Chimerix Inc (CMRX) 2013 Q1 法說會逐字稿

Welcome to Chimerix first-quarter earnings conference call. This call is being webcast live on the Investors section of Chimerix's website at IR.Chimerix.com. This call is property of Chimerix, and recordings, reproduction or transmission of this call without the express written consent of Chimerix is strictly prohibited.

As a reminder, today's call is being recorded. You may listen to a webcast replay of this call by going to the Investors section of Chimerix's website.

Before we begin I will read Chimerix safe harbor regarding forward-looking statements. During the course of this conference call, the Company will be making certain forward-looking statements such as statements relating to the Phase 3 SUPPRESS trial of CMX 001 and related matters. These statements involve risks and uncertainties that may cause actual results to differ materially from those projected in the forward-looking statements. These risks and uncertainties are discussed from time to time by Chimerix and are more fully set forth in the reports that Chimerix files with any Securities and Exchange Commission, including its registration statement on Form S-1 that was originally filed with the Securities and Exchange Commission on March 8, 2013 and amendments thereto.

All forward-looking statements made on this call speak only as of the time they are made and Chimerix undertakes no obligation to update these statements to reflect subsequent events or circumstances.

I would now like to turn the call over to Kenneth Moch, Chimerix President and CEO.

Thank you, Ashley, and good morning, everyone. On behalf of all my colleagues at Chimerix, I am very pleased to welcome all of you on the phone to our first investor call and to also welcome many of you as new investors in Chimerix.

Joining me today at Chimerix's corporate offices are several corporate officers; specifically, Michelle Berrey, our Chief Medical Officer; Tim Trost, our Chief Financial Officer; and Mike Rogers, our Chief Development Officer.

Since the beginning of the year, Chimerix has achieved significant progress in important corporate and clinical milestones. On the financial front, the key accomplishment was the successful completion of our initial public offering, generating $117.9 million in gross proceeds.

On the clinical front, we continue to make significant progress in advancing our lead antiviral compound, CMX001, to the start of the Phase 3 SUPPRESS trial for the prevention of the cytomegalovirus, or CMV, in adults who are immunosuppressed because they have received a hematopoietic stem cell transplant, which is often referred to as a bone marrow transplant.

During the first quarter, the FDA granted fast-track designation to the CMX001 for this indication and we recently announced a final study design for the Phase 3 SUPPRESS trial. The primary use of our IPO proceeds will be to fund SUPPRESS, which we plan to initiate later this year.

As many of you are new investors in Chimerix, we thought it beneficial to begin our first investor call with a brief overview of the Company. We are, as you know, a biopharmaceutical company developing novel oral antiviral therapeutics that have the potential to significantly transform patient care in areas of high unmet medical need.

We have advanced two compounds into clinical development, CMX001 and CMX157. Since licensing CMX157 to Merck in July 2012 for their development as a potential treatment for HIV, we have focused our efforts on CMX001. CMX001 is an orally-administered drug that delivers high concentrations of a potent antiviral compound into cells. It is being developed as the first broad-spectrum antiviral against a class of viruses called double-stranded DNA viruses. These viruses are commonly transmitted in childhood and early adulthood, and generally remain latent inside individuals with a functioning immune system.

However, in immunocompromised patients, such as stem cell or solid organ transplant recipients, or people who are immunosuppressed by drugs they are receiving to treat other diseases, certain of these double-stranded DNA viruses can reactivate and cause viral infections which are associated with significant morbidity, mortality, graft rejection and co-infection with other viruses, fungus and bacteria.

Our first area of focus for CMX001 has been, again, cytomegalovirus, a double-stranded DNA herpes virus that is found in approximately 65% of the US population and which is a key cause of complications in immunosuppressed patients. Chimerix has completed Phase 2 clinical development of CMX001 for the prevention of CMV in stem cell transplant recipients, for which there are no approved drugs. In this Phase 2 trial, CMX001 demonstrated a favorable safety and tolerability profile, as well as clear indications of efficacy.

As I already mentioned, we plan to initiate the Phase 3 SUPPRESS trial later this year for the prevention of CMV infection in high risk stem cell transplant recipients. Michelle Berrey will provide more details on the SUPPRESS trial later in this call.

