Infinity Pharmaceuticals Inc (INFI) 2016 Q4 法說會逐字稿

Ladies and gentlemen, thank you for standing by. Welcome to the Infinity Pharmaceuticals conference call to discuss the Company's financial results for the full year 2016. My name is Amanda and I will be your operator for today's call.

(Operator Instructions)

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, Senior Director of Investor Relations and Corporate Communications at Infinity. Please go ahead.

Thanks, Amanda, and good afternoon, everyone. Welcome to today's call to discuss our recent business progress and review our fourth-quarter 2016 and full-year financial results. With me here today are Adelene Perkins, Chief Executive Officer; Jeff Kutok, Chief Scientific Officer; Claudio Dansky Ullmann, Senior Vice President, Clinical Development; Dr. Joe Pearlberg, the Medical Lead for our IPI-549 Program; and Larry Bloch, President. 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 objectives, the therapeutic potential of our product candidates, our strategic plans and strategies, and financial projections. Our actual results may differ materially from what we project today due to a number of important factors, including the considerations described in the risk factor section of our annual report on Form 10-K for the full year 2016, and in other filings we may make with the SEC.

These forward-looking statements represent our views as of only today. We caution you we may not update them in the future, whether as a result of new information, future events, or otherwise. Now I'd like to turn the call over to Adelene.

Thanks, Jaren. Good afternoon, everyone, and thanks for joining us on today's call, particularly those of you who are battling today's nor-eastern blizzard. We're particularly pleased with the progress we're making with IPI-549, the first and only selective PI3-kinase gamma inhibitor in clinical development.

Our Phase 1 study in patients with advanced solid tumors is enrolling ahead of schedule. We are maintaining strong fiscal discipline, and we have an experienced team in place that's executing with a great sense of urgency to deliver meaningful data within our two-year test runway. Today, we will review our progress in advancing IPI-549, and also review our full-year 2016 financial results.

We had a number of key accomplishments last year that position us to make important progress this year. Last November our preclinical data, which established the objective for our ongoing clinical study, were reported in back-to-back publications in Nature.

We also entered a clinical trial collaboration with BMS for the supply of Opdivo, a PD-1 immune checkpoint inhibitor, for the combination component of our study, which we initiated in December. Enrollment in this first combination cohort was completed in January, and we are well on our way to completing enrollment in the second combination cohort.

We are excited about IPI-549 because it represents a unique immuno-oncology approach, by reprogramming macrophages within the tumor micro-environment, converting them from a pro-tumor to an anti-tumor phenotype. Our preclinical data, which we'll review momentarily, provides compelling rationale for our Phase 1 study and underscores the potential for IPI-549 to serve as the backbone for a wide spectrum of combination therapies for the treatment of solid tumors.

The Phase 1 study is evaluating IPI-549, both as a monotherapy and in combination with Opdivo in a broad range of patients with advanced solid tumors. The primary objective of this study is to establish the safety profile of IPI-549 as a monotherapy and in combination with a checkpoint inhibitor. We're very encouraged by the tolerability of IPI-549. At doses that provide near complete suppression of PI3-kinase gamma, as no patients have discontinued treatment due to drug-related side effects to date.

The current dose-escalation phases of the study evaluating IPI-549 as a monotherapy and in combination is very important, because it enables us to learn about the safety, pharmacodynamic, and pharmacokinetic profile of IPI-549, and determine the optimal doses to evaluate in our expansion cohort. Through these expansion cohorts, we will generate additional data for monotherapy treatments and also a combination of IPI-549 in Opdivo in specific types of solid tumors, including non-small cell lung cancer, melanoma, and head and neck cancer.

We had the honor of presenting our preclinical and early clinical data in peer-reviewed forum that enable us to share our findings and seek feedback from highly regarded scientists and clinicians. Less than two months ago at the plenary session of the PI3-kinase Keystone Symposia, we presented a summary of our recent publications in Nature, along with the Phase 1 data from the first nine patients previously presented at the AACR Triple Meeting in New York last September.

Additionally, an update of the Phase 1 monotherapy data were presented in a plenary session at the International Congress on Targeted Cancer Therapies, or TAT, last week. And we're looking forward to sharing updated data from the ongoing monotherapy module, as well as initial data from the combination-dose escalation module at the AACR Annual Meeting next month. These data will be reviewed during both an oral education session on Saturday, April 1, and in a poster session on Tuesday, April 4.

