Five Prime Therapeutics Inc
Q4 2014 Earnings Call Transcript

Published: 18 Mar 2015

[Operator:]

Good day, ladies and gentlemen, and welcome to Five Prime Therapeutics' 2014 Fourth Quarter Earnings Conference Call. [Operator Instructions] I would now like to hand the conference over to Mr. Aron Knickerbocker, Chief Business Officer. Sir, you may begin.

[Aron Knickerbocker:]

Good afternoon and thank you for joining us. On behalf of Five Prime Therapeutics, I'd like to welcome everyone to our conference call to discuss financial and operational results for the fourth quarter and the full year 2014. Joining me today are Dr. Rusty Williams, Chief Executive Officer; Dr. Julie Hambleton, Chief Medical Officer; and Marc Belsky, Chief Financial Officer. During today's call, Rusty will begin with introductory remarks on our progress during the quarter. Julie will then give you an update on our clinical programs. I will provide an update on our collaborations. And then Marc will discuss our financial results. Finally, we will conclude the call with a Q&A session. 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. And with that, I'll now turn the call over to Rusty.

[Rusty Williams:]

Thanks, Aron. Good afternoon everyone and thanks for joining us. I'm really pleased to report that during 2014 we achieved many important milestones and made tremendous progress in our pipeline and in our research programs. As you know, we began the year with just two candidates in the clinic and now our pipeline has grown to three clinical-stage therapeutics that are being tested in 11 indications. Over the course of the year we significantly expanded our presence in immuno-oncology, signing two separate collaboration agreements with Bristol-Myers Squibb, obviously an established leader in the States. The most recent collaboration with Bristol, which we announced in November, is a clinical trial collaboration in multiple tumor types, combining our CSF1 receptor antibody FPA008 with BMS's PD1 antibody nivolumab. In March of 2014 we also announced the discovery collaboration with BMS that's focused on two immune checkpoint pathways. Furthermore, on the research and discovery front, we've made great progress in our internal immuno-oncology program which has led to the identification of promising antibody targets as well as ligand traps. Turning to our clinical pipeline for just a minute, I'd like to highlight some of the 2014 accomplishments in the development programs of our unpartnered antibody assets FPA008 and FPA144. In November 2014 we reported a phase one healthy volunteer study for FPA008 at the American College of Rheumatology Annual Meeting. These data show that FPA008 was well-tolerated in doses up to 3mg/kilogram and resulted in modulation of key biomarkers that may indicate the potential for clinical benefit. Clearly we'll provide an update on this ongoing study. Given the growing body of data regarding the CSF1 receptor pathway and its potential role in cancer, we've expanded development of FPA008 into six different cancers that we'll evaluate in the nivolumab combination study with BMS. We're also initiating clinical development of FPA008 in pigmented villonodular synovitis, PVNS, a tumor driven by the CSF1 receptor pathway. We expect both trials to begin in mid-2015. So as you can see, we're excited about the potential for FPA008 and have greatly expanded our development efforts around this therapeutic antibody. We're also proud to now have a third therapeutic candidate in a clinical trial. During the fourth quarter we initiated the phase one study for FPA144, our anti-FGF receptor 2b antibody. We're developing FPA144 for a subset of patients of gastric cancer, and we expect preliminary safety data from this trial by the end of the year. Now regarding -- I'm sorry -- FP-1039, our FGF ligand trap, we expect our partner GlaxoSmithKline to report the first data from the ongoing phase 1b trial at a scientific meeting by yearend. GSK continues to enroll patients with squamous non-small cell lung cancer and mesothelioma in the three arms of the study. And in one arm, GSK has already completed dose escalation and has begun dose expansion. As I look ahead, I'm excited that we have the team and the resources to deliver on important milestones in the coming quarters. With that, I'd like to turn the call over to Julie to give a more detailed update on our clinical programs.

