Infinity Pharmaceuticals Inc (INFI) 2012 Q4 法說會逐字稿

Ladies and gentlemen, thank you for standing by, and welcome to the Infinity Pharmaceuticals' conference call to discuss the Company's full-year 2012 financial results. My name is Kate, and I will be your operator for today's call. At this time, all participants are in a listen only mode. There will be a question and answer session to follow. Please be advised that this call is being recorded at Infinity's request.

At this time, I would like to introduce your host for today's call Ms. Jaren Madden, Director of Investor Relations and Corporate Communications at Infinity. Please go ahead.

Thank you, Kate, and good afternoon, everyone.

Welcome to today's call to discuss our recent business progress and review our full-year 2012 financial results. With me here today are Adelene Perkins, President and Chief Executive Officer, Julian Adams, President of R&D, and Larry Bloch, CFO and CBO. Following our remarks, we will open up the call for Q&A. The press release issued earlier today details our results and is available on our website at infi.com.

Please note that during this call we may make forward-looking statements about our future expectations and plans, including clinical development milestones, the therapeutic potential of our pilot candidates and financial projections. It is possible that our actual results may differ materially from what we project today, due to the considerations described in the risk factors section of our annual report on Form 10-K for 2012 and our subsequent filings with the SEC. While these forward-looking statements represent our views as of today, they should not be relied upon in the future as representing our then current views. We may update the statements in the future, but are not taking on an obligation to do so.

And with that, I would like to turn the call over to Adelene.

Thanks, Jaren. Welcome, everyone, and thank you for joining us on the call today.

This is an exciting time at Infinity. We made important advances in 2012 which provides a strong foundation for the continued progress we expect to make this year. Our vision of building a sustainable fully-integrated Biopharmaceutical company based on three strategic pillars, a promising pipeline, an experienced team and solid financial foundation. I will take a moment to reflect on our strength in each of these three pillars.

Last year we rebalanced our portfolio, resulting in a pipeline that is now stronger than ever. We have increased our focus on our lead PI3 kinase inhibitor, IPI-145 based on early encouraging Phase I data in patients with hematologic malignancies, and also based on Phase I data from a study in healthy subjects that enabled the initiation of Phase II development in inflammation. Additionally, we continued our research efforts to advance our understanding of the biology of PI3 kinase, and to identify additional product candidates, which led to the selection of our second PI3 kinase inhibitor, IPI-443.

Looking ahead, we are focused on aggressively advancing our portfolio of product development candidates, and expanding it through both our ongoing internal discovery efforts and the evaluation of strategic in-licensing opportunities to further build our pipeline.

The key determinant of our ability to advance a great science in building strong product pipeline is the quality of our team. Last year, we added depth and experience to our team to further prepare us for the potentially transformative clinical and business opportunities ahead. We have a strong culture of collaboration, and are leveraging the cross-functional alignment of all of our teams, from discovery and clinical, through new product planning and finance to ensure that we make good strategic decisions under conditions of uncertainty, informed by the breadth of disciplines required to successfully develop and commercialize new drugs. Finally, we have taking measures to increase Infinity's ownership, and thus value creation potential of our product pipeline and to strengthen our financial position.

Last year, we restructured our two strategic alliances, and successfully completed two financings. As a result, we now have world-wide rights to all of our programs, and we started the year with a strong balance sheet of over $325 million in cash and investments. We appreciate the support of our investor base and our resulting financial strength, which together with full ownership of our programs enables us to independently drive our products through key value inflection points. We hope that 2013 will be as transformative for Infinity as 2012 was, as we are better positioned than ever before to realize our mission of building a sustainable fully integrated Biotech Company.

With that, I will turn the call over to Julian to review our pipeline.

Thank you, Adelene.

We are very pleased with the progress we have made with our PI3 kinase and HR protein 90 programs over the past few months, and we anticipate reporting data from both of these programs later this year. This afternoon, I will review our pipeline within with a focus on IPI-145, our potent oral PI3 kinase delta gamma inhibitor.

At this stage of development IPI-145 continues to be the most exciting program I have ever worked on in my career. Last year we reported encouraging preliminary data at ASH, demonstrating that IPI-145 was well-tolerated with a potentially broad therapeutic window. These data indicated that IPI-145 was clinically active, and each dose evaluated from 8 milligrams through 75 milligrams twice daily, or b.i.d.

