Good morning, and welcome to Cara Therapeutics' 2022 Virtual Notalgia Paresthetica Event. Before we begin, let me remind you that today's presentation will include forward-looking statements made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Please see slide two of the accompanying presentation in our SEC filings for important risk factors that could cause our actual performance and results to differ materially from those expressed or implied in these forward-looking statements. We undertake no obligation to update or revise the information provided on this webinar as a result of new information or future results or developments. Participating from Cara Therapeutics today will be Chris Posner, Cara's President and Chief Executive Officer, Dr. Joana Goncalves, Cara's Chief Medical Officer, and Eric Vandal, SVP of Commercial. We're delighted to also be joined by two highly accomplished key opinion leaders, Dr. Zoe Draelos and Dr. Brian Kim. Dr. Draelos is the Founder and President of the Dermatology Consulting Services, PLLC. She's in solo practice in High Point, North Carolina, and she's a Consulting Professor of Dermatology at Duke University. Dr. Kim is the Vice Chair of Research at the Icahn School of Medicine at Mount Sinai in New York, Site Chair of Mount Sinai West and Morningside, and Director of the Mark Lebwohl Center for Neuroinflammation and Sensation. Today's event is expected to run until approximately 12:15 P.M. Eastern Time. Following the presentations, we will host a Q&A session. If you'd like to submit a question, you may do so at any time during the webinar by typing your question into the Ask the Question field. A replay of the webinar will be available on the investor section of Cara Therapeutics' website later today. With that, I will turn it over to Chris for his introductory remarks. Thanks, Iris, and good afternoon, everyone. Thank you for joining our virtual NP event. Today's deep dive into our Notalgia Paresthetica Program showcases our continued execution and validation of our long-term strategy. We are excited to show more on how oral difelikefalin is proving to be the broad-based value driver in this strategy. Our mission is to be the leader in chronic pruritus, and with this mission, we are creating a differentiated company. Our singular focus is on treating this distressing, underserved condition that affects millions of patients across many diseases. We have an anchor product approval, KORSUVA injection, that's gaining traction as a first-of-its-kind treatment for moderate to severe pruritus in hemodialysis patients. We are rapidly advancing our oral formulation of difelikefalin and creating a new platform for treatments addressing pruritus in multiple disease categories, including systemic, such as advanced chronic kidney disease with or without dialysis or primary biliary cholangitis, dermatologic, such as atopic dermatitis, and lastly, neurologic, such as notalgia paresthetica. We are confident that our efforts to deliver treatments to pruritus patients across these three categories will help build a sustainable growth company for the long term. Today, we will focus exclusively on our exciting progress addressing the third disease category, pruritus of neurological origin. NP, which is treated by medical dermatologists, is a nerve disorder characterized by chronic pruritus of the upper to middle back. This under-recognized and undertreated condition is challenging to manage and burdensome for patients who suffer from diminished quality of life and well-being. Currently, no treatments are approved for NP and conventional options have little effect. You will hear more from two experts in the field about the unmet need and clinical presentation of NP, as well as the scientific and clinical rationale for difelikefalin as a potential treatment. Recent positive top-line results in our KOMFORT phase II proof of concept trial in notalgia paresthetica validate oral difelikefalin's potential broad applicability in chronic pruritus and more specifically in NP. In a moment, Dr. Jo Goncalves, our Chief Medical Officer, will provide a detailed recap on our KOMFORT trial results. Overall, what you will find today is that our strategy is hitting on all cylinders. Our NP program broadens the potential for DFK to cover a spectrum of pruritus-causing diseases, and it expands our potential offering for dermatologists who continue to look for answers for patients with challenging chronic pruritus like NP. I'd now like to turn it over to Dr. Zoe Draelos for an expert clinical overview of NP. I will rejoin you when we conclude with a Q&A session to answer your questions. Over to you, Dr. Draelos. Thank you, Chris. I'm happy to talk about notalgia paresthetica and really understanding the itch, which is difficult to understand if you don't have an itch you cannot scratch. In my clinical experience, patients really describe notalgia paresthetica as an itch that cannot be reached. It's the itch that drives patients nuts. It's the itch that requires a collection of back scratchers and the itch that seeks the door jamb. When I see someone, like I'm walking through an airport, and I see somebody scratching against a door frame, I think, ha, notalgia paresthetica is the right diagnosis. It's such an annoying condition simply because you cannot scratch that itch, and that's a very, very uncomfortable feeling for many people. When patients present with notalgia paresthetica, it's usually an itch at the base of the shoulder blade. We're not exactly sure why the condition occurs, though. However, it may be related to the fact that the shoulder blade rubbing over the skin can cause some skin or neurologic damage. Some patients with notalgia paresthetica are unable to sleep, and the varying intensity of the itch can change with activity. Many patients find that notalgia paresthetica decreases their quality of life, affects their ability to work because they're unable to concentrate due to the itch. In my clinical experience, some patients even comment on increased suicidal ideation. Probably the most poignant description one of my patients gave me of notalgia paresthetica was the desire to unzip his skin, take it off at night, and put it on the chair just because he wanted to relax. Indeed, an itch that you cannot scratch can drive you crazy and create a great deal of stress in your life. Visually, notalgia paresthetica is characterized by increased pigmentation over the area at the base of the shoulder blade, and it is also characterized by thickened skin, a characteristic in dermatology known as lichenification. The clinical presentation of notalgia paresthetica is based on a variety of symptoms. Patients may present with chronic intermittent paroxysmal itching, or they may have other sensations such as tingling, numbness, or burning. Some patients comment that the area has a cold sensation, or that there are pins and needles coming out of their back, much like your hand or leg when it goes to sleep. Some patients even comment on tenderness or more severe manifestations such as pain, hyperesthesia, or other paresthesias. Notalgia paresthetica can occur on the right base shoulder blade, left base shoulder blade, or both, and it usually lasts multiple years, with a mean duration between 21 months and three years. In my experience, however, notalgia paresthetica can last quite a bit longer and sometimes in people, a lifetime. Interestingly enough, it affects more women than men, but I believe it's really underdiagnosed, and I think the reason is that as dermatologists, we have no good treatment to offer patients who suffer from notalgia paresthetica. It might interest you to know that notalgia paresthetica accounts for 8% of chronic itch patients, and there is no currently approved on-label treatment, which is very dismaying for patients when they come to see the dermatologist, and they're told the treatment is indeed lacking. There are a variety of treatments for notalgia paresthetica, and the fact that there are so many different treatments, in my experience, means that there's one that doesn't work terribly well, and so people