Five Prime Therapeutics Inc
Q1 2018 Earnings Call Transcript

Published: 13 May 2018

[Operator:]

Good day, ladies and gentlemen and welcome to the Five Prime Therapeutics first quarter 2018 earnings call. As a reminder, this conference may be recorded. I would now like to introduce your host for today's conference, Heather Rowe, Senior Director, Investor Relations and Corporate Communications. You may begin.

[Heather Rowe:]

Good afternoon and thank you for joining us. I would like to welcome everyone to our conference call to discuss results for the first quarter 2018. We issued a press release this afternoon and also posted slides to accompany this presentation. The slides can be found under the Investor Relations section of our website under Events and Presentations. Joining me today are Aron Knickerbocker, Chief Executive Officer, Dr. Helen Collins, Chief Medical Officer, Dr. Bryan Irving, Senior Vice President of Research and Linda Rubinstein, Interim Chief Financial Officer. Today's conference call will include forward-looking statements under the Private Securities Litigation Reform Act of 1995, including statements regarding our research and development programs and financial outlook. Actual results may differ from those indicated by these forward-looking statements due to numerous factors, including those discussed in the Risk Factors section of our SEC filings. Our expectations and assumptions could change. While we may elect to update these forward-looking statements in the future, we specifically disclaim any obligation to do so, even if our views change. I will now turn the call over to Aron.

[Aron Knickerbocker:]

Thanks Heather and good afternoon. Thanks for joining us today to review our first quarter 2018. Highlights appear on slide three. During the quarter, we continued to advance our later stage clinical compounds, cabiralizumab and bemarituzumab, which I will call cabira and bema. The potential of our comprehensive IND engine continues to be validated as we fill our pipeline and the pipelines of our collaborators with new product candidates. The productivity of this engine is reflected in our progress with FPA150, our B7-H4 antibody, which recently under clinical development, FPT155, our CD80-Fc fusion protein, for which we expect to file an IND or foreign equivalent in the second half of the year and a wave of other programs that we have yet to disclose. This vibrant platform is not just for target discovery. We strategically assembled a fully integrated suite of capabilities, including multiple state-of-the-art antibody technologies that we implement in parallel to increase our speed in generating product candidates. This engine continues to yield valuable targets and therapeutics for our partners as well. In the quarter, UCB licensed an undisclosed fibrosis target and BMS entered the clinic with a fully human monoclonal antibody targeting TIM-3, an immune checkpoint inhibitor that is known to limit the duration and magnitude of T cell responses. This is a strong testament to the power of our IND engine. We have chosen to focus on I-O, yet the breadth of this engine extends far beyond I-O. In fact, we have used it to find targets in many disease contexts, including fibrosis, respiratory disease, muscle diseases and more. Our pipeline, as shown on slide four, is progressing into late stage development while simultaneously expanding. I will start with cabira, our CSF-1R antibody, which reduces and reprograms tumor-associated macrophages. The rationale for targeting macrophages in the tumor microenvironment was further validated in a paper that just appeared in the May 1 issue of Cell Reports that showed that CSF-1R-positive macrophages play a vital role in pancreatic tumor maintenance and suppression of T cells. Last fall, we and BMS presented data that demonstrated deep and durable responses in late-line patients with pancreatic cancer. These data are unprecedented for immuno-oncology agents in this patient population. Anti-PD-1 agents have not demonstrated efficacy in patients with microsatellite