Because of its potential as a broad-spectrum antiviral, we are already working to demonstrate the activity of CMX001 against other double-stranded DNA viruses. We have completed enrollment of a Phase 2 study in stem cell transplant recipients in which we are evaluating CMX001 as a preemptive therapy for adenovirus, another double-stranded DNA virus which is often fatal and has no approved therapies. We expect to announce data from this study later this year.

As you can imagine, we are extremely encouraged by CMX001's clinical data thus far and look forward to progressing CMX001 further through clinical development and to bringing this vital therapy to the many critical ill patients in dire need.

With that brief introduction, I would now like to turn the call over to Tim Trost, our CFO, to review the financials for the first quarter.

Thank you, Ken. Earlier today, we issued a press release detailing our financial results for Q1 2013. We reported a net loss of $9.1 million, which, when coupled with the $25.5 million in accretion of redeemable convertible preferred stock, resulted in a net loss of $22.58 per basic and diluted share for the first quarter of 2013.

For the first quarter of 2012, we had a net loss of $6.9 million, which, when coupled with the $0.9 million and accretion of redeemable convertible preferred stock, resulted in a net loss of $5.14 per basic and diluted share.

The increase in net loss per basic and diluted share in the first quarter of 2013 compared to the prior year is primarily due to the increase in accretion of redeemable convertible preferred stock.

Revenues for the first quarter of 2013 were $1.8 million compared to $3.1 million for the same period in 2012. Revenues for both periods consist of contract revenue from our contract with the Biomedical Advanced Research and Development Authority, or BARDA, for the development of CMX001 as a medical countermeasure against smallpox.

The decrease in revenue for the first quarter of 2013 compared to the prior year is a reflection of us nearing completion of the base segment of our BARDA contract. We are currently in discussions with BARDA regarding subsequent segments of the contract.

Operating expenses for the first quarter of 2013 were $8.3 million compared to $8.6 million for the same period in 2012. Research and development expenses were $6.5 million for the first quarter of 2013 compared to $6.6 million for the same period in 2012. We expect research and development expenses to increase throughout the rest of 2013 as we initiate our Phase 3 SUPPRESS trial for CMX001.

General and administrative expenses were $1.8 million for the first quarter of 2013 compared to $1.9 million for the same period in 2012.

Interest expense increased to $400,000 in the first quarter of 2013 compared to $100,000 in the same period in 2012. The increase was due to a higher amount of venture debt carried in the first quarter of 2013 compared with the prior-year period as a result of a drawdown of a $12 million second tranche of venture debt in the third quarter of 2012.

Cash, cash equivalents and short-term investments were $22.9 million at March 31, 2013 compared to $29.8 million at December 31, 2012.

Following the completion of our recent IPO, our pro forma balance sheet, also as of March 31, 2013, shows $134.1 million in cash, cash equivalents and short-term investments, $14.3 million in debt and 25.7 million outstanding shares of common stock. As a reminder, the first quarter results, as well as this morning's announcement, are available on the Investors section of our website. I would now like to turn the call over to our Chief Medical Officer, Michelle Berrey.

Thank you, Tim. We were pleased to recently announce the final study design for our Phase 3 study for CMX001 for the prevention of CMV infection. Following the successful Phase 2 study of CMX001 as a potential prevention of CMV infection in patients who had recently undergone a stem cell transplant, we began conversations with the FDA to agree on a study design for a registrational trial. In May 2012, we held our end of Phase 2 meeting with our FDA review team, and over the following months, have come to an agreement on the population, specifics and timing of the primary and multiple secondary endpoints, as well as the dose and duration of CMX001.

The initial study design considered by Chimerix and the FDA included two active doses of CMX001 -- 100 milligrams twice weekly and 75 milligrams twice weekly -- to be carried forward into the Phase 3 trial in order to mitigate the risk of gastrointestinal side effects. However, in the intervening months, we've received results from a Phase 1 trial of CMX001 administered with food. We now believe that by administering CMX001 with food, in addition to the use of the safety monitoring and management plan, or SMMP, we have addressed the risk of premature discontinuation of CMX001 due to G.I. events. We are very comfortable with the decision to explore a single dose of CMX001 in SUPPRESS, 100 milligrams administered twice weekly.