try and combine multiple therapies. That doesn't work very well. Conventional therapies that we use for itching, such as oral antihistamines or topical corticosteroids, really don't work very well in notalgia paresthetica because it's more than just the itch. Some dermatologists have used capsaicin as a first-line treatment. This is a derivative of chili peppers. Basically, what this does is it's a sensitizer that confuses the skin, doesn't necessarily get at the root of the problem. Other anecdotal off-label therapies to which there are no robust clinical studies include topical anesthetics like topical lidocaine. It doesn't work terribly well, however, because the problem really isn't on the skin surface. Other topical medications such as tacrolimus or intralesional steroids, they don't work terribly well either for the same reason. Neuromodulators such as botulinum toxin A have been used, with not long-term great effect. Gabapentin, oxcarbazepine, amitriptyline, an antidepressant, really isn't a condition related totally to depression. Those don't work terribly well. Surgical modalities like surgical decompression, vertebral local anesthetic blocks, transcutaneous electrical nerve stimulation or TENS, and electrical muscle stimulation or EMS don't work terribly well either because this isn't totally a nerve or muscle problem. Phototherapy, such as UVB radiation, has been tried. Also, manipulations such as spinal manipulation, physical therapy, osteopathic manipulative therapy, and acupuncture have been tried, and then cryotherapy, which is basically freezing the skin. You can see we have a wide variety of treatments from anesthetics to neuromodulators to antidepressants to surgical intervention to phototherapy to physical therapy to freezing therapy. The fact that we have so many different treatments means that none of them work terribly well. In summary, what can we say about notalgia paresthetica? Well, just imagine an itch you can't reach, you can't scratch. Itching is one of the most potent sensates that humans feel. The problem with itching is it just provokes the need to scratch. With notalgia paresthetica, however, it may be an itch that doesn't go away quickly, if ever. Going to the dermatologist seeking treatment for a life-ruining ailment and being told there is no treatment is very depressing, not only for the dermatologist, but also for the poor patient. Therefore, I am very excited as a dermatologist about the potential for a new effective treatment for notalgia paresthetica. Now I would like to hand it over to Dr. Brian Kim for his comments. Thank you to Zoe for the nice overview of notalgia paresthetica. I'll be talking now about difelikefalin and its potential mechanism of action in notalgia paresthetica. We're going to specifically try to understand itch in notalgia paresthetica by talking about the sensory nervous system. Notalgia paresthetica is a truly neuropathic itch disorder. There are no FDA-approved treatments. Off-label treatments are either ineffective or have tolerability issues. Because it is a neuropathic itch disorder, the itch actually starts from the nervous system, and therefore, anti-inflammatory agents demonstrate poor efficacy. Although there are a number of neuromodulatory drugs that are used in notalgia paresthetica, they are limited in terms of their tolerability, and efficacy as well. In terms of the pathogenesis of notalgia paresthetica, like many other neuropathic itch conditions, it is likely secondary to mechanical irritation or even damage along the spinal cord, where there are nerve fibers that enter from the periphery. There are a number of different conditions in which there can be a physical damage to these nerves, and notalgia paresthetica is one of them. It's primarily thought that notalgia paresthetica is caused by compression of these dorsal branches that come into the thoracic and perhaps even spinal portion of the spinal column, and that this leads to circumscribed pruritus between the scapula in the middle or slightly lateral portion of the back. It's usually unilateral, occasionally bilateral. This is a very common condition that's malformed. It's thought to be why in many ways the back scratcher was invented. If we actually break it down in terms of what's actually happening from the skin all the way up to the brain, how does itch actually occur? We know that molecules such as histamine, which is actually an inflammatory molecule, can actually trigger itch by acting on sensory neurons within the skin. These sensory neurons go into the spinal cord. You have a series of what we refer to as interneurons within the spinal cord that then relay and activate projection neurons that go all the way up to the brain, and that's how we perceive itch. It's this very rapid signal from the skin all the way up to the brain through the circuit that we get itch sensation. As I mentioned earlier, you can have damage to these nerves between the dorsal root ganglion, the DRG, and the spinal cord that results in this kind of neuropathic itch. Notwithstanding how this occurs, if you actually get this kind of signal, what can actually happen, and what we often forget, is that within the spinal cord, you actually activate what we refer to as an efferent neuron. This is a neuron that goes out to your skeletal muscles, and you can actually then activate contraction and then that results in kind of the scratching motion. It actually can be a reflex. In other words, you don't need the brain to activate this kind of circuit, though of course the brain is there to perceive it. Of course you can consciously scratch, but even unconsciously you can scratch. You can imagine if there's damage to these nerves that this can result in a kind of autonomously firing kind of process here. What we're talking today about kappa opioid receptor molecules that actually can directly stimulate kappa opioid receptors such as difelikefalin. How does this exactly occur? What is the biology? There's been a lot of great work by many other laboratories here that have identified that there are kappa opioid receptors on these peripheral itch sensory neurons. They're within the spinal cord. They're also within the brain. At every level, it's actually appreciated that activating these kappa opioid receptors, whether it's difelikefalin or other agonists, results in alleviation of itch. The way this works is still not entirely understood, but it's thought that either directly on the nerves that mediate itch, kappa opioids serve to suppress itch in that fashion. Or we also think another possibility here is that other mechanosensory neurons that sense mechanical stimulation can be activated by difelikefalin to then suppress itch by gating out itch sensation from these other nerves. This is slightly different. You're not acting on the nerves that mediate itch. Rather, you act on other nerves that serve to suppress itch. I talked a lot about the nervous system and how neuropathic itch may occur, but we all of us actually intuitively understand itch more from the standpoint of how inflammation leads to itching conditions like eczema. In this case, you have immune cells that produce cytokines that are color labeled here, and these cytokines can actually directly cause damage to the skin barrier. Also what we know now is that these cytokines can directly stimulate sensory neurons to mediate itch. In other words, these inflammatory cytokines that we thought of as being firewalled off into the immune system actually can cross into the nervous system and act as neurotransmitters. Whether you have neuropathic itch or whether you have inflammatory itch, all itch has to go through your nervous system to reach your brain and for it to be perceived. What we think of now is that anti-inflammatory agents, although effective in inflammatory itch, are not going to be so effective in neuropathic itch because you really don't have the immune system as part of the major equation. You have the nervous system, again, as I mentioned, somewhat autonomously firing and causing itch. The idea here is that we really need to put the nervous system front and