So -- and I think we've said this fairly consistently over the last year that, as we come up on midyear, we would be hoping to present a snapshot of the Part B, and that's still our intention. So as we said earlier, the Part A arm update should be fairly comprehensive by midyear. But we do hope to be in a position to give an initial update or snapshot, if you like, of what we're beginning to see in Part B.

Got it. Thank you. And then, the second one on the data for Part A1, which we are expecting to see in the middle of the year. So could you please help us understand what answers will get from the efficacy point of view? And how we should interpret the data when they become available? Because, the way I understand it, we are looking at tumors, which traditionally do not respond to an anti-PD-1, (inaudible) therapy. And I think biopsy may not be a major part of this Part A1, so if you could help us understand how much data we will have on efficacy? And then, how should interpret -- how should we interpret the data from the target engagement point of view?

Absolutely. And obviously, the first answer to the question is, we'll share the full update midyear. But I do think it's important, and again I think we've been pretty consistent in guiding to first things first, if you like, with Part A1, which is, it's a monotherapy dose escalation. We're looking principally at safety of the Probody. This is the first experience we've had by putting a Probody into cancer patients, and so some very basic questions we are looking to answer, safety, tolerability, some basic platform questions, including how the Probody behaves in circulation. And when it comes to activity, you're absolutely right to point out that the patient population in Part A is not directed or designed to demonstrate efficacy of CX-072, because this is PD naive patients for whom PD agents are not otherwise available. So it will by definition be a varied mix and heterogeneous and late-stage patient population. I think, we've said previously that, any evidence of clinical activity of the Probody in that patient population we would consider upside.

Got it. Got it. And then from the point of view of starting any expansion cohort, if you see any activity, do you see that as a 2018 event or more like a '19 event for this program?

Well, just to clarify that, Part D is, of course, already underway, as we mentioned. And we're not guiding currently on when we would be in a position to present data on Part D. We'll provide additional guidance as the year progresses. It's obviously something that we'll look at as the year progresses also is the potential initiation of additional Part Ds, if you like, depending upon how the data comes out for Part A.

And our next question comes from the line of Christopher Marai with Nomura.

First, just on the Pfizer agreement termination. I wanted to further clarify, I know you had said it was regarding really just platform realignment on their end. Just regarding any of the data that maybe they had access to on your platform, overall? Have they looked at any current clinical data or the Probody technology? Or could you maybe comment further on any of that?

Hey, Chris, good question. Let me be completely clear that Pfizer hasn't seen any of our clinical data. The data that they have access to is data that was generated within the collaboration and additional pre-clinical data that we published in various formats.

Okay. Thank you. And then a quick follow-up. Just regarding the data that we're going to see next from Part A. How much will you be able to really determine regarding next half forward for the asset based on this next readout? Is this something that you'd be expected to provide some color on at the time of the data or will we need to wait more for the Part C and D components of the trials readout?

Yes. It's a little hard to comment right now on that, and we'll provide further guidance as the year progresses.

And our next question comes from the line of Biren Amin with Jefferies

Maybe if I could just start on the Part B for 072. Do you think we can see safety data where we can get readthrough on the value of the Probody?

Hey Biren, the question was on Part D?

Part B.

Part B. Well, obviously, the design of that arm, the combination with AbbVie is to some extent as with Part A. The first question that we're asking there is safety -- is the safety and tolerability of ipi at various CX-072 doses, initially at the label full dose of ipi. So yes, we think the safety from initial safety data from that arm as it emerges has the potential to be quite significant.

Got it. And then as it relates to the Part C with Zelboraf. When can we expect data in 2019, do you think early part of the year versus later? I'm just trying to get a sense on timing there and how is that cohort enrolling?

I don't really want to be any more precise at this point, if you don't mind. As we mentioned on the call, we continue to believe that the clinical question that we're asking there is an important one and a relevant one. We are having to go outside U.S. and principally to Eastern Europe to find the patients, and we are enrolling. It's been a little slower than what we perhaps initially expected. And we just have to see how it goes as the year progresses.

Got it. And then maybe if I could ask a question on 2009, the expansion cohort. Which tumor types are you going into for that expansion cohort? And how was expression or how was expression defined in this cohort?

Yes. So I think you are talking about the A2 cohort. So, again, just to recap. So Part A is monotherapy, 3-plus-3 dose escalation to MTD. Part A2 is exploring the higher-end of that dose range in CD166 positive patients, the same indications. So the same 7 indications that we're selecting patients for the very high expression, which is defined as 3-plus by immunohistochemistry. And we're actually using an in-house developed antibody, an IFC assay, to screen those patients that's the work that we've done ourselves.

And our next question comes from the line of Boris Peaker with Cowen.

My first question is on the 072 plus Zelboraf combo arm. I'm just curious, is the key goal of the study to show that 072 plus Zelboraf doublet combo is better tolerated than the triplet combo with the MEK. And if you so, will you have actually enough patients to make this determination?