Following successful screening, SUPPRESS subjects will be randomized to receive 100 milligram doses of CMX001 twice weekly or placebo. We anticipate enrolling 450 patients who have evidence of prior CMV infection, with approximately 300 of the 450 enrolled subjects receiving CMX001, maintaining the two-to-one ratio in the original study design. This two-to-one randomization will provide a larger number of patients for our safety database, will be exposed to the dose and duration of CMX001 intended for our final label.

In addition, recruitment for the trial may be accelerated by increasing the likelihood of a single patient being randomized to active CMX001 versus placebo.

In SUPPRESS, we will begin dosing of CMX001 or placebo shortly after subjects received their transplant, not after engraftment. Waiting to begin dosing until after engraftment was a safety precaution that had been included in our Phase 2 study and in other recent studies of investigational agents for CMV prevention related to the bone marrow toxicity seen with ganciclovir. The safety data to date on CMX001 has not shown a risk of hematologic toxicity or bone marrow suppression, allowing for initiation of dosing closer to day zero, the day of transplant. Early dosing is an important change in SUPPRESS from the Phase 2 trial as the period of highest risk of reactivation of CMV and the other herpes viruses is the first 100 days after transplant.

Initiation of dosing of CMX001 earlier in the post-transplant period may provide protection from CMV reactivation to patients at risk of very early CMV disease, while capturing the events in the first weeks after transplant in patients on the placebo arm. This new early dosing of CMX001 should have a positive effect on the ability of the SUPPRESS trial to demonstrate a statistically significant reduction in CMV reactivation.

In addition to capturing the early events between transplant and engraftment, we saw in Phase 2 that a majority of CMV reactivation events occurred in the first two weeks after beginning dosing, when subjects were less likely to have achieved effective concentrations of CMX001. By beginning dosing earlier, optimal drug concentrations will be achieved earlier in the period of highest risk of CMV disease.

As reviewed, SUPPRESS subjects will received CMX001 or placebo from as early as three days after transplant and will receive CMX001 or placebo through week 14, the period of highest risk of CMV reactivation. We will continue to monitor all patients through week 24 for evidence of CMV disease or for CMV in the blood at levels high enough to require preemptive therapy. Trials of other agents explored for prevention of CMV have noted an increased risk of late CMV events occurring after the first 14 weeks of highest risk.

In our Phase 2 trial in CMV prevention, we followed patients through week 22 and we did not observe an increased rate of late CMV events. In the CMX001 arm receiving 100 milligrams twice weekly, one of the 50 subjects had a positive CMV PCR at week 21.

The recently approved Roche TaqMan real-time polymerase chain reaction assay, or PCR, will be used to monitor levels of CMV in the blood, with a single measurement in the blood greater than or equal to 1000 copies per mL considered a failure of CMV prevention in any enrolled subject. In addition, subjects who are at risk of rapid progression to CMV disease, in particular those recipients of umbilical cord blood stem cells, will have a lower threshold for initiation of an antiviral reaching the primary endpoint with any CMV level in the blood greater than or equal to 150 copies per mL, the lower limit of quantification of the assay.

SUPPRESS is designed to demonstrate the superiority of 100 milligrams twice weekly of CMX001 over placebo in the prevention of CMV infection. Because there are no approved antivirals for the prevention of CMV in stem cell transplant recipients, a placebo control is appropriate. This superiority design allows us to collect the maximum of safety and tolerability data for CMX001. In addition, a superiority design carries fewer operational and regulatory risks than the noninferiority trial.

Failure to prevent CMV reactivation through week 24 is the primary endpoint for the trial. The study is powered to detect a 50% decrease in CMV reactivation in the 300 subjects receiving CMX001 versus 150 subjects randomized to placebo.

We have begun identification of clinical sites for SUPPRESS and anticipate approximately 40 sites will be involved in clinical conduct. Dosing is expected to begin in the third quarter of this year. Data from SUPPRESS are anticipated in 2015 and, if positive, may support accelerated approval of CMX001 for the prevention of CMV infection.

Conversations with the FDA regarding a path to traditional approval are continuing and could include a second study of CMX001 in CMV prevention in pediatric stem cell transplant recipients or in solid organ transplant recipients.

In summary, we are enthusiastic about this outcome from discussions with our FDA review team, and we are eager to begin study conduct for the SUPPRESS trial later this year.

Now I'd like to turn the call over to the operator for any Q&A.

(Operator Instructions) Philip Nadeau, Cowen and Company.