center, and activation of the nervous system results in neuropathic or neurogenic itch, where independent of the immune system, you can have itch occurring, all the time. This is where difelikefalin really comes in in my mind and its mechanism of action. We've actually studied this actually in the context of inflammatory itch to first understand whether this is even, a possibility in terms of blocking the nervous system in the setting of inflammation, but then we can infer from this back to what this really does to the nervous system. We use a mouse model of atopic dermatitis, where we actually treat mice with a compound called MC903, which results very reliably in atopic dermatitis-like disease in mice, clinically, histologically, and immunologically. We know that if we actually do RNA sequencing of the skin in this mouse model, we see key cytokines and various different factors upregulated as reported in human atopic dermatitis. Most importantly for us here on the right, if we look at scratching bouts on the Y-axis over time in days in the X-axis, what we find is that these mice are very spontaneously and continuously quite itchy, you know, as measured by very, very robust scratching. Here what we did, shown on the upper left here, is that we actually induced this atopic dermatitis-like disease in our mice, and we also simultaneously treated them with difelikefalin twice a day intraperitoneally. This is very robust systemic delivery of the drug to these mice. What we found is that if we actually go actually counterclockwise here, is that immune cell infiltrate in the skin was completely unaffected. We'd use flow cytometry to look at various different kinds of immune cells, global populations of CD45+ immune cells, as well as ILC2s and CD4+ T cells, which are thought to be pathogenic in atopic dermatitis, and we saw no effect. Furthermore, if we measure the skin thickness over time, we saw no effect as well, shown here in the lower right. One of the most striking findings that we found was that with treatment with DFK, we found very, very robust, rapid, even right out of the gate, shown in red with DFK treatment, reduction in terms of the scratching bouts compared to the control vehicle-treated mice shown in black. We see robust, rapid reduction in terms of the itch. Now, as I mentioned, if we put the sensory nervous system front and center, we pull out the sensory neurons from the dorsal root ganglia, and we put them into an in vitro dish, and we do calcium imaging to look at activation of these sensory neurons. Now, these are just globally just looking at a whole population of sensory neurons. What we find is that over time, once we introduce the DFK, we see spikes in the calcium shown here on the left, indicating that in fact, sensory neurons can be activated by difelikefalin. One of the interesting things is that when we look at the whole population and we compare to sensory neurons that are activated by other itch-inducing molecules such as chloroquine or histamine, we find that the small diameter neurons are the ones that are activated, and indeed, some of them are activated by DFK. However, what we find is that as we get to the larger diameter neurons, particularly the medium diameter neurons, which tend to be not itch neurons, we find that they're activated more by DFK than the other molecules. Indicating back to our original concept that DFK or difelikefalin may actually serve to suppress itch by acting on other sensory neurons. The simple way to say this is we feel that difelikefalin is truly a neuromodulator. The point being here is that the role of difelikefalin in neuropathic itch largely may derive from a strong neuromodulatory action on suppressing itch, which we have found even in an inflammatory mouse model. Difelikefalin's mechanism of action is well suited, therefore, to potentially address even neuropathic itch and may be even better suited in some ways for neuropathic itch. The way we think about itch in general is there's inflammatory itch on the left on a spectrum to neurogenic itch. All forms of itch involve some level of both, though some are much more inflammatory in nature. For instance, the mosquito bite or even atopic dermatitis itch may be much more inflammatory. While other forms of neuropathic itch, where there's damage to nerve fibers such as the brachioradial pruritus on the right, are much more, neuropathic in origin and may be particularly well-suited to be treated with, neuromodulatory agents such as, difelikefalin. Thank you all for listening, and I'll now hand it over to Jo. Thank you, Brian, and good afternoon to all. I'll be presenting our clinical data from the KOMFORT phase II study. I'll review the endpoints I previously presented as well as new data, namely some additional efficacy data points, the quality of life data, and data from the active extension period. As a reminder, the KOMFORT study was the first robust randomized placebo-controlled study in patients with notalgia paresthetica. The study assessed the efficacy of oral difelikefalin in reducing itch and the safety compared to placebo in patients with NP and moderate to severe pruritus. Patients were randomized to receive either oral difelikefalin at a dose of 2 mg or placebo twice daily for eight weeks. After the eight-week placebo control period, patients could enter a four-week active extension period whereby placebo patients were switched to difelikefalin, and patients who were originally randomized to difelikefalin could continue to receive difelikefalin for another four weeks. The primary endpoint was a change from baseline in the weekly mean of the daily 24-hour worst itch NRS score at week eight. Other endpoints include the four-point responder analysis, a complete responder analysis defined as a worst itch NRS score of zero or one for 70% of the daily scores for the week, which meant that patients needed to have a score of zero or one for at least five of the seven days of the week. Quality of life assessments including the Skindex-10 and MOS Sleep questionnaire and safety assessments. A total of 126 patients were randomized across the two groups. 90% of patients on placebo and approximately 80% of patients on difelikefalin completed the eight-week placebo-controlled period. The most common reason for discontinuations across both groups was due to adverse events. Dizziness and nausea were the most common AEs leading to discontinuation in the difelikefalin group and abdominal pain in the placebo group. Baseline patient demographics was very much aligned to the NP epidemiology data and what you previously heard from Dr. Draelos. A higher proportion of female patients with a mean age of 60 and the majority of patients were white. Patients had NP for a mean duration of eight years, and the baseline itch severity was severe, with a mean worst itch NRS of 7.6. The study met its primary endpoint with a statistically significant improvement in itch observed with oral difelikefalin versus placebo in the mean change from baseline in the worst itch NRS at week eight. Patients treated with DFK had a mean change of -4 versus -2.4 in the placebo arm at week eight. This graph shows the weekly data over eight weeks and demonstrates there was a statistically significant reduction in itch compared to placebo occurring at week one and sustained at all time points. Here we show the daily data during the first week. What we see is that the impact on itch reduction with difelikefalin occurs even earlier at day one, with daily separation from placebo throughout the first week, with statistical significance at all time points except day two. A significantly greater proportion of patients on difelikefalin achieved a four-point improvement in their worst itch NRS score compared to placebo. As you know, this is the endpoint that regulators will be looking at in pivotal trials. 