Nektar Therapeutics (NKTR) Q3 2020 Earnings Call Transcript

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Nektar Therapeutics (NASDAQ:NKTR)
Q3 2020 Earnings Call
Nov 5, 2020, 5:00 p.m. ET

Contents:

  • Prepared Remarks
  • Questions and Answers
  • Call Participants

Prepared Remarks:

Operator

Ladies and gentlemen, thank you for standing by, and welcome to the Nektar Therapeutics Third Quarter 2020 Financial Results. [Operator Instructions]

I would now like to hand the conference over to your speaker today, Ms. Jennifer Ruddock, Head of Corporate Affairs. Ma’am, you may begin.

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

Thank you, Crystal. Good afternoon, everyone, and thank you for joining us today. With us on the call are Howard Robin, our President and CEO; Gil Labrucherie, our COO; Dr. Jonathan Zalevsky, our Head of Research and Development; and Dr. Wei Lin, our Head of Development. On today’s call, we expect to make forward-looking statements regarding our business, including clinical trial enrollment and clinical trial results, timing and plans for future clinical trials, timing and plans for future clinical data presentations, the therapeutic potential of our drug candidates, outcomes and plans for health authority regulatory actions and decisions, estimates and predictions of the COVID-19 pandemic’s impact on our business and clinical trials, financial guidance and certain other statements regarding the future of our business.

Because these 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 the Form 10-Q that we filed on August 7, 2020, which is available at www.sec.gov. We undertake no obligation to update any of these forward-looking statements, whether as a result of new information, future developments or otherwise. A webcast replay of this call will be available on the IR page at Nektar’s website at nektar.com. Before turning over the call to Howard, as we are all dialing in from separate locations, I will moderate the Q&A session for our team, so we can avoid technical issues during the session. We appreciate your patience as we work to ensure that there are no technology disruptions for all of those listening.

With that said, I will hand the call over to our President and CEO, Howard Robin. Howard?

Howard W. RobinChief Executive Officer, President

Thank you, Jennifer, and thank you to everyone for joining us on the call today. Over the past quarter, we’ve continued to advance our joint development program for bempeg with our partner, Bristol-Myers Squibb, including the start of two new studies in Q3, a phase III registrational study in adjuvant melanoma patients that Nektar is sponsoring and a new Phase I/II study that BMS is sponsoring, which expands the development of bempeg in renal cell carcinoma with a triplet regimen of bempeg plus nivo in combination with a TKI agent. The bempeg joint development program with BMS now has six separate studies ongoing for our lead cytokine candidate, including five registrational studies. The registrational program for bempeg collectively aims to benefit quite a large patient population across melanoma, renal cell carcinoma and bladder cancer. And this joint development program for bempeg plus nivo reflects a large investment into bempeg, and it underscores the excitement for how this unique and differentiated IL-2 agent may serve as an important backbone therapy with the checkpoint inhibitor, nivolumab, for the treatment of solid tumors.

We’re also advancing our development of bempeg with the checkpoint inhibitor pembrolizumab in the PROPEL study in non-small cell lung cancer, which is one of the largest solid tumor opportunities for bempeg. We are well ahead of our enrollment projections for the PROPEL study, and I’ll let Wei share more about this program — more about the progress that we’ve made in the program in that study in a moment. Next week at SITC, we will present several new data sets from our immune-oncology pipeline, including updated PIVOT-02 data for bempeg in melanoma with more than 30 months of follow-up for those patients as well as the first data for our NKTR-255 program, our IL-15 candidate. As you know, for PIVOT-02, we reported very strong results for bempeg plus nivo in this cohort at last year’s SITC with a high complete response rate of 34%, with 42% of patients experiencing a 100% reduction of their RECIST target lesions. And importantly, we recently reported that after 21 months, the cohort had not yet reached a median PFS. These results led to a breakthrough therapy designation for bempeg and two large Phase III studies in melanoma, one in first-line metastatic melanoma and one in the adjuvant setting. The addressable market opportunity for bempeg in these two areas is quite significant as a reference, combined OPDIVO and KEYTRUDA sales in this setting are approximately $2 billion. We’re excited to share these updated results from the PIVOT-02 melanoma patients next week at SITC.

We continue to be impressed with the efficacy benefit demonstrated by bempeg plus nivo in this study, and we maintain great optimism as we await the Phase III data readout. Our ultimate goal with bempeg plus nivo is to establish a new treatment paradigm in melanoma for the betterment of patients. And Nektar will host an analyst event on November 11 with key oncology experts to discuss these data as well as our additional SITC presentations, and we hope you’ll join us for that discussion. We’ve also recently initiated a second Phase I/II study of NKTR-255, our IL-15 program and the next cytokine in our pipeline. The new trial will evaluate NKTR-255 in patients with solid tumors. This adds to the ongoing Phase I study for NKTR-255 in patients with non-Hodgkin’s lymphoma and multiple myeloma. As a reminder, unlike other IL-15 approaches, NKTR-255 was designed to harness the full biology of the IL-15 pathway, meaning that NKTR-255 is specifically designed to capture all of the receptor-ligand interactions available for targeting the IL-15 agonist pathway. We believe this gives NKTR-255 the ability to act as a significant expander of natural killer cells as well as the ability to promote the survival and expansion of memory CD8+ T cells. Natural killer cell agents are currently gaining great interest as this cancer cell killing mechanism is designed to boost and restore the immune response in patients, which can enable them to more effectively fight their cancer.

For NKTR-358, we presented new data yesterday at the American College of Rheumatology conference, and I know many of you listened to that presentation. Most notably, we observed a dose-dependent increase in T regulatory cells in lupus patients treated with NKTR-358, with a corresponding order of magnitude of reduction in disease symptomology. In Q3, Lilly started a Phase II study in patients with lupus, and they are also planning a second Phase II study in patients with ulcerative colitis. These are in addition to Lilly’s two ongoing Phase Ib studies of NKTR-358 in atopic dermatitis and psoriasis. NKTR-358 is a first-in-class investigational Treg stimulating agents, which is designed to correct an underlying immune imbalance in patients with autoimmune conditions, many of whom experienced reduced numbers and impaired function of their own T regulatory cells. We are very pleased that Lilly is advancing NKTR-358, and we look forward to the continued expansion of this development program. As all of you know, we continue to navigate the evolving COVID-19 landscape, and I’m very proud of our employees who are working hard to ensure the least amount of interruption to our business. To that end, I’m pleased to report that we remain largely on track with our previously discussed trial time lines and were reviewed — that were reviewed on our August financial results call. As I stated earlier, we remain highly focused on the five ongoing registrational oncology studies with bempeg plus nivolumab. These are the first-in-line metastatic melanoma study, the first-line bladder cancer study, the first-line renal cell carcinoma study and the muscle-invasive bladder cancer study and the adjuvant melanoma study. We will provide a thorough review of the entire bempeg registrational program momentarily, but I’d like to mention a few time line highlights from the registrational program for the PROPEL study in non-small cell lung cancer.

