Design Therapeutics, Inc.

Good afternoon, and welcome to Design'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, and please be advised that this call is being recorded at the company's request. I would now like to turn the call over to Dr. Shawn Jeffries, Chief Operating Officer of Design Therapeutics. Sir, you may begin.

Thank you. Welcome, and thank you to everyone for joining us today. We are pleased to share with you these initial results from our phase one multiple ascending dose study of DT216 for the treatment of Friedreich ataxia. Earlier today, we issued a press release outlining initial data from this study. The slides that we'll be using during today's call will be available along with a recording of this call in the investor section of our website at designtx.com. With me on the call today are President and CEO Joao Sifert and Chief Medical Officer Dr. Jae Kim. During this call, we will be using forward-looking statements related to our current expectations and plans, including our program development plans, which are subject to risks and uncertainties. Actual results may differ materially due to various important factors, including those described in the risk factor section of our most recently filed 10-Q. These statements represent our views as of this call and should not be relied upon as representing our views as of any date in the future, and we undertake no obligation to publicly update any forward-looking statements. On slide three, serious inherited degenerative diseases affect millions of people across the globe, and research has identified nucleotide repeats in the genome as the underlying cause of a number of these diseases. However, there are currently no therapeutic options that address their root cause. At Design, we're approaching the problem of genetic disease differently. Our founding scientific breakthrough showed the potential of a small molecule genomic medicine that works with a patient's natural genome, allowing the patient's own cells to make the gene product that it needs. We call these gene-tacked small molecules. These are designed to harness an individual's natural genome to either dial up or dial down the expression of an individual mutant gene to address the root cause of inherited nucleotide repeat diseases while retaining the favorable pharmaceutical properties of a small molecule. We're evaluating our lead gene tax small molecule, DT216, for the treatment of one such degenerative disease, Friedreich ataxia, or FA. By way of background on slide four, FA is a monogenic disease caused by a homozygous GAA repeat expansion in the first intron of the frataxin gene. These repeats act like a roadblock and prevent the normal transcription of frataxin, a gene important for mitochondrial function. Lower frataxin levels cause earlier onset and faster progression of FA symptoms. The main clinical manifestations of FA are shown on the right side of the slide and involve multiple organs, including central and peripheral nervous systems, heart, pancreas, and importantly, skeletal muscle. Before we get into the data, I'd like to review the therapeutic hypothesis of DT216 as a treatment for people living with FA. As outlined on slide 5, DT216 is a novel gene-tax small molecule designed using our platform technology. The illustration on the left-hand side depicts the impairment of frataxin transcription due to the GAA repeat expansion mutation that causes FA. These long stretches of GAA repeats reduce frataxin transcription, leading to all the disease manifestations of FA. On the right-hand side, we designed DT216 as a heterobifunctional small gene-tacked molecule where one end of the molecule binds into the minor groove of intact double-stranded DNA in a sequence-specific fashion, targeting the GAA repeats. The other end of the molecule binds and recruits the transcriptional elongation complex by interacting with BRD4, enabling transcription through the intronic GAA repeat expansion and restoring the expression of a patient's own natural frataxin. The intronic GAA repeats are subsequently removed through the normal splicing process, and the endogenous for taxin mRNA is translated into normal functional protein. Therefore, transcription of mature endogenous for taxin mRNA serves as a key biomarker of pharmacology in our clinical studies. With that, I'd like to turn the call over to Jae Kim, our chief medical officer. Jae is a cardiologist and has decades of successful development of therapeutics, including multiple genomic medicines. He joined design in early 2022 and leads our clinical programs. Jay?