41% of patients on difelikefalin achieved a four-point response at week eighttwo compared to 18% on placebo. Statistical separation from placebo was seen as early as week two and sustained through week eight. Approximately 25% of patients treated with difelikefalin experienced a complete response at week eight, versus 5% of patients receiving placebo with a P value of 0.008. As I mentioned earlier, patients needed to score zero or one in their worst itch NRS for at least five of the seven days during the week to be defined as a complete responder. As you can see from this graph, statistical separation from placebo started at week two and was sustained until week eight in this endpoint. Quality of life was assessed using the Skindex-10 tool, which measures the effect of itch on three domains, disease, mood, and social functioning. There was statistically significant separation at weeks one, two, four and then numerical separation at week eight. The impact of itch on sleep was assessed using the Itch MOS Sleep Disturbance Subscale, which is a validated scale to measure sleep disturbance caused by itching. This tool assesses sleep on a zero to 100 scale, with higher scores denoting a worse response. A score of greater than or equal to 40 indicates that sleep is disturbed some to all of the time. Here we present patients with a baseline score of greater than or equal to 40. A numerical separation of difelikefalin compared to placebo was observed at all time points. Now we move on to presenting data for the active extension period. 55 of the 57 patients who were on placebo and completed the placebo-controlled period continued into the active extension period and were switched to difelikefalin. I'll refer to this group as the placebo DFK group. 48 of the 49 patients who were originally randomized to DFK during the placebo-controlled period and completed the eight weeks moved forward into the active extension period and continued to receive DFK. I'll refer to this group as the DFK DFK group. In the active extension period, two patients in the placebo DFK group discontinued to AE. All 48 patients in the DFK DFK group completed the four-week active extension period with no discontinuations. A similar reduction in itch was observed in patients who switched from placebo to DFK in the active extension period to the patients who were originally randomized to difelikefalin in the placebo-controlled period. Really confirming the efficacy of difelikefalin with this new cohort of patients. In addition, we see maintenance of effect in the reduction of itch, as assessed by the mean change in the worst itch NRS in patients who were originally randomized to difelikefalin and continued difelikefalin until week 12. Similarly, an improvement in itch observed in the four-point responder analysis in patients who switched from placebo to difelikefalin, with 59% of patients achieving a four-point response at week 12. Patients in the DFK-DFK group maintained their efficacy, with 71% of patients achieving a four-point improvement in their worst itch NRS at week 12. Again, we see a consistent effect in the complete response analysis with approximately one-third of patients achieving a complete response in their worst itch NRS at week 12 across both the groups. Moving on to the safety data. Approximately one-half of the patients on placebo and difelikefalin reported a treatment emergent adverse event in the placebo-controlled period. During the active extension period, 30% of patients in the placebo DFK group reported an AE, and 25% of patients in the DFK-DFK group reported an AE. AEs were mostly mild or moderate in severity. There were no SAEs reported throughout the 12 weeks. During the placebo-controlled period, 12 patients on difelikefalin and 4 patients on placebo discontinued due to an adverse event. The most common reason for discontinuation in the difelikefalin group were dizziness and nausea, and abdominal pain was the main reason in the placebo group. During the active extension period, two patients in the placebo DFK arm discontinued. One patient discontinued due to constipation and dizziness, and one patient discontinued due to GI adverse events. The most commonly reported treatment-emergent adverse events that occurred at a frequency equal to or greater than 5% in either group are shown in this table. Nausea and abdominal pain were the most commonly reported adverse events and with a similar incidence across the two groups. Headache, dizziness, constipation, and increased urine output were reported more frequently in the DFK group compared to placebo. These events are consistent with what has been reported across studies with oral difelikefalin. The adverse event of increased urine output is largely due to an aquaretic effect, which has been well described with kappa receptor agonists. These adverse events were all mild in severity with no clinical consequence. During the active extension period, constipation was the only AE that was reported at a frequency of at least 5%. 3 patients in the placebo DFK group reported AEs of constipation. There were no AEs of constipation reported in the DFK-DFK group. To conclude, oral difelikefalin demonstrated a strong antipruritic effect in patients with notalgia paresthetica. The study met the primary endpoint with strong statistical significance. The onset of action was rapid, with significant improvement observed at day one and sustained through week 12. There was a significantly greater proportion of patients on difelikefalin compared to placebo, who achieved at least a four-point improvement as well as a complete response in the worst itch NRS, starting at week two until week eight. This robust reduction in pruritus was further maintained until week 12. Patients who were originally randomized to placebo and switched to difelikefalin in the active extension period experienced similar efficacy to patients who were originally randomized to difelikefalin, confirming difelikefalin's antipruritic effect in another cohort of patients. An improvement in quality of life, including sleep, was observed with difelikefalin compared to placebo. Difelikefalin was well-tolerated, with adverse events occurring more frequently when difelikefalin is first initiated. Difelikefalin demonstrated a favorable safety profile for patients with NP at the 2-mg twice-daily dose. The data in the NP patient population confirms two important points. One, it confirms the mechanism of action that Dr. Kim showed in his pre-clinical data that DFK has strong neuromodulatory antipruritic effects. Two, it confirms the potential for DFK to work broadly as an antipruritic drug across disease areas, regardless of the underlying etiology of chronic itch. We look forward to engaging with the FDA by quarter four of this year on the path forward for the NP clinical program. Thanks for your attention, and I'll hand over to Eric now. Thanks, Jo, and good afternoon, everyone. I'm gonna take the next few minutes to discuss the commercial opportunity for oral difelikefalin in notalgia paresthetica or NP patients. When discussing the commercial opportunity of a product, let's first start with the relevant patient population in the United States. Currently in the U.S., 13% of adults, approximately 34 million people, suffer from chronic pruritus. 8% of these patients, or approximately 2.7 million people with chronic pruritus, suffer from a neuropathic itch, which includes NP. Not all of these patients are diagnosed and treated for NP. We estimate that 24% of these patients, or 650,000 patients, have been diagnosed with NP and are under a dermatologist care. Therefore, we believe the addressable patient population of NP is currently around 650,000 patients. However, this is a conservative estimate as NP is widely underdiagnosed. This market has not been developed with physician and patient education as there are no FDA-approved therapies for treating pruritus associated with NP. As you heard earlier, what it's like to suffer from NP, the pruritus associated with NP is not your average itch that most of us have experienced, like an insect bite or mild poison ivy. That type of itch will often go away quickly with little or no intervention or treatment. Typically, that type of itch has little to no impact on your daily life. The pruritus from notalgia paresthetica is, however, completely different. As you already heard, it is a chronic, often severe neuropathic itch that typically presents in the middle of the patient's back, which makes it extremely difficult to scratch or apply topical treatments. It can be often unrelenting to the patient, and in a patient survey, 83% of the patients said they itch daily. 