We now have three registrational studies for bempeg, where we can see our first data readouts in the same time line. These are the metastatic melanoma study, the cisplatin-ineligible bladder cancer study and the metastatic RCC study. For the metastatic melanoma study, which is being run by BMS, as we previously stated last quarter, because of COVID-19 delays in that study, we expect to report the first data in late 2021 or early 2022. The study has three endpoints: ORR, PFS and OS. These are sequential endpoints, and PFS is the endpoint designed to support a full approval. For the bladder cancer study, we expect a similar time line reporting ORR and the duration of response in the first part of 2022. And for RCC, we expect that our first interim analysis for overall survival around the same time. In non-small cell lung cancer, we are actively enrolling patients into the ongoing PROPEL study of bempeg plus Merck’s pembrolizumab, which is the established standard of care in this setting. These data will inform our strategy for a registrational program for bempeg in first-line non-small cell lung cancer. And there’s been a significant investigator interest in this study, and as a result, we’ve seen a recent increase in patient enrollment. We now expect that we will have preliminary ORR data in the first part of 2021 for approximately 30 patients with a minimum of two scans on treatment from the non-small cell lung cancer cohorts of this study.

You’ll recall that our original thought was that we would have data available for only 10 to 20 patients. So we’re very pleased with the speed of enrollment. We ended the third quarter with a strong balance sheet, with over $1.2 billion in cash and investments and no debt. Our strong financial position allows us to focus on advancing our pipeline of auto-immunocology candidates, including lead cytokine programs, IL-2 and IL-15, which have broad applicability in a wide range of tumor types.

And I will now turn over the call to Wei to review the bempeg development program in more detail.

Wei LinSenior Vice President and Head of Development

Thank you, Howard. I’d like to review the progress and time lines for our bempeg registrational program, which includes five separate registrational studies designed to position bempeg as the standard of care in front-line metastatic and adjuvant settings in melanoma as well as the kidney cancer and bladder cancer. Let me begin with the first-line metastatic melanoma study, which has been run by our partner, BMS. This summer, BMS successfully restarted enrollment activities for the study in many countries. Since then, they have been able to bring more investigational sites online in effort to remedy time lost as a result of the COVID-19 pause. As Howard mentioned earlier, we have received a breakthrough therapy destination for bempeg plus nivo based on the high complete response rate we observed in the first-line melanoma population. In the Phase III study, we have three endpoints: overall response rate or ORR; progression-free survival or PFS; and overall survival, OS.

The first readout will be an interim look comparing the ORR in the doublet arm of bempeg plus nivo to the ORR in the nivo monotherapy arm and will include about 2/3 of the patients in the study who have at least six months of follow-up. This endpoint was designed for a potential early accelerated approval submission for the doublet, which would enable us to bring this innovative therapy to patients more quickly if approved. The application for full approval of bempeg in the U.S. and in Europe will be based on PFS and OS. Because of our high complete response rate, many of you have asked whether we could use this as an endpoint for registration instead of ORR. After discussion with multiple global health authorities, BMS and Nektar have made the decision to leave the current protocol intact with existing endpoints. So this study continues with original three endpoints of ORR, PFS and OS. The original design of the study assumes a median PFS for the nivolumab arm to be comparable to the 6.7 months observed in the CheckMate 067 study. For our study, based upon its original design, the PFS analysis is projected to occur about six to seven months after the ORR analysis. However, PFS is an event-driven analysis and a number of other factors could impact this timing as well, including the time needed to review the data by independent blinded readout review. With respect to the registrational study in first-line metastatic bladder cancer, we reached our enrollment goal in September for the study. As a reminder, the primary endpoints in the study are ORR and duration of response as determined by central radiology review for about 110 metastatic bladder cancer patients who have a confined PD-L1-positive baseline score of 10 or lower, which will serve as a basis for a potential accelerated approval filing.

The duration of response is a critical part — important endpoint in this cisplatin-ineligible patient population because this endpoint was the differentiating factor that led to accelerated approvals for single-agent checkpoint inhibitors in this setting. As compared to a gemcitabine carboplatin combination standard-of-care regimen, for this study, we are planning a minimum follow-up of 18 months to better assess the duration of response. This brings the time line for our first data for this study to the first part of 2022. For the first-line renal cell carcinoma study, we remain on track with our enrollment projections for the study, which means we also expect to achieve the first interim analysis on the primary endpoint of overall survival in the first quarter of 2022, consistent with our prior guidance. Based upon the early guide that generated for bempeg plus nivo in renal cell carcinoma, BMS and Nektar have formulated a comprehensive approach for the development of bempeg in this indication. To this end and as Howard stated earlier, in addition to the ongoing Phase III study, BMS recently started a Phase I/II study in this setting, which includes a tyrosine kinase inhibitor. The new study reevaluated triplet combination of bempeg and nivolumab plus either axitinib or cabozantinib and will then be expanding to a second part, which will compare the triplet of bempeg, nivo plus a TKI to the doublet of nivo plus TKI in patients with RCC. The muscle-invasive bladder cancer study, which has been run by BMS, is enrolling approximately 540 patients who will receive bempeg plus nivolumab or nivolumab monotherapy for a 12-month treatment period following surgery.