[Julie Hambleton:]

Thank you, Rusty. And good afternoon everyone. I'll begin with FPA008. By inhibiting the CSF1 receptor, FPA008 targets monocytes and macrophages which are elevated or activated in multiple disease settings. In cancer, macrophages suppress the immune system's ability to kill cancer cells. In joint diseases such as PVNS and RA, macrophages play a central role in the disease process. Last year in our phase one trial, we completed testing in healthy volunteers and reported safety pharmacokinetic and biomarker data at the 2014 ATR Annual Scientific Meeting. FPA008 was well-tolerated up to 3mg/kg with modulation of biomarkers that may guide dose selection for subsequent trials and may correlate with potential benefit in patients. We observed a dose-dependent suppression of the subset of monocytes in blood called CD16-positive monocyte, and reduction of bone turnover markers which reflect macrophage activity within the bone. Lastly, pharmacokinetic data support dosing intervals or two weeks or more. The phase one trial has advanced to open-label dosing of RA patients who have active disease and are on a stable dose of methotrexate, in order to confirm the safety profile and optimize dosing in this patient population. Based on the data from this open-label portion in RA patients, the trial may then advance into a small randomized, double-blind, placebo-controlled portion. While the primary endpoint of this part of the trial is safety, key secondary endpoints include clinical signs and symptoms such as ACR scores and magnetic resonance imaging. We plan to report preliminary open-label data in RA patients by the end of the year. The dosing biomarker and safety information just reviewed allows us to expand the development of FPA008 into additional indications. As Rusty described, Five Prime is planning a phase 1a/1b study with BMS to evaluate the combination of FPA008 with nivolumab in multiple cancer settings. We have evidence that FPA008 may enhance the anti-tumor activity of PD1 pathway inhibitors. Preclinical data indicate that combining inhibitors of the CSF1R and PD1 pathways may lead to an enhanced anti-tumor immune response compared to either approach alone. In the phase 1a part of the planned study, we will evaluate the safety and tolerability of increasing doses of FPA008 in combination with the approved dose of nivolumab. Once we determine the optimal combination, we will evaluate preliminary efficacy of this combination in patients with non-small cell lung cancer, melanoma, head and neck cancer, pancreatic cancer, colorectal cancer, and malignant glioma. We plan to begin this trial in mid-2015 and expect preliminary safety data from the phase 1a part by the end of 2015 or early 2016. We also recently disclosed that Five Prime intends to develop FPA008 in PVNS. PVNS is a rare CSF1 driven tumor associated with significant morbidity in a subset of patients. We believe the inhibition of CSF1R with FPA008 will reduce joint infiltration by monocytes and macrophages which form bulk of the tumor mass. We plan to begin our phase one/two clinical trial by midyear and anticipate preliminary efficacy data from the phase 1 portion could be available by the end of 2015 or early 2016. Turning next to FPA144. We initiated dosing in our phase 1a/1b clinical trial in December. We are currently enrolling patients with a variety of solid tumors to assess safety and tolerability and to identify the outcome of those to take forward [ph] into gastric cancer patients. For the phase 1b part, we will enroll gastric cancer patients whose tumors show evidence of FGF receptors to gene amplification or FGF receptor 2b protein over-expression as identified by molecular diagnostic assays. Approximately 5% of gastric tumors have FGF receptor 2 gene amplification and additional gastric tumors may have protein over-expression without gene amplification. Both are associated with lower overall survival. FPA144 is a targeted agent for selected patient populations with a high unmet need and has potential for an accelerated development path. We engineered FPA144 to have enhanced ADCC that [inaudible] killer cells more effectively than the native antibody. We have seen tumor regressions with single-agent FPA144 in preclinical models of FGF receptor 2 gene-amplified gastric cancer, so we plan to evaluate this therapeutic initially as a monotherapy. With regards to our partnered product FP-1039, the ongoing phase 1b is a free-on-trial that GSK is conducting in two different studies of lung cancer. Arms A and B are enrolling patients with newly diagnosed or recurrent squamous non-small cell lung cancer whose tumors have amplification of the FGF receptor 1 gene. Arm C of the trial is enrolling patients with newly diagnosed mesothelioma, a tumor in which the FGF2 ligand is over-expressed. GSK has been testing increasing doses of FP-1039 in combination with standard chemotherapy, and once the optimal combination has been determined for each arm, GSK will -- patients will be enrolled to the expansion part of the trial to assess efficacy. GSK has now completed dose escalation in one of the three arms and has begun expansion in that arm. GSK anticipates presenting preliminary data at a scientific meeting by the end of the year. At this point I'd like to turn the call over to Aron to discuss our collaborations.