We are also hosting an event for the investment community on Saturday evening, April 1, during which time study investigators will be available to speak about their experience treating patients with IPI-549.

As we look ahead, we expect to make progress in the following three key areas this year. First, we will complete our monotherapy and combination dose-escalation modules. We anticipate completing the monotherapy dose escalation in the first half of the year, and the combination dose escalation in the second half of the year.

Second, we will begin enrolling patients in both the monotherapy and combination expansion cohorts in the second half of 2017. And third, we will report updated Phase 1 data throughout the year, first, at the AACR annual meeting next month, and then in a peer-reviewed forum in the second half of 2017.

Before we provide a more detailed review of IPI-549, I'd like to highlight the promotion of two key people to our executive leadership team: Claudio Dansky Ullmann, our Senior Vice President of Clinical Development; and Jeff Kutok, our Chief Scientific Officer. Claudio has led our clinical development team since joining the Company in 2015. He has more than 30 years experience in developing medicine at Millennium Takeda, as well as at the National Cancer Institute.

During this time, Claudio participated in and led numerous early stage in late-stage clinical trials, including studies evaluating treatments for lung and head/neck cancers, melanoma, and other solid tumors. His extensive work at the NCI focused on immuno-oncology and drug resistance.

Jeff Kutok has played an instrumental role in overseeing our biology and translational science efforts since joining Infinity in 2010, including leading the Infinity team that advanced IPI-549 into clinical development and co-authored our recent back-to-back publications in Nature on PI3-kinase gamma and IPI-549. His experience in translational research and in the medical pathologist at Harvard Medical School and Brigham and Women's Hospital is a perfect complement to our clinical team.

And with these introductions, I'm going to turn the call over to Jeff to summarize our pre-clinical data, followed by Claudio, who will review our clinical study. It's been a pleasure to work with Jeff and Claudio, and we look forward to their continued contributions in advancing IPI-549.

Thanks, Adelene, and good afternoon, everyone. Our discovery of IPI-549 provides us the unique and exciting opportunity to be the first to explore the potential therapeutic benefit of this highly selective PI3K-gamma inhibitor. Through research collaborations with colleagues at the University of California, San Diego, and Memorial Sloan Kettering, we've learned that PI3K-gamma is highly expressed in tumor-associated macrophages, and that the blockade of PI3K-gamma signaling by treatment with IPI-549 results in reprogramming macrophages.

This reprogramming shifts macrophages in the tumor micro-environment from the M2, or pro-tumor, phenotype to the M1, or anti-tumor, phenotype, and increases the number of T cells that attack the tumor and the production of pro-inflammatory cytokines. In terms of activity observed pre-clinically, we've demonstrated dose-dependent single-agent anti-tumor activity in multiple solid tumor models, including models of lung cancer, melanoma, head and neck cancer, colon cancer, and breast cancer.

Additionally, in preclinical models, treatment with IPI-549 in combination with a checkpoint inhibitor showed greater tumor growth inhibition and improved survival rates, including a greater number of complete tumor regressions when compared to treatments with either IPI-549 or the checkpoint inhibitor alone. The combination treatment resulted in long-lasting anti-tumor immune memory, as evidenced by the lack of tumor growth upon re-challenge with the same tumor in the absence of any treatment.

While it's encouraging to observe the synergistic activity of IPI-549 with checkpoint inhibition, resistance to checkpoint blockade therapy represents another challenge. Our preclinical data demonstrate that increased pro-tumor M2 macrophages are associated with resistance to checkpoint inhibitor monotherapy, and treatment with IPI-549 in combination with checkpoint inhibitors is able to overcome this resistance by reprogramming macrophages from the M2 pro-tumor phenotype to the M1 anti-tumor phenotype.

The key takeaways from our preclinical findings are as follows. First, inhibition of PI3K-gamma plays a key role in reprogramming tumor-associated macrophages; second, we have demonstrated monotherapy and combination activity of IPI-549 in multiple preclinical models of cancer; and third, we have shown that treatment with IPI-549 can overcome resistance to checkpoint inhibition. This collective body of research represents important contributions to the field of immuno-oncology.