The study is actively recruiting patients and more sites have been initiated throughout this year. As this study is longer, we expect the first data readout to be in 2024. Finally, for the adjuvant melanoma study, in Q3, we initiated this important additional Phase III registrational trial well ahead of schedule, and the study is now actively enrolling. As Howard stated, this study provides us with an opportunity to position bempeg as a new standard of care for the treatment of melanoma, and it significantly increases the number of patients that can potentially benefit from this agent. The trial will enroll 950 patients for the 12-month treatment period postsurgery and an endpoint of event-free survival. Initial data from this study are expected in 2024 as well. For PROPEL, our study in non-small cell lung cancer in combination with pembrolizumab, we’ve had great interest in the study from leading thoracic cancer centers in the U.S. and Europe. And consequently, we have surpassed our expected enrollment in the last few months. We now expect that we will have more data for each of the P less than 1%, 1% to 49% and 50% and greater PD-L1 from this study with data from approximately 30 patients who have had two scans or more available in the first part of 2020 from approximately 30 patients who have had two scans or more available in the first part of 2021. Finally, as we noted last week, we have initiated a proof-of-concept clinical study of bempeg for the treatment of COVID-19 patients.

As we now know, the United States continued to hit all-time highs in new daily coronavirus cases. We saw an opportunity to evaluate bempeg to potentially address an underlying phenomenon being observed in patients who go on to have more severe disease. And that is the observation of low baseline lymphocyte counts in these patients that may be a result of a lack of an adequate adaptive immune response to the viral infection. Our first study sites are now open in Texas and Florida with another plant in Pennsylvania at Temple. We’re hopeful that bempeg could provide a unique approach and early intervention to patients who need to generate a more robust T cell response to this virus.

Now I would like to hand the call over to JZ to discuss more on our NKTR-358 and NKTR-255 programs.

Jonathan ZalevskyChief Research and Development Officer

Thanks, Wei. Let me begin with a brief update on NKTR-358. Many autoimmune disorders, including systemic lupus, are associated with decreased Treg numbers, reduced Treg function and/or reduced production of interleukin-2. Treg deficiencies are important in the pathogenesis of these autoimmune diseases. With NKTR-358, our goal is to address these Treg abnormalities and to develop an IL-2-like molecule that could selectively stimulate Tregs in a more effective manner than native IL-2. At ACR yesterday, we shared new data from our Phase Ib study evaluating NKTR-358 in patients with mild-to-moderate lupus. And I’d like to call out a few key takeaways. As we reported at EULAR earlier in the year, NKTR-358 led to a selective, dose-dependent expansion of CD25 bright Tregs. This was maintained through multiple administrations. In the data yesterday, we showed that NKTR-358 resulted in dose-dependent and increased Treg activation markers and genes associated with Treg functionality. For the first time, we also reported on disease activity that was observed in patients treated with NKTR-358. The study enrolled patients with mild-to-moderate disease, and the patients only received three doses of NKTR-358. So it was very short in treatment duration. And in our analysis, we looked at a subset of patients who had moderate disease activity with CLASI-A activity scores that were greater than or equal to 4.

In these patients, NKTR-358 led to a dose-dependent reduction in CLASI-A score from baseline. Notably, patients at all dose levels with NKTR-358 experienced a reduction in CLASI-A, while the placebo patients did not. And seven of 18 patients had a four or more point score reduction by day 43 as compared to their baseline scores. And one patient, at the highest dose level of 24 micrograms per kilogram, experienced a reduction in CLASI-A score from 22 at baseline to five by day 43, two weeks after the last dose of NKTR-358. And this is very exciting. To see that NKTR-358 demonstrated a dose-dependent reduction in CLASI-A composite clinical scores in patients with moderate SLE after only three treatment cycles and complements well what we’re seeing with the PK data for NKTR-358 exposure and the PD data for Treg induction. Overall, we’re very excited about these data at ACR 2020 because we have now demonstrated that in SLE patients, NKTR-358 can produce a much larger magnitude of Treg increase than low-dose IL 2. The effect of NKTR-358 are dose-dependent, and we can detect molecular, cellular and clinical changes in these patients after treatment. The promising results from our Phase I studies of NKTR-358 led to the initiation of planning of a number of studies by our partner, Eli Lilly.

These include two separate Phase Ib studies in atopic dermatitis and psoriasis; the new Phase II study in lupus patients, which started in Q3; and a Phase II study being planned in ulcerative colitis. In the Phase II study in lupus, patients are being randomized to one of three dose levels of NKTR-358 or placebo, and the treatments are given on an every 2-week regimen for a treatment period of 24 weeks. The primary endpoint in the Phase II study is the reduction in the SLEDAI-2K scale. Secondary endpoints include the percent of patients who achieve an SRI-4 response, BILAG-based BICLA response and a level of low disease as defined by the lupus low disease activity state or LLDAS. We will also characterize PK, CD and immunogenicity in treated patients. The endpoints will be measured at week 24, and we expect the study to be completed within 18 to 24 months. Now let’s turn to NKTR-255, our IL-15 agonist program and our next cytokine therapy in clinical development. As Howard stated earlier, the IL-15 mechanism is being recognized by the scientific community as critically important for the engagement of natural killer cell biology in the treatment of cancer. And as you know, this area of research is generating much excitement. NKTR-255 is designed to capture the full biology of the IL-15 pathway because both proliferation of NK cells as well as the expansion of CD8 memory T cell. And this provides us with a wide range of potential development pathways for NKTR-255 in both liquid and solid tumors. And even virology has demonstrated in our early research collaboration with Gilead.

Given NKTR-255’s pharmacological profile, we are advancing forward on multiple fronts with this program. We are currently conducting a Phase I study in patients with relapsed/refractory hematologic malignancy. Although this study enrollment has been a little slower than we’d like because of COVID-19 challenges at Phase I study sites, we have recently brought on new sites, and the study is back on track. We expect to complete the dose escalation monotherapy portion of the study in the first quarter of 2021. After dose escalation, the study will expand into several arms that will evaluate NKTR-255 as a monotherapy in NHL and will also evaluate NKTR-255 in combination with daratumumab in multiple myeloma and in combination with rituximab in NHL. We expect to enroll approximately 60 patients in this part of the study. We are also very pleased to report today that we recently entered into a new drug supply collaboration with Janssen. Janssen will supply DARZALEX FASPRO, their new subcutaneous version of daratumumab, which was approved for multiple myeloma in May of this year, and we look forward to evaluating the combination of NKTR-255 and plus DARZALEX FASPRO in multiple myeloma patients in our ongoing trial. And as mentioned, we expect to open the daratumumab combination cohort as well as the rituximab combination cohort after completing the dose escalation portion of the trial in the first quarter 2021.