Hey, Boris. Again, I would point here to kind of the first-things-first philosophy, where what we know about atezolizumab plus vemurafenib in this patient population is of course that it has tremendous efficacy potential, but it is very, very poorly tolerated. And moreover, it's a clear example where adding PD-L1 blockade on top of another mechanism, in this case BRAF, which is in and of itself relatively well tolerated, you add PD-L1 on top of that and very severe toxicities emerge. So the clinical question is, can we [damp] down that toxicity that does appear to be driven in large part by PD-L1 blockade? Can we damp that down with the PD-L1 Probody? So that -- if we can, we think that's an important platform-proven concept. If that then results in our ability to dose fully in terms of the actual dose or the length -- the duration of dosing to maximize the efficacy potential. There is the possibility that, that efficacy could beat the MEK doublet or could potentially beat the triplet. We don't know. But that's something that we hold out some hope for. But we're really -- it's important to recognize that, that first question that we're asking we think is a very important clinical question to answer.

Got you. And in answering that question, I'm just curious since the subgroup is based on Eastern European patients, how different is the overall standard of care? Would that somehow impact the result versus the U.S. standard of care for these patients?

Well, the standard of care, obviously, is different in the sense that these agents are not available in certain locations, which is how we can actually provide access to our experimental therapies for patients. I don't really want to comment right now any more than that. It's a good question.

Okay. So lastly, for the data from Part A, which we expect in mid-2018, I'm just curious, what would you consider to be a good result, like, what should we as investors set as a kind of a line in the sand?

Yes. I'd just reiterate that it's safety first. It's platform behavior second. And then, anything beyond that we will consider to be upside.

And our next question comes from the line of Mara Goldstein with Cantor Fitzgerald.

I had a question on 2029, the anti-CD-1 Probody drug conjugate. The IND or rather the Phase I, will you include both solid and liquid tumors in that initial IND? And do you anticipate the dosing schedules will be consistent between those 2 tumor types?

Yes, Mara, it's Debanjan. Thanks for the question. We haven't disclosed any details on the clinical plan for 2029. What we've disclosed is, we expect to file an IND in the first half of this year. Obviously, as time progresses, we will describe more about the actual clinical design of that study.

Okay. And if I could just ask on the Pfizer collaboration and the decision against or rather the decision to make the second and third targets that just occurred. What happens then to those targets as well as the EGFR target that was previously returned to you? Do you have current plans for them or will you be entertaining that?

So we get the targets back and can develop Probody drug conjugates against those targets. What we don't get access to are the underlying antibodies that are Pfizer-derived antibodies, and we also do not get access to their linker-toxin technology. But we do get -- those targets are returned and we can move those forward, if that's our choice.

And our next question comes from the line of Robert Driscoll with Wedbush Securities.

Just a general one to begin with. Is there anything different about dosing a PDC versus an ADC, especially with regards to potentially mitigating the off-target tox?

Hey, Robert. The answer is, no. We've -- in fact, it is a good general question, because if, in fact, if we take an even more general question and ask about Probodies in general, we have from the early days of the company, designed Probodies -- Probody drug conjugates and other modalities so that we can dose them on the same schedules as typical -- their antibody, their corresponding -- underlying antibodies. So those scheduled -- those amounts are in the same ballpark. With the PDCs, of course, given that the typical toxicities seen in the clinic are a function principally of payload. What we're exploring with CD166 and CD71 is, first of all, what the MTDs would actually look like for the Probodies. And second of all, approaching or at those MTDs, what the level of activities or molecules would be, but the dosing schedules are very conventional.

Got it. And then just lastly. Just wondered how you're thinking about clinical development of CX-188, the PD-1. Would you do something similarly comprehensive as the CX-072 or fast-track it through development or even offer it up for partnering?

Not -- it's an important question, but we're not providing any guidance on that just yet. We will, as the year progresses.

And our next question comes from the line of Ying Huang with Bank of America Lynch

Sean, maybe going back to the disclosure on the A1 portion in midyear, can you remind us if you can release data of all doses? And also if that's the case, how many patients in total would we see at that point? And then, secondly, as you mentioned, the most important data probably will be on safety. So we can see that from [only marked] PD-L1 therapy. Typically the Grade 3 adverse events rate are maybe somewhere 10% to 15%. What do you think will be considered a clinically meaningful improvement over that?

Ying, good to hear from you. So with regard to number of patients, I think as we guided previously, the A1 dose escalation, again, 3-plus-3 design. The dose range is spelled in our prior poster presentations. And so you can without too much difficulty get to a computation of a number of about 20 to 30 patients based on study design. And we -- when I say that we will present a comprehensive -- our goal is to present a comprehensive overview of that arm, as the data develops in the coming months. Yes, that would include data from the full dose escalation range, that will be our goal. With regards to the safety question. When we think of safety, you're absolutely right, the PD-L1 and/or PD-1 inhibitors are relatively well tolerated compared to, for example, CTLA-4. And I think we've -- I think we've been very consistent in saying over the last year that, we're not necessarily expecting to demonstrate that PD-L1 monotherapy in this initial arm, the Probody monotherapy is substantially safer than the underlying antibody because the numbers are so small and event rate is small. That actually relates -- that relates more to the question that was asked earlier on by Mohit about -- I think about where he was (inaudible) about safety in B1, where the safety signal should be more acute. So when we say safety in A, we're really are talking more about the fundamental safety of this novel platform technology in patients, if you see what I mean.

Ladies and gentlemen, that concludes today's question-and-answer session. So with that, I would like to turn the call back over to Debanjan Ray for closing remarks.

This concludes our call and Q&A session. Thank you very much.

Ladies and gentlemen, thank you for participating in today's conference. This does conclude the program, and you may all disconnect. Everyone, have a wonderful day.