Thank you, Sean. Before we dive into the DC216 multiple ACE and EGO study, let's first discuss an observational study that design conducted, shown on slide 6. We developed procedures and methods to measure endogenous potassium mRNA and protein in skeletal muscle to enable evaluation and clinical activity directly in tissues relevant for disease symptoms. we biopsied three populations, normal healthy volunteer controls, heterozygous FA carriers, and FA patients. It is important to emphasize that carriers who have only one mutant allele with a GAA repeat expansion are phenotypically normal and clinically healthy. The plot on the left illustrates interquartile ranges in tenths and ninetieth percentiles. The biopsy data show that endogenous protaxin mRNA across the three populations are significantly different from each other. The interquartile range of SA patients, shown in blue, do not overlap with that of clinically normal carriers, shown in purple, demonstrating that protaxin mRNA levels from these two populations are largely distinct. We believe that the data supports use of our muscle protaxin mRNA assay as a sensitive indicator of clinical activity in SA. with the ability to discriminate clinically meaningful changes in endogenous frataxin mRNA expression. We would like to also propose that any significant increase in endogenous frataxin may be clinically meaningful, especially increases in frataxin mRNA beyond the upper portal of FA patients or into the carrier range. I would like to now discuss frataxin protein on slide seven. On the left plot, we show protaxin protein measurements in carrier and SA patients using our measurements from muscle biopsy samples. In contrast with mRNA, protaxin protein measurements were much more variable and had substantial overlap between the SA patient and carrier population. On the right plot, We show the intra-individual variability from the 11 FA patients who underwent two biopsies approximately three days apart, with percent change in protaxin protein shown between the two visits. The red lines show more than half of FA patients had 25% or more visit-to-visit variation, with intra-individual coefficient of variation of 69%, which is beyond the range typically acceptable for a reasonable assay. This variability substantially limited the utility of these frataxin protein measurements in skeletal muscle. In summary, this observational data provides context for frataxin measurements using the procedures and methods developed in our DC216 Multiple Ascending Dose Study. On slide eight, I will now review the design and rationale of our DT216 phase one program in SA patients. The completed single ascending dose study evaluated IV doses ranging from 25 to 600 milligrams of DT216. As we previously shared, there were injection sites for most thrombocobitis events in the SAD study, and these were only observed at the highest dose levels, at 400 and 600 milligrams. As a result, our Phase I MADS study, shown on the right, explored initial multiple doses of 100, 200, and 300 milligrams, shown in blue, green, and orange respectively. These doses were selected based upon anticipated tissue exposures projected to be in the therapeutic range and injection site tolerability guided by our single ascending dose experience. Participants were randomized, double-blinded, to either DT216 or matching placebo administered as three weekly IV injections. The MAD study was designed to assess safety and tolerability and pharmacokinetics of multiple doses of intravenously administered DT216. Exploratory clinical activity was measured by levels of endogenous protaxin mRNA in muscle biopsies, taken at pre-dose baseline, and then two days and seven days after the third weekly dose. Muscle biopsies were performed in the 200 and 300 milligram cohorts only. All initial data we will walk through today is based upon a data cutoff of August 7th. The study is fully enrolled but currently ongoing. with blinded PK and PD data available in full 100 and 200 milligram dose cohorts and 11 of 14 participants in the 300 milligram dose cohort. Safety data remain blinded. Baseline characteristics of the enrolled population are detailed on slide nine. A total of 29 adults with clinically diagnosed FA with genetically confirmed homozygous GDAD repeat expansion mutations were enrolled in this study. As you can see, the study enrolled a representative sample of symptomatic SA patients distributed across the dose code works. MAD study safety data aligned with the treatment assignment are summarized on slide 10. Multiple doses of DT216 were generally well-tolerated, but injection site reactions were observed. There were no serious AEs and no discontinuations due to treatment-related adverse events. All AEs were mild or moderate and none were severe. There were five events of injection site thrombocobitis. Four of these events were mild and one was considered moderate. These events in the MAG study were observed across the three-dose cohorts, and we will provide further perspective on these injection site reactions in the summary. There were otherwise no new clinically significant safety observations. As we review the biopsy data in the next few slides, note that two participants did not return for post-dose biopsies due to acute COVID. Slide 11 summarizes the plasma pharmacokinetics of three weekly doses of BP216. As shown in the left panel, plasma BP216 levels were approximately dose proportional. The first and third dose PK profiles were also similar, showing a lack of significant drug accumulation at the three doses. On the right, average DT216 concentrations measured in skeletal muscle were approximately 8 to 10 nanomolar two days after the third weekly dose on both the 200 and 300 milligram cohorts. Muscle PK declined to approximately 1 nanomolar at seven days after the third weekly dose. These DT216 concentrations in muscle were lower than projected based on non-clinical studies in animals, but were sufficient to drive substantial pharmacology, as we will show in the next slide. Slide 12 summarizes the clinical activity of DT216 in skeletal muscle by measurement of endogenous frataxin mRNA. The left panel shows mean percent change from baseline in protaxin mRNA in 200 and 300 milligram cohorts. Protaxin mRNA expression in muscles was significantly increased from baseline at two days after the third weekly dose of 300 milligrams shown in the left orange bar compared to placebo shown in the left gray bar with a p-value less than 0.05. Protaxin mRNA increased 30% with DT216 treatment, which corresponded to levels in the 75th percentile, or the top upper quartile of reference FA patients from our observational study. We also observed durable increases in protaxin expression with a positive trend in increased protaxin mRNA seven days post-dose, as shown in the right-hand orange bar. The right panel shows a waterfall plot of individual FA patients' protaxin mRNA and muscle. Increases in individual protaxin mRNA show adaptive response across individuals that favors the DT215 treatment, using ranges from the observational study referenced Protaxin mRNA by percentiles is overlaid in the lower blue shaded area for FA patients and the upper purple shaded area for clinically healthy carriers. Treatment with DT216 restored protaxin mRNA in muscle to what we believe is a clinically normal range for one patient in the 300 milligram dose group. with approximately half of DT216 treated patients' response above or approximately at the upper quartile of reference SA patients. For context, higher potassium expression among SA patients previously has been shown to be associated with myelin disease. Additionally, exploratory statistical analyses demonstrated a significant DT216 dose-response trend and tissue exposure-response relationship for muscle protaxin mRNA, both at p-values less than 0.05, adding to the multiple lines of evidence that protaxin mRNA increase in muscle with DT216 treatment is a robust finding. On slide 13, we summarized additional exploratory evaluations. On the left, we assessed muscle protaxin protein in the MAG study, and these measurements were highly variable, consistent with findings from the observational study. We did not detect an observable protaxin protein signal above the measurement noise. These results were therefore inconclusive due to assay variability. On the right, we evaluated protaxin mRNA in PBMCs. In the MADS study, we observed a transient increase of protaxin mRNA in PBMCs 24 hours after the dose, which was consistent with and confirms the results from the single-dose study. As of this data snapshot, the PBMC protein results are not yet available. Turning to slide 14, in summary, we are enthusiastic that this phase one multiple-ASCII study has demonstrated proof of concept. showing clinical activity of DP216 in skeletal muscle of SA patients of relevant disease-affected tissue. We observed significant endogenous protaxin mRNA increase two days after the third dose at P less than 0.05, with trends in durable increases to seven days. Increases in protaxin mRNA corresponded with levels in the observational study that might portend less severe disease. A significant dose-response trend and exposure-response correlation in skeletal muscle, both at P less than 0.05, adds to the internal consistency of the evidence in support of DT216's ability to reverse the transcriptional block of endogenous protaxin mRNA expression that is the root cause of FA. DT216 levels in multiple biopsies were lower than projected from animal studies, but substantial and dose-proportional pharmacology was observed in human disease exposures. Multiple doses of DT216 were generally well-tolerated with a favorable systemic profile. Local injections by thrombocobitis occurred across the three-dose cohort, and Joao will provide additional perspective on how we plan to advance DT216 for the treatment of that patient. And with that, I'd like to turn the call over to Joao Siefert, our CEO.