On April 1, I will review our IPI-549 program during an oral educational session at the AACR annual meeting. It's an honor to be invited to share our innovative chemistry, preclinical research, and clinical data in this forum, and I hope to see many of you there. Our preclinical discoveries provide the foundation for our ongoing clinical study Phase 1 of IPI-549, which I will now turn to Claudio to review in more detail.

Thank you, Jeff. I'm really pleased to update you on our progress with IPI-549. There is a growing need for treatment options for patients who do not respond to current immunotherapies, including checkpoint inhibitors. Even when there is an initial response to checkpoint blockade, resistance often subsequently develops. Given our preclinical data demonstrating that IPI-549 can overcome resistance to checkpoint blockade, I'm very excited about where we stand today and what we could accomplish in the future.

While it's still early days, I want to share with you a few reasons I believe in the therapeutic potential of IPI-549, while our investigators have been so supportive, and why our study has been progressing ahead of schedule. First, IPI-549 is the first and only selective PI3-kinase gamma inhibitor in the clinic. The unique mechanism of action of reprogramming macrophages to create a more favorable tumor micro-environment and facilitate an anti-tumor immune response makes IPI-549 a great partner for combination with today's immunotherapies.

Second, the preclinical data supporting this first-in-class therapy provides a compelling rationale for our ongoing Phase 1 study. Third, as once-daily oral therapy, IPI-549 is easy to administer. And fourth, the safety profile today is excellent, and no patients have discontinued treatment due to drug-related adverse events.

This treatment study is designed to determine the safety, recommended Phase 2 dose, and activity of IPI-549 in approximately 135 patients. The study includes four distinct modules, which I will now review.

The first module is a monotherapy dose-escalation phase in patients with advanced solid tumors. This first module allows us to define the safety, tolerability, pharmacokinetic and pharmacodynamic profile of IPI-549, and to determine a recommended single-agent Phase 2 dose. We have completed patient enrollment in five dose-escalation cohorts, evaluating once-daily doses of IPI-549 ranging from 10 milligrams to 40 milligrams.

We are extremely pleased with the safety, PK and PD data observed today. We're near complete suppression of PI3-kinase gamma, no serious drug-related side effects have been observed, no dose-limiting toxicities have been reported, no patients have discontinued treatment due to drug-related side effects, and the maximum tolerated dose has not been reached. This monotherapy safety data represents a significant derisking for our program.

Based on our PK and PD data, which showed significant suppression of PI3-kinase gamma at 20 milligrams once daily, we felt confident in initiating the second module of our study early last December. The goal of the second dose-escalation module is to demonstrate that IPI-549 and Opdivo can be safely combined and to establish a recommended Phase 2 dose for this combinations.

We initiated the first combination cohort at 20 milligrams IPI-549; that's the standard regimen of Opdivo. We continued enrollment in the first combination cohort in January and have already enrolled the majority of patients in our second cohort evaluating 30 milligrams IPI-549 with Opdivo. Demonstrating the safety of this combination represents a key derisking event for the program, and will enable us to more formally test the efficacy of this combination in the disease-specific expansion cohorts.

Our monotherapy and combination expansion cohorts represent the third and fourth modules of our study. Module 3, our monotherapy expansion cohort, provides an opportunity to generate more simulation data in a greater number of patients with a variety of solid tumors, advanced solid tumors. Since this is an all canvas cohort, we also have the opportunity to learn about additional potential indications for IPI-549.

The fourth module will evaluate IPI-549 in combination with Opdivo in patients with specific types of cancer, including non-small cell lung cancer, melanoma, and squamous cell carcinoma of the head and neck. In addition, involvement to the disease-specific cohorts we serve for patients who have demonstrated initial resistance or those who initially responded, but subsequently developed resistance to checkpoint therapy. This fourth module is a direct test of whether IPI-549 can overcome checkpoint resistance as demonstrated in pre-clinical models and published in Nature.

Translational research will be critical to helping us better understand how IPI-549 works in patients and will inform future studies. To that end, I want to emphasize that pre-treatment and all treatment biopsies are mandatory for all expansion cohorts so that we can better understand the tumor basics of patients who respond and identified biomarkers of response and resistance.