stable or MSS pancreatic cancer. Based on our encouraging Phase 1 data, BMS initiated a randomized open label Phase 2 trial in second-line pancreatic cancer in the first quarter. This triggered a $25 million milestone payment to Five Prime. Slide five shows you the estimated incidence of pancreatic cancer by line of therapy in major markets. Beyond I-O, we are also studying cabira in diffuse PVNS, a rare disease that causes benign tumors in the joints. Because PVNS is a chronic, non-lethal disease, we changed the dosing schedule in our ongoing Phase 1/2 trial from every two weeks to four weeks with the goal of reducing irritating side effects such as eyelid swelling and itching, while preserving the efficacy we have already observed with cabira in PVNS. Based on what data we see from this study, we plan to announce by the end of this year whether we will proceed to a pivotal trial in 2019. As shown on slide six, we estimate the prevalence of diffuse PVNS to be about 67,500 patients in the U.S., EU5 and Japan, a significant opportunity for us in a chronic indication. Now I will discuss the bema program. Bema, also known as FPA144, is currently in a Phase 1 safety lead-in portion of our Phase 1/3 FIGHT trial in combination with chemotherapy in first-line gastric cancer. We plan to move into the Phase 3 portion of the trial in the second half of the year. Our collaboration with Zai Lab in Greater China is an important strategic component of our bema program since we expect about half of the patients in the trial to come from this geographic region. This collaboration is expected to reduce our trial costs and speed up enrollment. We have recently refined and are raising our estimates on the number of patients expected to be FGFR2b-positive in the U.S., Europe, Japan, Korea and China and you could see our revised assumptions on slide seven. Also, we don't expect to compete with Herceptin since HIR2 and FGFR2b overexpression in gastric cancer tend to be mutually exclusive and we are excluding HIR2-positive patients from the FIGHT trial. We are also very excited about FPA150, our first-in-class B7-H4 antibody which recently began a Phase 1 monotherapy trial in solid tumors. Given this is first-in-class therapeutic targeted checkpoint pathway for which there are no other drugs in clinical development, we were invited to make an oral presentation at the AACR Annual Meeting in April. We showed FPA150 demonstrated dose-dependent anti-tumor activity in vivo as a monotherapy and elicited complete tumor regressions in pre-clinical models when given in combination with PD-1 blockade. Beyond FPA150, we are excited about the next wave of targets that reprogram cells in the tumor microenvironment and Bryan will cover these shortly. I have great confidence in the future of Five Prime. Our pipeline is expanding, we are transitioning toward late stage development and we have a strong balance sheet with $389 million in cash. Moreover, we have multiple levers available to us to advance our programs and finance the company allowing us to remain agile and to adapt to the needs of the company over time. This provides us with optionality across our pipeline. We have a history of successful deal-making to support both discovery and product development. These deals are valuable because they generate cash, broaden and accelerate development and provide us access to global patient populations and markets. Consistent with this history, we are constantly scanning the landscape for business development opportunities that maximize shareholder value. In any potential strategic alliance, one of our primary objectives would be to maintain a U.S. commercial presence. During the quarter, we also announced an executive change. Marc Belsky, our former Chief Financial Officer, left Five Prime to pursue another opportunity. An executive search is ongoing. In the meantime, I would like to introduce Linda Rubinstein, our interim CFO. She will discuss our financials later in the call. For now, I will turn the call over to Helen to talk more about our clinical programs.