We have introduced a robust biomarker program into the Phase I NKTR-255 study, which is measuring its effect on multiple immune cell populations that we know are important for tumor control. We’re especially focused on the expansion of NK cell, analysis of NK cell subsets as well as their activation and function and expansion of CD8 T cells. With initial patients treated in our Phase I study, we have already observed evidence of target engagement of the IL-15 pathway, and we look forward to sharing more details on this next week at SITC. We are also very excited that we recently initiated our second Phase I/II study of NKTR-255 to evaluate the combination with cetuximab in two distinct groups of highly refractory second and third-line patients with metastatic colorectal cancer or metastatic head and neck cancer. The overall study will enroll up to 75 patients and will include a dose escalation component for the combination regimen, which will then be expanded into dedicated expansion cohorts for head and neck and colorectal cancer. We’re building significant momentum with the NKTR-255 program, and we look forward to presenting early translational data from the initial dose escalation cohorts in our first-in-human Phase I study at SITC next week.

With that, I will now turn the call over to Gil for a review of the financials.

Gil M. LabrucherieChief Operating Officer and Chief Financial Officer

Great. Thank you, JZ, and good afternoon, everyone. On this call, I will review our 2020 financial guidance. Starting with our strong financial position, we ended the quarter with $1.2 billion in cash and investments and no debt on our balance sheet. We still plan to end 2020 with over $1 billion in cash and investments. Now turning to our annual financial guidance. Our full year 2020 GAAP revenue projection remains between $140 million and $145 million. This includes $50 million of milestone payments from BMS and $90 million to $95 million of royalties, product sales and other revenue. Under the BMS collaboration, we recognized a $25 million milestone for the start of the muscle-invasive bladder cancer study in Q1 and recognized a second $25 million milestone related to the start of the adjuvant melanoma study in Q2. For our GAAP R&D expense guidance, we now anticipate 2020 GAAP R&D expense will range between $415 million and $425 million, which includes approximately $60 million of noncash depreciation and stock compensation expense.

This decrease in our R&D expense forecast is a result of a number of factors, including the timing of R&D expenditures for certain of our earlier-stage and non-oncology programs due to COVID, lower-than-projected noncash stock compensation and depreciation expense, and reduced travel and other costs due to the impact of the COVID-19 pandemic. Our G&A expense for 2020 is still projected to be between $105 million and $115 million, which includes approximately $45 million of noncash stock compensation and depreciation expense. Finally, due to the impact of the COVID-19 pandemic on the financial markets and lower-than-expected yields on our investment portfolio, we now project that interest income will be approximately $20 million for 2020. Importantly, we have not experienced any significant realized or unrealized losses on our portfolio of investments. We continue to closely manage our operating expenses and remain highly focused on the execution of our broad portfolio of research and development programs. And as I stated earlier, we still plan to end 2020 with over $1 billion in cash and investments.

And with that, I’ll open the call to questions. Operator?

Questions and Answers:

Operator

[Operator Instructions] Our first question comes from Peter Lawson from Barclays. Your line is open.

WaleedBarclays — Analyst

This is Waleed [Phonetic] on for Peter. Thank you for taking my question. Just a question here on your PIVOT study in frontline melanoma, just how we should be thinking about the bar here for efficacy? What would be considered positive results in your pivotal data that could help support approval?

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

Thanks, Waleed. Wei, I’m going to ask you to answer that.

Wei LinSenior Vice President and Head of Development

Yes, sure. I think the way we kind of look at this data is really looking at the control arm, which is the standard care right now is the nivolumab. And so our comparator is set up very well and it’s well recognized worldwide and would serve as a basis for worldwide registration. So our registrational strategy really is — it’s a 2-step process. One is we’re going to aim for accelerated approval based on ORR, and then followed by a full approval based on progression-free survival with subsequent supplement by overall survival. So it’s really looking at these two benchmark numbers. So nivolumab in this setting, the baseline response rate is around 40%. So we would like to clear that with ORR. That’s roughly 10% to 15% higher than response rate of nivolumab single agent. I think then we can demonstrate unequivocally in a statistically significant fashion that we have a superior response rate compared to nivolumab. So that, together with durable response and the safety profile, that will be the final package that will enable a third approval for — based on ORR.

Now subsequently, the progression-free survivor, PFS, which would allow us to gain full approval will be, not only a second shot at goal, but also a potential conversion if we were to gain third approval based on ORR. And that will be benchmarked against the six to seven months PFS that’s been observed historically for nivolumab in this setting. And so as many of you will recognize that we’ve been generally early phase data in PIVOT-02 and specifically with regard to our melanoma cohort, the patients who were enrolled in that cohort have actually experienced fairly phenomenal benefit from the combination of bempeg plus nivolumab with. I think at the last prior earnings call, with even 21 months of follow-up, we have not reached the median progression-free survival. So at the upcoming SITC, we’ll be providing even further update with longer follow-up. And so all of us are certainly very encouraged by the data from PIVOT-02. And if the Phase III registrational study were to be able to replicate the data from PIVOT-02, then we should have a fairly significant margin improvement in PFS compared with nivolumab single agent. And that would bring huge value in extension of survival for patients with first-line metastatic melanoma.

WaleedBarclays — Analyst

Great. Thank you for taking my question.

Operator

Our next question comes from Alexander Duncan from Piper Sandler. Your line is open.

Alexander DuncanPiper Sandler — Analyst

Hi. Thank you for taking my question. One on bempeg and one on 255. So for bempeg, the recent uptake in PROPEL enrollment is great to see. Just curious to understand the dynamics here a little bit more if you can elaborate on that. Is this largely due to discontinuation of the nivo-bempeg trial? And secondly for the 255 monotherapy, dose escalation update at SITC, what safety signals are you paying particularly close attention to? And then whether or not you identify the MTD, how are you going to use the 255 monotherapy biomarker data to inform safe-dose selection to use with the combination cohorts? I guess my question here is what’s your confidence that the combination of 255 and RITUXAN, for example, won’t potentiate an adverse event such as infections and liver mets. Thank you.

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

Thanks, Alex. Wei, I’m going to ask you to answer the first part of the question about the PROPEL study. And then, JZ, I’ll ask you to take the second one. Thank you.

