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Calithera Biosciences Inc (NASDAQ:CALA)
Q3 2019 Earnings Call
Nov 12, 2019, 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 Calithera Biosciences' Third Quarter 2019 Earnings Conference Call. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question-and-answer session. [Operator Instructions]

I would now like to hand the conference over to your speaker today, Jennifer McNealey, VP of Investor Relations. Thank you, and please go ahead, ma'am.

Jennifer McNealey -- Vice President of Investor Relations

Thank you, Chris. Good afternoon, everyone. Welcome to our third quarter 2019 conference call. Joining me today are Susan Molineaux, our Founder, President and CEO; Keith Orford, Chief Medical Officer; and Stephanie Wong, Senior Vice President of Finance.

We have issued our press release, and it can be accessed through our website at calithera.com.

Before we begin, I'd like to remind you that today's discussion will include statements about future expectations, plans and prospects that constitute forward-looking statements for the purposes of the Safe Harbor provisions under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those in the risk factors discussed -- in the Risk Factors section of our quarterly report on 10-Q filed with the SEC.

In addition, any forward-looking statements represent our views only as of today, and should not be relied upon as representing our views of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so even if our views change. Please note that this call is being recorded.

And with that, I'll turn the call over to Susan.

Susan M. Molineaux -- Co-Founder, CEO, President & Director

Thanks, Jennifer. Good afternoon, everyone, and thank you for joining us today on our third quarter 2019 conference call. At Calithera, we are building an integrated biotechnology company that develops novel small molecule oncometabolism drugs, drugs that are targeting tumor and immune cell metabolism pathways for the treatment of cancer and other diseases. By building a pipeline of novel therapeutic product candidates, we are creating multiple opportunities to positively impact clinical outcomes for patients and drive development programs toward commercialization.

We are the first company to take a selective glutaminase inhibitor into the clinic and the first to demonstrate clinical activity in cancer patients. Based on the compelling results for the ENTRATA study in renal cell carcinoma, which we presented at the European Society for Medical Oncology or ESMO Meeting in September. We believe we have demonstrated proof of concept for the treatment of renal cell carcinoma.

We have now fully enrolled to telaglenastat CANTATA trial, a study with registration potential in renal cell carcinoma patients. This moves us a step closer to becoming a commercial biotechnology company. We are pleased with the enrollment of CANTATA ahead of schedule, and we are grateful to the investigators and patients who helped us exceed our enrollment goal. We are on track to report top line efficacy and safety data from the trial in the second half of 2020. In parallel, we are making the necessary investments in key areas, such as regulatory, quality and manufacturing to ensure access for patients and a successful product launch if telaglenastat is approved.

Our arginase inhibitor INCB001158 or 1158 is the first arginase inhibitor to enter the clinic. Arginase is an immunosuppressive enzyme expressed by immune cells in the tumor microenvironment. At the ESMO Meeting, the first efficacy data for this compound were presented in an oral session. In this study we were evaluating 1158 as a monotherapy and in combination with pembrolizumab, a PD-1 inhibitor.

We are pleased that we observed responses in microsatellite stable, or MSS, colorectal carcinoma, a disease that has been shown historically to be virtually unresponsive to PD-1 and PD-L1 inhibitors. We're pleased with the progress of this program as we seek to develop a first-in-class product for patients with multiple types of solid tumors.

Beyond telaglenastat and 1158, we have a broad pipeline and a productive R&D team. We remain focused on producing novel drug candidates with the potential to be highly differentiated new therapies in areas of unmet need. This quarter we announced a new program targeting IL4I1. IL4I1 is an enzyme with phenylalanine oxidase activity, primarily expressed by tumor cells and antigen preventing cells, and produces hydrogen peroxide, which is an inhibitor of T-cell function.

IL4I1 expression has been correlated with poor outcomes in several tumor types, it has a potential role in immune invasion and may decrease the ability of checkpoint therapy to stimulate an anti-tumor response -- immune response. IL4I1 expression is elevated in multiple tumor types with particularly high expression in ovarian and B-cell tumors. We have developed an investigational first-in-class, potent and orally bioavailable IL4I1 inhibitor. Preclinical data were presented at the Society for Immunotherapy of Cancer or SITC last weekend, and demonstrated that our novel small molecule inhibitor of IL4I1 has single agent anti-tumor activity in syngeneic mouse tumor models and augments the activity of checkpoint inhibitors. We are excited for this new target, and look forward to updating you on the progress of this program.