Good morning and thanks for taking my questions. Michelle, a couple for you. First, what do you need to do before SUPPRESS can be initiated? Is it just a matter of locating sites and getting through IRBs, or is there anything else logistical that you need to achieve?

Good morning. Thanks for the question. For us to begin initiation of dosing, we need to get through the IRBs, as you mentioned. Many of these academic centers have multiple IRB reviews, so we have begun submission of the protocol to the IRBs and ethics committees. And after that, just site initiations. So that is all that is outstanding at this point.

Okay, great. And then on the statistics on the trial, can you remind us, since it is a single study, do you need to achieve p less than 0.01, or is there a different criteria for the p-value?

No, it is a p of less than 0.05. The superiority trial, though (inaudible) -- correlates with a single-sided p of 0.025.

Okay, great. And then just one last question. Can you give us some update on your pediatric plan? What is the Company's most recent thinking in how it could secure a pediatric label?

Our plan is, again, to unblind the data from the Phase 2 study of adenovirus preemption with CMX001 that we completed enrollment for in December of 2012. We should have those data available in the second half of 2013.

As soon as those data are unblinded, we will go back to our review team with a plan for pediatric, which potentially could encompass adenovirus and CMV prevention for pediatrics. But we are waiting until we see those data to finalize our plans.

A second study to achieve traditional approval for CMV prevention could be accomplished through potentially a pediatrics trial in stem cell transplant recipients or potentially in a study of solid organ transplant recipients.

Great. Thanks for taking my questions.

Katherine Xu, William Blair.

Good morning, everyone. Just curious, for the European side for the SUPPRESS design, have you talked with European authorities? And also, given your interactions historically, what would you think their reactions would be?

And also on the pediatric, the adenovirus pediatric study that you are going to release data later this year, was CMV some kind of a secondary endpoint, and are you looking at it rigorously there? You mentioned that you might be able to get both adeno and CMV from this study, this [small] study.

Good morning, Katherine. It's Michelle. For the pediatrics adenovirus trial, adenovirus was the only virus that was considered in an endpoint there. But what we found from our studies in pediatric stem cell transplant recipients, and specifically in the 350 expanded access trial, was that children are much more likely to have multiple double-stranded DNA viral infections.

This opportunity is something that we are considering as part of our Phase 3 design if we were to go forward with a pediatric CMV prevention trial, and it is possible that we could incorporate multiple double-stranded DNA viral endpoints in a Phase 3 design. That is something that we, again, have to be discussing with the FDA review team later in this year after we unblind that adenovirus data.

At the same time, we plan to take our pediatrics plan to Europe to have our first official conversations with the EMA regarding going forward with development in Europe. We have had off-the-record conversations with many of the key opinion leaders in stem cell transplant infectious disease in Europe, and find that their approaches are very similar to those in the US. Our study design has been reviewed by many of the European KOLs. So we do believe that the SUPPRESS trial design would be acceptable.

But again, that would be part of a conversation with European regulatory authorities at the time that we take our pediatrics plan to Europe. So at this point we don't have an official stance on whether or not we would be enrolling patients in SUPPRESS in Europe.

Thanks for that clarification. So later this year, if we see very good data -- let's say some mortality benefit from the adenovirus study, pediatric and some adults -- if there is a striking benefit, what are your plans going to be?

It is a great questions, and again, it was a trial that was not intended as a registrational trial. There are 48 patients who were enrolled at the time that adenovirus was detected in the blood. So again, it was a preemption trial. Patients who progressed with either symptoms or increasing levels of adenovirus in the blood were allowed to go on to open-label therapy. So we do have both clinical and virologic endpoints for the trial.

If we did have a successful adenovirus trial, there are certainly mechanisms for an early approval for an indication that has a mortality endpoint and does not have any alternative therapy. But again, this trial was not designed as a registrational trial.

If we do have a positive clinical endpoint, we will certainly be having conversations with the regulatory authorities regarding making the drug available through one mechanism or another for these children who are at increased risk of an early mortality based on adenovirus infection. So we are keeping all options open at this point.

Thank you.

David Friedman, Morgan Stanley.

Thanks for taking the question. I just wanted to see if you could talk a little bit about some of the questions you are thinking about as you are analyzing the compassionate use and treatment sort of EIND data and how you expect to use that data set going forward.

