Good morning, and welcome to NGM Biopharmaceuticals's Conference Call. At this time, all participants are in a listen-only mode. There will be a question and answer session after the prepared remarks. As a reminder, today's call is being recorded. I would now like to turn the call over to Brian Schoelkopf, Head of Investor Relations at NGM Biopharmaceuticals. You may begin. Thank you, operator, and good morning, everyone. Thank you for joining us to discuss the top-line efficacy and safety data from our phase II CATALINA trial evaluating treatment with NGM621 in patients with geographic atrophy, or GA, secondary to age-related macular degeneration. During this call, we will refer to our press release issued this morning, as well as accompanying slides, which are available in the Investors and Media section of our corporate website at ngmbio.com. This morning, you will be hearing from Dr. David Woodhouse, NGM Bio's Chief Executive Officer, and Dr. Hsiao D. Lieu, our Chief Medical Officer. Dr. Erin Henry, our Head of Ophthalmology, Clinical Development, and Siobhan Nolan-Mangini, our President and Chief Financial Officer, will join us for the question and answer session. We remind you that during this call, we will be making forward-looking statements, including those detailed on slide two and any other statements that relate to future events or our future performance rather than historical fact. These forward-looking statements involve numerous risks and uncertainties that could cause actual events, performance, and results to differ materially from those described. These risks and uncertainties are identified and described on slide two and in today's press release, as well as under the caption Risk Factors in our quarterly report on Form 10-Q for the quarter ended June 30, 2022, which can be found on our website. 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 our CEO, David Woodhouse. Thanks, Brian, and good morning, everyone. Thank you for joining our call. Earlier this morning, we announced top-line data from CATALINA, our 56-week phase II trial evaluating NGM621 compared to sham control in patients with GA secondary to age-related macular degeneration. NGM621 is a humanized IgG1 monoclonal antibody we designed to inhibit activity of complement C3 with the goal of reducing disease progression in patients with GA. To summarize the key takeaways from this top-line readout, as we announced in our press release this morning, CATALINA did not meet the primary endpoint of a statistically significant rate of change in GA lesion area over 52 weeks versus sham, as assessed by the slope analysis. We are surprised and, of course, disappointed that the study did not meet its primary endpoint and are still analyzing the data to determine what additional learnings we can glean from the trial through secondary and post-hoc analyses. Xiao will describe some of these early analyses in greater detail in a moment. Briefly, in a pre-specified secondary analysis using the MMRM method, NGM621 dosed every four weeks and every eight weeks showed a treatment effect with a Q4 arm achieving an effect rate of 19.8% and a nominal P value of 0.027 at the 24-week time point. While this effect was diminished at 52 weeks, we nevertheless are encouraged by the signal we saw using MMRM. Furthermore, to investigate unexpected baseline characteristics we observed in patients in the sham arm, we undertook post-hoc subgroup analyses to adjust for the inherent complexities of large GA lesions, including their measurement challenges that may have introduced unexpected variability into the CATALINA results across all arms. The results of these additional analyses revealed some intriguing findings that we believe warrant further exploration. This is something we'll be discussing with our partner, Merck, as we further digest the data and determine next steps. On the safety front, as we expected, NGM621 demonstrated a favorable safety and tolerability profile in the study with no evidence of increased CNV conversions compared to sham, and in fact, numerically fewer cases of CNV in NGM621 treated patients. In addition, there were no drug-related serious adverse events. Given the retinal community's focus on CNV conversion and other key safety parameters, including intraocular inflammation, we're encouraged by the clean safety profile NGM621 demonstrated in CATALINA. I'll now turn the call over to Dr. Hsiao D. Lieu, our Chief Medical Officer, to present the CATALINA results in more detail. Hsiao? Thank you, David, and good morning, everyone. I wanted to start with just some quick disease background. GA is an age-related progressive retinal degenerative disease that is associated with an irreversible loss of vision. It is the leading cause of blindness in the developed world, and there are currently no approved treatments for the disease. As GA progresses, patients lose their central vision. Severely limited vision can have a devastating impact on everyday functioning and on quality of life. Now I will review the CATALINA study design. CATALINA enrolled 320 patients diagnosed with GA secondary to AMD in one or both eyes. The primary objectives of this multi-center randomized double-mask sham-controlled study were to evaluate the efficacy and safety