Activity was observed in patients with both P-cell and T-cell malignancies, including chronic lymphocytic leukemia, indolent non-Hodgkin lymphoma, mantle cell lymphoma, Hodgkin lymphoma and T-cell lymphoma. Currently, we are completing our dose exploration and optimizing -- and optimization efforts, and planning for the initiation of at least two additional trials this year of IPI-145 in patients with the hematologic malignancies.

Today we announced that the maximum tolerated dose of IPI-145 has been defined at 75 milligrams b.i.d. The dose-limiting toxicities observed at 100 milligrams b.i.d., which per protocol are defined in the first cycle of treatment, were an incident of Grade 3 rash and an incident of Grade 3 ALC elevation. These were consistent with the adverse events previously reported at ASH. I am pleased to add that both patients' DLTs resolved, and per protocol were dosed-reduced and remained on the study at 75 milligrams b.i.d.

With the MTD defined, we are now able to leverage the adaptive approach of our Phase I trial to initiate additional planned expansion cohorts. These cohorts allow us to increase our patient experience in a broad range of hematologic malignancies and further optimize the dose of IPI-145, as we advance the program towards registrations studies. To that end, we have just opened 5 expansion cohorts, with approximately 30 patients each to further evaluate the safety, pharmacokinetics, biomarkers and activity of IPI-145 at 75 milligrams b.i.d.

I will now take a moment to describe these five cohorts. The first two new expansion cohorts are designed to confirm the initial activity reported at ASH, and the other three are intended as signal finding cohorts to explore malignancies in which there is strong mechanistic rationale for PI3 kinase delta and gamma inhibition.

First, we are enrolling another cohort of patients with chronic lymphocytic leukemia, indolent non-Hodgkin lymphoma and mantle cell lymphoma. As you know in July of 2012, we initiated our first cohort expansion at a dose of 25 milligrams based on activity observed at our lowest doses of 8, 15, and 25 milligrams in our dose escalation. Based on the tolerability and activity reported at ASH, we believe that 25 milligrams b.i.d. may be an appropriate dose for the chronic hematologic malignancies.

At this dose, the PK profile of IPI-145 indicates full inhibition of PI3 kinase delta, as well as partial inhibition of PI3 kinase gamma. Importantly, the second cohort at 75 milligrams BID provides us with the opportunity to further evaluate IPI-145 at a higher dose in these same indications, and thereby evaluate whether or not there is an enhanced benefit to treating patients at this higher dose.

Second, we are enrolling a cohort of patients with T-cell lymphomas, which allows us to explore the initial activity reported at ASH. Finally, we are enrolling patients in three signal finding cohorts in malignancies for which there is a compelling scientific rationale in the following indications; aggressive B cell lymphomas, including patients with diffuse large B cell lymphoma; myeloid neoplasms including patients with acute myeloid leukemia; high-risk myelodysplastic syndromes, myelofibrosis; and CML in accelerated phase or blast crisis; and finally, in T-cell and B-cell acute lymphoblastic leukemia/lymphoma.

We have submitted abstracts to ASCO, and plan to report updated data from the Phase I study during the year. The data contained in these abstracts will represent data as of November 20, 2012, which is the same data cutoff we used for our ASH presentation last December. If the ASCO abstracts are accepted, presentations would then include updated data on tolerability and activity including duration of response from the Phase I dose escalation and 25 milligram b.i.d. expansion cohort. In addition, we will report on initial data from patients enrolled on the newly initiated expansion cohorts at 75 milligrams b.i.d. The evolving data, together with input from our advisers and discussions with regulatory authorities, will guide our later stage development plan and registration strategy for IPI-145.

Beyond hematologic malignancies, we are developing 145 in inflammation including our Phase IIa trial in mild -- in patients with mild allergic asthma. This is a randomized double-blind placebo-controlled crossover study designed to evaluate the safety, pharmacokinetics, biomarkers, and activity of multiple doses of IPI-145 in approximately 30 patients.

The trial is intended as a signal finding study using antigen provocation to induce broncho constriction The activity end points include improvement in forced expiratory volume in one second or FEV1, a standard measure of lung function, airway hyper-responsiveness, and markers of inflammation. We expect to provide an update on this trial in the second half of this year, which will inform our development path forward in asthma.