Also with the SITC meeting, we presented preclinical data on CB-708, our oral small molecule CD73 inhibitor. CD73 is an enzyme that synthesizes the immunosuppressive agent, adenosine, and is over-expressed in multiple tumor types. We remain interested in the adenosine pathway and our timing for entering clinical development will depend in part on partnership discussions that are ongoing.

And with that I will pass the call over to Keith for an update on clinical programs.

Keith Orford -- Chief Medical Officer

Thank you, Susan. Let's begin with a more detailed update on telaglenastat, our glutaminase inhibitor and our most advanced product candidate. We are currently focused on forging a clinical and potentially commercial path for telaglenastat in renal cell carcinoma. In the quarter, we announced completion of enrollment of CANTATA, a global randomized double-blind trial of telaglenastat in combination with cabozantinib, in second and third line RCC patients. CANTATA enrolled 445 patients ahead of schedule, demonstrating the significant unmet need for advanced RCC patients in the second and third line setting. CANTATA is designed to evaluate the efficacy and safety of telaglenastat in combination with cabozantinib versus placebo plus cabozantinib in clear cell RCC patients, who have previously received one or two prior lines of therapy, including at least one prior anti-angiogenic agent or the ipilimumab-nivolumab combination.

Patients are being randomized in a 1:1 ratio to either telaglenastat plus cabozantinib or placebo plus cabozantinib. Patients who are stratified by IMDC risk category and prior treatment with anti-PD-1, PD-L1 therapy. The primary endpoint is progression-free survival by independent review. Overall survival will be assessed as a key secondary endpoint. The trial has the potential to serve as a registration trial, and we remain on track to report top line results of CANTATA in the second half of 2020.

The ENTRATA data were presented at ESMO in Barcelona in September. ENTRATA is a small-randomized, double-blind trial, which was designed as a proof-of-concept study to evaluate the efficacy and safety of telaglenastat in combination with everolimus. To summarize the results presented, the trial enrolled 69 advanced clear cell RCC patients, who had been previously treated with at least two prior lines of systemic therapy, including at least one VEGF receptor-targeted tyrosine kinase inhibitor. Patients were randomized to either telaglenastat plus everolimus, or placebo plus everolimus. The primary endpoint is investigator-assessed progression-free survival. Overall survival is a secondary endpoint.

The statistical design reflected the studies -- the small study size and was appropriate for a proof-of-concept Phase 2 study. The patients enrolled were heavily pretreated, poor prognosis population with a median of three prior lines of therapy for advanced metastatic disease, including 70% with two or more prior TKIs and 88% having received prior PD-1 or PD-L1 therapy.

When added to everolimus, telaglenastat doubled the median PFS to 3.8 months as compared to 1.9 months for everolimus alone, and reduced the risk of disease progression or death by 36% for hazard ratio of 0.64 with a p-value of 0.079 one-sided. The secondary endpoint of overall survival is not yet mature. We believe the ENTRATA trial demonstrates proof of concept for telaglenastat in the treatment of RCC.

Late last year, we announced two new clinical trial collaborations to evaluate Pfizer's CDK4/6 inhibitor palbociclib also known as IBRANCE and the PARP inhibitor talazoparib, also known as TALZENNA, each in combination with Calithera's glutaminase inhibitor, telaglenastat. Each of these combination protocols are now open and enrolling patients into the dose escalation cohorts.

We also believe telaglenastat has the potential to be developed in patients with NRF2/KEAP1 mutations. Multiple in vivo preclinical models have demonstrated that activation of this pathway through a loss of function KEAP1 mutation or a gain of function NRF2 mutation accelerates tumor formation and spread. In addition to making tumor models more aggressive, the activation of the NRF2/KEAP1 pathway in these models also makes them sensitive to the inhibition of glutaminase activity by telaglenastat.

An NCI-sponsored study testing this hypothesis is currently ongoing in solid tumors. Recently presented clinical data demonstrate that activation of this pathway, either through the loss of KEAP1 function or activation of NRF2 results in very poor outcomes in non-small cell lung cancer patients receiving front-line standard of care chemotherapy or chemoimmunotherapy. Based on these recently presented data and the unmet need in this population, we are designing a randomized Phase 2 trial in lung cancer patients, which we expect to begin in the first half of 2020.