of NGM621 compared to sham control. Patients were randomized to one of four treatment groups in a ratio of 2: 1, to receive intravitreal injections of NGM621 or sham injections every four weeks or every eiqht weeks for a total of 52 weeks. Patients were monitored for safety for an additional four weeks after treatment completion for a total of 56 weeks on the trial. The primary efficacy endpoint was the rate of change in GA lesion area as measured by fundus autofluorescence or FAF imaging over 52 weeks of treatment. The sham arms were pooled for the final analysis. Moving next to the inclusion criteria for the trial. Patients 55 years or older with a confirmed diagnosis of GA secondary to AMD could be enrolled in CATALINA. The study allowed inclusion of patients with foveal and non-foveal involved lesions. Patients needed to have a total GA area in this study, in their study eye between 2.5 square millimeters -17.5 square millimeters. If multifocal, at least one lesion needed to be greater than or equal to 1.25 square millimeters. The presence of banded or diffuse junctional hyperautofluorescence was required and finally, there needed to be no evidence of current or prior CNV in the study eye. Patients with CNV in their fellow eye were permitted to enroll if their diagnosis was two years or more prior. We limited these participants to no more than 25% of the CATALINA study population. Per the two-to-one, two-to-one randomization, 108 patients were randomized to the NGM621 Q4 cohort. 105 patients were randomized to the NGM621 Q8 cohort and 107 patients were randomized to sham. We had a very good compliance to treatment in the trial with an overall compliance rate in the range of 98%-99%. Patient demographics and baseline ocular characteristics were generally balanced across the treatment and sham arms, with the exception of baseline GA lesion area, which was 7.02 for the Q4 arm, 7.62 for the Q8 arm, and 7.75 for the sham. Now turning to the top line results. The primary endpoint was a slope analysis evaluating the rate of change in the GA lesion area over 52 weeks. The study did not meet its primary endpoint. At 52 weeks, there was only a modest effect in both treatment arms with the NGM621 Q4 and Q8 arms showing a reduction at 6.3% and 6.5% respectively. We also conducted a pre-specified secondary analysis of the primary endpoint using MMRM, the other commonly used method to analyze GA lesion change. This pre-specified secondary analysis was a change from baseline in GA lesion area using MMRM, a standard statistical methodology that adjusts for covariates such as baseline GA lesion area. With MMRM, the overall results at week 24 and week 52 showed a greater separation between the treatment versus sham arms than we observed using a slope analysis. At week 24, treatment effect in the NGM621 Q4 and Q8 arms were 19.8% and 15.6% respectively, with the Q4 arm demonstrating a nominal P value of less than Research Associate $0.05. While the MMRM results appear to be numerically larger than the slope analysis at 24 weeks, they also showed a relative treatment attenuation from week 24 to week 52. This prompted us to sequentially examine other factors that may have contributed to the trial not meeting its primary endpoint. One observation was that the sham arm lesion growth was noticeably different between the first and second six months. This is contrary to what we would expect based on natural history that suggests lesions normally grow at a steady linear rate over time, and which led us to explore what variables were driving this observation. An interesting observation in this study is that we have many patients with large baseline complex lesions. As you can see on this slide, these complex lesions appear to have an irregular morphology with many accompanying satellite lesions. As you can imagine, these complex lesions may have inherent challenges to grading consistency, particularly when they exceed the ETDRS grid or image window at baseline. We believe these inherent complexity of large GA lesions, including challenges in measurement, appear to have introduced unexpected variability into the trial results across all arms, which may have contributed to the trial not meeting its primary endpoint. We conducted post-hoc subgroup analyses excluding the top quartile patients with lesion measuring greater than 9.64 square millimeters at baseline, calculated using both MMRM and slope analyses. In these subgroup analyses, by including only the three quartiles patients with lesion measuring less than 9.64 square millimeters at baseline, the GA lesion area size of the patient across all arms became more balanced at baseline, and the sham arm appeared more in line with what would have been expected based on natural history. At 24 weeks, using the MMRM method on the selected subgroup, the rate of reduction in GA lesion area was 17.8% and 15.3% for the Q4 and Q8-week dosing groups, respectively, and at 52 weeks was 13.9% and 12% respectively. The 52-week findings are consistent when calculated using a slope analysis, Q4 week at 13.7% and Q8 week at 12%. Now I will describe the overall CATALINA safety findings, starting with CNV conversion, a safety consideration that has been consistently observed in other GA trials. In this