[Helen Collins:]

Thank you Aron. We continue to be pleased with the progress across our three ongoing clinical programs. I will start on slide eight with cabiralizumab, our antibody to the CSF-1 receptor on macrophages that we are studying in oncology and PVNS. We are combining cabira's CSF-1R inhibition with the BMS's PD-1 inhibitor Opdivo to reduce and re-polarize immunosuppressive tumor-associated macrophages and remove the PD-1 inhibition on CD8-positive T cells. Based on the pancreatic data we reported last fall, physicians are enthusiastic about the potential for this combination in this hard-to-treat patient population. They emphasize to us that PD-1 inhibitors haven't shown efficacy in microsatellite stable pancreatic cancer and objective durable responses are completely unexpected with systemic treatment that doesn't include a chemotherapy backbone. As Aron mentioned, a large unmet need remains for pancreatic cancer. The chemotherapy combination of Onivyde and 5-FU with Leucovorin in second-line and later patients reported an objective response rate of only 7.7% and an overall survival of 6 months. In comparison, as you can see on slide nine in the cabira plus Opdivo data, we saw confirmed objective response rate of 13% in the first 31 evaluable patients enrolled and durabilities of those responses lasted from five to nine months at the time of data cutoff. Responses were also accompanied by declines in the tumor marker of CA19-9, indicating that we are reducing tumor cells, not just reducing macrophages. In response to these promising data, we enrolled additional patients with late-stage pancreatic cancer to bring the total to more than 60 patients. These newly enrolled patients are all undergoing baseline and on-treatment biopsies with the goal of providing a greater understanding of which patients are more likely to benefit from the cabira-Opdivo combination. Given these durable responses in late-stage pancreatic cancer, BMS has advanced into a Phase 2 randomized trial in approximately 160 second-line patients. Their trial has four arms with roughly 40 patients per arm and you can see the trial design on slide 10. We believe this trial design is the ideal way to quickly determine a path forward for the cabira-Opdivo combination. The study tests the combination alone, the combination added to standard chemotherapy regimens which are used either first or second line and importantly, also includes a control arm of standard chemotherapy alone. There's a strong scientific rationale for combining cabira and Opdivo with chemotherapy. Nonclinical data demonstrates synergy when CSF-1R and PD-1 antibodies are combined with chemotherapy in pancreatic cancer models. And we like this trial design because it has a randomization scheme and an active standard of care comparator and includes overall survival rate as an endpoint. We have maintained there's a strong rationale for targeting macrophages, particularly in tumors that do not respond to PD-1 therapy. This rationale was recently underscored in the Cell Reports paper that Aron mentioned earlier, in which researchers from the U.K. identified that CSF-1R-positive macrophages play a vital role in pancreatic tumor maintenance and suppression of T cells. Their research indicates that inhibiting CSF-1R depletes macrophages, loosens the stroma and makes tumors more immunogenic. This paper also reported reduced survival among patients with pancreatic cancer whose tumors had high macrophage content and low T cells. BMS is also supporting several investigator-sponsored trials evaluating additional combinations with cabira and Opdivo, such as with radiotherapy and with anti-CD40 in cancers beyond pancreatic, such as lung, renal and melanoma. We recently announced that an abstract featuring cabira-Opdivo pharmacodynamics and genomic profiling data from our ongoing Phase 1 trial was accepted for a poster presentation and also selected for a poster discussion at the 2018 ASCO Annual Meeting. As the title denotes, this abstract is focused on selected initial biomarker data being generated from this trial. Cabira is also being studied as a monotherapy in an ongoing Phase 2 trial in patients with PVNS, which is a non-malignant tumor of the joints. The trial design can be seen on slide 11. At ASCO last year, we presented preliminary Phase 2 data that demonstrated efficacy with dosing every two weeks. Some patients discontinued treatment due to tolerability such as eyelid swelling and itching, so we are enrolling up to 30 additional patients to test a less frequent dosing schedule and obtain additional data on improvement in functional outcome measurements. Data from these extra patients will help inform our go/ no-go decision on a pivotal trial which we expect to make by the end of this year. Let's turn our attention now to bemarituzumab, also known as FPA144. As shown on slide 12, bema targets FGF2b overexpressing tumors and is designed to enhance ADCC. We recently initiated a Phase 1/3 global registrational trial called the FIGHT trial. This past December we dosed the first patient in the safety lead-in portion of the trial and expect to begin the Phase 3 portion later this year. The trial design can be found on slide 13. We designed this trial to achieve frontline approval for bema in patients with FGFR2b overexpressing advanced stage gastric or GE junction cancer. The FIGHT trial design is a gold standard double-blind placebo-controlled trial without a crossover and overall survival is its primary endpoint. It will compare bema plus modified FOLFOX6 chemotherapy to placebo plus modified FOLFOX6 in the 10% of patients whose tumors overexpress FGFR2b. Bema is a targeted therapy and we are using state-of-the-art diagnostic tools to help us identify these patients, both through noninvasive blood-based tests and tissue biopsies. A bema trial in progress abstract was accepted for a poster presentation at ASCO. In April, we closed the Phase 1 monotherapy trial studying bema and bladder cancer after evaluating the feasibility and timing of activating clinical sites, the rate of patient enrollment in the trial and the landscape of potential alternative treatment options. So moving on to FPA150, our first-in-class B7-H4 antibody, as shown on slide 14. We have designed this antibody to have two potential mechanisms of action. It releases the checkpoint blockade that B7-H4 puts on the T Effector cell and is engineered to have enhanced ADCC. B7-H4 is overexpressed in multiple solid tumors, including breast, bladder, ovarian and endometrial cancer. Because FPA150 is also a targeted therapy, we are developing an IHC assay to identify patients who might benefit most from treatment. In March we initiated a Phase 1 monotherapy dose escalation trial of FPA150. Once the dose is selected, we plan to open expansion cohorts to enroll patients whose tumors overexpress B7-H4. Our investigators are enthusiastic about enrolling patients and developing this drug since it's a first-in-class checkpoint inhibitor against B7-H4 and despite hundreds of I-O trials to-date, there are no I-O therapies approved in breast, ovarian or endometrial cancer. You can see the trial design on slide 15. I will now turn the call over to Bryan to review our research efforts.