We are pleased to share the initial data from our monotherapy and combination dose-escalation modules at the AACR annual meeting next month. As Jeff mentioned, he will review our IPI-549 forum during an oral educational session on Saturday, April 1, which will include an overview of our clinical data. Then we will provide a more detailed review of our clinical data during a poster session on Tuesday, April 4.

While our abstract is embargoed by AACR until March 31, we can tell you that we're planning to provide an update on 15 patients in module one of our monotherapy dose escalation, as well as at least 6 patients in module two our combination dose escalation. The presentation will be focused on safety, pharmacokinetic, and pharmacodynamic data.

I look forward to seeing many of you at the AACR and to sharing additional clinical updates with you at medical [meetings] the second half of 2017. Now Larry will review our 2016 financial results.

Thank you, Claudio. What you've heard from the Infinity team is a great deal of enthusiasm for IPI-549, which is rooted in compelling science, the excitement of advancing potential first-in-class oral therapy, and the tremendous support of our investigators. We expect a data-rich 2017 and have the financial resources to complete all four modules of our clinical study within our current cash runway, which extends into the first quarter of 2019.

I'll now summarize our financial results for the full year 2016. Revenue during 2016 was $18.7 million and was related to our previous collaboration agreement with AbbVie for duvelisib. Revenue during 2015 was $109.1 million, all of which related to the AbbVie collaboration.

In 2016, we also recorded a nonrecurring gain on AbbVie's opt-out of the duvelisib collaboration of $112.2 million. This nonrecurring gain represents the remaining deferred revenue of $112.2 million, as of June 24, 2016, from the previous collaboration with AbbVie for duvelisib. The AbbVie opt-out is irrevocable, and we have no further obligation to continue to provide AbbVie with any services. Additionally, we did not record any gains during 2015.

R&D spend for 2016 was $119.6 million compared to $199.1 million for 2015. The decrease in R&D expense year over year was primarily related to a 2015 exercise option payment to Takeda, our restructuring activities, and a reduction in clinical development expenses for duvelisib.

General and administrative expense was $42.2 million for 2016 compared to $37.1 million for 2015. The year-over-year increase in G&A expense is primarily due to restructuring activities.

Net loss for 2016 was $30.1 million, or a basic and diluted loss per common share of $0.61, compared to a net loss of $128.4 million, or basic and diluted loss per common share of $2.62 for the same period in 2015. At December 31, 2016, we had total cash, cash equivalents, and available-for-sale securities of $92.1 million, compared to $245.2 million at December 31, 2015, and $112.3 million at September 30, 2016.

I will also review the 2017 financial guidance that we provided in January, and it remains unchanged. We expect net loss for 2017 to range from $40 million to $50 million, and we expect to end 2017 with a year-end cash and investment balance ranging from $40 million to $50 million.

Based on current operating plans, we expect our existing cash, cash equivalents, and available-for-sale securities at December 31, 2016, will provide cash flow rate into the first quarter of 2019. Our cash runway expectations exclude additional funding or business development activities.

We're off to a very strong start in 2017 and expect to make continued progress in our Phase 1 study throughout the year. We look forward to providing updated data from our clinical study next month at AACR, as well as additional data updates throughout the year as we pursue our goal of bringing considerable benefits to patients. We hope to see many of you at AACR meeting in just a few weeks. And now we're happy to take your questions.

(Operator Instructions)

Anupam Rama, JPMorgan.

Hi guys, it's Eric in for Anupam this afternoon. I hope you guys are staying warm and dry. Thanks for taking the question. Claudio, you noted expectations of presenting data from six patients from the Opdivo combination in AACR. Is that inclusive of patients who would be evaluable for [resis] responses in addition to initial safety, PK, PD? And I have a follow up.

Yes, as you recognize, the key focus on the dose escalation, as we explore the combination is the safety, because that's the key issue that we want to be able to say that we have a viable combination to move forward. Obviously, we are going to look into [particular] signals, depending on what type of patients we get and what they have been prior exposure to checkpoint inhibitors in that particular cohort. And if those are usual responders or not, or expected to respond or not to checkpoint [blockade].

So we may be looking at that type of activity, but I think we should emphasize that, that should not be the focus in terms of the dose escalation, and that it should be mainly efficacy. Hopefully, we will have at least a very or stronger read-out once we move forward with expansion cohorts in very defined tumor types.