trial, if the investigator suspected CNV conversion in the study eye, he or she was required to take an OCT and FAF and submit it to the central reading center for confirmation. Once confirmed, the investigator had the option to treat with anti-VEGF. Study eye CNV over the course of the trial was low overall. The incidence in both the sham and treatment arms are in line with natural history studies. The incidence of CNV conversion in NGM621 treated patients was actually numerically lower, with 2.8% in the Q4 arm, 1.9% in the Q8 arm, and 3.8% in the sham control group. There was no disagreement between investigators and the reading center on the occurrence of CNV conversions. Importantly, while approximately 18.6% of patients had a diagnosis of CNV in the fellow eye at baseline, an additional 4.2% of the fellow eyes developed CNV over the study. This rate is similar to what we saw for the study eye sham arm and in line with natural history for this group. Intraocular inflammation is always a safety category of interest in retina studies, and we did not detect any significant differences between the treatment arms compared to sham. All cases of anterior chamber cells were mild and resolved. As to the instance of eye inflammation, that patient had mild bilateral eye inflammation, which resolved with topical steroid drops. From an intraocular inflammation perspective, NGM621 appears to have been well-tolerated in the study. None of the SAEs were deemed by the investigators to be related to NGM621. There were two cases of retinal artery occlusion. One had a documented emboli, and the other had suggested systemic vasculopathy from chronic atherosclerosis and a history of smoking. Overall, NGM621 demonstrated a favorable safety and tolerability profile in the study. To summarize the key takeaways from the CATALINA trial, the study did not meet its primary endpoint. Pre-specified MMRM analysis showed reduction in lesion growth rate at 24 weeks with a nominal P value of less than 0.05 for the Q4 arm that diminished at week 52. Additional post-hoc exploratory subgroup analysis that excluded the top quartile showed potentially encouraging finding that we believe warrant further exploration. NGM621 did not increase CNV conversion. Finally, NGM621 showed a clean safety profile. To conclude, I would like to extend a special thank you to the CATALINA phase II study sites, investigators, and more importantly, the GA patients who participated in this trial to help advance our understanding of NGM621 as a potential treatment for GA. I would like now to turn the call back to David. Thank you. Thank you, Hsiao. Well, we'll continue to evaluate the potential of NGM621. Before I conclude today, I'd like to take a moment to touch upon a number of upcoming milestones across our pipeline. On the oncology front, we're currently enrolling patients with advanced solid tumors in our ongoing phase I/II trial of NGM707 and expect to report monotherapy dose escalation data from this trial towards the end of this year. NGM707 is our ILT2/ILT4 dual antagonist antibody and part of our myeloid reprogramming and checkpoint inhibition portfolio. We also continue to enroll patients with advanced solid tumors in ongoing phase I trials of the other two programs in that portfolio, NGM831, an ILT3 antagonist antibody, and NGM438, a LAIR-1 antagonist antibody. We expect to share initial data from these trials next year. For NGM120, our GFRAL antagonist antibody for cancer, we have ongoing proof-of-concept trials in both metastatic pancreatic cancer and prostate cancer and look forward to sharing updates through the course of next year. Finally, in our NASH portfolio, we anticipate a readout from the ALPINE 4 study of aldafermin in patients with stage four liver fibrosis in the first half of 2023. In addition, Merck continues to enroll in its global phase II-B study of MK-3655 in patients with NASH and F2-F3 liver fibrosis. We designed MK-3655 to mimic FGF21 biology in a format that allows for once monthly dosing. We continue to have a healthy cash position and expect to report that we had $300 million on the balance sheet as of the end of the third quarter, and with a cash runway that we expect will fund planned activities through anticipated data readouts in 2023 across our oncology portfolio. In closing, we're still digging into these complex top-line CATALINA findings. They're obviously not as positive or straightforward as we'd hoped. That said, based on our learnings from the trial thus far, we believe we owe it to the GA patients and to the retina clinician community to comprehensively evaluate and understand the results so that we can more fully assess the potential of NGM621 to treat this difficult disease. I'd like to echo my thanks to all the patients, investigators, and clinical trial staff who participated in the CATALINA study. In addition, I wanna thank the NGM Bio team for their exemplary work and dedication executing this trial. As a company, we remain as committed as ever to our mission of delivering life-changing medicines for patients. Thank you all again for joining today's call and for your support of NGM Bio. We look forward to providing you with further updates in the months to come. I would now like to open the call for questions. Operator? Thank