Wei LinSenior Vice President and Head of Development

Yes. Thanks. Yes. So PROPEL study, as you know, is a study that we hope that would actually engage registration study in first-line non-small cell lung cancer. And to that end, we’re trying to generate data, currently with the doublet of bempeg plus pembrolizumab, building upon the foundation of pembrolizumab as the current standard care in PD-L1-positive patients. So right now, with the COVID pandemic happening, everyone has experienced challenges in enrollment. And our study team has really navigated this extraordinarily well. As we have shared earlier in an earlier earnings call with the PROPEL study, while we were planning to open the sites in both Europe as well as in the U.S., we had some challenges because the first wave of pandemic in Europe coincided with our plan to initiate the sites. But we were very vigilant in both working with the sites, finding out the best time to open the sites. And while initially we had a delay in opening the sites in Europe, but as soon as the first wave of pandemic passed, we’re able to get our sites up going, and the enrollment has been really, really brisk. I think that just reflects — while pembro has really brought a huge improvement in overall survival for patients suffering from non-small cell lung cancer. Its benefit is still limited with monotherapy to about two years or so.

So there’s still a tremendous need for these patients for better improved therapy and especially for things that are chemo-sparring. And hence — and that’s reflected by how well this study has enrolled after we have gotten the sites in the U.S. and in Europe up and going. So we’ve seen a gradual improvement for the combination and also is reflecting the need that the doctor continues to see in spite of the pembro monotherapy being a wonderful established standard of care to really build upon that and really improve that and extending patient’s life in its indications. So we’re certainly enthused about the study, enthused about the data we’re able to deliver next year and also the potential — the data and evaluating the possibility of a Phase III to follow up on that data analysis.

Jonathan ZalevskyChief Research and Development Officer

Thanks, Wei. And Alex, thank you for the question. So regarding 255, so as you know, this is the first-in-human study. And in the dose escalation part, we’re taking patients with pretty advanced disease, either non-Hodgkin’s lymphoma or multiple myeloma and treating them with escalating doses of NKTR-255 delivered intravenously. Now what we’re looking for in terms of the safety signals are things that both were informed from our preclinical toxicology and other studies but also what we know experience-wise from the groups of involvement in others that have also used IL-15 as an agent clinically. So we’re looking for those same kinds of effects. We’re studying key cytokine-related toxicities and adverse events. We’re looking at secondary cytokines, which are essential because, of course, we expect IL-15 agonism of cells that express IL-15 receptor complexes to induce cytokine responses. And we’re also studying the downstream cellular dynamics associated with IL-15. And as you know, it can have a lot of homeostatic effects. So you were asking if the MTD in the study has been reached, and it did not. We’re still dose escalating.

And we have a very rich biomarker program that we can use to inform dose selection. And this is, again, a page of the playbook that we played, for example, with bempeg where we have a lot of markers that assess the target engagement of IL-15 with its receptors. And you can assess that, both in the national killer cell compartment in terms of cellular response changes, activation, functional changes of the cells as well as their subsets as well as in the CD8 compartment, and then you can assess that both in the blood as well as in secondary tissues as well. So we use all of those things to inform our dose selection and give us a very, very clear confidence that we have engaged target or getting the kind of pharmacodynamic response that we want. So then when we identify a go-forward recommended Phase II dose for the expansion cohort, you’re absolutely right. We’re going to pay a lot of attention to what happens when we combine either of daratumumab or rituximab. And in that case, as you know, these are both antibodies that have an IgG1. They’re are also antibodies that are known to have something like a tumor lysis syndrome. It can be seen when you have a very rapid lysis of B cells, for example, with rituximab, when it clears them so quickly, with clearance either through the liver or through the spleen in the fixed tissue cells.

So we’ll be looking very closely at those things. We’ll be looking very closely at the cellular changes and also monitoring the patients very, very closely to ensure that we’re not seeing any kind of adverse events of the combination because, in fact, we try to do the exact opposite, which is substantially improve cell clearance not just in the blood compartments, but particularly in the secondary lymphoid compartments where these tumors reside.

Alexander DuncanPiper Sandler — Analyst

Thank you for answering my question.

Operator

Thank you. And our next question comes from Jessica Fye from JPMorgan. Your line is open.

Daniel WolleJPMorgan — Analyst

This is Daniel for Jessica Fye. Thank you for taking my question. Staying with 255, you stated that you’re going in colorectal cancer in head and neck initially in solid tumors. Can you help us think about the opportunity of 255 in solid tumors? Why you’re able to choose those two different tumor types? And then do you see combination as an ideal approach for this program as you advance it forward? Or is there an opportunity to evaluate it as a monotherapy as well?

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

Yes. Thanks. Wei, I’m going to ask you to take that.

Wei LinSenior Vice President and Head of Development

Sure. Yes. So we really see tremendous opportunity in solid tumors for — in IL-2 agents like 255 because now monoclonal antibody has become the standard of care in cancer, in general, but both in heme and solid tumors. And in fact, one of the first-approved monoclonal antibody in any cancer type was Herceptin in HER2-positive breast cancer. So there’s a long history, a tradition of monoclonal antibody analysis become well-established standard of care in many, many tumor types. And as we think about how to develop 255 within the solid tumor space, we really look at which are the indications where the usage of a monoclonal antibody still remain not in first line but in later line and whether standard of care is still — leaves a lot of room for improvement. And that’s what really threw us to really cetuximab in the indication of head and neck cancer as well as colorectal cancer. Specifically in head and neck cancer, for quite a while, cetuximab initially was approved as monotherapy in a late-line setting but eventually moved to the first-line setting based on the EXTREME trial. And then the regimen of cetuximab plus platinum chemotherapy plus 5-FU have become in standard of care in head and neck cancer in the first-line setting for quite a while until more recent times when pembrolizumab plus chemotherapy has improved upon that standard of care. And then — so then the use of cetuximab had returned back to a later-line use monotherapy. And with that change, it creates an opportunity to really improve upon the late-line benefit that the cetuximab really brings. If you take a look in the late-line setting, cetuximab as monotherapy only has about a 15% response rate.

And so that obviously leaves a lot of room for improvement. And MOA of our 255 molecule is really to expand the NK cells, which are so critical in executing the ADCC activity of these monoclonal antibodies, including cetuximab. So the MOA strongly supports the hypothesis that addition of 255 by expanding the NK cell population would significantly enhance the activities of ADCC antibody like cetuximab and improve upon the 15% response rate in late-line head and neck cancer. So that’s sort of the rationale we decided to pick cetuximab as one of the — in head and neck cancer as one of the first indication to pursue. In addition, a similar kind of situation plays out in colorectal cancer. Now worldwide, colorectal cancer is a much bigger disease. Now the — cetuximab use, it’s somewhat divided. So to a large extent, cetuximab is either used in first-line or second-line setting together with a chemotherapy regimen. It’s full fury. Now but in some centers as well as some investigators use cetuximab as a single agent as well. So due to the variety of different use, we also saw an opportunity to really combine with cetuximab as a single agent in combination with 255 to improve upon the benefit that single agent has. And again, it’s in the 15% range in terms of single-agent activity in colorectal cancer in a later-line setting. And were we to be successful there, it leaves room for us to move into an earlier line setting, where it’s in combination with chemotherapy as well.

