Enliven Therapeutics Inc (ELVN) 2020 Q2 法說會逐字稿

Ladies and gentlemen, thank you for standing by and welcome to the Imara, Inc. Q2 earnings conference call and webcast. At this time, all participant lines are in a listen-only mode. (Operator Instructions). Please be advised that today's conference is being recorded. (Operator Instructions) I would now like to hand the conference over to your speaker today, Mike Gray, Chief Financial and Chief Operating Officer. Thank you. Please go ahead, sir.

Okay. Thanks, Gigi. Good morning, everyone, and welcome to Imara's second quarter 2020 conference call. I'd like to begin by reminding everyone that various statements that we make during this conference call about the company's future expectations, plans, and prospects constitute forward-looking statements for purposes of the Safe Harbor provisions under the Private Securities Litigation Reform Act of 1995.

Actual results or events could differ materially from those expressed or implied by these forward-looking statements as a result of various important factors including those set forth in the Risk Factors section of our most recent quarterly report on Form 10-Q that we filed with the SEC this morning and any other filings that we may make with the SEC.

Any forward-looking statements made on this call represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so even if our views change. Therefore, you should not rely on these forward-looking statements as representing our views as of any date subsequent to today.

With that, I'll turn the call over to Imara's President and CEO, Rahul Ballal. I'll return following the whole discussion to review our second quarter financial results, and then we'll open the call for questions. Rahul?

Thank you, Mike. Good morning, everyone, and thanks for joining our second quarter 2020 conference call. The second quarter was a productive time for Imara as we made significant progress across the business and accomplished several of the key objectives that we set for ourselves in 2020. Most notably, we initiated our Phase 2b trial for the treatment of patients with sickle cell disease, known as the Ardent trial as well as our Phase 2b trial for the treatment of patients with beta-thalassemia known as a Forte trial.

We've activated multiple clinical sites and have been screening patients in each of these trials. And despite the challenges with COVID-19, I'm pleased to report that we dosed the first patient in the Ardent trial for sickle cell disease yesterday. We've also continued to progress our ongoing clinical trials, including our Phase 2a trial of adult patients with sickle cell disease as well as our open label extension or OLE trial, which allows patients from the Phase 2a trial to continue into a four-year study to evaluate the long-term safety and tolerability of IMR-687.

I'll spend some time on this call reviewing preliminary data from this open-label extension trial, which we publicly disclosed today for the first time. Our Phase 2a interim data was previously presented at the EHA Annual Congress in June. We also made important progress on the regulatory front over the last few months as we were granted Orphan Drug, Fast Track, and Rare Pediatric designations by the FDA for the treatment of patients with beta-thalassemia. We believe that these are important designations as we continue to develop the development of IMR-687 for this disease.

We also made significant progress on our advocacy and community support efforts, having announced the first program under our real impact community support initiative during the second quarter. This program, which includes grant funding to support non-profit, community-based organizations serving patients and families impacted by sickle cell disease and beta-thalassemia awarded 25 grants of approximately 5,000 each to each community base organization in 13 states.

The grant funding was increased by 25% from original plans due to the particularly strong demand for COVID-19-related relief. Advocacy and community support are both important to Imara's core mission, and we expect that we will continue and expand the real impact initiatives going forward.

I would now like to spend a few minutes updating you on our Phase 2a trial in sickle cell disease and then take a deeper look at interim data from two patients from our Phase 2a open-label extension trial. Beginning with the Phase 2a, we presented interim results for IMR-687 in adult patients with sickle cell disease at the virtual EHA Annual Congress in June.

In the higher dose cohort, where patients started a 100 milligram per day for three months and were then dose escalated to 200 [milligram] a day for three months, IMR-687 monotherapy showed a statistically significant increase in F-cells, which are red blood cells containing fetal hemoglobin as well as a dose-dependent increase in fetal hemoglobin levels.

We believe that this data provide important proof-of-concept for the potential for IMR-687 to be developed as an oral, once-a-day, disease-modifying treatment for sickle cell disease. We completed enrollment of this clinical trial during the first quarter of 2020 and expect to report top-line data from the Phase 2a trial in the fourth quarter of 2020. We are also conducting a four-year open-label extension clinical trial, which allows patients completing the Phase 2a to enroll in a long-term safety and tolerability study of IMR-687.