you. As a reminder, to ask a question, you will need to press star one one on your telephone. Please stand by while we compile the Q&A roster. Our first question comes from Steven Seedhouse with Raymond James. Your line is now open. Good morning. Thanks for taking the question. I wanted to ask about foveal versus non-foveal subgroup analysis. Have you had a chance to conduct that, and does that tell you anything about differential effect in foveal versus non-foveal? Yeah, that's a good question, Steven. Thanks for asking it. We have taken a preliminary look at that. It looks like we don't see any outsized effect in the non-foveal population, which I think is interesting. We're learning a lot about this disease. I know we've seen kind of mixed results. Some trials have shown more of an effect, some not as much of a differentiation. We seem to fall in the category we didn't see much differentiation. Okay. I mean, at this point, I guess I'm just interested in sort of looking forward, what options are available to you. Can you just talk about if you have any future development plans for NGM621 systemic administration? Is that something you're interested in? In other words, could this disappointing effect just be, you know, a PK/PD issue in the eye that wouldn't necessarily impair activity of this antibody and systemic disease? And then I wanted to also just clarify, like, do you anticipate continuing development of NGM621 in GA or is that unlikely? It sounded like that might depend on some of these exploratory analyses. Yeah, let me hit the second part first, and then I'll come back to systemic use. Yeah, it is too early. We're digging in. I'd say, you know, between now and the Retina Society in the beginning of November, we'll be doing additional analyses. We obviously have to evaluate these results with Merck, and so it's just too early to be definitive about next steps of 621 in ophthalmology. As it relates to the systemic use, we don't have any current plans to go into systemic use with 621, but we have prepared it as a molecule in the sense that we've done a phase I safety study with systemic administration. It's teed up to go if we'd like to do that. Our conversations to date with Merck have suggested that's not an area they would go into. If they were to not option the program, that's something we could consider at the time. Okay. My last question just to expand on, I'll ask it so you could expand maybe on the Merck dynamic. If Merck does not opt in for GA, does the molecule essentially return to you indefinitely for any future development in either GA or any other indication? Yeah, it's a great question. I'm gonna hand it over to Siobhan to answer that one. Sure. Hey, Steve. It's nice to hear from you. Obviously it's early to speculate, but if Merck does not exercise its license to option NGM621, then NGM retains its worldwide rights to the program. At this point, we most likely try to pursue a partner for the program given our portfolio. We do think there could be interest there, but obviously it's quite early. Okay. Thanks for taking the questions. Appreciate you guys hosting the call, with the update this morning. Thank you. Our next question comes from the line of Paul Choi with Goldman Sachs. Your line is now open. Hi. Thank you and good morning. My first question is, you know, as you've done the various analyses, can you maybe give your thoughts on as to why the, you know, treatment, the effect size changed between months zero to six versus six to 12? You know, any impact from trial conduct side, or is your thinking that's probably more PK/PD related? I had a follow-up question. Sure. Yeah. That's certainly something we're continuing to dig into, but Hsiao, maybe you can take that one. Thank you. We don't think that there's any trial conduct issue in this trial. Right now, you know, because we have seen efficacy at week 24, we don't think there's an issue with PK/PD. What we think is going on is when we look at our top quartile, that there are a few patients with these very large complex lesion. When you measure these large complex lesion, it's very difficult and very challenging, and that causes the variability. We believe this variability is what caused the attenuation between week 24 and week 52. The other point I would like to make is looking at the p-value at week 24 and week 52. At week 24, you can see the p-value less than 0.05. What that means is if we repeat this experiment, that there's less 5% chance we will get a different result at week 24, versus at week 52, when a p-value is as high as 0.4, that means if we repeat this experiment, there's a 40% chance we'll get a different result. Okay. Thank you for that. As a follow-up, just with regard to your analysis that you did with regard to the quartiles versus the lower top quartiles versus the lower three quartiles, were there any other characteristics beyond lesion size that in your mixed models or other analyses that suggested could be a contributing factor? Yeah, it's a great question, Paul. It's something we're continuing to look at. I think it's still early. It's the type of thing we're digging into in anticipation of the Retina Society. We're working in concert with Dr. Charles Wyckoff, who's one of our key advisors, and