67% of those patients reported that the therapies they tried were not helpful. The pruritus is severe enough that in many NP patients it can impact the patient's emotions or mood, for example, being irritable in up to 70% of the patients. It can also impact the patient's ability to sleep, as reported by 40% of the patients. Because there are no approved therapies and the products tried off-label are often reported as not helpful, pruritus from NP is truly unmet medical need. Now that we understand from NP patients that most of the products they try do not help with their itching, what did dermatologists do to try to help these patients, even with their limited options? To gain a better understanding of this, we conducted a qualitative market research study with a group of dermatologists to find out what they currently do to manage NP and what they saw as their biggest needs to treat these patients. As you heard earlier, because there are no approved treatments, dermatologists will try multiple approaches, generally with limited success. This was echoed by dermatologists in our primary market research. The dermatologists in our study said they will typically try topical agents such as topical corticosteroids or capsaicin. Efficacy of these agents can be limited, and they are often difficult to apply in the middle of the patient's back, particularly if that patient does not have a caregiver readily available. Dermatologists will also try oral agents such as gabapentin or pregabalin. Sometimes these drugs can be used in combination with the topical products. The dermatologists in that study stated these products lacked predictable efficacy, and they are also concerned with the side effect profile of these agents in a typically older patient population like NP. When none of these conservative treatments work, dermatologists will sometimes consider trying other therapies such as nerve block, BOTOX, or phototherapy. These treatment options are limited, particularly since they often require a referral to another specialist, or they might be difficult to get insurance coverage for. Given the limited armamentarium that dermatologists have, where do they see the biggest unmet needs when treating NP patients? Dermatologists in our study expressed frustration by the lack of efficacy of the therapies they currently use off-label. Therefore, their most significant unmet need is for a medication that is specifically indicated for NP. Dermatologists second highest unmet need is for oral treatments that are safe. Currently used oral agents often have side effects that are not desirable for the older patient population. To summarize, we are very excited about the opportunity of oral DFK as a potential treatment for NP because oral DFK can address a significant patient population that is widely underdiagnosed. There are no approved therapies to treat pruritus related to NP. Dermatologists are looking for a product that is approved for NP with demonstrated safety and efficacy in this patient population, and they are looking for an oral product that is easier for patients to use, given the location of the itch. In short, we feel oral DFK could potentially help meet a significant unmet medical need. Thank you for listening, and I will turn the presentation back over to Chris. Well, thanks, Eric, and now we're ready to take your questions. Let me turn it over to Kevin, who will open up the line for Q&A. Kevin? Good morning. My name is Kevin. I'll be your conference facilitator. As a reminder, if you would like to ask a question, you can type the question into the question and answer section on the webcast. If you are dialed in on the phone line, you can simply press star and the number one one on your telephone keypad. Please mute all other devices to avoid any interference or background noise. One moment before our first question. Our first question comes from Daniel Wolle with JP Morgan. Your line is open. Good morning, everyone. Thank you for taking our question. I have a couple of questions. First, does the data from the active extension period, particularly in the DFK to DFK patient group, indicate a deepening of response with longer treatment? If so, what is the biological rationale for such an observation? I have a couple of other questions. Okay, thanks, Daniel. Let me address that. We do have to interpret the data in the active extension period with caution. It is active and open, so all patients are on steady drug, and they know that. There is quite a bit of bias that is introduced at that stage. I think what we like to conclude from that data is that the efficacy is sustained up to the 12-week period. Okay. Maybe for the physicians, like other pruritus indications, are NP patients subdivided by their itch into mild, moderate, or severe groups? Dr. Draelos, why don't we start with you? I think you can divide them into mild, moderate, and severe, but that is largely done for research purposes. When a patient comes in and they have an itch, the fact that they've sought medical care doesn't matter whether it's mild, moderate, severe, it's an itch. An itch is one of the most noxious sensory stimuli. If you think about it, when you have an itch, you just have to scratch it. It doesn't really matter if it's mild, moderate, or severe, you still have to scratch it. For the purposes of inclusion into a study, for the purposes of grading itch, you have to have some kind of monikers. If a patient comes into my practice and says, "I've got this horrible itch on my back," and you ask them, "Is it mild, moderate, or severe?" Everyone's gonna tell you it's severe. It's just a bad itch. I think that those designations are not clinically relevant. Got it. Dr. Kim, any thoughts from you? Yeah, absolutely. Dr. Kim, any additional thoughts? Yeah. Can you guys hear me okay? Yeah. Yeah. I think that for NP, I actually think a lot of people have NP, and they're not gonna show up to the dermatologist. I think what we would classify as mild, moderate, severe is gonna be skewed already when you're seeing it from the lens of a dermatologist for diagnosis. They're all gonna be at minimum moderate. The mild to moderate population is probably pretty big, and oftentimes those individuals know they're itchy on the back. They don't know that it's something that should be addressed. Yes, we classify in clinical trials, but that does not mean that it necessarily is capturing the whole population. I hope if that makes sense. Got it. Yes, it does. I guess following up on for the company, how does that fit the 650,000 addressable patients when you don't need to classify them by this grouping? Yeah. It makes sense it fits that 650,000 because that classifies all patients that are diagnosed and treated by a dermatologist based on the data. That would cover basically what Dr. Draelos was saying of patients that show up to dermatologists seeking treatment. Okay. Got it. One last question. Given the findings shown here by Dr. Kim in animal models of AD, where DFK doesn't seem to drive changes in inflammatory mediators, how should we think about the company's efforts in atopic dermatitis? How much of the itch in AD is neuropathic versus inflammatory? Thank you very much. Dr. Kim? Sure. I'll just address it from this clinical end, that all itch has to go through the peripheral nerve. To some degree, all itch is a neuropathic process. When we say neuropathic itch, we mean that it's primarily neuropathic, and meaning that it's primarily that the nerves have gone awry. In theory, you could actually neuromodulate your way out of anything. It's just that with atopic dermatitis, I think if you have tremendous amount of inflammation in, you know, moderate to severe, particularly severe cases, it can be much more challenging to neuromodulate your way out of it. I think that's why I'll leave it to the company. I think the strategy