So I think now it’s — because both head and neck and colorectal cancer offers opportunity to leverage the monoclonal antibody ADCC MOA and has well-established standard of care in use in a later-line setting and with the efficacy bar that leaves tremendous room for improvement, those were the reasons where you kind of take these indication and pick cetuximab as a combination partner to start out with. Now if we generate the proof of concept with cetuximab in head and neck cancer or in colorectal cancer, that would allow us to move forward after demonstrating this proof of concept based on this MOA to expand the combination to other ADCC-based monoclonal antibodies in solid tumor as well as the generation data in heme allowing us to move forward in heme malignancies as well. So — and to build upon that, and I think 255 really has huge potential and improve upon the current standard of care, which is in wide use of ADCC monoclonal antibodies that cover so many different tumor types.

Daniel WolleJPMorgan — Analyst

Thank you for answering my question.

Operator

And our next question comes from George Farmer from BMO Capital Markets. Your line is open.

George FarmerBMO Capital Markets — Analyst

Hi, good afternoon. Thank you for taking my question. Wei, can you comment a bit on what the bar for success would be in PROPEL? 30 patients that are basically going to be distributed among different PD-L1 subgroups, are you expecting to see any differences there? And I know 30 patients is a good number to hit, but it’s spread across all these different subgroups. It might get a little thin per subgroup. And then, JZ, I know there was some discussion about this yesterday. But could you talk about the significance of the CLASI-A score and how that relates to SLEDAI score in lupus and how we can think about the two different scoring systems?

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

Thanks, George. Wei, do you want to?

Wei LinSenior Vice President and Head of Development

Sure. Yes, I’ll take the first part of the question. Yes. Thanks for that great question. So it’s something we’ve thought a lot about because that the registrational goal decision is an important decision for development of any drug. For bempeg, in particular and for the PROPEL study, as you well know that the current standard of care really segments that population in the first-line metastatic non-small cell lung cancer population into three subgroups. And that’s less than 1% of PD-L1 expression, 1% to 49% and 50% above. And then we have either early phase data or registrational data that we can use to benchmark against the historical numbers that pembrolizumab has in each of the subpopulations. So first of all, looking at the population of less than 1%, pembrolizumab as a single agent-based on the early phase data really had a response rate of 7% to 8%. So really in the single-digit range in the 5% to 10% range, and that’s what we expect. Right? So that’s a benchmark for that population of patients. For the 1% to 49%, the response rate is typically hovering around 17% or so from past trials, specifically KEYNOTE-042.

And so we’re really looking at a benchmark of pembrolizumab in that population patients of 1% to 49%, ranging about 15% to 20% response rate. And then finally, the benchmark for the 50% above PD-L1 expression subgroup, looking at data from KEYNOTE-024 as well as 42, we’re looking at the numbers that are really in the 40% to 50% range. So that’s the baseline response rate for monotherapy pembrolizumab. So I think to your point, because of these subgroups, we have — when we do generate the 30-plus patient worth of data, we’d be looking at data by segmenting into each of these subgroups. And this would help us to really understand fully how our drug works and also help us to design our registrational study. So I think what we — now the registrational study for a doublet of pembro plus bempeg, pitting that against pembrolizumab monotherapy, will be limited to the 1%-above population because pembro mono is not approved in less than 1%. However, I think the less than 1% data generating from PROPEL will be extremely informative because I think IL-2 being known as a proinflammatory cytokine is expected to inflame the tumor. As we have shown in our early phase data from PIVOT-02 on treatment biopsies, for instance, in our bladder cancer trial, we were able to demonstrate that seven out of 10 patients who previously was PD-L1 negative, meaning PD-L1 expression less than 1%, we’re able to convert to PD-L1 positive after treatment, just one cycle treatment of bempeg.

And so the — I think if this is where we really hope to be able to see similar phenomenon in non-small cell lung cancer in the PROPEL study. And hence, while the pembro monotherapy is approved in a broad spectrum of patients, I think probably the subgroup that would be most informative to us will be the less than 1% as well as the 1% to 48% — 1% to 49% because, number one, those benchmarks are low; number two is those benchmarks are actually fairly low, such that if we demonstrate a cyclical improvement of, say, a doubling of the response rate, then we know that the bempeg as a molecule has really followed through its MOA as we have seen in other tumor types of inflaming the tumor especially in the PD-L1 low expressing or at the nonexpressing tumors to really engage and inflame the tumor, allowing that to be sensitive to a checkpoint inhibitor, such as pembrolizumab. So we’d be definitely looking at the data in a very nuanced way, dissecting out each subgroups and interpreting them separately and looking for really robust signals that will allow us to have confidence that we have a combination of bempeg plus pembro that can significantly improve upon the benefit that pembrolizumab monotherapy is delivering to patients in first-line non-small cell lung cancer. Thanks.

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

And JZ, do you want to take the CLASI-A versus SLEDAI question that…

Jonathan ZalevskyChief Research and Development Officer

Yes. George, thanks for the question. So you asked about the CLASI versus SLEDAI kind of how they’re related. And so to start off with the CLASI is a score that specifically zeros in on the cutaneous manifestations of lupus disease, so really looking at the skin. It’s not directly linked to the psoriasis SLEDAI, but we always use CLASI along with those other instruments because we use them to characterize lupus patients. But there is one important connection, and remember, lupus patients are characterized by their secondary organ involvement, and the SLEDAI as well as BILAG, they both take into account the additional accessory tissues. And since these are multicomponent scales, you get scoring ranging of everything from the presence or absence of autoantibodies to the presence or absence of secondary organ involvement and then the subcutaneous lupus that will contribute to the SLEDAI score. So there is a level of relationship. Now we really focused in on it because we know that there is a really good long-standing biology about Tregs and Treg action, particularly in the skin. You know that with Lilly, we are currently in the process of two Phase Ib studies that focus on dermal application, right? So there, we’re treating patients in one study with atopic dermatitis; and in another study, we’re treating patients with psoriasis.