We are also planning to begin a Phase II trial in rheumatoid arthritis. This double-blind randomized placebo-controlled trial will be designed to evaluate the safety and activity of multiple doses of IPI-145 in patients with moderate to severe rheumatoid arthritis. This will be a robust trial that if positive, could enable us to move directly to Phase III development. We will provide additional details about this trial once patient enrollment begins.

In addition to our clinical efforts, we have ongoing research programs directed to identifying additional PI3 kinase inhibitors that will complement IPI-145. Earlier this year, we named our second PI3 kinase product candidate, IPI-443 which is also a potent oral delta gamma inhibitor. Throughout this year, we will be conducting nonclinical studies designed to help us better understanding the pre-clinical profile of 443 and enable Phase I development. IPI-433 has the potential to provide us with important strategic flexibility and optionality, as we pursue our dual development pathways for our PI3 kinase franchise in both hematology and inflammation.

I will now provide a quick update on two trials of our potent selective Hsp90 inhibitor, retaspimycin hydrochloride. Our Phase II double-blind randomized placebo-controlled trial of retaspimycin hydrochloride plus docetaxel in patients with non-small cell lung cancer is now fully enrolled. This trial has 226 second or third line patients who are heavy smokers and who are naive to docetaxel treatment has two primary end -- two co-primary endpoints; overall survival in the total population, and overall survival in patients with squamous cell histology. We will also be prospectively testing the relationship between survival and a predictive CLIA-certified lab biomarker not previously described, which was originally identified by our in-house molecular pathology group. Top line overall survival data from this trial is expected in the first half of 2013.

Our second trial is an exploratory Phase Ib/2 trial evaluating retaspimycin hydrochloride plus everolimus in non-small cell lung cancer patients whose tumors have activating KRAS mutations. We also anticipate reporting top line data from this ongoing trial in the first half of this year. In summary, we have continued to make strong progress advancing our pipeline, and look forward to reporting data this year that could lead to multiple registration studies.

With that, let me turn the call over to Larry to review our financial results.

Thank you, Julian.

I will briefly review our financial results for the full-year 2012. Total revenue for the full year 2012 was $47.1 million, compared to $92.8 million for 2011. In 2012, revenue consisted of $45 million related to reimbursed R&D services, and $2.1 million related to the amortization of deferred revenue for the grant of rights and licenses under our previous strategic alliance with Purdue and Mundipharma. This compares to $88.5 million and $4.3 million, respectively for 2011.

R&D expense was $118.6 million, compared to $108.6 million for 2011. The increase in R&D expense in 2012, compared to 2011 was primarily due to the restructuring agreement with Millennium last December, which recorded the full lease payment of $15 million payable in installments, as well as development milestones paid to Millennium for IPI-145 and IPI-443. Under restructuring, Infinity regained US rights to all its PI3 kinase inhibitors.

G&A expense was $27.9 million, compared to $22.7 million for the same period in 2011. The increase in G&A expense year-over-year was primarily due to a higher stock-based compensation expense, early commercial development activities, and corporate development activities. In 2012, we recorded a nonrecurring gain of $46.6 million which was triggered by the restructuring of our previous strategic alliance with Purdue and Mundipharma. On this restructuring, we have gained ex-US development and commercialization rights to all our PI3K kinase inhibitors.

Net loss for the full-year 2012 was $54 million, or basic and diluted loss per common share of $1.70, compared to $40 million or basic and diluted loss per common share of $1.50 for 2011. And as of December 31, 2012 we had total cash, cash equivalents, and available for sale securities of $326.6 million, compared to $115.9 million as of December 31, 2011. In the absence of additional funding or business development activities and based on our current operating plans, we expect our current cash and investments to provide us with a cash run way into 2015. Importantly, we have the financial resources necessary to see our ongoing trials through their next key inflection points.

With that, I will turn the call over to our operator for questions.

(Operator Instructions)

Our first question comes from the line of Michael Yee with RBC Capital Markets. Your line is open

Hi, good afternoon. Thanks for the question. One, as you think about opening these cohorts, these five cohorts, you are looking at your competitors who are ahead of you, speeding along, one of them may be an accelerated filing later this year or next year. How do you think about your path to market? Do you think you could turn some of those five cohorts into an expanded cohort and file? Or are one of those five cohorts, a great unmet medical need?