[Aron Knickerbocker:]

Thank you, Julie. As Rusty mentioned at the beginning of the call, during the first quarter of 2014 we were pleased to announce our immuno-oncology discovery collaboration with BMS and two undisclosed immune checkpoint pathways. In addition to its $20 million upfront payment, $21 million equity stake BMS took in Five Prime, and the $9.5 million research funding, we're also eligible to receive up to $300 million in future development, regulatory and sales-based milestone payments per collaboration target. And importantly, Five Prime is free to pursue all other pathways in immuno-oncology outside of the collaboration. Additionally, during the year we broadened our relationship with GSK. In the third quarter, GSK took a commercial license to an undisclosed muscle disease target that we identified using our proprietary target discovery platform. GSK also expanded our respiratory collaboration from its original scope to include two new target discovery programs. And while I'm discussing our collaborations, I'd also like to provide some additional color on the clinical trial agreement with BMS for FPA008. It's important to note that this is a clinical trial collaboration, not a license or option agreement. And we retain full ownership of FPA008. We will run the trial working closely with BMS and BMS is funding most of the trial including third-party costs. In addition, BMS paid Five Prime a one-time payment of $30 million in exchange for a time-limited right of first refusal that's only triggered if we decide to out-license the product. We and BMS also agreed to work exclusively with each other on CSF1R and PD1, the PDL1 inhibitor combinations, through the same time period as the right of first refusal. We work really well with BMS and this new clinical collaboration builds on the strong relationship that we previously established through our immuno-oncology discovery collaboration. Our track record of establishing new collaborations and expanding existing alliances continue to provide clear evidence that world-leading pharmaceutical companies value our platform and the asset it generates. It also speaks to the breadth of our capabilities to identify novel promising targets and therapeutic candidates in a variety of disease areas. We'll continue to evaluate partnering opportunities in 2015. And at this point I'll turn the call over to Marc to discuss our financials.

[Marc Belsky:]

Thank you, Aron. In the fourth quarter of 2014, Five Prime had a net loss of $11.8 million or $0.55 per basic and diluted share, compared to a net loss of $7.3 million or $0.43 per basic and diluted share for the fourth quarter of 2013. Full year 2014 net loss was $37.4 million or $1.79 per basic and diluted share, compared to a net loss of $28.9 million or $5.23 per basic and diluted share for 2013. The net increase in net loss was primarily related to advancing the FPA144 program into a phase one clinical trial and expanding internal immuno-oncology discovery efforts. Collaboration revenue was $4.6 million for the fourth quarter of 2014, compared to $3.8 million for the fourth quarter of 2013, primarily due to revenue recognized under the immuno-oncology research collaboration with BMS. Collaboration revenue for the full year increased by $5.4 million to $19.2 million in 2014 from $13.8 million in 2013, primarily due to revenue recognized under our collaborations with UCD, GSK and BMS. Research and development expenses were $12.6 million for the fourth quarter of 2014, compared to $8.1 million for the same period in 2013. Full year research and development expenses increased to $43.2 million in 2014 from $32.8 million in 2013. This increase was primarily related to advancing the FPA144 program into a phase one clinical trial and expanding our internal immuno-oncology research. General and administrative expenses were $4 million for the fourth quarter of 2014, compared to $3 million for the same period of 2013. Full year 2014 general and administrative expenses were $13.6 million, compared to $10.4 million in 2013. This increase was primarily due to public company related expenses and non-cash stock-based compensation and cash compensation. Cash, cash equivalents and marketable securities as of December 31st, 2014 were $149.1 million, compared to $75.7 million as of yearend 2013. We expect full year 2015 net cash use in operating activities to be less than $65 million. Taking into account the equity offering we completed in January 2015 which netted approximately $79 million, we estimate ending 2015 with more than $160 million in cash, cash equivalents and marketable securities. We expect to have cash to fund operations into the first half of 2018 without entering into any additional collaboration agreement or receiving any future milestone payments. This provides us runway through efficacy data milestones for all of our current clinical programs. And with that, I'll turn the call back over to Rusty.

[Rusty Williams:]

Thanks, Marc. We feel we've made incredible progress in all our research and clinical programs last year and continued to establish and expand strong collaborations with leading pharmaceutical companies. We look forward to carrying our momentum throughout 2015. We're now happy to take your questions. I want to mention that, also joining us today, Dr. Bob Sikorski, Vice President of Global Clinical Development, Five Prime; and Dr. Brian Wong, our Vice President and Head of Immuno-Oncology research. So, operator, I'll turn the call back over to you to open the Q&A session.