we'll be presenting at the Retina Society to dig into that. We don't have anything further to add at this point. Okay. Thanks, David. I'll hop back in queue. Okay, thanks, Paul. Thank you. Our next question comes from Mayank Mamtani with B. Riley. Your line is now open. Good morning. Thanks for taking my question. Maybe just staying focused on the learnings there, you know, incremental at the Retina Society in early November, like, can you comment on what more you could present? Also, for example, was BCVA looked at already and, you know, based on the basis of the subgroup analysis you conducted, was there any interesting signal on BCVA? If you could comment on that, and then I have a follow-up. Yeah. Thanks for the question, Mayank. We have looked at BCVA as it's a safety output of the study, and that's actually the only kind of functional related measurement we've looked at. We didn't see a treatment effect at this point. We haven't looked at it kind of on a subgroup analysis. It's already a pretty noisy measurement, so as you slice the patient population further, it makes it even noisier. It will be relating to your question, you know, this is just the top line results, and so there's quite a bit of additional data we'll be able to gather from the study over time. You know, once we get to The Retina Society, which is pretty soon, I'm sure we'll have other forums to present those data. You know, our style is we obviously wanna contribute as much to this study to the GA community as possible, and so we'll find ways to do that over time. Okay. Thank you. Then on CNV conversion, how you evaluated relative to maybe how we've seen in other studies. Could you just comment on the protocol there and how was anti-VEGF therapy administered? Was it until the CNV was resolved, or was it maybe as only a small number of those? Can you just comment on that? Sure. I'll let Dr. Erin Henry, our Head of Ophthalmology, answer that one. Hi there. The protocol defined the method that investigators should take if they suspected CNV. If they suspected CNV when they were evaluating a patient, they were to do additional imaging that included fluorescein angiography and OCT images and submit it to the central reading center. The central reading center then confirms whether or not it was a case of CNV. It could be called a CNV conversion by either fluorescein or OCT. The investigator was able to treat with anti-VEGF at their discretion. We didn't enforce a particular protocol, and each investigator was able to use the anti-VEGF in the best manner that they thought possible. They continued to provide additional monitoring and imaging for the remainder of the time the patient was in the study. Great. Then on the Merck collaboration, maybe for Siobhan, can you just clarify how much of the overlap on portfolio remains? I know oncology is completely out of that collaboration, but can you just summarize what outstanding work that is remaining with them in terms of pipeline programs beyond NGM621? Sure. I'd be happy to. Beyond NGM621, of which Merck will have about a quarter to make their option decision, they also are looking at two preclinical ophthalmology programs that we're working on in collaboration with them. We also have some very early-stage discovery programs with an earlier option period, specifically in cardiovascular. Think of that as like specifically in heart failure. Obviously, as David mentioned earlier, Merck is running a global phase II-B study right now in NASH for MK-3655, which they have already optioned. Everything else in the NGM portfolio is then wholly owned by NGM. That's in oncology as well as aldafermin. Okay. I'll hop back in the queue. Thanks, David, for taking my question. Thank you. Our next question comes from Anvita Gupta with Cowen. Your line is now open. Hi, guys. This is Anvita on for Ritu this morning. In terms of the analyses that we can expect at the Retina meeting, could you give us some color on the breadth of the analyses we can expect? Then what kind of data from these analyses would make you want to continue the development of 621? Thank you. Yeah. Thanks for the question, Anvita. I'd love to answer more specifically, but the short answer is, you know, we are literally digging into it, and so it's, I wouldn't wanna give any indication we have specifics at this point. I think sort of an obvious one is along the lines of digging in further to the quartile analysis. That seems to be quite interesting to us given the complexity of these large lesions. But that's about as far as we can describe at that point. I do think there's rich information here. Just can't get more specific than that. Thank you. Our next question comes from the line of Dennis Ding with Jefferies. Your line is now open. Dennis Ding with Jefferies, your line is now open. Please check your mute button. Hi. Thanks for squeezing me in, guys. Just one question from me, and it's not on GA. As we think about the company, can you just right size for investors how to think about the path forward for the company and just help us understand the catalyst path over the next 12 months? I know you had a catalyst slide, but what is your message to the Street in terms of what are the most promising assets and readouts in your view? Thanks. Yeah. Thanks for the question, Dennis. Yeah, I think as those of you who've been following NGM for a while have noticed, we've been pivoting towards oncology for the last couple of years, and that continues. Because of the Merck option on NGM621, you know, either way, we'd intended to really focus on oncology going forward. We've got four wholly owned programs in that area, four shots on goal. They cover both this myeloid reprogramming strategy and then some very novel biology around a GDF15 pathway that we think plays a role in cancer. What we're planning to roll out, starting at the end of this year with NGM707 but into next year is really that first clinical data from all of those programs. 