And then my second question is on your five studies. You also previously alluded possibly opening two other cohorts as well, maybe in combination. Maybe you could talk a little bit about where we stand on that? Thanks.

Thanks, Michael, for your question. I think the expansion of the five cohorts is really part of the Phase I investigation, and is not anticipated to provide the basis of a regulatory filing. I don't think the size of the cohort, nor the composite safety data would be sufficient at this time. But it does allow us to very thoroughly investigate the activity of the drug, IPI-145 in the indolent malignancies, as well as the more aggressive malignancies, and gives us a basis for which to plan aggressively the next trials, to initiate conversations with Ad boards of KOLs and investigators, as well as start engaging the agency, both the FDA and the AMA to determine the threshold and the trial design and comparators and the necessary elements for registration studies.

And that really speaks to your second question, Michael. There will be, an addition to these five expansion cohorts, we do anticipate opening two additional trials which will be follow-on trials from these expansion cohorts. And we are in the process of determining whether they might have a registration path associated with them.

And we haven't discussed it, but we are well aware that ultimately there is a need also to look at combination studies. So all of these are part of our thinking. We just haven't voiced this over today. But rest assured, we are leaving no stone unturned with this program.

Okay, okay. Thank you very much.

Our next question comes from the line of Cory Kasimov with JPMorgan. Your line is open.

Good afternoon, thanks for taking the question. Julian, I wonder if you could talk a little bit more about this adaptive approach you are using, and how you may compare the low and high doses to inform your next step, considering you are looking at three indications with both those doses. The other one is, obviously, all at the high-dose. And then second question is, if you can provide us an update on how you're thinking about your partnering strategy, now that you have made this next step in determining the MTD? Thanks. Thanks.

Yes, so the adaptive approach was always foreseen when we wrote the trial, and we had accounted for enrolling up to five cohorts. What was different in this trial is, and was not anticipated at the very start, is that we would see such activity, as we saw at the low -- at the lowest doses. And therefore, elected to expand the 25-milligram cohort in CLL and lymphoma and mantle cell lymphoma.

For certain diseases, particularly the aggressive lymphomas, the T-cell malignancies, we fully anticipate that a further suppression of gamma, which we assert is important in these heme malignancies should be investigated at the MTD or the biologically optimal dose, to fully suppress delta and suppress gamma as much as possible. And by doing so, it behooves us also to reinvestigate CLL in lymphoma, just to see if we have deeper and faster responses, enhanced responses, as I alluded to, and will that make a difference?

Because the field still needs a better understanding of what inhibition of delta and gamma. We are the only ones -- the pioneers sort of forging the way here, and we would like to very much understand the interplay of these two iso forms of PI3 kinase. With respect to partnering, Larry?

Sure. Cory, thanks for your questions. In regard to partnering, we feel there is really two motivations for partnering. One is that to access capital necessary to prosecute the clinical campaign, and eventually the commercial campaign, assuming we are able to get regulatory approval.

And the second one is to access capabilities, in order to execute with the financial resources. And we do continue to have ongoing discussions with the potential partners, but as we said today, we believe that we have all the financial and operational resources to really fully explore the breadth of activity for IPI-145, both in the heme malignancies and in inflammatory disorders through these next value inflection points. And that is our plan -- again, we are open to having discussions, we have those discussions ongoing. But we are in no way inhibited from fully prosecuting independently, which is our current plan.

All right, great. Thanks a lot.

Our next question comes from the line of Marshall Urist with Morgan Stanley. Your line is open.

Yes. Hi, good afternoon, thanks for taking the questions. So a few for me. So first Julian, just on the MTD determination, I mean you mentioned rash and ALT, both things that we have seen before, certainly saw in the data at ASH. So just try to understand a little bit better, was that because you saw them in the first cycle? And related to that, it seems like from a gamma perspective, 75 probably does leave some efficacy on the table from the gamma perspective. So just trying to think about why -- why not trying either a protocol modification or some other way to kind of push on?

Yes, your first point is exactly right. The protocol DLTs are defined in the first cycle. And you are right, we have seen sporadic events like rash and transaminase elevations. What we haven't yet shared with the world is sort of the PK profile of 75 and 100, and those data will be probably provided by the ASCO time frame.