The OLE trial was initially designed, so the patients were administered a daily dose of 100 milligram of IMR-687 and in the second quarter of 2020, a protocol amendment increased that daily dose to 200 milligrams. If patients were on a HU and the Phase 2a trial, they continued on the same dose of HU for the OLE trial. As the Phase 2a trial nears completion, we have seen increased enrollment in the OLE trial, with six of eight currently enrolled patients having started the OLE since the beginning of June.

We plan to analyze data from the OLE patients at approximately six month intervals, and two patients have already crossed that threshold to date. I will summarize data on these patients next. Patient number one, completed one year of treatment on the OLE trial in June of 2020. This patient was originally randomized to the monotherapy sub-study of the Phase 2a trial and received 100 milligram/200 milligram of IMR-687 for six months through May 2019. The patient then transitioned to the OLE trial in June of 2019 after a pre-specified washout period of about a month.

As of June 2020, the patient has been on IMR-687 for 18 months, six months as part of the Phase 2a trial and one year as part of the OLE trial. This patient is not on HU therapy. We examine this patient across clinical outcomes in sickle cell disease associated biomarkers. For VOCs, we compare the 18-month period while the patient was on IMR-687 to the patient's medical records for the 18 months prior to IMR-687 use. In the 18 months prior to IMR-687, the patient reported 38 VOCs versus 17 during the 18 months of IMR-687, which is a 55% decrease on IMR-687.

Specifically, reported VOCs that resulted in emergency department visits decreased by 55% from 22 to 10 events and reported VOCs that led to outpatient visits dropped 50% from 14 to 7 events. [The] reported VOCs that resulted in hospitalizations decreased from two in the 18 months period prior to IMR-687 to zero during the 18 months on IMR-687. We also look more carefully at the patients reported VOCs during the [18-month] span the patient has been on IMR-687.

In the first six months of this 18-month period, the patient reported nine VOCs. In the next six months, the patient reported six VOCs. And in the last and most recent six months, the patient reported only two VOCs. Additionally, VOCs that resulted in emergency department visits dropped from five in the first and second six-month periods to zero in the most recent six-month period.

As defined in the trial protocol, patients on the OLE trial are administered the ASCQ-Me questionnaire at the 12 months visit. ASCQ-Me is an independent, NIH-validated sickle cell questionnaire that reports patient outcomes across emotional, social functioning, pain, stiffness sleep, pain episode frequency, and pain episode severity domains.

This patient completed the questionnaire and showed improvement in five of the seven domains when compared to ASCQ-Me scores at the start of the Phase 2a trial. This included improvement in two key measures, pain episode frequency and pain episode severity. There was no change from baseline in the social functioning domain. And the emotional domain score was the only domain score to worsen when compared to the baseline Phase 2 trial measurements.

But we also observed improvement across sickle cell associated biomarkers in the first patient. when comparing the patient lab values from the most recent OLE visit to the patient's baseline lab values at the start of the Phase 2a trial, we observed an absolute increase in F-cells of 20.2% points, an absolute increase in HbF of 3.9% points, and also saw hemoglobin increase by 1 gram per deciliter.

There were also improvements across markers of hemolysis, namely decreases in percent reticulocytes, absolute reticulocyte count, indirect bilirubin, and LDH. A table detailing this biomarker data is included in the 10-Q we filed this morning. I will now turn to patient 2. Patient 2 completed six months on the OLE trial in August. This patient entered the Phase 2a trial as part of the hydroxyurea or HU combination arm and was randomized the placebo dose group, and thus never received IMR-687 as part of the Phase 2a trial. The patient has remained on stable dose of HU since initiation of the Phase 2a trial and while on this OLE trial, which started 14 months after completing the Phase 2a.

We also examined this patient across clinical outcomes and sickle cell associated biomarkers. For reported VOCs we reviewed medical records prior to and during the OLE period. During the six-month period prior to the OLE trial and while on a stable dose of HU, the patient had 15 reported VOCs that required outpatient visits. During the six-month period on the OLE trial and while on combination HU and IMR-687, the patient had zero VOCs.

In addition to observing zero VOCs we also saw an improvement across sickle cell associated biomarkers in the second patient. When comparing to lab the patient's lab values from the start of the OLE trial to the most recent visit in July 2020, we observed an absolute increase in upsell percentage of 21.2 points and an absolute increase in HbF percentage of 9 points.