[Bryan Irving:]

Thank you Helen. I am on slide 16. At Five Prime, our success in identifying novel targets arises from our ability to probe the fundamental roles that thousands of extracellular signaling proteins play in virtually any disease process. Our scientists have produced nearly all known secreted proteins and cell service receptors and have developed novel screens to interrogate their function in medically relevant in vitro and in vivo models. In an agnostic fashion, similar to genetic screenings, we can determine which proteins alter the underlying mechanism of disease in ways that produce the desired therapeutic benefit. Our immuno-oncology screens have identified targets which previously unappreciated roles in modulating or regulating immune function in ways that others cannot. And as Aron noted earlier, we also have state-of-the-art technologies to generate drug candidates against these novel targets. We are excited about our next wave of I-O programs. Our most mature preclinical program is FPT155, a first-in-class CD80-Fc fusion protein engineered to activate T cells through multiple mechanisms. You can see it on slide 17. FPT155, which I will refer to as 155, was identified as a highly potent activator of tumor immunity in our in vivo tumor screens. CD80 is a costimulatory molecule expressed on antigen-presenting cells that primarily regulates the activity of the dominant costimulatory receptor CD28. 155 uses the binding interactions of soluble CD80 to first directly engage CD28 to enhance its costimulatory activity, importantly though without the super agonism that was observed with the CD28-targeted antibody. And second, to block CTLA-4 from competing for endogenous CD80, thus allowing CD28 signaling to prevail in T cell activation. We think the direct interaction with CD28 should differentiate it from CTLA-4 blocking antibodies. 155 stimulates anti-tumor immunity in vivo and efficiently costimulates primary human T cells in vitro, but only in the presence of T cell antigen receptor engagement. Work done in preclinical models with 155 suggests this agent has the potential to induce strong single-agent anti-tumor activity and synergistic efficacy when combined with anti-PD-1 therapies. And we are on track to file an IND application or foreign equivalent for 155 in the second half of this year. Beyond 155, we are studying multiple additional targets that are at various stages of preclinical development. We anticipate our future product pipeline to remain robust as we expand our I-O screenings that fuel our IND engine and we continue to pursue the development of additional treatments for patients both on our own and with partners. Now I will turn the call over to Linda to review our financials.

[Linda Rubinstein:]

Thank you Bryan. The full details of our financial results can be found in the press release issued this afternoon as well as slides 18 and 19. We ended Q1 with a strong balance sheet. Cash, cash equivalents and marketable securities totaled $389 million on March 31, 2018, compared to $293 million on December 31, 2017. This increase over the prior quarter reflects $108 million in net cash proceeds from our equity offering in January. Net loss for the first quarter of 2018 was $20 million or $0.63 per basic and diluted share. Collaboration and license revenue was $32 million for the quarter, including a $25 million milestone earned under the cabira collaboration agreement on BMS's initiation of its Phase 2 clinical trial. This is an increase over last year's revenue of $10.1 million. R&D expenses totaled $44 million for the quarter. The increase over R&D expenses of $33.8 million in the first quarter of 2017 was primarily related to increased spending on our bema program, including the initiation of the Phase 1 portion of the FIGHT trial and the initiation of our FPA150 Phase 1 trial. G&A expenses totaled $10 million for the quarter, which was flat year-over-year. Looking ahead, we continue to expect full year 2018 net cash used in operating activities to be less than $135 million. We estimate ending 2018 with approximately $250 million in cash, cash equivalents and marketable securities. I will now turn the call back to Aron for closing remarks.

[Aron Knickerbocker:]

Thank you Linda. So as you heard during this call, we advanced our clinical programs throughout the quarter and we will continue this momentum throughout the rest of the year. You can see our expected milestones on slide 20. We are moving toward late-stage clinical development with the FIGHT trial being our first registrational trial. In addition, our IND engine continues to fill our and our collaborators' pipelines and we are well capitalized. Moreover, we are a financially disciplined company and have multiple levers to fund the company. So I am very confident in the future of Five Prime. Finally, before we open up the call for questions, I really want to thank the patients and investigators participating in our clinical trials, our Five Prime employees and our strategic collaborators. And with that, I will now open the call up to questions.