But I can assure you that at 75, we are getting quite a substantial suppression of gamma. So we don't feel like we are leaving a lot on the table. And it is very important that we really do follow the patients, so that it is not just getting them through the first cycle. But it is now -- the game is about duration of response as well.

So we want to make sure the drug is very well-tolerated, and we can manage patients for a long time on the study. So duration of the response, we are very happy with the initial response. Number of responses, albeit in a small number of patients, we want to enhance that experience in terms of response, and get a response rate. But make sure that that it is a durable response that patients can be maintained for a long time on study.

Okay. Understood. Just wanted to get your updated thoughts on gamma. You have obviously seen more longer sort of follow-ups from the patients of sort of the ASH vintage. And just your kind of updated thoughts on AT 75, can you give us a sense of how much gamma inhibition are we seeing? It doesn't seem like that that will get us to the IC, certainly not the IC-90, so just wanted to get a sense of how much gamma inhibition do you think you need or want, would be the other way to think about it in -- when we think about T-cell lymphoma, and the TL/ALL as well?

So I can't give you a precise answer on that. We will be providing more guidance on that at ASCO. Suffice it to say, that we think that gamma is very important, because there is high expression of both delta and gamma in these malignancies. And so, the science that we are following, in terms of looking at database of -- databases in these malignancies and expression of delta and gamma, certainly looks like delta and gamma co-amplify each other, and cooperate in these malignancies. So, delta has clearly been shown to be important. And then we think we are at a very professional dose of gamma inhibition, and we will provide more details at ASCO.

Okay, perfect. And then just one last one which was just -- wanted to understand a little bit better what your plan is in terms of interactions with the FDA, and what you kind of feel like you need to initiate those discussions and think of next steps? Is a decent amount of duration from the 25 expansion cohort enough? Do you want to wait for these cohorts right now, maybe in some of the bigger unmet need populations to think about going to the FDA? Just wanted to get a better sense of, what you think the critical path is to getting there from a data perspective?

Yes. In general, it is good to meet with them early and often. But it is also important to bring them data, and not just have a theoretical conversation. So we are thoughtfully considering the timing and the data we will present to the FDA in a propitious -- with propitious timing that doesn't hold back our clinical development, but is in alignment with what the agency's expectations, and as well as our clinical investigators. So again, stay tuned over the year. It will become very clear how we are prosecuting the program.

Okay, great. Thanks.

Our next question comes from the line of Jason Kantor with Credit Suisse. Your line is open.

Hi, thanks for taking the question. I have just two really. One of your competitors got this breakthrough therapy designation. Is this something that you could also likely get? Is there some criteria? Have you talked to FDA about this? Does this offer you an accelerated path forward potentially, as well?

Well, first of all, I would like to congratulate, Pharmacyclics I think its good for the field, and it shows a very attentive FDA that looks at data, particularly their data in mantle cell, which unequivocally shows, it is meritorious of a breakthrough designation. We will look at our own data and make the same kinds of judgments, and present our data to the agency at the appropriate times. And if we merit it, maybe we will be next in line. It is impossible to -- I certainly don't want to speak for the agency or for the data yet -- that we don't have in hand.

So and with regard to the data, will we see the data on all patients for the full expansion of the 25 cohort at ASCO?

Yes, we should. At ASH we had 55 patients enrolled. So imagine that all 55 patients, the maturity of those data will be included at -- for the ASCO presentation, again if we are accepted. And then the ongoing enrollment of the five cohorts -- to the extent that those data are mature, we will present whatever we have as of the few weeks cut off before ASCO.

Now is there any, -- with regard to the ASCO abstract, you said that what you submitted to the ASCO abstract was the same data cutoff for the presentation that you had at ASH. Is there a risk that ASCO just doesn't accept it because you submitted no new data in the abstract? Or is that fairly standard?

I would say it is fairly standard, but I cannot speak for the adjudicators at ASCO.

Okay. But you will provide us with data that is updated as of as close to ASCO as possible when we get to that time?

Well, at ASCO, we will provide you with the data. That is the forum.

Right.

The medical forum and peer-reviewed forum for which we will be able to present the most updated version of our data.

Okay. Thank you.

Our next question comes from the line of Ian Somaiya with Piper Jaffray. Your line is open.