Specifically, the baseline HbF increased from 20.7 to 29.7 during the OLE study. We also saw an increase in hemoglobin of 0.8 grams per deciliter. As with patient 1, there were improvements across markers of hemolysis, namely decreases in percent reticulocytes, absolute reticulocyte count, indirect bilirubin and LDH. A table detailing this biomarker data is included in the 10-Q we filed this morning.

We do caution that this data is based upon only two patients at specified intervals in the OLE trial and reported VOCs for the comparative periods prior to the treatment of IMR-687, are based on a review of the patient's medical records and thus is not a statistical approach. However, we are encouraged by the potential value of longer-duration IMR-687 administration in these patients.

I would now like to turn to the Phase 2b Ardent trial in patients with sickle cell disease. We initiated the Ardent trial during the second quarter. And despite COVID-19 challenges, we are very pleased to have announced yesterday that the first patient was randomized and dosed in this study.

In addition to the activated sites, we have progressed regulatory submissions seeking approval to conduct the Phase 2b trial in 13 countries and believe that we are laying the foundation of the global footprint in which the study will operate. The Ardent Phase 2b will enroll approximately 99 patients with sickle cell disease and is a double-blind randomized trial where patients will be stratified by use of hydroxyurea as well as by [region].

We are utilizing weight-based dosing to maximize exposure across a wide range of patient weights, resulting in doses that include 300 milligram and 400 milligram. Recall that 200 milligram was the top dose in our Phase 2a trial and this trial tests higher doses and extended duration with IMR-687. The planned primary efficacy endpoint is to evaluate the proportion of patients with fetal hemoglobin response, defined as an increase of HbF of 3% or greater from baseline to week 24 versus placebo, and the trial is powered for statistical significance for this endpoint.

Patients will continue on treatment through 52 weeks to provide data for planned secondary and additional endpoints, including evaluation of IMR 687 versus placebo on VOCs, HbF associated biomarkers, indices of red cell hemolysis, white blood cell adhesion, and quality of life measures. We plan to conduct a pre-specified interim analysis when 33 patients have reached 24 weeks of treatment and currently expect to report interim data from this trial in the first half of 2021.

I would now like to turn to the Phase 2b Forte trial in beta-thalassemia that we initiated during the second quarter and are actively screening in. The Forte trial is a randomized, double-blind, placebo-controlled, Phase 2b trial in adult patients with beta-thalassemia. We've activated sites for this trial and expect to dose the first patient in the near term. In addition, we have progressed regulatory submissions seeking approval to conduct the trial in 14 different countries. The trial will evaluate the safety and tolerability of IMR-687 in approximately 60 transfusion dependent patients and 16 non-transfusion dependent patients.

Additionally, for transfusion-dependent patients, we plan to evaluate the effect of IMR-687 versus placebo on transfusion burden and the change in iron load as a result of transfusion during the trial and in comparison to recorded rates in the 12 weeks prior to initiation. The Forte trial will also examine additional exploratory efficacy endpoints as well as safety and PK endpoints. Like our Ardent Phase 2b trial for sickle cell, we plan to utilize weight-based dosing with potential doses as high as 400 milligram.

Safety and tolerability will be assessed after 24 weeks of dosing. And there are pre-specified protocol-driven analyses planned in the trial with the first such analysis being conducted with 30 patients have reached 24 weeks of dosing and an additional interim analysis being conducted with 30 patients have reached 36 weeks of dosing. Currently expect to report interim data from this trial in the first half of 2021. However, like the Ardent trial in sickle cell disease, I caution you that we are still evaluating the impact of the COVID-19 pandemic on these trials and therefore our estimated timelines for both trials could be delayed.

I'll touch briefly on our pediatric development program for sickle cell disease next. Most notably, we have been able to accelerate our originally planned time line to initiate this clinical program, primarily due to advancements in our oral solution formulation, which includes promising pre-clinical stability data and progress in scaling up third party manufacturing. Oral solutions are generally preferred in younger patients. It will enable dosing to be more customized based on weight, age, and other parameters.

We currently anticipate initiating the clinical program in the first half of 2021, approximately six months ahead of our previous expectations. We plan to conduct a single ascending dose trial and expand the program to a multiple dose extension study in adolescents in younger children.