Next, the arginase program. INCB001158, also known as 1158, is an investigational first-in-class immuno-oncology metabolic checkpoint inhibitor targeting arginase, an immunosuppressive enzyme secreted by myeloid-derived suppressor cells, or MDSCs, to block T-cell activation in tumors. A 1158 is being developed with Incyte in a co-development, co-commercialization collaboration. The 1158 data were presented at ESMO in September.

In this study, 1158 is being evaluated as monotherapy and in combination with pembrolizumab across eight cohorts of patients with different types of metastatic or locally advanced cancers not amenable to local therapy. A dose escalation with monotherapy to find their recommended Phase 2 dose of 1158 was followed by expansion in three cohorts, non-small cell lung cancer, colorectal cancer and the basket of solid tumors. Following the dose escalation of 1158 in combination with pembro, eight cohorts were expanded. Four enrolled patient populations that were PD-1 naive and four enrolled patient populations that were PD-1 refractory. PD-1 refractory patients had to be on a checkpoint inhibitor based therapy and failing to derive benefit at the time of study entry, which means that they had active disease progression or prolong stable disease without a[Phonetic] response.

The colorectal monotherapy and MSS colorectal combo cohorts advanced to Simon stage 2, and data on both cohorts were presented at ESMO. The PD-1, PDL-1 naive had a NK[Phonetic] cohort has also advanced to stage 2 and is actively enrolling. As the colorectal cohorts were the most mature at the time of data cut off, they were the focus of the presentation.

First, the combination colorectal data. Among 43 responsive valuable MSS colorectal patients, who had received a median of three prior therapies, three patients achieved a confirmed partial response. The response rate of 7% compares favorably to the historical overall response rate of zero to 1% in second and third line MSS CRC patients treated with checkpoint inhibitor therapies. Two of the three responders were ongoing at the time of data cut-off with a duration of response of 2.4 plus and seven plus months respectively. The third responder had a duration of response of 6.7 months.

The six month PFS rate for the cohort was 20%, which compares favorably to six month PFS rates observed in patients treated with single agent checkpoint inhibitors. We were also pleased to see increases in total intratumoral CD8 positive cells, following treatment with 1158 plus pembrolizumab in MSS colorectal cancer patients with the increases occurring most notably among those patients that derive clinical benefit.

Now the monotherapy results. 1158 inhibited plasma arginase activity at all doses, and induce dose-related increases in plasma arginine, including a mean threefold increase at the recommended Phase 2 dose of 100 milligrams BID. Among 33 response of valuable MSS colorectal cancer patients, one patient treated with 1158 alone achieved a confirmed partial response lasting seven months and one patients achieved stable disease lasting seven months. Both of these patients progress on their immediately preceding line of therapy in less than six months. The overall disease control rate for the monotherapy MSS CRC cohort was 27%.

A second ongoing clinical trial is evaluating 1158 in combination with three different chemotherapy regimens, FOLFOX, gemcitabine/cisplatin or paclitaxel, in patients with ovarian, endometrial, colorectal, gastroesophageal and biliary tract cancers. An additional trial in multiple myeloma patients, treating patients with 1158 plus daratumumab or daratumumab alone is also ongoing. We are pleased with the progress of this program, and we continue -- and we look forward to additional data updates from the 1158 program in the future.

We are also developing an arginase inhibitor outside of oncology. CB-280 is a novel arginase inhibitor in the -- in development for the treatment of cystic fibrosis. Under our collaboration agreement with Incyte, we retained worldwide rights to develop arginase inhibitors in specific non-oncology, rare disease indications, including cystic fibrosis. Arginase has been proposed to be critical in the pathophysiology of cystic fibrosis and several other non-oncology diseases.

CF patients have neutrophil infiltrates in their lungs, and these neutrophils secrete high levels of arginase. High arginase activity depletes arginine, which in turn depletes nitric oxide. Nitric oxide, or NO, is known to have potent antimicrobial activity and has been shown to improve lung function when administered to CF patients. We hypothesize that inhibition of arginase with CB-280 can restore normal arginine and NO levels, and improve lung function in CF patients, a concept that is supported by previous proof-of-concept clinical trials.