Well, thanks, Jay. So let's turn to slide 15. We're very encouraged by the initial results from our Phase I Multiple Ascending Dose Study, which confirmed clinical activity of DT216 and support its continued development as a potential disease-modifying treatment for frederic ataxia. However, we elected to complete the dose escalation in this phase one study of the 300 milligram cohort due to concern for potential worsening of injection-side thrombophlebitis at higher doses with multiple administrations. We have since turned our focus to developing DT216 with an improved formulation which we expect will enable exploring the full pharmacodynamic potential in long-term treatment of FA. We have conducted non-clinical studies that show that the injection site reactions were attributable to the excipients in the current formulation. And we have since shown that an improved ET216 formulation had favorable injection site tolerability following multiple intravenous administrations in animals and enabled dosing to increase tissue exposure. We're now conducting bridging non-clinical studies so we can resume clinical development and expect to begin a multiple-dose Phase I clinical trial to assess safety, pharmacokinetics, and pharmacodynamics of the improved DT216 formulation in the second half of 2024, with initial clinical data in the first half of 2025. I understand that this hiatus before we can resume clinical development of DT216 is disappointing to the FA community, especially after showing clinical activity in phase one. But we're confident in our path forward and remain highly committed to bringing disease-modifying treatments to those suffering with FA. We look forward to keeping you updated on our progress along the way. Before I review our pipeline progress and upcoming milestones, I wish to thank all the SA patients, their caregivers, and other volunteers who participated in our studies, the Friedreich Ataxia Research Alliance, or FARA, and of course, our great team here at Design Therapeutics. Turning on to slide 16. So as we look ahead, we're very excited about the future of design because we believe the confirmation of clinical activity of our SA gene tag molecule supports the therapeutic potential of a broader gene type pipeline and platform, with multiple novel small molecules being advanced for the treatment of other nucleotide repeat expansion disorders. One such example is our program in Fuchs Endothelial Corneal Dystrophy, or FECD, a disease which affects millions of people and is the leading cause of corneal transplants in the United States. We're on track to submit a 9G later this year for our DT168 eye drop for Fuchs, and we look forward to sharing more in this program soon. As our other pipeline programs continue to advance, we anticipate having three programs in the clinic over the next three years. With that, thanks for joining us today, and we'd be happy to take your questions. Thank you. Operator?