at first, I think, is better to get a population that's been less well addressed, which is in the more kind of low moderate to high mild, which actually is a much bigger population. Yeah. Let me just add to that as well. Absolutely, Brian. Daniel, as you recall in our atopic dermatitis phase II study, the greatest treatment effect in AD was seen in the mild to moderate patients. Exactly to what Brian was saying, you know, the moderate to severe, a lot of systemic inflammation on board. Because the drug has a stronger neuromodulatory action, it now, you know, makes a lot of sense, why we saw the data that we saw in the clinical phase II study. That's why we're focusing on those patients, and that's the positioning of the drug, where we seem to be best suited in the mild to moderate patients. Great. Thank you again for taking my questions. One moment before our next question. Our next question comes from Annabel Samimy with Stifel. Your line is open. Hi. Thanks for taking my question and for all the detail. I guess a follow-up question on the extension data. I guess given the neuronal activity, is there any chance for like remodeling of the neuronal pathways that you could get a longer term effect? Or on the flip side, could there be any remodeling of the pathway such that you lose effect over time? This is kind of a question for Dr. Kim. I'm not sure if you've done any kind of analysis based on that, but you know, based on the extension data that you did see continued activity. I was just curious about that aspect of it and have some follow-up. Thanks. I guess I'll take that. Yeah. Well, the short answer is we don't know long-term, right? One of the things I think that's interesting is that this pathway seems to be a little bit broader. We're not just blocking a specific itch signal, which is typically the case. What we're actually doing is suppressing a variety of different itch signals. I actually think that this is a rather broad pathway, and it's less susceptible to kinda things kinda wiggling around it. Whether that translates to real durability, you know, I don't wanna be too, you know, forceful in terms of my opinion on that. I think you never know what's gonna happen long term. Maybe again, on the extension data, we saw that there was a reduction in some of the AEs, compared to, I mean, as far as the percentages compared to the first part. Is there anything that was done differently, like setting expectations differently, or did patients just seem to start tolerating the therapy better? Is there anything that you can do ahead of time to be able to manage some of the nausea or GI issues that they feel? Thanks. Yeah. No, good question. I think always, you know, you typically see when patients go on to active extension periods, it's usually sort of the hardier patients who continue on. They may be patients who maybe more tolerate adverse events a little bit better. Nothing was done differently, Annabel, in that part of the study. You know, patients obviously all knew that they were going onto study drug. As far as information regarding tolerability, it remains the same as the first part. Okay, great. Maybe I can ask. I'm not sure that you know this right now specifically for difelikefalin, but as these patients itch less or scratch themselves less, I mean, do you see any chance for reversal of the skin thickening or the lesions that they have on their back with the calming of the itch, and will this possibly be incorporated into any future endpoints of subsequent trials? Yeah, I can answer that. Why don't we actually have Dr. Draelos answer that? Yes. Thank you. Okay. Yes. You know, lichenification that occurs, which is the thickening of the skin on the back, the coarsening of the dermatoglyphics, the dyspigmentation that occurs, all of those are due to repetitive scratching of the skin. Once the itch resolves and there's no drive to scratch, the skin will indeed normalize. The mark that many NP patients have that is indicative of the diagnosis of their disease will resolve, and they should be able to return to normal skin appearance and normal life without standing and scratching every door post that they come by. Maybe I can address from a kind of trial perspective. We did not include it as an endpoint in the phase II study and certainly up for discussion in our phase III program. Okay, great. One last question with regard to the phase III program. I think the last time you spoke about NP and the next steps with FDA, you discussed additional dose finding. Is it possible to move into a phase III with dose finding, and can you gather anything from the prior phase II trials in AD or CKD, non-dialysis CKD that you can incorporate or gather for these lower doses? Thanks. Yeah. No, excellent. For sure, we've always said we need to do some dose finding. This was obviously just one dose at the highest dose. Indeed we can glean some information that we collected in both the CKD and the AD study regarding the doses. We'll take that all into consideration in choosing the dose for the next step. We would like to, you know, move and accelerate the program as fast as we can into a phase III program. Looking at ways that we could do that, and that, of course, will be a discussion with the FDA, which we will be meeting and hope to meet before the end of the year. Okay, great. Thanks a lot. All right. Why don't we take a question from the webcast? The first one is, maybe, Dr. Draelos, you can answer it. Does this condition get worse over time without treatment? Is that likely due to an itch scratch cycle and/or worsening of the underlying mechanical nerve damage? Maybe Dr. Draelos, you can start on that. Yes, I'm happy to answer that. I think the course of NP is variable person to person. Certainly, there are other factors that can make itch worse, like stress in one's life, other emotional issues, depression, et cetera. So the disease and any itch tends to be stress-mediated to some degree. Usually, people with NP have a course that gets worse over time. The reason is whatever the cause is, it's magnified over time. We don't know exactly what the cause is. Many people have theorized that the scapula rubbing against the skin itself causes neurologic damage. It is interesting that in some people the disease does resolve and indeed go away. It's really hard to predict the course, but certainly controlling it early, you might think would lead to less neurologic damage that would lead to less skin changes that might lead to earlier resolution. I think treating the disease early in its course definitely has a place and an oral medication that would induce relief, I think would bring the disease under control much earlier for many of the sufferers. Great. Thank you. Let's take another question from the online platform. Maybe Dr. Kim, you can start us off on this, and then, Jo, maybe you have an opinion on this as well. Given the efficacy signal in NP, what other neuropathic itch conditions may make sense to explore? And Jo, maybe for you, do you simply enroll a broader neuropathic itch population in your registrational studies? Maybe Dr. Kim, we'll start with you. Yeah. I'll answer that, and I'll expound a little bit upon the last question that Dr. Draelos answered as well, which is that they're kind of related in the sense that the itch can get worse over time, so leaving it untreated is not a good idea. There's some concern that the itch can actually generalize as well. That neuropathic itch. There's a concept that neuropathic itch, like notalgia paresthetica, can actually generalize, and that some of these individuals who even have chronic pruritus of unknown origin actually, in fact, started that way. There's that concern. Then also related to that is that notalgia paresthetica is actually in a family of neuropathic itch disorders that are all related to kind of damage, chronic wear and tear to the spinal column. This also includes a condition called brachioradial pruritus, where there's actually itching on the arms very characteristically. It's very much neuropathic. Then also scalp pruritus as well. A very common problem is scalp pruritus. It's