Thanks. Just two questions from me. First, just on the combination, I know the question was asked previously. But it is early days, but I think we are all looking forward to the pursuit of novel combinations in the hematology field. And from a mechanistic standpoint, just rationale, can you point to what combinations make more sense than others?

It is a subject of great discussion and research in our laboratories. So, we are trying to make that determination, both from first principles, from experimental work, and eventually from clinical studies. Obviously, this is an era where new targeted therapies look very exciting. And I would hazard a guess, that what we are trying to do is replace the more toxic standard chemotherapy, DNA damaging agents, alkaloiding agents and the like.

And one can imagine all sorts of combinations that meet -- that require exploration. I still confess that none of these agents has presented themselves as a cure. So the goal is really to induce deep remissions, minimal residual disease, and have patients live a long time with their cancer and not succumb to their cancer eventually.

And the other question I had was just on a recent publication which spoke more to a more prominent role of the potential alpha sub unit of PI3 kinase in the myeloma. Is that something you would agree with? Does it sort of directionally point you away from myeloma, in the pursuit for your drug?

I would not make any assumptions. Delta and gamma are also highly expressed in myeloma. It is not clear to me what is the driver in myeloma, if PI3 kinase at all is a driver there. I would just submit that this is a very different disease in a very different micro environment. And I would -- probably not sufficiently explored to draw any final conclusions.

Okay. Thank you very much.

Sure.

(Operator Instructions)

Our next question comes from the line of Joel Sendek with Stifel Nicolaus. Your line is open.

Thanks a lot, a couple questions. Let's see -- first I am wondering if you could answer this, maybe we have to wait for ASCO. But can you tell us if there is any new AEs, and if there were any Grade 4 or 5 AEs?

I think you are right, with the assumption that you have to wait for ASCO. (Multiple Speakers) One-off comments about patients.

Got it. Okay. Well, I figured I would try anyway. A couple more -- I noticed in the five Phase Is that you went through in the press release and on the call, the one disease that appears to be missing relative to where you got responses at ASH was Hodgkin's lymphoma, and I am wondering why that might be?

You are right. It is a -- if we should come upon Hodgkin lymphoma, they would form part of the aggressive B cell lymphomas. So, we probably will see more of the diffuse large B cell lymphoma, of both the ABC and germinal-centered lymphomas, just because of prevalence. Hodgkin's patients in adults are very rare. But certainly, we would not turn away Hodgkin's patients.

Okay, got it. And then, just a quick one on the finance outlook. You mentioned that $15 million R&D payment. So, if I back that out of the fourth quarter number, that it puts you in R&D spend of about $25 million run rate. Is that what we should use and build off of for our modeling for this year?

Yes. So we gave our guidance early this year at JPMorgan, and operating expenses of $115 million to $125 million. That incorporates, obviously, some of the aggressive prosecution of the PI3K franchise that Julian went through with you. So that is not all of that, obviously, can be reflected in the Q4, which kind of is a baseline from which we are building on for 2013.

Got it, okay. And then my final question is, you are talking about these two additional trials, at least two additional trials, should we -- and then you gave a date of 2013 as the general date. I mean, is it fair to say those are -- would be back end of the year, or might you be lucky enough to start those sooner rather than later? Maybe possible in the first half?

We will comment on those trials as we announce them with patient enrollment. We don't forecast month to month.

In our guidance, we try to be -- provide a clarity that was feasible to provide. And so in the first half, for the IPI-145 heme malignancy focus, we committed to expanding the five expansion cohorts, and defining the Phase II dose in the first half. But in the balance of the year we committed to at least the two additional trials. We are moving as expeditiously as possible, but it could be any time in the balance of the year.

And let me just point out, the most important is not the first patient in, it is last patient out. So when we -- (Laughter). Seriously, when we designed the trial, we have to look at the landscape, what will be one or two years down the road. And therefore, there is no imperative for us to rush into a trial in any particular quarter. It is really about designing the right trial, executing flawlessly in collecting the data, and reporting on the data, getting database lock, and being able to announce a successful trial down the road.

Understood, okay, thanks a lot.

I am not showing any further questions at this time. I would like to turn the call back over to Ms. Adelene Perkins for closing remarks.

Thank you everyone for joining us today, and we look forward to providing you with further updates on our clinical trials throughout the year. Have a good night.

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