I'll just remind you, Eric, that in the dose escalation, it's all comers so we don't have the homogeneity of patients in the tumor type that all have progressed on a PD-1 at the recommended Phase 2 dose. So as Claudio outlined, the modules one and two really are about safety, and three and four get to efficacy.

Got it. With the initial focus here still being around dosing, short of reaching an [NTD], what measures are you looking at to establish or, solidify a biologically effective dose with 549, both as monotherapy but also in combination with Opdivo? Thanks.

Joe Pearlberg gets to take that question.

Thank you, Adelene, short of an NTD for both the monotherapy, as well as the combination dose-escalation arms of the study, we're going to really look at the totality of all of the data, which will include safety, tolerability, the PK, and PD data to make a decision for each of those respective cohorts with respect to a recommended Phase 2 dose.

Got it. Thank you. Thanks for taking the questions.

Thanks, Eric.

Katherine Xu, William Blair.

Hi, good afternoon. I'm just wondering what is the effective toxicity of 549? Does that include [mono] supression or any others?

So Katherine, we will just remind you that to date, we haven't seen any side effects, and that will be discussed in more detail in the upcoming AACR presentation. But Joe can share with you what was presented at the last AACR meeting in September on that.

Thank you, Adelene. At the presentation in September of 2016, we presented data on nine patients. What we reported at that time there were no drug-related SAEs, there were no DLTs, and most of the adverse events have been low grade, that is Grade 1, Grade 2.

And in fact, going back even further, the preclinical data package really did not suggest anything concerning in terms of toxicity. And since this is a first-in-class compound, IPI-549 in targeting the gamma isoform of PI3K, it's distinct, it's unique from the other isoforms. We are very well aware of the side effect profile that's associated with inhibiting the delta isoform of PI3K. We're also aware of the side effect profile of inhibiting the alpha isoform of PI3K.

And I'll also add our investigators are very well experienced in the field of immuno-oncology. So they and we are very keen with regard to the [expective] toxicity of the immuno-therapeutic agents, and we're going to present a complete safety profile of IPI-549 in a couple of weeks at the AACR meeting, which we look forward to.

Great, and then from the preclinical data or the data that you've seen so far in the clinic, do you see 549 could convert to PDL negative tumors to positives toward that direction? And also, when you talk about overcoming resistance to anti-PD1, can you -- is there any characterization of those resistance? For example, is this [inverse refactory]? Are there any specification on those and are there any differential activities against the potential different phenotypes of resistance?

Jeff can take that one.

This is Jeff. Let me start by answering your second question with respect to the overcoming of resistance in our preclinical models. The models that we looked at that were resistant to checkpoint inhibition had a very unique phenotype, and it was that they were very rich in M2 tumor-associated macrophages.

And we showed that there was a differential sensitivity between sensitive and insensitive tumors, depending on the level of the M2 macrophages. And we subsequently showed that in combination with a checkpoint inhibitor, IPI-549 was able to effectively reverse the M2 to M1 ratio, and subsequently activated a anti-tumor T-cell response.

So the preclinical data pointed to a myeloid-rich tumor, which would potentially be insensitive to checkpoint inhibition. So this is something that, as Claudio alluded to, we're going to be actively pursuing in the clinic, in answer to whether 549 can reverse this resistance. And your first question, could you repeat it for me please?

Does it convert PDLs negative to PDL positive?

Yes, so it's an interesting question. Often the response of a tumor to increasing PDL1 is mediated through interferon gamma responses. It's an adaptive resistance concept that [true partle] has put forward. And we have shown that there is an increase in gamma interferon induction preclinically with 549 treatment, and we have shown that there is an increase in PDL1 expression in the tumors in our preclinical study. So it's possible that in the clinic, we will increase the PDL1 level on tumors with 549 treatment.

Thank you.

Thanks, Katherine.

Mike King, JMP Securities.

Good afternoon. Thank you for taking my call. This is Patrick for Mike King. Just have some quick questions regarding upcoming data. What data point should investors be most watching for, and how should investors think about the [odds of] success for 549? Thank you.