[Operator:]

Thank you, sir. [Operator Instructions] Your first question comes from Brian Abrahams from Wells Fargo. Your line is open, please go ahead.

[Brian Abrahams:]

Hey. Thanks for taking my questions. And congrats on all the progress and productivity this past year.

[Rusty Williams:]

Thanks, Brian.

[Brian Abrahams:]

A couple of questions on the 008 PD1 combo plans. To what extent have the diseases like colorectal cancer and pancreatic cancer, I guess the more exploratory indications, how -- to what extent of those have been clearly associated with tumor-associated macrophages or -- and/or have preclinical support for this concept of PD1 plus CSF1 receptor inhibition? And then, on the PD1 sensitive tumors, what population should we think about you guys potentially exploring there? Will those -- will that be second line or later line following nivo failure? Or what's sort of the path forward in the potentially PD1 sensitive tumor types?

[Rusty Williams:]

Okay. Thanks, Brian. I think to break that question into two parts. The first part is the rationale in the exploratory set of tumors, pancreatic, colorectal and glioblastoma that we've disclosed we'll be combining with nivolumab. So the rationale for those tumors, first of all, with pancreatic, there's a very strong rationale in pancreatic. It's based really on two observations. One is it is a tumor that's rich in tumor-associated macrophages. And second, preclinical data, there was a beautiful study last summer by David Dinardo [ph] at Washington University showing synergy in blocking CSF1 receptor and blocking checkpoints. And the synergy is based on the fact that the CSF1 receptor inhibition led to reduction of TAM [ph], increase in CD8 cells in the tumor, decrease in T-reg [ph] cells in the tumor, and in combination with checkpoint inhibitors, there was a synergy in tumor shrinkage. So that's the compelling preclinical data plus the clinical observation that there are macrophages in the pancreatic cancer. Now, colon cancer is a little bit more conjectural. We have some KOLs who are advocates for that, but I will have to say that one, of all the ones on our list of six, is probably the most conjectural. And then finally, you know, malignant glioma, there has been some report of single-agent activity with respect to CSF1 receptor inhibition. Also there are TAMs [p] in that tumor. And there's, you know, we think there are other data that are suggestive of the fact that a combination may be efficacious there. Now I'm going to let Julie answer the second part of your question.

[Julie Hambleton:]

Yes. Thanks, Rusty, and hi, Brian. Regarding your question about combination in the PD1 sensitive tumors. So as you know, we will be looking at non-small cell lung cancer, melanoma and head/neck. Certainly nivolumab now has approval in both non-small cell lung cancer and melanoma, and with that non-small cell lung cancer specifically in squamous, although we will be looking at tumor histologies in addition to squamous. We do have interest with BMS in exploring some of these settings in which patients don't have a good response to nivolumab as single agents. So you made reference to the nivo-resistant settings, so to speak. We have not fully disclosed all the details of the trial, that's not yet finalized. But once we do so, we'll be able to spend more time with you discussing all the different arms in this trial.

[Brian Abrahams:]

Great. And then one quick follow-up if I may, on 144, how should we think about what we might learn from the data in all-comer solid tumors? Do you have any sense yet in this early dosing whether you might be able to reach exposures equivalent to those that showed activity in the xenographs [ph] with acceptable epithelial toxicities? Thanks.

[Julie Hambleton:]

Yes, you're welcome. Yes. So as you know, we are dose-escalating in all-solid tumor patients, and we do believe that we'll be able to achieve exposures that correlate with potentially efficacious levels based on our non-clinical studies. And this just allows us to move more quickly into dose escalation and identifying more active doses as we get additional sites up and running who have seen more of the gastric cancer patients, before we launch into specifically selecting these gastric cancer patients. We are selecting tumors in the dose escalation portion of the trial, to look forward to the over-expression. However, we don't expect to find many of those tumors to be selected in the instance of having over-expression of FGF receptor 2b. But we'd certainly be able to characterize the pharmacokinetics and safety on these all-solid tumors.

[Brian Abrahams:]

Thanks so much.

[Operator:]

Thank you --

[Rusty Williams:]

Thank you, Brian.