Earlier in the year, we initiated a Phase 1 clinical trial. This first-in-human Phase 1 trial, evaluating the safety, tolerability and pharmacokinetic profile of oral CB-280 in healthy volunteers is now successfully complete. A Phase 1b clinical study in CF patients, which is expected to start enrollment in the first half of 2020 will test multiple doses of CB-280 compared to placebo in approximately 30 adults CF patients to determine a safe dose range for CB-280 in CF patients.

Patients with any CFTR mutational status will be eligible for the study. Patients will receive CB-280 or placebo for 14 days, lung function as well as sputum microbes will be evaluated. A dose-finding expansion of this study is planned in which additional cohorts of patients will receive different doses of CB-280, or placebo for 28 days in order to select the optimal dose of CB-280. For the entire study patients will continue their existing therapies for CF, including CFTR modulators.

With that, I'll pass it over to Stephanie for an update on our financials.

Stephanie Wong -- Senior Vice President of Finance and Secretary

Thank you, Keith, and good afternoon everyone. Detailed financial results for the third quarter 2019 were included in today's press release. I will briefly review our results on this call.

Calithera ended the quarter well capitalized following our secondary offering in June, where we raised gross proceeds of $58 million. We believe our cash position enables us to drive our clinical programs to meaningful value inflection point. Cash and investments were $133.6 million at September 30th, 2019. Research and development expenses were $17.2 million for the third quarter 2019, compared to $16.4 million for the same period in 2018. The increase from 2018 to 2019 was primarily due to the telaglenastat program, including for the CANTATA trial, which completed enrollment in the third quarter.

General and administrative expenses were $3.9 million for the third quarter 2019 compared to $3.1 million for the same period in 2018. The increase of $0.8 million primarily related to higher professional services and personnel related costs. Net loss for the third quarter 2019 was $20.3 million or $0.38 per share.

And with that, I will now return the call back over to Susan.

Susan M. Molineaux -- Co-Founder, CEO, President & Director

Thank you, Stephanie. And with that, operator, we're happy to open the line for questions.

Questions and Answers:

Operator

Thank you. [Operator Instructions] And our first question comes from the line of Jonathan Chang with SVB Leerink. Your line is now open.

Jonathan Chang -- SVB Leerink -- Analyst

Hi, guys. Thanks for taking my questions. First question. In the prepared remarks, I thought I heard something on the business development front. Was this in reference to CB-708? Did I hear that correctly? And can you elaborate on this?

Susan M. Molineaux -- Co-Founder, CEO, President & Director

We just mentioned that the clinical trial time line for CB-708 will be dependent in part on ongoing conversations with partners.

Jonathan Chang -- SVB Leerink -- Analyst

Got it. Any color you can add to, I guess, what a potential partnership could look like? Or what you guys are interested in getting from a potential partner?

Susan M. Molineaux -- Co-Founder, CEO, President & Director

I think you can reference our partnership with Incyte. We were very happy to share clinical development costs in order to take our arginase compound into cancer patients. And we feel that program targeting CD-73 has some of the similar aspects and could benefit from a partner at this point.

Jonathan Chang -- SVB Leerink -- Analyst

Got it. Second question on the ENTRATA study, when could we see a survival update?

Keith Orford -- Chief Medical Officer

Yes. So we -- as we've talked about before those data are not yet mature, and we'll continue to follow those data and provide an update when it's available. And just historically, what we've done is to kind of give an announcement on that when it's been accepted into a meeting. And we would expect that to happen sometime in 2020.

Jonathan Chang -- SVB Leerink -- Analyst

Got it. Thanks for taking my questions.

Operator

Thank you. And our next question comes from the line of Mohit Bansal with Citi. Your line is now open.

Chan -- Citi -- Analyst

This is Chan on for Mohit. I have one for Susan. Based on the comments that enrollment for CANTATA was ahead of schedule. Can you maybe share how the pace or cadence events have trended thus far? Or maybe what are the puts and takes for data to be unveiled in 3Q versus 4Q next year?

Susan M. Molineaux -- Co-Founder, CEO, President & Director

So this is an event-driven trial. So after the last patient is in, which happened obviously in third quarter, we're just counting events. And so -- and we see in this certain number of events, we then go ahead and analyze the data. So we can't give guidance more than the second half of next year, because it's event-driven and we don't know what that pace of events will be.

So this is a trial design with cabozantinib as the control arm. And while the populations have changed since then because of new therapies, I can just comment that the historical PFS for cabozantinib alone in second line patients -- were primarily second line patients was 7.4 months. And that's an anchoring number. But we cannot predict what the cabozantinib PFS will be in our current population accurately because again therapies have changed and the population has moved.

Chan -- Citi -- Analyst

Thanks, Susan. I have one more for Keith maybe. Keith, I was looking through the slide deck that was -- that came out in October. It looks like you guys compared CD8 level responders for 1158. But have you guys also taken a look at T-cell exhaustion markers like increased TIM-3 or LAG-3 levels? Couple of studies have linked higher TIM-3 with non-response?

Keith Orford -- Chief Medical Officer

Yes. That's a great question. So to-date, our biomarker program is really focused on CD8 positivity. We don't have a more extensive report although[Phonetic] there's interest in looking more exhaustively at a number of markers maybe using multicolor immunofluorescence. So those are things that are in the plan to do, but we haven't done to-date.

Chan -- Citi -- Analyst

Thanks guys. That's it for me.

Keith Orford -- Chief Medical Officer

Okay.

Operator

Thank you. And our next question comes from the line of Matt Phipps with William Blair. Your line is now open.

Matt Phipps -- William Blair -- Analyst

Good afternoon. Thanks for taking my question. So interested on the NRF2/KEAP1 mutation trial. You mentioned a randomized Phase 2 starting next year. But can you give us details on the trials? Is that second line? Is that versus chemo? What's the -- any additional term design you guys have yet?

Keith Orford -- Chief Medical Officer

Yes, so the design is -- will be announced when we're -- when we've actually announced the opening of this study, so we can give more detail at this point. I think it's worth noting though that just looking at the data that have been presented in terms of the prognosis for these patients receiving standard of care therapy as early as frontline, they do very, very poorly. So one could imagine a study as early as frontline given that -- those poor outcomes, but that's something we can provide more detail on when the study is opened.

Matt Phipps -- William Blair -- Analyst

Okay, Keith. And have you guys seen any data from that NCI study?

Keith Orford -- Chief Medical Officer

No, that data -- that study is just getting started. So we don't have any data at this point.

Matt Phipps -- William Blair -- Analyst

Got it. And Keith also on CB-280, do you have any kind of data maybe for preclinical 708 oral therapies as systemic small molecules having enough concentration like as humongous as helium. How do you look at that when you trying to select dosage for the CF patient trial?

Keith Orford -- Chief Medical Officer

Right. Yes, so from our preclinical data, I mean, we -- the drug is highly soluble and distributes well within animals. So we have every reason to expect that we will be able to achieve sufficient exposure. I think it's worth noting that in patients -- CF patients, who were treated with high levels of oral or IV arginine, there were positive effects on lung function as well as on NO production in that setting. And so, in that case at least arginine is able to get into the right place and we would expect CB-280 will be as well.

Matt Phipps -- William Blair -- Analyst

Got it. Thanks, Keith.

Keith Orford -- Chief Medical Officer

Thanks, Matt.

Operator

Thank you. And our next question comes from the line of Jim Birchenough with Wells Fargo Securities. Your line is now open.

Nick -- Wells Fargo Securities -- Analyst

Good afternoon, it's Nick in for Jim this afternoon. Just a quick one on CANTATA. Is there any opportunity for an interim review now that the trial is fully enrolled?

Keith Orford -- Chief Medical Officer

No. Hi, Nick. We -- the study was designed without an interim. Given the speed of enrollment and the time line for the readout, there was really no opportunity for an interim to impact, for example, for the enrollment. So the first read of the data will be when top line results in the second half of 2020.

Nick -- Wells Fargo Securities -- Analyst

Okay. Thank you. And then, I noticed ASH, there's going to be data from the MD Anderson Group or Telaglenastat in MDS. I noticed looking at the abstract clearly the data appear quite positive. But how do you think of these data? And do the data support continued development in MDS?

Keith Orford -- Chief Medical Officer

Yes. We think the data are very interesting. And those are data that we continue to discuss with them through the collaboration. So, no plans at this point as to -- we have nothing to announce at this time, but we do agree that the data are very interesting.

Nick -- Wells Fargo Securities -- Analyst

Okay. And then I had a question on [Indecipherable] in osimertinib trial combining telaglenastat and osimertinib in EGFR-mutated cancers. Do you have any insight into the potential timing of data from that trial? And can you just educate us on what the overlap is between EGFR mutations and the KEAP1 mutations?

Keith Orford -- Chief Medical Officer

So, in terms of the timing, unfortunately SITC is a great mechanism in order to generate data through -- in collaboration with NCI, but the timing is something that's out of our control. So we expect from what we've heard that it will enroll at a reasonable rate, but it's something that -- it's tough for us to provide any real guidance around.

In terms of the mutations, they can coexist or they can be coincident, but they're not -- I would say that the NRF/KEAP mutations tend to be somewhat less frequent in EGFR mutant patients. So I wouldn't expect that that would be a great source of data to kind of provide insight into the NRF/KEAP hypothesis. But I mean there has been a recent publication that EGFR mutant patients do poorly. Their prognosis is poor if they also have activation of that pathway. So it does happen and it does continue to look like a poor prognosis factor, but the frequency is somewhat less than you'd expect by chance.

Nick -- Wells Fargo Securities -- Analyst

Okay. Thank you. And then moving to 1158 if I may. I believe that at the ESMO Meeting, you've indicated that the squamous cell head and neck had also achieved the target to the Simon 2 stage. When do you think you'll be able to present the data from that head and neck cohort?

Keith Orford -- Chief Medical Officer

Yes, so that cohort has moved to Stage 2. So, it passed the first bar, which was to go from Stage 1 to Stage 2. And that continues to enroll currently. So, I think the timing for presenting those data is hard to say. We want to let the data mature to a reasonable extent, and particularly with an I/O therapy we'll we want to see the durability of those data. So -- but we expect to be able to present those data at some point in collaboration with Incyte.

Nick -- Wells Fargo Securities -- Analyst

Okay. And then on the microsatellite stable CRC, I think you had indicated really that given the level of activity probably you need a biomarker to move forward. Has there been any progress on thoughts what that biomarker might be?

Keith Orford -- Chief Medical Officer

Right. So, yes, given the -- what we've seen so far, we think it's encouraging evidence of activity. But I think for a true development path, we would need to really be able to better identify the subset of patients that are deriving value or likely to derive value. Those efforts are -- remain ongoing. So, nothing to report at this point in terms of the development of a new biomarker, but that's certainly an active project.

Nick -- Wells Fargo Securities -- Analyst

Okay. Great, thank you very much.

Keith Orford -- Chief Medical Officer

Yes. Thank you.

Operator

Thank you. And our last quarter comes the line of Sean Kang with H.C. Wainwright. Your line is now open.

Sean Kang -- H.C. Wainwright -- Analyst

Hi, thank you for taking my question. This is Sean for [Indecipherable] H.C. Wainwright. I just have a quick one regarding R&D expense. I noticed that there was about like 18% decline in R&D expense for this quarter compared to second quarter 2019. Would you say this is more of an like temporary decline considering you guys are planning like clinical studies next year?

Susan M. Molineaux -- Co-Founder, CEO, President & Director

Hi, Sean. Thanks for the question. I can't -- we haven't really commented on trends from quarter-to-quarter. I can tell you that in March we gave cash guidance of $75 million to $85 million, and that contemplated the CANTATA enrollment of 445 patients. So, what you're seeing is not really something specific that I can comment on, but the cash guidance is something that we are aligned to.

Sean Kang -- H.C. Wainwright -- Analyst

Okay. That's good enough. That's all for now. thank you.

Operator

Thank you. And this concludes today's question-and-answer session. I would now like to turn the call back to Jennifer McNealey for any closing remarks.

Stephanie Wong -- Senior Vice President of Finance and Secretary

Thank you, Chris, and thank you all for joining us today. And have a great evening and feel free to reach out to us for follow-up questions if you have anything that we didn't cover today. Thank you.

Operator

[Operator Closing Remarks]

Duration: 33 minutes

Call participants:

Jennifer McNealey -- Vice President of Investor Relations

Susan M. Molineaux -- Co-Founder, CEO, President & Director

Keith Orford -- Chief Medical Officer

Stephanie Wong -- Senior Vice President of Finance and Secretary

Jonathan Chang -- SVB Leerink -- Analyst

Chan -- Citi -- Analyst

Matt Phipps -- William Blair -- Analyst

Nick -- Wells Fargo Securities -- Analyst

Sean Kang -- H.C. Wainwright -- Analyst

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