So the most important data in the first module, the dose escalation of our Phase 1 study, is the tolerability and determining the recommended Phase 2 dose to take into the expansion cohorts. We'll be able to explore efficacy in, particularly in the combination with Opdivo, more homogeneous patient population. And those cohorts will begin in the second half of this year.

And to add to that, we're going to present the pharmacodynamic data that it's clearly showing how, at least in the areas we're measuring, how we're achieving meaningful suppressive concentrations of our target. So I think that's very relevant as we move forward.

Okay, also about duvelisib, I know it's licensed to you with TM, but maybe you can remind us how the trial is set up for [security] to ofatumamab, and what is the milestone payment at (inaudible)? Thank you.

Sure Patrick, so the DUO trial, which is evaluating duvelisib versus ofatumumab has an PFS endpoint and that trial is now being run by Verastem. If the trial is successful, they will owe us $6 million milestone. And then subsequently, if they file and have an NDA accepted, a $22 million milestone.

Okay, makes sense. Thank you.

(Operator Instructions)

Jim Birchenough, Wells Fargo Securities.

Hi, thanks for taking our questions. This is Yanan in for Jim. So first of all for the AACR data presentation, I'm wondering if we are going to see data for the biomarker for M1, M2 conversions from tumor biopsies?

I would just turn it over to Claudio to answer. I would just remind you that we are not collecting the biopsies until we get to the expansion cohort phase.

So to complement, so basically the answer is no because we are not maintaining biopsies at this point either for the monotherapy dose escalation or for the combination dose escalation. So we will not have that data to present.

Great, thanks, and you mentioned that you have achieved near complete inhibition of PI3K-gamma. Have you talked about at what dose level that occurred?

Yes, I can comment and then Joe can comment. As we move forward in the different dose escalation, we have been doing almost as much as possible real-time assessment. So as we said in our initial remarks, we already see meaningful suppression of 20 milligrams in the monotherapy dose escalation. And then we're obviously following the same story for 30 milligrams and we're waiting for the 40 milligrams data. But basically we can say confidently that we are achieving good levels of suppression even at 20 milligrams.

Now as Joe was referring earlier, once we have the complete data set of all the dose escalation cohorts, we will look at the totality of the data and see how that performed in terms of (inaudible) [suppression].

Great, last two quick questions. One is you mentioned enrollment was ahead of schedule. Could you talk about whether that's true for both the monotherapy portion in addition to the combination portion? Also, have you gotten certain KOL feedback after you provided the data at TAT? Thanks.

This is Joe Pearlberg; I'll answer the first part of the question, and the answer is yes, for the monotherapy and combination dose-escalation arms, enrollment is ahead of schedule. And now I will now turn to Claudio with regard to the investigator feedback from the TAT conference.

At TAT, one of our -- the main enroller actually, Tony Tolcher presented data in the oral session, and also Jeff Wolchok presented some of the preclinical rationale in his work lecture. We had very positive feedback from investigators in relation to what they saw in terms of the data, where we are with the program, and the potential directions where the product could go as we move forward. If that's the question you're asking.

Yes.

And Yanan, I think both the enthusiasm from TAT and to Joe's response about a enrolling ahead of schedule, it's we believe due to some of the reasons Claudio mentioned earlier, that it's an easy-to-administer oral drug, it's been well tolerated. For any who are interested in this whole M2 to M1 reprogramming, we have the -- it's the only PS3-kinase gamma inhibitor in development and for patients who progress on a checkpoint inhibitor, there are few options. So we think there are a lot of sustainable reasons why that's true for both the monotherapy arm and the combination arm of the trial.

And also, as -- maybe as a measure for you regarding involvement, as you recognize with all the competition from different trends and different combinations, the fact that we opened enrollment for the combination cohort in mid December, we continued enrollment of the six patients by the first half of January this year. So I think that speaks to the robustness or strong support that we get from investigators about our trial.

Great. Thanks for taking the questions and congratulations on the progress. Thanks.

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

Thanks, Amanda. We're looking forward to presenting our data at AACR in Washington, DC and hope to see many of you there, along with our IPI-549 study investigators at our investor event on Saturday evening, April 1. Please mark it on your calendars, and Jaren will follow-up with the details. We hope you all have a good evening, and stay safe from the storm. And thanks again for joining today's call.