And even if you remember from David’s presentation yesterday, he showed that low-dose IL-2 showed quite a bit of efficacy in patients with psoriasis and other skin diseases because he showed that large table of phenotypes of patients treated in TRANSREG study. So really, we’re both extremely excited and encouraged that we saw dose-dependent reduction in CLASI. The effect was really quite pronounced. As you saw one patient that was enrolled in the study had a pretty severe skin evolving with the 22-score baseline. And that patient had a 17-point reduction in their CLASI over the course of treatment. That patient was enrolled at the highest dose level of NKTR-358. So it’s a very encouraging piece of information, and it’s very, very consistent with the dose-dependent relationship we see in Tregs, and it’s one of the main reasons why we’re so excited that we’re now in the Phase IIb dose-range finding study with Lilly. That study began just a couple of months ago in the summertime, and it’s currently enrolling patients. And a second Phase II study is around the corner as well in ulcerative colitis and additional ones will follow next year. Thanks, George.

Operator

Thank you [Operator Instructions] And our next question comes from Difei Yang from Mizuho. Your line is open.

Alex BouillouxMizuho — Analyst

Hi. Good afternoon, everyone. This is Alex on for Difei. Thank you for taking my questions. And apologies if this was addressed already, but quick question on non-small cell lung cancer and bempeg combo with pembro. Assuming you show positive data here in the upcoming readouts, what would be the strategy going forward? And would there be an opportunity to pursue kind of an accelerated pathway to approval?

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

Thanks, Alex. Wei, I’ll ask you to comment again briefly on that.

Wei LinSenior Vice President and Head of Development

Sure. Yes. So I think — I mean it’s a great idea. It’s certainly something that we would be willing to interest in for — with the health authorities. Now the — historically, in the first-line setting, there has not been an example of accelerated approval based on just a response rate, certainly not — with exception of like a TKI such as [Indecipherable] so it’s something that we will have to explore with the health authorities, and it really depends on the robustness of the data we generate from PROPEL.

Operator

Thank you. And our next question comes from Arlinda Lee from Canaccord. Your line is open.

Arlinda LeeCanaccord — Analyst

Hi. Thank you for taking my questions. Sorry about that. On 358, given the potentially broad applicability of the Treg mechanism that you’re [Indecipherable] presented yesterday, I’m kind of curious about how you guys chose the first two indications. And is there a sense to explore others as well?

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

Thanks, Elanda. JZ, I’m going to ask you to answer that.

Jonathan ZalevskyChief Research and Development Officer

Yes. Arlinda, great question. So about the indications for Treg. So there’s definitely very large realm of autoimmune indications in chronic inflammatory diseases where you can consider the Treg mechanism. And it kind of sort of breaks apart into some of the different pathobiologies. So one of the key reasons why we focused on SLE as the first indication is that’s a disease that has a very clear and characteristic dysfunction in the Treg compartment. So those patients have, especially as they get more severe in the disease progression, they have both a drop in Treg levels, and then the Tregs that have recovered from those patients are far less suppressive so they’re much less functionally active. Now if you also remember, David talked about T follicular helper cells yesterday. Tregs antagonize those cells and T follicular helper cells are the main T cells that drive the germinal cellular reaction, which leads to antibody production, which in autoimmune diseases is really detrimental because it leads to autoantibody production. And in those same patients that have a drop in Treg, they have an expansion of T follicular helper cells. So that was one of the very strong reasons why some of those early studies in the earliest cases of treating lupus patients with low-dose IL-2 specifically to reduce a Treg increase in those patients led to some of the very encouraging results that have been reported. And that’s now been replicated in multiple studies.

But low-dose IL-2, you can really only achieve so much of a Treg normalization. So really with NKTR-358, we can reach far, far higher levels of Treg elevation and sustain those levels for much longer periods of time than is possible with low dose IL-2. So that’s why this is a key lead indication for us. Second indication is ulcerative colitis. And actually, this is very interesting because you see as also another disease that’s highly known to be characterized by Treg biology, and this is biology, it’s a gut access, where you have a lot of Treg function associated with the lamina and other kinds of compartments where you’re regulating pathologic T cell responses in that disease. And unlike a disease like lupus, which has autoantibodies, disease like UC has much less, but it has underlying chronic inflammation with pathogenic T cells. And here, we know that Tregs can restore those pathogenic T cell responses. It’s also very notable, Arlinda, that the earliest discovery of the FoxP3 cell, the cell that was originally coined T suppressor cell but later learned to be a Treg, actually came from studies in EAE, which is the mouse model of UC. So it’s a very, very important related — and also TNBS as well.

So it’s very, very, very nice correlation that links to that. And then beyond these two lead indications, we’re also evaluating with Eli Lilly, a number of other indications. In the collaboration that we struck with Lilly, Lilly will be running four Phase II studies, of which the first one has started. And the second one was just recently announced just yesterday and getting covered today with UC. And so there’ll be two other studies that are starting, and we’ll see more of those coming next year. We’ll be sampling different indications. So it will be different than these first 2. And we’ll really be focusing in all of the places where Treg biology and intervention with 358, we would expect scientifically to have a very strong effect of controlling the disease. Thank you.

Operator

Thank you. Our next question comes from Jay Olson from Oppenheimer. Your line is open.

Jay OlsonOppenheimer — Analyst

Hi. Thank you for taking my questions. And congrats on the 358 update yesterday. I had a question about, it seems like a dose-dependent increase in NK cells. And I was wondering how you would interpret those findings.

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

JZ, I’ll ask you to take that.

Jonathan ZalevskyChief Research and Development Officer

Yes. Thanks, Jay, for the question. So we do observe low-level increases in NK cells. And we only really observed that at the highest dose level tested, 24-microgram per kilogram dose level. Now it’s also important to note that what we presented yesterday was we dove into the NK subsets. And so there are several, but the two primary types that occur in humans are the CD56 bright, CD16 dim subset. These are the ones that cannot participate in ADCC. They cannot bind to Fc because they lack the CD16 receptor. And then there’s the CD56 dim, CD16 bright. And the 16 dim — sorry, the 56 dim, 16 bright are the majority of the NK cells in the body. They’re also the ones that are the most hyperactive, and they possess the CD16, so they bind Fc and antibody receptors. And what you saw in our presentation is we saw very little change in that compartment, where we saw the majority of change in the 56 bright, 16 dim. And actually, a lot of scientists consider those to be like regulatory NK cells. And why they’re coined that way is because we don’t secrete killer cytokines or inflammatory cytokines in response to stimulus. So they’re almost a kind of cell that is the opposite function that you have with the traditional NK cells. So that’s one important component.