[Operator:]

Our next question comes from Michael Schmidt from Leerink Partners. Your line is open, please go ahead.

[Michael Schmidt:]

Hey, good afternoon actually, and thanks for taking my questions.

[Rusty Williams:]

Sure, Michael.

[Michael Schmidt:]

On FPA008, on the nivolumab combination trials, I was wondering if you are planning to use biomarkers in any way prospectively to, you know, to look at different patient subsets?

[Rusty Williams:]

Thanks, Michael. So, prospectively, we don't plan to use biomarkers. But the biomarkers will be the really key part of this trial because we do plan to learn a lot in the trial, the measurements we have made in the tumors and the circulation, in terms of mechanisms and being able to predict in the future which indications are best. And so, you know, for example, we'll be measuring markers for TAMs [ph], for T cells, for T-reg [ph] cells, and checkpoints, et cetera, and happy to go into those in more detail at another time with you, but anyway, that's what we'll be measuring in conjunction with this trial. Very important aspect of the trial that -- with BMS and we are working on.

[Michael Schmidt:]

Yes, makes sense. And I guess based on the mechanism, would you expect the difference, if you combine FPA008 with either a PD1 antibody or a PD1 antibody?

[Rusty Williams:]

So the question about whether a PD1 or PDL1 antibody would be different in terms of combination with FPA008, you know, theoretically we and BMS believe that they're roughly the same mechanistically.

[Michael Schmidt:]

Yeah.

[Rusty Williams:]

We might be wrong about that, but that's the way we view it. And so we do think, however, that FPA008 has the potential to combine with other immuno-oncology agents beyond the PD1, PDL1 pathway, and we have some preclinical data suggesting that's true and there are other data in the literature that are publicly available suggesting that's the case.

[Michael Schmidt:]

Got it. And then a question on the planned PVNS study. You mentioned potentially having initial data by yearend. Could you just comment on, you know, on the design of that initial phase one study, you know, how many patients do you expect to have treated by yearend and sort of what efficacy measures might you be able to present initially?

[Julie Hambleton:]

Yeah, thanks, Michael. This is Julie, and I'll comment on that. What we have put out is that this is a phase one and phase two combined study. In the phase one component, we will be doing a few dose cohort levels of exploration, looking at optimizing the dosing. Based on our healthy volunteers, as you know, we've only administered two doses of the drug. Because this tumor is a CSF1 driven tumor, we believe that these patients will derive some clinical benefit, that we expect to see some tumor shrinkage, and that will be on dosing for longer periods of time. So we'll do some of that dose exploration in the phase one component. And that's part of the preliminary data that we expect to be able to share by the end of this year or early 2016. Again because this is a CSF1 driven tumor, we do expect to see some tumor modulation at that early phase of the study, before we then launch into a larger phase two component at one set dose.

[Michael Schmidt:]

Got it. It's great. Thank you so much. And congrats on the progress.

[Rusty Williams:]

Thank you, Michael.

[Operator:]

Thank you. Our next question comes from Eun Yang from Jefferies. Your line is open, please go ahead.

[Eun Yang:]

Thank you. A follow-on question on PVNS, for 008. This indication could be the fastest way to get the product to market. And based on [inaudible] preliminary data in less than 20 patients with over response rate of 80% [ph], it's highly encouraging. So, during the decision [inaudible] indication, do you have any indication from the FDA what would be required for approval aside from overall response rate?

[Rusty Williams:]

Eun, thanks for the question. Julie again will comment on it.

[Julie Hambleton:]

Yes, thank you. So as we generate these data, obviously when we feel we have an adequate data set, we will discuss this with the FDA to actually talk about what our registrational path would look like. At the current time, you're right, it may be overall response rate, duration of response. But certainly the FDA may want to see additional data. So we can't comment on that at this point in time.

[Eun Yang:]

Okay. And then a question on RA. So, currently in phase 1b dose finding study, you are enrolling active RA patients on methotrexate. [Inaudible] is expected by yearend, are we going to see if there is going to be any additive or synergistic effect of -- to methotrexate?