Thank you. To ask a question, please press star 1 1 on your phone and wait for your name to be announced. To withdraw your question, please press star 1 1 again. Standby as we compile the Q&A roster.

One moment please for our first question.

Our first question will come from Yasmeen Rahimi of Piper Sandler. Your line is open.

Hi, team. Thank you so much for the update. A few questions for you. Maybe the first question to ask is, do you plan on, I mean, we understand that you're going to work through coming up with a new formulation and work is in progress and you're going to expedite the development in terms of being in the clinic. But how do you overcome sort of the variability with protein levels and what the next steps are? So I think we learned now, which we didn't know, that there's quite a bit of variability for taxon levels in the protein. So how do you overcome that even with a new formulation? Do you think that we will get a definitive answer of gene taxability to restore protein levels? Two, would the new formulation allow you to go to dose higher beyond 300? And then how would your design with the new formulation differ from the current study that you conducted? Sorry for the multi-pronged question, but I appreciate color on those topics, please.

OK. Thanks, Yas, as well. I'll start with one of your questions. So we have, in fact, identified formulation that is better tolerated, and we've tested this in animal and multiple studies. So we're really moving forward with developing so we can resume clinical development of DT216. As for the biomarker, obviously, there has been You know, currently and so far, the method and procedures we use to measure protaxin protein and muscle have issued variability, and of course, we'll continue to work on this and potentially other approaches as we continue to develop DT216. But I think it's important to underscore that the mRNA is, in fact, the actual direct evidence of pharmacology of DT216, which is restoring the transcription of protaxin at the DNA level, making RNA. And in this case, this was very clearly demonstrating that this current exposure of DT216 was sufficient to elicit a significant response in frataxin mRNA in muscle, skeletal muscle, which is an affected tissue in the disease, FA. And this was dose-related. So as we look ahead with a formulation that is not limited by injection site tolerability, we can both plan to dose patients both at higher doses if needed and also for longer-term treatment, which is the ultimate goal for treating NFA. As we progress in the development of D216, we'll continue to provide updates, and as we come closer to the beginning of clinical studies in the second half of 2024, we'll provide more specifics in both the study design as well as potential assessment of biomarkers.

Thank you so much, João. I'll jump back into the queue.

Thank you. Thank you. One moment, please, for our next question. Our next question will come from the line of Laura Chico of Wedbush. Your line is open.

Hey, good afternoon. Thanks for taking the question. I guess I have two, just kind of following up on the last question with respect to excipients. Could you just clarify a little bit more about kind of your understanding of what's actually causing these thrombolytic events. And I guess, why was this initial excipient chosen and what could be confidence in the alternatives that you're pursuing there? And then I have one quick follow up.

Yeah, so obviously the excipients used in the current formulation are suitable for clinical use. But as we proceeded with dose escalation, larger volumes, these started to show signals of intravascular tolerability at the superficial vein right at the site where they're injected. So it's hard to know exactly what's taking place, but we, generally speaking, think that this is the combination of the physical chemical characteristics of the whole formulation, so the mixture of excipients. When tested in animals in the vehicle group, you see the same effect. So without the drug in the formulation, you see the same effects in tolerability in the veins of animals. So with the new formulation, we've modified the excipient composition. And when tested now in animals again, we see that these are well-tolerated both with and without the drug in the formulation. So that's basically what gives us the sort of the has helped us decide to move the program now focusing on the improved formulation. that will essentially open up the possibility of exploring the full pharmacodynamic potential both through, you know, dose ranging and duration of treatment. So, you have a second question, I guess, on the biomarker, right? I'll turn it over to Sean.