really this kind of nexus of injury to the upper kind of back over time, not acute injury, but chronic wear and tear, and that these are all kind of related. Those are the ones that are actually very closely related. Again, the concern is that some of these things can actually generalize. From a clinical perspective in our studies and, you know, what we aim to do, for now, the data that we've generated is notalgia paresthetica. We'll have a discussion with the FDA and get a better sense of what the next development step would be and, you know, which patients would we limit those studies to. Great. Thank you both. Let's go back to the phone lines. One moment for our next question. Yes. We have the next question from the phone. Our next question comes from Sumant Kulkarni with Canaccord Genuity. Your line is open. Good afternoon. Thanks for taking my questions. I have three. The first two are for the experts, and the third is for the company. First, when diagnosing an itch, is NP the last stop by a process of elimination and location of the itch, or could there be other types of unexplained itch? In other words, you know, how confident are physicians in the clinical community of a definitive diagnosis of NP? Maybe we'll start with Dr. Draelos and then, maybe Dr. Kim. Well, NP is very difficult to diagnose because it's characteristically at the base of the scapula, either unilaterally or bilaterally on the back. There are no other itches that really present quite like that. There are itches that present in other body areas, but not so characteristically. Patients will give you a history that's fairly consistent. They have the spot on their back that they cannot reach, and it itches. Indeed, that is a place where it's very difficult to reach to scratch. Many of those patients will also present to the clinic bringing a back scratcher. That's a clue even before you ask a past medical history from them. When they come with a back scratcher, you know what the diagnosis is at the door. Finally, on physical exam, it's very characteristic to see the lichenified hyperpigmented skin. It's in a well-defined area about the size of the palm, usually at the base of one or both scapulae. The diagnosis, I would say, is fairly easy to make. There aren't a lot of other things that would fit in the differential, actually, for this localized type of itch on the back in this location. Yeah. I'll just chime in. I think I only see itch, so I don't find this particularly challenging at all to diagnose. I think we overly focus on the physical attributes of dermatologic conditions, naturally. When it comes to itch, it's a sensory pathology, so I don't really feel that I even have to see the hyperpigmentation. My personal preference wouldn't be that that is overly emphasized. A conceptual question. In terms of preclinical models, are there known cases of NP in other animals or non-human primates? Are they any good alternatives to mouse models? It's a good question. I'm not aware of NP. The only animals I would wanna consider is primates for this. I suspect that this condition is arising from the kind of modern epidemic of inactivity and bad posture and bad kind of occupational habits. I would suspect that this would be much less likely in other species. Got it. Lastly, for the company, given no product is specifically approved for NP, how many phase III trials do you think would be necessary as part of an NDA package? If more than one is required, do you plan to run them simultaneously? Thanks, Sumant. There will, of course, be a discussion with the FDA, and, you know, we'll obviously follow their guidance. We expect it likely to. Study at this stage and what we typically do with our phase III, we usually try and stagger them, try to run them as close together, but sometimes just staggering for operational efficiency. Thank you. One moment for our next question. Our next question comes from Jason Gerberry, Bank of America. Your line is open. Hey, thanks for taking my questions. My questions are for the doctors on the call. Just trying to get some of these patient numbers, a sanity check, really. Can you give us a sense of how many NP patients you manage in a given year? You know, what proportion you'd say are candidates for systemic pharmacotherapy? Maybe if you can kind of give a split of topical, non-topical treatment options as they're currently kind of divided out. My follow-up question is more or less how you envision using a drug like oral KORSUVA. Would it be more PRN as needed, or do you see it more as a chronic treatment for these patients? Thanks. Maybe we'll start with Dr. Draelos. I think treatment for NP, basically, you would start out treating it chronically, and you wanna be sure that all the skin findings resolve and you have the disease under control. Then maybe after six months to a year, you might want to take a short drug holiday and see what happens. If it's incompletely re-treated, you will need additional treatment. That actually is also a position, though. Excuse me. The reason is we don't know anything about drug holidays, and we don't know anything about year-long treatments with interposed periods of drug holidays and remission. I have to say that that's just basically my clinical gestalt, not based on any particular research study that's been done to date. I do think that the population of NP is very underrepresented in the dermatologist's office, and the reason is topicals do not work. I haven't found a topical yet that works well. Some people with NP might be misdiagnosed with eczema by a family practitioner, and a topical corticosteroid works, but if it's true NP, topical corticosteroids do not work. I think NP patients get tired of going to the dermatologist or to a general doctor and seeking medical care for a condition where they get no improvement. I think if it were known that there was a treatment for the, quote, "itchy back syndrome," people would come to the dermatologist and identify themselves. I probably, in my current practice, maybe see one patient every two weeks. Usually those are people who are at wits' end. I think there are a lot of people who have NP where it lowers their quality of life, but they just don't seek medical care because of it, because there isn't anything to offer. If consumers knew that there was an approved oral medication for NP, I believe they would come to the dermatologist. I believe that they would request a prescription. I think NP is a lot like rosacea. Years and years and years ago, rosacea was very underdiagnosed because we had nothing to treat it with. Then MetroGel was discovered. Galderma really put rosacea on the map, made it a disease. People understand now if your face is red and stays red, you need to seek the help of a dermatologist. I think that same model would apply to NP, where people now realize NP is a recognized disease condition. Remember, itch was not even recognized by the FDA as a diagnosis that you could use for a patient visit several years ago. You know, itch wasn't a disease, it was a symptom. Now itch is now recognized as a disease. NP is recognized as a disease. I think that will create a market for this medication much bigger than the current population of identified NP patients who are under dermatologic care. Great. Dr. Kim, maybe you have some thoughts as well. Yeah, I agree. I already kinda hinted at this. I think that we see a very skewed population in dermatology. I see an even more skewed population. I don't think I see as much NP because they tend to I do see a lot of itch patients, but I only see about a couple a month. I think that a lot of them actually don't even know to actually make it to me unless they're very, very severe. I think that most of them sit kind of in the moderate range, maybe even a ton in the mild. I think if there's a drug for it will explode. I think it could be almost problematic because you'd have so many people suddenly recognizing that what they have. They're not really getting diagnosed by their physicians necessarily. A lot of them are probably getting actually filtered out and don't even make it to dermatology from primary