Good morning, David. Our 350 trial, was an expanded access trial that had the same requirements as emergency INDs in the US. So patients had to have a life-threatening infection with a double-stranded DNA virus and no alternative therapies.

What we found from those -- the first looks at those 210 patients enrolled in study 350 were a wide variety of double-stranded DNA infections, and a proportion of patients, even adult patients, who were infected with more than one double-stranded DNA infection. We found anecdotal reports of patients who have cleared virus including, some cases of JC virus and patients with PML.

We are continuing to look specifically at JC virus and BK virus, again, because of our interest in CMX001 and its potential activity against polyomaviruses. We recently presented some data on the adenovirus, as well, from the 350 study, showing that compared to historical event rates, we had superior outcomes in patients who began therapy with CMX001 during a time of only viremia, prior to development of adenovirus symptoms. So again, those are anecdotal cases, small case series, and not in a controlled setting.

So those are examples of potential further indications that we may be able to pursue based on these early proof-of-concept cases. So we look forward to presenting more of these data at scientific conferences later in the year, as well as moving forward with publications of these data sets. We are additionally having conversations with our medical advisors regarding designs of possible proof-of-concept studies to continue to move forward with multiple indications for CMX001.

Thank you.

Josh Schimmer, Lazard Capital.

Good morning. Thanks for taking the questions. First, could you give us an update on the adenovirus assay in the Phase 2 preemptive study? And what specifically needs to happen in that trial going forward to be able to lock the database and report results?

Good morning, Josh. Yes, so the adenovirus assay specifically, because we do not have any other therapies available for adenovirus, we've not seen the same advances in the sensitivity and specificity of an assay. So we don't have a commercially available adenovirus assay.

So we are continuing to move forward with getting closer to locking our safety database and efficacy database for that adenovirus trial. We are trucking along our scheduled timelines to lock that database, don't expect any delays there.

The difference with adenovirus versus CMV is that we don't have as tight a correlation with adenovirus viremia leading to disease. It has not been established as a valid surrogate, as we have with CMV, which is why for our SUPPRESS trial, we are able to use CMV viremia as a surrogate marker for progression to disease. We're not quite there with adenovirus. That is one of the goals of the Phase 2 trial, was to establish that link between adenovirus viremia and progression to disease.

So is the assay still being revised or improved, or is the assay itself locked and at this point it is more of a correlation analysis? I'm just trying to understand what the next steps are until data as it pertains to both the assay as well as the study.

Yes, so the assay that we used in the trial is the assay that will be used for that virologic analysis. That is not to say that there won't be another assay or improvements on that assay prior to any use of an adenovirus viremia endpoint in subsequent trials or moving forward in therapeutic intervention.

So I think, as far as analysis of the Phase 2 data, we are locked in on the use of our current assay. But we are continuing to work to get the diagnostic groups in developing more sensitive and specific assays, and again, showing a clinical correlation of adenovirus viremia with risk of progression to disseminated adenovirus or adenovirus pneumonitis.

Okay. What is the duration of evaluation in that study, I guess? I think it finished enrollment in December. Maybe just help us understand the (inaudible).

Yes, so the duration of therapy could be up to 12 weeks for those patients. And then it really has been collection of data and QC of data. As soon as those QC events are locked up, we will be able to lock the database. So we are, as I mentioned earlier, still on track for a second-half 2013 unblinding of those data, and should be able to get those to both the FDA and to our European regulatory counterparts by the end of this year.

Got it. Maybe one more quick question. What is it that the SUPPRESS study lacks in order to gain full FDA approval? And what do you think the different potential studies, (inaudible) or solid organ, will be able to provide in terms of information to gain that full approval?

It is a great question. Currently, our agreement with the FDA is that if the SUPPRESS study were to produce positive data, that that would be sufficient for accelerated approval because of our use of a surrogate marker, or CMV viremia, as an endpoint.

However, we are collecting clinical endpoints within SUPPRESS. And if we were to have sufficient evidence for clinical benefit through those clinical endpoints, that is a possibility.

It is much more likely that we would require a second trial that has a higher likelihood of having clinical events. That second trial could be in pediatric stem cell transplant recipients, again, with a primary indication of CMV prevention. As I mentioned, the pediatric population are much more likely to have additional double-stranded DNA viruses, so they are more likely to have multiple clinical endpoints that could be demonstrated to be decreased by the intervention of CMX001.