[Operator:]

[Operator Instructions]. And our first question comes from the line of Robyn Karnauskas from Citi. You may begin.

[Greg Harrison:]

Hi. This is Greg Harrison, on for Robyn. Thank you for taking the questions. I am curious on PVNS. What do you need to see in Phase 2 to make the decision to move on to Phase 3? Do you need to see a complete absence of the edema? Or is there a certain rate that could be acceptable relative to the previous dose?

[Helen Collins:]

So I will take that question. That's a good question. We haven't said specifically. I think we have had conversations with regulatory agencies about how a Phase 3 trial design probably needs to be and I think as you have heard us say before, we think that we have clearly demonstrated the efficacy of this drug, which of course makes sense based on its mechanism of action and the real question's going to be the durability of that efficacy, which is indirectly related to tolerability. So again, I am not trying to evade your question but we haven't actually specifically talked about what that bar would be.

[Aron Knickerbocker:]

That said, we will be making a disclosure by the end of the year of our plans for this program and whether or not we will proceed to a pivotal trial. If that's a go, then we would initiate the pivotal trial in early 2019.

[Helen Collins:]

The one other color I will just add is, again, some of my being vague is because the patients really have a huge say in this, right. So they are the ones that decide is the edema such that, because edema is not a toxicity that we require people to discontinue. So it's really the patients making that risk/benefit decision. Is the edema bad enough, worse or better than the effects of their PVNS? And also is it reversible? We know it's reversible, but how long it takes to reverse.

[Greg Harrison:]

Okay. That makes sense. So is it more based on tolerability and discontinuation rather than the actual existence of the side effects?

[Helen Collins:]

I will go out on a limb and project and say yes because, again, it's the durability of response. So to get durability response, patients are going to have to stay on drug. I mean, they certainly can delay for a while but we know they can't delay indefinitely. So yes, it's discontinuation rate.

[Greg Harrison:]

Okay. Thank you.

[Operator:]

And our next question comes from the line of Kennen MacKay from RBC Capital. You may begin.

[Justin Burns:]

Hi. This is Justin, on for Kennen. In regards to the ongoing cabira plus Opdivo trial, first off, congratulations on completing enrollment there. In your press release, it looks like only one-third of patients are being assessed for tissue biomarkers. Can you provide some color on to why only a third of the patients? Is this possibly based on tumor indications?

[Helen Collins:]

So again, this is Helen. I will answer that. The trial was designed that way initially so that there's 30 patients in each of the tumor cohorts in the combination in the expansion arms. And that was done, again, really just trying to do the balance between expeditious enrollments, because as you may know required biopsies sometimes slow enrollment and then getting the data. The dose escalation Phase 1 has all patients getting baseline and on-treatment biopsies as does the additional pancreatic cancer patients that we are talking about. So we think that if you look at it that way, we are going to have probably about 100 patients that have baseline and on-treatment biopsies. So we think that that's going to be very informative.

[Justin Burns:]

Great. Thank you for the color.

[Operator:]

And our next question comes from the line of Christopher Marai from Nomura Instinet. You may begin.

[Allen Cha:]

This is Allen Cha, on for Chris. Congrats on all the progress. I have got a couple on the FPA150. First, can you give us a rough estimate with respect to when we might see data on the single-agent activity and how fast we can get to interim proof of concept, like just a rough estimate? And second, can you give us some color on the type and range of response that you need to see and whatever else that gets the patients to move forward? And third and last, it seems like you will only be testing in pretreated patients in the Phase 1. Will you be specifically screening for certain prior treatments and any plans for testing treatment naïve patients? That's all. Thank you.

[Helen Collins:]

So goodness, so let me start with the data. I think Phase 1 trials are, again, the primary endpoints and the primary objective is safety, right. Obviously, we do want to see some sign of activity as well, but number one is safety. Having said that, as I said during the prepared notes, the investigators are very enthusiastic about this because both it's a first-in-class and second because specifically, it's going to be right now, at least for tumors that don't have an approved PD-1. So we do anticipate this to enroll quickly. In terms of when we will actually get data that we will be talking about publicly though, it's probably going to be sometime in 2019, even the second half of 2019. In terms of what level of responses we need to move forward, we haven't said that specifically about these tumors. Again most Phase 1 trials, you have to take patients who don't have available therapy. So that's typical of a Phase 1 study. And of course that also means that fairly low responses are of interest usually. And again I don't know you want to add to that, Aron, if you have something?