Lastly, during the second quarter, we began pre-clinical studies to explore IMR-687 for the treatment of heart failure with preserved ejection fraction, or HFpEF in collaboration with the Necker Institute in Paris, France. Published literature suggests that inhibition of PDE9 and resulting increases in cyclic GMP through the natriuretic peptide modulation pathway can serve as an attractive target for prevention and treatment of cardiovascular disease, including HFpEF. In connection with this program, we formed a advisory board co-chaired by Dr. Thomas Wang, MD at UT Southwestern Medical Center, and Dr. Deepak Gupta, MD at the Vanderbilt University Medical Center.

In addition, they have assembled a group of key opinion leaders in heart failure from Vanderbilt, UT Southwestern, the Mayo Clinic, and Northwestern University to further advise about potential development of IMR-687 in this indication. We believe that HFpEF is a natural pipeline extension for IMR-687.

Thank you, and I will now hand back to Mike to review our second quarter financial results.

Thanks, Rahul. Second quarter results can be found in the press release that we issued this morning, and I'll summarize that briefly below. More details are also included within the 10-Q that we filed with the SEC, also earlier this morning. R&D expenses were $7.9 million for the second quarter of 2020 as compared to $4.4 million for the second quarter of 2019. The increase of $3.5 million was primarily related to the conduct of the company's clinical trials and manufacturing of clinical materials related to the development of IMR-687, as well as increased personnel-related and other R&D operating costs.

G&A expenses were $2.4 million for the second quarter of 2020 as compared to $1.2 million for the second quarter of 2019. The increase of $1.2 million is primarily due to increased personnel-related and other G&A operating expenses as a result of our operating [more] as a public company. Net loss attributable to common stockholders was $10.2 million or $0.59 per share for the second quarter of 2020 as compared to a net loss of $5.4 million or $7.68 per share for the second quarter of 2019. We ended the second quarter with cash, cash equivalents and investments of $106.3 million, and we expect this will be sufficient to fund our planned operations into mid-2022.

That concludes our prepared remarks. Gigi, could you open the line for questions, please?

(Operator Instructions) Matthew Harrison, Morgan Stanley. Your line is now open.

Hello, everyone. This is Kostas on for Matthew. Two questions from me. The first one has to do with the VOCs you observed and a decrease in the VOCs in the Phase 2a, our open label study. And I'm wondering how should we think about the powering of Phase 2b on VOCs? Will you be able to demonstrate [a] statistical signal there or you haven't powered the Phase 2b study for VOCs [deduction]?

It's a good question and thank you for asking it. The study is powered to show a 3% increase in fetal hemoglobin or greater in 35% of patients on active versus placebo. It is not statistically powered to show VOC as a endpoint. However, in discussions with the FDA at our Type B Meeting, they were clear that they would consider 3% as a potential surrogate endpoint for approval.

And in addition, they commented that we -- they would like to see trends in secondary clinical outcomes including VOCs, ACS, and a number of different clinical outcomes. And so with that meeting in mind, we powered the primary endpoint as delineated and we will be looking for those important trends that you noted in VOCs and across other clinical outcomes. I will say that the duration of the study is an important component of the Phase 2b.

And as we saw [and] granted only two patients, a longer duration of IMR-687 is potentially promising. And so as you know, that 2b study is a one year duration study versus a six-month study. So we are hopeful that, that will further allow us to see some of those potential clinical outcomes be valuable.

Thank you, and that's very helpful. And the second question is on the heart failure program. I'm wondering how much work do you need to do before you could move it through the clinic?

And secondly, literature suggests that, common heart failure includes the eye manifestations. And I'm wondering whether or how you are thinking about the adverse events, the TI adverse events you have seen with IMR-685 with relation to the heart failure manifestations in relation to TI. So do you expect the adverse events you saw with 687 to be a roadblock in developing these [compound] in the heart failure setting? Thank you.

So let me give you some perspective on heart failure. Again, it's good question. It's early days for the company in heart failure. We have obviously focused very carefully on our hemoglobinopathies approach, which includes sickle cell and beta-thalassemia. Part of the rationale in heart failure preserved EF is a seminal paper by Dr. David Cassette of Hopkins talked about PD9 overexpression being a component in heart failure with preserved EF pre-clinical models.