That’s why we presented that data, Jay, to show the delineation and that this is really a subset-specific effect. The other important point is that what we learned is very consistent with what’s been known and studied with the use of IL-2 throughout many historical uses. So we’ve always seen that, that 56 bright, CD16 dim subset is much more sensitive to IL-2 than the other NK subset. And we’ve also seen the same NK cells elevated in multiple studies of low dose IL-2 and not just the studies from David Klatzmann lab, even in Kohn Koreth’s studies in chronic graft-versus-host disease patients. We also saw an expansion of NK cells, only the 56 bright subset. And they really haven’t led to any sequela. So it’s something that we’ll be following in all of our studies because obviously, in Phase II, we will be going to a much longer treatment duration. And so we’ll be studying that very, very closely. But so far, it doesn’t look like that seems to have any clinically negative significance at all.

Operator

Thank you. And our next question comes from Paul Choi from Goldman Sachs. Your line is open.

Corinne JenkinsGoldman Sachs — Analyst

Hi. This is Corinne Jenkins on for Paul. I was hoping you could talk a little bit about your strategy in melanoma. I think you’re going to have potentially a combination in adjuvant but also two separate combinations in metastatic melanoma. I was just hoping you could talk a little bit more about how you think about all of those kind of in the same indication.

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

Yes. Thanks, Corinne. Wei, I’m going to ask you to comment on this. Thanks.

Wei LinSenior Vice President and Head of Development

Sure. Yes. Maybe can you elaborate what you mean by two different combinations in metastatic?

Corinne JenkinsGoldman Sachs — Analyst

Bempeg, next week. So I was just hoping, pending obviously positive data, but how would you think about development and kind of how those combinations worked together in that market?

Wei LinSenior Vice President and Head of Development

Sorry, I didn’t catch the first part of what you were saying.

Corinne JenkinsGoldman Sachs — Analyst

Wei, With the SITC data of NKTR-262 and bempeg, plus your ongoing bempeg plus nivo studies in metastatic melanoma, how are you thinking about that?

Wei LinSenior Vice President and Head of Development

Right. Right. So yes. So the 262, right now, the patient population being addressed is in the post IO setting, so relapsed/refractory to IO versus the bempeg plus nivo combination that is really being developed in the first-line metastatic melanoma. So the — I think — so the thinking there is really in the first-line setting, we’re trying to improve upon the standard of care, which is the nivolumab single agent build on top of that by introducing a combination doublet of bempeg plus nivolumab and really displacing nivo as standard care in that setting. Now after the patient who has failed IO therapy in the first-line setting, whether it be check inhibitor or PD-L1 plus a CTLA-4 combination, I think those are the patients being — really being addressed with the two combinations that are currently in our REVEAL study. That’s the 262 program. These two combinations are the 262 molecule, which is a toll-like receptor 7/8 in combination with bempeg, or the second combination is a triplet of 262 plus bempeg plus nivolumab. So that’s a triple combination. And either combination is really designed to address a patient who have progressed on a checkpoint inhibitor in the first-line setting, whether the addition of a toll-like receptor agonist, which would ignite the innate immunity. Because, so far, I think if you think about whether you’re talk about CTLA-4 or you’re talking about a PD-L1 agent or you’re talking about a bempeg agent, which is IL-2 targeting T cells, all of these are really trying to harness the body’s adaptive immunity in the fight against cancer.

And the 262 agent and any toll-like receptor agent is really going the other side, really try to trigger immune response — trying to trigger adapting immunity through the activation of innate immunity first. So — and I think there’s been some data with other toll-like receptor agents that seem to indicate that’s a viable strategy to really reignite the immune response and really to pull in the adapting immunity by first engaging and activating the innate immunity to these intratumor injection of toll-like receptor agonist. So — and I think what our strategy is really unique on is really, while the 262 or toll-like receptor strategy is being done by others as well, we have the unique opportunity to add an IL-2 agents like bempeg to really additional — provide the additional boost to that immunity. So really, you get an enhancement of the immune response that’s associated with checkpoint inhibitors like nivolumab, and you get a double enhancement on the one hand with a toll-like receptor agonist such as 262, so really trying to inflame the tumor and the immune response by activating the innate immunity. And on the other hand, you’re also adding an agent like bempeg, which really enhances adapting immunity.

So with this combination, it’s I think one of the unique combinations that only Nektar can really do that really leverages and trying to activate the immune response in an IO relapsed/refractory setting by activating both the adaptive as well as the innate immunity. I hope that helps to answer your questions.

Operator

And that does conclude our question-and-answer session for today’s conference. I’d now like to turn the call back over to Howard Robin for any closing remarks.

Howard W. RobinChief Executive Officer, President

Well, thank you, everyone, for joining us today. And I’d like to first thank our incredible employees for their continued hard work and tireless efforts during these challenging times. Their dedication to advancing our clinical studies while keeping our business on track to make me especially proud. As I stated earlier, we’re well positioned with a strong balance sheet, a maturing portfolio of immuno-oncology and immunology programs, and we thank our shareholders for their ongoing support and look forward to continuing to provide you with updates on our progress. And please join us at our analyst event on November 11. And lastly, we sincerely hope that you and your families stay safe and healthy throughout the coming months. So thank you very much for joining us today.

Operator

[Operator Closing Remarks]

Duration: 74 minutes

Call participants:

Jennifer RuddockSenior Vice President, Strategy and Corporate Affairs

Howard W. RobinChief Executive Officer, President

Wei LinSenior Vice President and Head of Development

Jonathan ZalevskyChief Research and Development Officer

Gil M. LabrucherieChief Operating Officer and Chief Financial Officer

WaleedBarclays — Analyst

Alexander DuncanPiper Sandler — Analyst

Daniel WolleJPMorgan — Analyst

George FarmerBMO Capital Markets — Analyst

Alex BouillouxMizuho — Analyst

Arlinda LeeCanaccord — Analyst

Jay OlsonOppenheimer — Analyst

Corinne JenkinsGoldman Sachs — Analyst

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