707 monotherapy dose escalation at a meeting later this year. As I mentioned in my prepared remarks, you know, there should be data across the board for these programs. You're kind of asking the question, what's your favorite child? It probably depends on the day. There is some target validation with NGM707 for the ILT4 target from Merck's MK-4830 to the anti-ILT4. That's one that we're pushing forward as quickly as possible. That's why it's in the lead in that myeloid reprogramming portfolio. We are also quite interested in the LAIR-1 program, for instance, NGM438. As novel biology, we're basically in the front on that, and so that's another one to keep an eye on. NGM120, we have these interesting proof of concept studies in pancreatic cancer and prostate that we're also hopeful we can define in 2023, you know, what the path forward is for that program as well. As a follow-up, you know, you guys have $300 million in cash. Can you remind us your quarterly burn, and how do you prioritize spending across all these different oncology programs? How much are you willing to spend on some of these more risky targets? Thanks. That's a great question. You're right. We had $300 million in cash as of September thirtieth. At this point, we believe we have the resources to fund in particular these oncology programs through proof of concept data while also remaining committed to the discovery engine that produced all of these programs. You know, we've also identified levers. You can imagine we're always scenario planning so that we think we could extend runway further with really keeping our focus narrowed onto these oncology programs that David was just talking about and really funding those specifically. You can imagine that that's something we're in the process of executing now. Yeah, it's also worth mentioning that because they're wholly owned, we have the option of business development across the portfolio. You know, that's been our history as a company of funding approximately 50% of our capital needs from business development, 50% from capital markets. It's just another way to think of our profile going forward as well. Thank you. Our next question comes from the line of Swapnil Malekar with Piper Sandler. Your line is now open. Hey. Thank you for taking my questions. First one is, like, can you tell us, like, how many patients and how many injections of anti-VEGF were received across the active and the placebo arms of to treat the CNVs? That's a very specific question. I'm looking around. I know we know the compliance rate, but, maybe, Erin, do you have anything to comment on that? I'll say that these CNV conversions happened across the course of the study, and the investigators had the opportunity to treat with anti-VEGF as they saw fit. In many of these instances, there was no diminishment of visual acuity, and so there was variability in how many anti-VEGF injections they chose. I think Retina Society is probably the better place to get into more of those details, but what I can tell you is that all conversions received anti-VEGF. Got it. Okay. Then based on the natural history, we know that the extrafoveal lesions progress faster. In theory, a C3 inhibitor should have a greater effect on extrafoveal lesions. In your case, you are seeing a more effect of a higher magnitude on foveal lesions. Can you like help us explain why that difference might be? Well, maybe just to clarify. First of all, I don't think it's possible that extrafoveal lesions can show a greater effect, but there's been some mixed data in the landscape related to that. You know, this is the type of thing as we've dug into it, we don't see an obvious difference in terms of the effect on extrafoveal lesions. It's kinda one of these areas where we have to dig in. I think if you look across the different data sets, though, there is kind of a mixed bag, as I said. I wouldn't take that as gospel yet. As evidenced, I mean, I think Iveric Bio took that strategy, and it didn't necessarily pan out in their last phase III trial. We'll I'm sure disclose it at some point and just to contribute it to the community to make sure we can seek out the natural history overall for these types of populations. Thank you. Thank you. I'm currently showing no further questions at this time. I'd like to hand the call back over to David Woodhouse for closing remarks. Okay. Well, thank you, operator, and thank you all for joining today. We look forward to providing more updates and seeing many of you in the months ahead. Today's conference call. Thank you for participating. You may now disconnect.