care. Got it. Thank you. One moment for our next question. Our next question comes from Joseph Stringer with Needham. Your line is open. Hi. Thanks for taking my questions. A few from us. First one for the company. You went into the segmentation of the market, 650 threshold patients, U.S., that are under Derm care. You had this figure with 73% who are not on medication. I was just curious if you could further comment on what percent of that 73% who are not on meds have either tried various types of medication and sort of inadequate responders and have sort of gone off medication or, you know, what percent just had never started medication and are just sort of in wait and see mode managing on their own. Then question for Dr. Kim and Dr. Draelos. What's your view on in regards to the Cara's phase II NP trial here, how representative are the NP patients from that trial in terms of baseline disease characteristics? How representative are those patients of the real world NP patients, so to speak? Lastly, just given the phase II data to date in NP, what percent of your NP patients would you prescribe the drug in? Thank you. I'll start first with the question regarding the 73% of the patients. That information comes from a study that was conducted with talking to NP patients. If you look in that same study, 67% of the patients said they tried therapies and they didn't work. The vast majority of those patients, that 73% that are no longer on therapy, tried therapy, but it was ineffective, so they've stopped. You even heard that in the patient videos that we started up front, that a lot of those patients tried a number of things and now they've stopped therapy because nothing's effective for them. I would expect that most of that 73% were on therapy at one point, but then stopped because of ineffective treatment or side effects. Great. Draelos Dr. Draelos, if you wanna jump in here. Yes. There was a question of how representative were the patients enrolled in the study of those I see in my practice. I would say because of the inclusion/exclusion criteria, they might have been a little more severe. It's usually assumed that if it works on more severe patients, the medication will also work on more milder patients. I think the efficacy seen in the trials will probably nicely correlate to what's seen in the clinic. The other question was, is what percentage of my patients would I prescribe this drug for if it came to market? I would use it 100% of patients because it's the only on-label medication that we have for NP. That's important because off-label medications aren't usually covered, on-label medications are. I really think for practicing dermatologists, having something on label for NP would be a huge breakthrough. Great. Dr. Kim, your thoughts? Yeah. There's a SlicerDicer function on Epic, and if you use it, you'll find that most of these patients have blasted through antihistamines, gabapentin and topical steroids, which topical steroids are useless. Antihistamines are useless. Two of the drugs that the majority of will have received are not even useful. Yeah, I agree with Dr. Draelos. 100% of the patients would get it because the other things don't really work very well. Lastly, the trials always skew more severe, as we've been talking about. I think it'll be if we're too literal about the trial as we translate to the clinic, you'll have patients being very frustrated who won't be able to get the medicine is actually my primary concern. Great. Okay. Let's take a question from, you know, sort of a closing question from the online platform, and that is start out with you, Jo. Can you frame qualitatively the importance of complete response? And are these patients truly itch-free? And maybe we'll have, Dr. Draelos and Dr. Kim comment as well, just around the importance of the concept of very low WI-NRS rating. Right. I'll just remind everyone about the definition that we used. We requested that patients, when they document in their daily diary, and they document daily for seven days, that five of the seven days, if they had entered a zero or one, then they would be considered a complete responder for that week. What we saw in the data is that by week eight of the double-blind treatment period, you had about a quarter of patients achieving that versus 5% on placebo. You really do see the separation from placebo because it's quite a high bar for patients to reach to be free or almost free of itch. You know, we were very pleased with the data and it was, yeah, very strong data. Great. Maybe we'll just have, Dr. Draelos and then Dr. Kim comment on the importance of reaching such a high bar from an itch-free perspective. Dr. Draelos? Yes. You know, an itch is an itch, and whether it's mild, moderate or severe, it's still annoying and it still needs to be scratched. Unfortunately, scratching NP only makes the condition worse. Whether you have mild, moderate or severe disease, you wanna get rid of the itch. If you told patients, "Well, you know, this drug works great, it'll get rid of half of your itch," that's not success because patients are still going to have that annoying symptom. It's really an all or none treatment. The high bar was necessary, the high bar was met. Itch is an all or none. Not everything in dermatology is atopic dermatitis, for example. You can have less excoriation, you can have less erythema. Psoriasis, you can have less scaling, but when it comes to itch, it's gotta be gone. There isn't such a thing as it's just half. It either itches or it doesn't. I think the bars that were put in place for the clinical trials in the phase II studies, et cetera, are very realistic for what you would see in the clinic. Great. Dr. Kim, any thoughts? Yeah, thank you. I think the itch-free state, you know, it's a very high bar. I don't think it's necessarily what should be held to the standard in terms of as a universal standard. I think it's a very high bar, and that's great. I think in the clinic, I have lots of patients who are on drugs with, you know, modest to moderate efficacy, and they won't come off of them either. I think it speaks to how unmet the need is, and I think we're talking about a condition that doesn't have an on-label drug. It's great that we can hit these huge bars, but I also don't think it's absolutely necessary. Great. Awesome. We've run out of time, so I will turn it over to Chris for his closing remarks. Yeah. Thanks, Iris, and especially wanna thank Dr. Draelos and Dr. Kim. I really appreciate your time on this call. Very informative. I certainly wanna thank everyone for joining today. You know, I'll say a couple things. Our core strategy is on target and on track, and we are working diligently to expand the applicability of oral difelikefalin across a spectrum of diseases causing chronic pruritus. This is the engine that's gonna drive Cara's value and growth. I'll emphasize a few key takeaways from today. You know, first, our NP program really showcases our expanding opportunities with oral difelikefalin. You know, our platform is addressing multiple indications, including now with NP, a larger footprint with diseases treated by dermatologists. Second, you know, there is a strong scientific rationale for oral difelikefalin in notalgia paresthetica and pruritus of neurological origin, certainly. Oral difelikefalin has a neuromodulatory mechanism of action, which allows it to potentially address itch in a way that anti-inflammatory mechanisms cannot, as Dr. Kim explained. Third, we have a clear clinical rationale and a real differentiated market opportunity, as you heard today. There are no approved treatments for pruritus and NP. Currently used treatments are mostly ineffective, and it leaves a significant patient population, like the ones you met at the opening, where we met three patients that are really in search of new and innovative options. With that, I'd like to thank everyone for joining us and for your participation today. We look very much forward to an exciting progress ahead. Thank you very much. Ladies and gentlemen, this concludes today's presentation. You may now disconnect and have a wonderful day.