[Julie Hambleton:]

Yes. So as you stated, these patients have active disease and they are on methotrexate. The requirement for the trial is that they're on a stable dose of methotrexate. Most have been on for a prolonged period of time with their active disease. So, at the open-label component of the trial, we do not have obviously a place-controlled, so we will be looking at the MRI scans at baseline, and then while on FPA008. We won't have the active comparator until -- or if we move forward into the small randomized component.

[Eun Yang:]

I see. So, don't have a comparator to the baseline, so, how many different doses of 008 are we going to see by yearend?

[Julie Hambleton:]

We have in the current protocol three doses that we plan to test. And that's approximately three patients in each of those cohorts. But we do have provisions to do additional dose exploration, which could be a dose level or maybe an additional dose administration. So we'll just make those decisions as the trial advances in this open-label component.

[Eun Yang:]

Okay. Thank you.

[Julie Hambleton:]

Yes.

[Rusty Williams:]

Thanks, Eun.

[Operator:]

Thank you. [Operator Instructions] And our next question comes from Jim Birchenough from BMO Capital Markets. Your line is open, please go ahead.

[Nick Abbott:]

Good afternoon. It's Nick in for Jim this afternoon. Thanks for taking my questions. Two questions, again on 008 I'm afraid. And the first one relates to the competitive landscape. Obviously Plexxikon has listed their phase three trial for PVNS. There are at least two antibodies already enrolling patients, PVNS, one from Roche and one from Novartis. So, do you happen to know anything about those antibodies, how your antibody compares? Novartis is testing two monthly dosing in their trial, for example. Do you think you can stretch to two monthly dosing? And then I have a follow-up. Thanks.

[Rusty Williams:]

Thanks, Nick. So the Roche antibody blocks receptor dimerization, our antibody blocks activation of the receptor by ligands. They're, in our view, roughly equivalent in terms of their effects. Certainly if you look at the effects on biomarkers like CD16-positive monocytes in circulation, it seems to be very similar -- they seem to be similar in in vitro studies as well. The doses that Roche has reported using in the clinic are higher than our doses, and we don't know if that's important or not. But one would expect them to back in similar ways. The Novartis antibody, by contrast, is different, because it's an antibody against the ligand CSF1. Now it might have the same effects in this particular setting, it's a little hard to say, but it doesn't block, if there is any IL34 involved in this tumor, because those are the two ligands, right, CSF1 and IL34? If there's any IL34 that's involved in promoting the expansion of these macrophages after they get in the joint, then their antibody would not block that. But the clinical data will be -- that will trump all of my conjectures.

[Nick Abbott:]

Thanks. And a follow-up, notwithstanding your answer to Michael's question earlier, macrophages can express PDL2 and -- sorry, PD ligand 2, I did say PDL2 -- I'm tripping off over myself. So the question really is, what do we know about PDL1 versus PDL 2 expression on macrophages and in particular sort of macrophages you find in tumors? And could therefore there be a benefit to targeting PD1 as opposed to PDL1? Thanks.

[Rusty Williams:]

I see. So your question is, would you get broader coverage by targeting PD1 as opposed to PDL1 -- about the two ligands. I'll let Brian Wong take a crack at this.

[Brian Wong:]

Hi, Jim. Watch out for tough questions. I really -- so I think what's been reported on macrophages and PDL2 is expressed along with other checkpoints actually, but also PDL1 can be expressed on macrophages in some settings. And at least from what we know from the preclinical data, they're so -- there's not enough information to be distinguished between the activity of the two, other than that PDL1 seems to be more predictive marker than PDL -- PDL1 seems to be more of a predictive marker than PDL2 in determining the response to PD1 therapy.

[Rusty Williams:]

But I think that, you know, you've answered the question for me, Nick, and that is theoretically, if you block PD1, might you get more coverage than by blocking PDL1. I think theoretically that's the case, but we don't have any data to actually show that.

[Nick Abbott:]

Okay, thanks. I'll look forward to data emerging during the year, it's going to be exciting.

[Rusty Williams:]

Okay. Thank you, Nick.

[Operator:]

Thank you. I'm showing no further questions at this time. I would like to hand the conference back over to Mr. Rusty Williams for closing remarks.

[Rusty Williams:]

Okay, thanks. Thanks to all of you for joining us today. And we look forward to updating you on our continued progress throughout the year.

[Operator:]

Ladies and gentlemen, thank you for participating in today's program. This concludes our conference. You may all disconnect. Have a wonderful day.