[Aron Knickerbocker:]

Yes. Well, you probably saw the trial design in the slide. So we will be getting into the selected cohorts we think early next year. And again, those are ovarian, endometrial, bladder and breast. And so we have got an IHC test ready to go. We can find those patients who overexpress this target. And given the mechanism or dual mechanisms of this drug, we would be looking for single-agent activity in that trial and it's an open label study so we will be seeing the data as they emerge. But again, this drug does two things. It turns off the checkpoint inhibition of the Effector T cells. It also acts as an ADCC-enhanced antibody to attract in K cells to kill the tumor cells that overexpress the target. So for those reasons, we would like to see single-agent activity just as we have seen single-agent activity with our other drugs in the clinic in Phase 1. So we look to establish a signal early and make decisions off of that.

[Allen Cha:]

Got it. That was very helpful. Thank you.

[Aron Knickerbocker:]

You are welcome.

[Operator:]

[Operator Instructions]. And our next question comes from the line of Jim Birchenough from Wells Fargo. You may begin.

[Nick Abbott:]

Good afternoon. It's Nick, in for Jim this afternoon. Maybe just starting off with the ASCO abstract title. What should we expect to see in that presentation? I mean, the title is very provocative, Tumor Immune Modulations and Support Future Clinical Applications.

[Aron Knickerbocker:]

Yes. Thanks, Nick. Well, unfortunately, the abstract hasn't published yet. So all we can say is what the title says and I assume you have got it right there in front of you. But it is providing evidence of on-target tumor immune modulation that we think is supportive of future clinical applications. But beyond that, we can't tell you more. There are a panel of biomarkers that have been assessed in these patients, both pre and on treatment, as Helen noted. And those are PD markers as well as genomic profiles of the tumors. But just have to stay tuned until the abstract is published next week and then the poster shown on June 4.

[Nick Abbott:]

Sorry. So should we just expect to see the on treatment as well as the pre data?

[Aron Knickerbocker:]

Yes.

[Nick Abbott:]

Okay.

[Aron Knickerbocker:]

But can't foreshadow what that is at this point.

[Nick Abbott:]

And then going to bema. Can you give us an update on when you think Zai will get regulatory approval? And given the market size, are they interested or able to explore other settings, neoadjuvant, for example?

[Aron Knickerbocker:]

You are talking about Zai in Greater China?

[Nick Abbott:]

Yes.

[Aron Knickerbocker:]

Yes. So we actually already filed the CTA in China. We are anticipating that Zai would begin enrolling patients later this year. But as for CFDA approval, are you asking about --?

[Nick Abbott:]

No. Just when would we expect them to begin to contribute patients.

[Aron Knickerbocker:]

Yes. Later this year is the target, by the end of the year.

[Nick Abbott:]

And then do they have the opportunity to explore other settings such as neoadjuvant, for example, like a window opportunity study?

[Aron Knickerbocker:]

Yes. Zai does have development rights in Greater China, as you are noting. So if they wanted to conduct such a study that would be in their purview to do that. We do have a joint development committee to coordinate and do things as expeditiously and efficiently as we can. But yes, they could do additional work.

[Nick Abbott:]

And the last one. So on FPA, I noticed you have a bladder cohort, yet you just recently terminated the bema bladder cohort. So what is the difference here?

[Aron Knickerbocker:]

Yes. You are talking about bema versus 150?

[Nick Abbott:]

Yes.

[Aron Knickerbocker:]

Yes. We think the target is more abundant for 150, the B7-H4 target as opposed to the FGFR2b target in bladder. So that's a key driver for us, just based on our initial IHC analysis and what's in the literature.

[Nick Abbott:]

Thank you very much.

[Aron Knickerbocker:]

You are welcome.

[Operator:]

Thank you. And I am actually showing no further questions at this time. So I would like to turn the call back to Mr. Aron Knickerbocker, Chief Executive Officer, for closing remarks.

[Aron Knickerbocker:]

Sure. Well, thank you all for joining us today and for your support of Five Prime and we look forward to updating you on future calls.

[Operator:]

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.