Yeah. Actually, before we get into that, Laura, you know, I think it's important to recognize that, you know, nonclinical species are particularly sensitive to these types of reactions because, you know, they're smaller and they have smaller veins. You know, we saw the reactions were much more mild in humans, but unfortunately, as we started to push the excipient volume, you know, we started to see some injection site reactions. You said you had a follow-up?

Yeah, I guess I just wanted to clarify. So if I'm understanding the timeline of events, then... the study would be restarted in 24 and data, I guess, can you just remind us what is the current cash runway expectation based on the operating plan? And does this really change meaningfully in terms of the R&D spend between now and data in 25? Thank you.

Okay. So we ended the quarter with $303 million in cash, and we've updated the guidance to cash through 2026. which enables us to execute on the current operating plan and the upcoming milestones.

Okay, thanks very much. Yeah, it does. Thank you.

Thanks, Lauren.

Thank you. And one moment, please, for our next question.

Our next question will come from Leonard Timoshev of RBC Capital Markets. Your line is open.

Right. Thanks. I just want to continue to build on the questions about the new formulation. I guess, can you help us understand maybe the decision to not advance into some phase two work with maybe longer follow-up, three months, maybe in whole blood for taxon, and then do the PK bridging work in parallel, just given the severity of the disease and the unmet need, why not move the programs in parallel? And then With the new formulation, do you have any initial thoughts on how much further you can push the exposure and how that may translate into mRNA increases? Thanks.

Okay, so it's a multi-pronged question. Thanks, Leo. So let me see if I answer your question. If there's something missing, please remind me to answer this. So as we came to the end of the MAD, it was exactly this decision. Should we start a Phase II trial and try to push the dose and work with this formulation, or should we make a switch over to the improved formulation? And the decision became clear in that in the MAD, we saw injection-side thrombocytitis even at the doses of 100, 200, and 300, although the events in and of themselves were mild or moderate and generally self-limited. We felt that there was a concern if you were to then push doses higher or treat longer, which is ultimately what's required for treating a chronic disease like FA, that this eventually could push the envelope in terms of injection site tolerability and could put a halt in the program prematurely, which is not related to the drug itself, right? So ultimately, what we want to develop is DT216, but it has to be within the context of a formulation. When you reformulate a drug, you have to test the drug under the current formulation, that standard drug development. And the sooner we start with that, the better off in terms of minimizing the hiatus between where we concluded now with phase one until we resume multiple dose testing in second half of 2024.

And Leo, to answer your second question, you know, you asked about, you know, how much more exposure can we get, you know, with an updated formulation. I just want to remind you that, you know, to this point, DT216 has been systemically very well tolerated, both in clinical trials, but also in our non-clinical studies where, you know, systemic tolerability, the NOAEL was really the top dose tested. So, I think the answer to that question is still to be determined. You know, we have an opportunity with the resolution of injection site reactions to continue to advance the dose, and so far, you know, the molecule has shown to be very well tolerated.

Got it. Thanks so much. Thank you.

Thank you. And one moment, please, for our next question. Our next question will come from Joseph Schwartz of Learing Partners.

Your line is open.

Thanks very much. So, my first question is, now that you've accumulated some experience in patients and you're able to compare it to what you've seen in animals, how useful would you say that the animal models are for predicting what you might see in patients in terms of the ISRs? How much better behaved is the new excipient? Can you quantify this in any way? And does your animal data to date suggest that you'll be able to dose higher or longer without seeing the same degree? Can you quantify that goal in any way? Thank you.