The other possibility is in solid organ transplant recipients. When CMV viremia is present in solid organ transplant recipients, there is a CMV syndrome; they are much more likely to be febrile and symptomatic. So that certainly is a strong possibility for a second trial to achieve traditional approval. Again, it doesn't have to be in the same population, just with the same indication of CMV prevention.

Great. Thanks very much.

[Kevin Moore, Accenture].

Yes, hello. My question is regarding -- so kind of a follow-up to the compassionate use trial conversation that was had before. And when we are looking at compassionate use, there is a lot of different double-stranded DNA indications that it was set out to look at, and I know a lot of them had to do with life-threatening diseases. But a lot of them, on the flip side, don't deal with life-threatening diseases, such as herpes simplex virus.

And I'm specifically interested if -- have you seen people who might have been co-infected with multiple DNA viruses and one of them including herpes simplex virus? And the reason I'm asking is because your initial study, where you looked at CMX001 in animal models showed that it was a potent inhibitor of herpes simplex, and it showed much more efficiency compared to acyclovir.

So I'm just wondering if anything has been done since then to follow up with that study, just to look at how effective your drug might be for that indication.

Thank you, Kevin, for the questions. And yes, in the 350 trial, as well as in the EINDs, we did have patients who were enrolled with the herpes viruses I and II. So if you will remember, there are eight different viruses within the herpes family, and we have demonstrated in vitro activity for CMX001 across all eight of those human herpes viruses, including the simplex viruses that have demonstrated resistance to acyclovir.

In order to be enrolled in the 350 trial or emergency INDS, there could not be any alternative therapies and patients did have to have a demonstrated infection with a double-stranded DNA virus. So we do have some data on acyclovir-resistant simplex. We have treated patients with herpes encephalitis, which is certainly associated with significant neurologic outcomes as well as potentially life-threatening complications. We do intend to continue to pull those data together for presentations and publication hopefully later in 2013.

Again, these are part of a broader database of evidence of activity in CMX001 against the herpes viruses, against adenovirus and for the polyomaviruses JC and BK virus. So we are continuing to move forward with all of these areas of exploration for CMX001.

Okay. I want to make sure that everybody on the call understands some of the verbiage that you've been using. Because when you talk about clearance of the virus, you are essentially meaning, when you are talking about BK and some of the other ones that you mentioned in the compassionate use trial, that that would essentially be like a functional cure.

So if we are talking about, like, for instance, what you've done with herpes encephalitis, if you actually cleared the virus -- which I'm not sure that you would say that you did, because that is a latent herpes virus that -- obviously, these are viruses that have no functional cure, that acyclovir and the current mode of treatment is just to suppress.

But I think the way some of the investors see this CMX001 is that it is an extreme suppressor, so meaning if the patient were to take it, that they would have no more viremia, that it would discontinue that the virus would still be there. Can you explain to me what exactly it's actually doing?

Absolutely. It is a very important point, that the herpes viruses are not curable. They can be cleared from a certain reservoir or cleared from a certain area that we are testing, or resuppressed at something like a mucosal vesicle or mucosal lesion; so that is resuppression. We do not and no therapy has been shown to completely clear a herpes virus from the human host.

What -- our hope is in patients who have a short-term immunosuppression and have an increased likelihood of progression to disease or complications of herpes viruses that we can resuppress the active replication of a herpes virus, particularly in those patients with short-term immunosuppression, such as around the time of a stem cell transplant, when we are waiting for the host immune response to recover.

In adenovirus, BK virus, JC virus, we may have an opportunity for clearance of those viruses. That's a very different scenario than the chronic latency that we see with the herpes viruses. So it's a good point of differentiation. However, we are still collecting those clinical endpoints and demonstrating the improved responses and ability of the host to control chronically the herpes virus [layer].

So I hope that was clear and explains again the consistent mechanism of either viral clearance or resuppression for the different double-stranded DNA viruses.

With that, I'll turn back over to Ken Moch, our CEO, if there are no further questions.

Actually, I believe there are no further questions.

There are no further questions.

All right. Listen, we thank you all for your participation in today's call and look forward to updating you again very soon. And with that, I think we are at the point of completion.

Ladies and gentlemen, this concludes today's presentation. Thank you once again for your participation. You may now disconnect. Everyone, have a great day.