So really at the beginning stage of looking at those pre-clinical models with the [Nektar] Institute of France, and we've assembled an advisory team of leading cardiologists to think through the translatability into the clinic. So just acknowledge that the target and the rationale behind moving into the indication is very strong. But for us as a company, it's early days as you think about moving into the clinic. So we wouldn't guide you on when we would move into the clinic. So we would just say that we've assembled what we think is a very stellar group of KOLs, that knows the pitfalls that have been in this space and is helping us think through that.

Okay, that's helpful. Thank you very much.

Thanks.

Thank you. Yigal Nochomovitz, Citigroup. Your line is now open.

Hey, Rahul, and Mike. Thanks for taking the questions. (multiple speakers) Rahul, can you just clarify what you said a second ago about the 3% that you [described] that you need to show 3% or better of the HbF benefit in at least 35% of the patients? I just didn't quite catch that.

Yeah, sure. So we have referenced the trial's being statistically powered to show a 3% or greater increase in fetal hemoglobin. And the 35% is the underlying math that is giving us that patient number. So we are hoping to see that 35% or greater patients in the active arm of IMR-687 versus the placebo arm are showing a 3% or greater increase in fetal hemoglobin. That is just the math behind the statistical powering and how we got to 99 patients who go [on].

Okay. So but for example, if you got some -- like 10% fetal hemoglobin increases in less than 35%, it could compensate right, for the mean -- for the whole population, I mean, right?

Well, so just to be clear, it's a responder-based analysis. So we wouldn't be looking necessarily at the means, of course, the mean data is very important, as you noted, but we'd be looking specifically at a responder analysis, which is how the powering of the trial is contemplated and done across the industry.

Okay. Okay. Got you. And then can you just provide a little bit more context on the 3%? I know this has been a recent debate among investors. Just where does the 3% come from? Some physicians we've spoken with have been interested in seeing a higher than 3% increase in HbF. Just like to get a better understanding of how that's setup?

Sure. So there's kind of two data points that we used. The first one is an extensive meta-analysis of 688 papers across the literature of fetal hemoglobin, both natural history data as well as hydroxyurea-treated patients. And in a meta-analysis that is in process of being published, we were able to show that changes in fetal hemoglobin of 1% or greater, had a material and quantitative impact on risk outcomes related to sickle cell disease. That set of literature will be published, and that's almost 700 papers.

The second data point, of course, is the seminal work from (inaudible) -- from the multi-center hydroxyurea study. And that shows, anywhere from 3.2% to 4% increases in fetal hemoglobin have clinical outcome value. And so when you triangulate both the meta analysis as well as for the hydroxyurea literature from the kind of seminal RCT, I think there is a relevant justification for 3% being what I would call the minimal clinical important difference that shows clinical outcomes. And of course, we have shown some early data today and that data is early and is in two patients.

But if you look at patient number 1, which showed a substantial reduction in VOCs as well as substantial reductions in reticulocyte counts, absolute [retics], and an increase of hemoglobin of one gram per deciliter, the change in fetal hemoglobin is only 3.9%. So when we start thinking about literature in the first two data points, when we started thinking about actual patient data with the acknowledgment that's only an N of one in that particular patient, smaller changes in fetal hemoglobin may have merit and may potentially be relevant to both VOCs and clinical outcomes.

And so of course, we have to generate the full Phase 2b data to get comfortable with that value proposition. But just looking at the OLE data already from a small number of patients, you can at least get comfortable that smaller changes in fuel hemoglobin over time may potentially lead to those clinical outcomes that everyone and patients, of course, desire the most.

That's super helpful. I think you mentioned there were more than two early patients. What -- are we going to see the data for the other ones by the end of the year?

Yeah. So, yep. Great question. So we have gotten quite a bit of interest in the OLEs as patients have finished up their duration of treatment on the Phase 2a and so we have eight patients on the OLE trial, six of eight of those patients started in June. And as I noted in the prepared remarks, we will be releasing data at six-month time points.

And so if you just do the math, six of those eight patients will have six-month time points at the end of December or early January, depending on what dates they fall. And we will report data shortly after that at six-month increments. And so that maybe the short answer would be early next year, we'll have at least six more patients of data, assuming they stay on the OLE trial, in addition to the two patients we talked about today, which we'll continue -- continually update.

And as you can imagine, Yigal knowing us, we have submitted and will submit these to medical meetings so that the full datasets, including ConMeds, opioid use, et cetera, et cetera, will be fully featured in a medical meeting. We just wanted to provide the summary both in the 10-Q and on the prepared remarks today.