Thanks, Joe. The current formulation had shown signs of thrombophobitis in animal studies. So we know the animals themselves, rodents and non-human primates, are a sensitive species, if you will, both sensitive species to detect any kind of vascular abnormalities or reactions. So in terms of the actual peripheral, the vein itself, that's the design we're trying to overcome. Systemic tolerability, which is the doses we pushed to in top studies, these were well in excess than we even deployed in the phase one trial. So from the systemic tolerability of, say, liver, kidney, et cetera, et cetera, we could have escalated the dose further beyond the 300 milligram dose level. So the only rate limiting was the injection site thrombofibitis, which in the MAD study and the SAD study themselves were not that severe, but we're really looking forward to a drug development and ultimately approval of a drug, hopefully, that is for chronic use. So as to how do we gain confidence that the improved formulation will not run into these issues, which is, of course, an important question, is one that we have explored already. We dose this in multiple doses in animals, in rodents, where we had seen injection-sized thrombophobitis. And so far, we have not encountered the same injection site thrombofibitis that we had observed with the current formulation. So being that these are more sensitive than humans to these reactions, we feel pretty confident that we have a formulation with improved characteristics. And that's why we decided to bring this forward in the bridging studies and ultimately developing and back into the clinic.

Okay, thank you. And then in terms of the FOOPS program, I was wondering, how are you thinking about the potential to have PD markers there? And what are the main technical challenges you think that you might have to overcome in order to demonstrate disease modification, target engagement potential in FOOPS?

Okay, I'll turn it over to Sean to answer that. Sean?

Yeah, thank you, Joe. Yeah, I mean, you know, Fuchs is, you know, also a genetic disease, you know, caused by a CTG repeat expansion in the, you know, in the intron of the TCF4 gene. So there's certainly multiple opportunities to look at, you know, genetic biomarkers in this disease. You know, the disease affects the corneal endothelium, and so being able to look at the corneal endothelium, you know, from... from patients, potentially post-surgical patients, is certainly an opportunity. We haven't provided definitive guidance on the endpoints in subsequent studies in our clinical program, but there certainly are multiple opportunities to examine pharmacology in disease-affected tissue.

Thank you. Thank you.

One moment, please, for our next question.

And we have a follow-up from Yasmine Rahimi of Piper Sandler. Your line is open.

Team, just a clarification question. Do you have to file an IND for the new product, for the new formulation, or there's no regulatory refiling of the IND needed? If you could just provide some color.

Yeah, of course, we'll work with the FDA prospectively to ensure that we're aligned on the development program. The expectation is a brand new formulation that requires a separate IND. But we have, of course, a fair amount of experience with VP216 itself, right? So we're tested both in animals and in people. And this gives us a lot of know-how and knowledge that we can reference in our development plans for DT216 going forward. And then, Joelle, yeah. Jay, Kim wanted to just add something. Yeah.

Yes, one additional point, Yasmeen, is that a new INB is a rather administrative step, you know, and that is in line with precedent for new formulations for DT216. revised formulations in the current day. There's a lot of diligence that has been done in the non-clinical arena that could be referenced in the new IND.

Thank you, Tim. And then when you look at the non-clinical data with the new formulation, are you able to quantify how much higher It is relative to 116. Is it like two times higher, three times higher, four times higher? Is there an opportunity to figure that out?

In terms of doses we can achieve?

Yeah.

Yeah. So just as a reminder, in the single ascending dose study, we had dose stations with single doses up to 600. Just right there you can see that theoretically we could have gone up to 600 milligram dosing in the math, so at least doubling just based on clinical data alone. Of course, as we progress with testing the new formulation forward, we can then adjust how much we can go. And as Sean mentioned earlier, when we tested this in toxicity studies, the top dose was actually the no adverse event level dose, meaning that we could escalate the dose in the tox studies all the way to the top dose tested. and systemically was well tolerated. So we think we have room to go. The question is how much do we need to go up? It may be not much actually as it turns out. So if you look at the data we presented today and look at the step up between the 200 and the 300 milligram dose cohorts, you see an increase in the mRNA response about 2.3 fold going from 200 to 300 in a very clear dose response relationship. I think bodes well to perhaps even modest increases in doses could elicit a greater protaxin response. Obviously, all this will be tested as we move forward.

Thank you so much, Tim.

Thank you. I see no further questions in the queue. I would now like to turn the conference back to Joelle Siefert for closing remarks.

Well, thank you everyone again for joining today in short notice. We look forward to keeping you apprised of our progress across the pipeline. Thank you. Have a good evening.

This concludes today's conference call. Thank you all for participating. You may now disconnect and have a pleasant day.