Okay, got you. And then, interesting on how heart failure -- have you already put in heart failure as a -- in your patents as a method of use for 687? Or is that, that would come down the road?

Yeah, that's something that's in the process. But I will just note that the Lundbeck license that we have, the exclusive license contemplates fields other than hemoglobinopathies. So we are covered based on an exclusive license with Lundbeck. The patent portfolio will expand to cover that on in due time.

Okay. Thank you very much.

Thanks, Yigal.

Thank you. Joseph Schwartz, SVB Leerink. Your line is now open.

Thanks very much, and congrats on all the progress and thanks for the super interesting update on the first two patients. I want to continue talking about that if we could and see if you could give us your sights, your insight into not only the change in fetal hemoglobin, which seems to get a lot of attention. But clinicians we talk to suggest that it's the absolute level that you end up at or operate at is really important. And it's interesting to me that these first two patients weren't at insignificant levels at baseline, yet they still had a lot of disease activity.

And so where do you think you'd like patients to end up considering that, that second patient was already in the 20s and had an increase of [nine], I think and had some serious benefits? The other patient had a lot more disease activity, was obviously lower, but got a even bigger benefit, perhaps from drug. And so how much of the benefit from 687 would you ascribe to fetal hemoglobin versus some potential other benefits? And are you going to be looking at any other biomarkers like P-selectin and VCAM? Thanks.

Yeah, it's a good question, Joe. First of all, thanks. Thanks for your time today. So let me try to break your question into two different segments. The first one is where do we want patients on the fetal hemoglobin spectrum and then two, what else are we looking for?

So to question number one, I think fundamentally, we believe at this time that increasing fetal hemoglobin by 3% or greater is an important organizing principle. So if that patient is for sake of discussion at 12.3, which is where the first patient was, were 20.7 where the second patient was. It's clear to us that patients have pathology up and down the spectrum of their fetal hemoglobin baseline.

And in fact, the best evidence of that is their interest in enrolling in clinical investigational clinical trials because they're not getting the benefit from where their fetal hemoglobin baseline is as a result of HU or as a result of no drug.

And so why we like the Phase 2b study is because we have stratified the study for hydroxyurea use. And so we'll be able to see two patients receive additional or better benefit when their own background HU as a additive benefit of IMR-687. And we will also see -- kind of the answer to your question, do benefit -- do patients benefit more when they start at 8% or 9% fetal hemoglobin and move up? Or are they still benefiting if their fetal hemoglobin for sake of discussion is around 3% or 4%.

I can't give you an answer to your question in terms of where the actual number in terms of fetal hemoglobin needs to be. All I can say is that we've seen that what are not huge changes in fetal hemoglobin of 3.9% in that [OLE] patient are substantial in terms of making differences. And I intuit, at least from the literature, the changes in fetal hemoglobin are kind of the organizing principle and of course, is the focus for the company is what we need to do and what we're powered to do in the Phase 2b.

The second part of your question is a really good one as well. And as you know from the IPO and from our pre-clinical data that's been published in peer-reviewed journals, there is a multi-modal potential for this drug that extends beyond fetal hemoglobin into some of the biomarkers, you noted, the selectins, the VCAM, ICAM, Myeloperoxidase. And so for these OLE. patients, we are going to actually start processing what we -- what's called the PDE sample for these patients over time. That process is a little bit longer.

Then the CBC and markers of hemolysis, and gathering the VOCs through just in the medical records. So we have those well documented. And so the best thing for us to do is to process those PDE samples in batches, and we will be doing that as part of some of those medical meeting submissions. And so while today I cannot comment on the changes in those values, I very much believe the preclinical data is directional for us and that there could be secondary advantages to this mechanism beyond fetal hemoglobin.

Of course, I don't have the data today to support that, but we will be generating the data to your question in the coming months.

Thanks for all the color.

Yep, thanks, Joe.

Thank you. At this time, I'm showing no further questions. I would like to turn the call back over to Rahul Ballal for closing remarks.

Thank you very much, Gigi. I just wanted to thank everyone for their excellent questions, their time on a Friday and the company is excited to continue to focus on execution and enabling these treatments to get to patients. Have a nice morning and a nice weekend. Thank you.

Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect.