Good afternoon, ladies and gentlemen, and thank you for standing by. Welcome to the Relmada Therapeutics, Inc First Quarter 2021 Financial Results Conference Call. At this time, all participants are in a listen only mode. A question and answer session will follow the formal presentation. I will now turn the conference over to your host, Timothy McCarthy with LifeSci Advisors. Thank you, operator, thank you all for joining us this afternoon. With me on today's call are Chief Executive Officer, Sergio Traversa, and Chief Accounting and Compliance Officer, Charles Ence. This afternoon, Relmada issued a news release providing a business update and announcing financial results for the first quarter ended March 31, 2021. Please note that certain information discussed on the call today is covered under the safe harbor provision of the Private Securities Litigation Reform Act. We caution listeners that during this call, Relmada's management team will be making forward-looking statements. Actual results could differ materially from those stated or implied by these forward-looking statements due to risks and uncertainties associated with the company's business. These forward-looking statements are qualified by the cautionary statements contained in Relmada's press release issued today and the company's SEC filings, including in the annual report on Form 10-K and subsequent filings. This conference call also contains time-sensitive information that is accurate only as of the date of this live broadcast, May 12th, 2021. Relmada undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call. Now, I'd like to turn the call over to Sergio. Sergio? Thank you, [Timothy McCarthy], and good afternoon to everyone. I'm pleased to welcome you to Relmada's first quarter 2021 conference call. On today's call, I will provide an update on the comprehensive development program for the treatment of depression, the REL-1017, and the upcoming milestones. I will turn the call over to Charles Ence, our Chief Accounting and Compliance Officer, and who is standing today for our CFO, Maged Shenouda, for a review of the financials. By the [June 5th] of the recent data that we presented at three recent scientific conferences. With that, I'll begin with an update on RELIANCE. That is the ongoing phase III program for REL-1017. It consists of the first placebo-controlled pivotal studies, RELIANCE I and RELIANCE II, which includes 364 participants per study at 25 sites. It also includes RELIANCE-OLS, that stands for, Long-Term Open-Label Safety study that is enrolling both rollover participants from the pivotal studies as well as de novo participants. This study are designed to evaluate REL-1017 as an adjunctive treatment for Major Depressive Disorder, MDD, and includes placebo and 25 mg of REL-1017. I just got somebody told me that I am breaking up, so I'll try to switch. Now it should be better. I was saying placebo and 25 mg of REL-1017, and both are on top of standard antidepressant treatment for participants who have already unsuccessfully tried a minimum of one up to three antidepressant therapy. The primary endpoint is change in MADRS score at day 20. Key secondary endpoints include change in MADRS score at day seven and change in CGI-S, the stage for severity, score at day 28. The first phase III trial, RELIANCE I, continues to enroll as expected, and additional sites are coming online nicely. We recently began enrolling participants into the second phase III trial, RELIANCE II, which is a mirror study of RELIANCE I. Top line data from these two trial are expected in the first half of next year. The RELIANCE-OLS is also underway and enrolling participants as planned. RELIANCE-OLS will include both participants from the pivotal studies as well as de novo participants. The data for this long-term open label safety study will be the part of the NDA filing package. We remain on track to initiate the study evaluating the use of our REL-1017 as a monotherapy for MDD during the current quarter. At a very high level, the most significant difference between this trial and the ongoing clinical studies is the patient population. The patient population plan for MDD monotherapy study will consist of people who are diagnosed with depression, and they are not currently taking standard antidepressant therapy. We anticipate the completion of this study by year-end 2021. Moving on, I would now like to provide an update on the Human Abuse Potential or the HAP studies. As we discussed previously, we discontinued Study 120 that was assessing REL-1017 versus oral ketamine as an active control. As part of a pre-planned blinded analysis of the initial study completers showed that a significant material group of participants did not respond to the active control ketamine. Most likely, this lack of response was due to the poor The bioavailability of oral ketamine, and this would have resulted in non-concluding findings, so we decided to stop it. We are now working toward initiating a new ketamine control study. We call it Study 126, which will use as an active comparator intravenous (IV) ketamine that has a established history as an effective positive control. We plan to complete this study by year-end of this year, so end of 2021. The second HAP study, the abuse study, is Study 124, is comparing REL-1017 to oxycodone. It's progressing as planned, and we continue to expect to complete the study by end of the current quarter. These HAP study are a standard component of the NDA submission for many CNS drugs and will inform the assessment of REL-1017 for the scheduling. The HAP studies also represent an important opportunity to add to the existing very strong body of literature that clearly differentiates REL-1017 from the parent drug, racemic methadone, and any potential perceived association with opioid effect or dissociative symptoms. I'm also happy to share that Relmada just completed presentation of a total of nine poster over three different scientific congresses. I will provide a brief overview of the data for REL-1017 that we presented. However, before I do that, I will turn the call over to Chuck for his review of the financial. Chuck. Thanks, Sergio. It's all you. Good afternoon, everyone. Today, we issued a press release announcing our business and financial results for the first quarter ended March 31st, 2021, which I will now review. For the first quarter ended March 31st, 2021, total research and development expense was approximately $14 million as compared to $4.5 million for the comparable period of 2020. The increase was primarily related to an increase in cost associated with the execution of a broader clinical program for REL-1017. Total general and administrative expense for the quarter ended March 31st, 2021, was approximately $8.4 million as compared to $5.5 million for the comparable period of 2020. The increase was primarily due to an increase in stock-based compensation. For the first quarter ended March 31st, 2021, we recorded a net loss of approximately $22.2 million or $1.34 for basic and diluted share, compared to a net loss of $10.7 million or $0.72 per basic and diluted share in the comparable period of 2020. On March 31st, 2021, the company had cash equivalents, and short-term investments of approximately $102.7 million compared to $117.1 million on December 31st, 2020. We continue to expect that this strong cash position will support us through at least the multiple data readouts we anticipate through the first half of 2022. I will now hand the call back to Sergio for further remarks on the most recent progress. Sergio? Thank you, Chuck. I appreciate it. As I mentioned, I'm happy to outline the recent data that we presented in nine posters across three different medical meetings. First, at the American Society for Pharmacology and Experimental Therapeutics, we share pre-clinical data that confirm a lack of any neurotoxic feature that potentially link to Olney's lesion. This was totally not a surprise, it's important because this effect has impacted safety and development of other NMDA receptor blockers like MK-801, these findings continue to support the consistent safety profile across pre-clinical and clinical studies. Next, at the Society of Biological Psychiatry, we share a total of six posters that outline new work to understand the underlying mechanism of REL-1017. What we find was very interesting and included additional support for a role in neural plasticity and insight regarding its binding to NMDAR subunits, in particular the GluN2D subunit, which appears to explain both the lack of dissociative side effect as well as the rapid and sustained antidepressant effect. Lastly, we share at the APA, the American Psychiatric Association, the data from the phase II study that showed that REL-1017 demonstrated a statistically significantly rapid and sustained efficacy with large effect size, in addition to favorable safety and tolerability profile and absence of any sign of withdrawal after ending treatment. In summary, the REL-1017 development program remains extremely active, and we anticipate multiple key data readouts over the next 12 months. Importantly, as Chuck noted, we have a strong balance sheet driving this robust R&D effort, and we have cash to support us through this expected data point. As always, I'm grateful to the Relmada team for their continued hard work and dedication to executing on our mission. I would also like to extend my sincere thanks to the participants and clinical partners involved in the REL-1017 clinical trials for their effort in advancing this important therapy through the clinic as expeditiously as possible. I do believe that now we can open up for questions and the operator, you can go ahead and open the line for questions. Thank you. Thank you. Our first question is from Andrew Tsai with Jefferies. Thanks. Good afternoon, congrats on all the progress, Sergio and team. My first question is on the oxycodone study, the data reading out soon. Very clear that all three doses need to be stat-safe versus esmethadone and it's similar to placebo. Can you describe just how similar esmethadone should be to placebo on the VAS liking score? From time to time, I think of a scenario where what happens if esmethadone is showing 60- 65 score, for example, just outside of the typical placebo range. How would we interpret that result, I guess? Thanks. Thank you, Andrew. Good afternoon, and thanks for the question. Well, look, it's a key question. oxycodone 40 mg, that is what we use as a comparator. It's not a very high dose, but it's high enough that is clearly likable by patients or people, participants that like to take a narcotic as a recreational drug abuse. As a CNS drug, you may expect, we may expect that it's not placebo, right? You're taking benzodiazepine or you take a sleeping pill, it's not placebo. You feel something. If this feeling will be pleasant or not is very difficult to say, although all the data that we have seen so far, nobody really likes it. We have treated over 100 patients and there is really no likability at all. If you really take in phase I, if you take a high dose like 150 mg and some patient experience nausea, That is not a very pleasant feeling. To answer directly your question, the most important is to differentiate all three doses of esmethadone from 40 mg of oxycodone. We don't expect to be very different from placebo. Also, it does not require that we are similar to placebo. I would focus everybody's attention to the oxycodone. Placebo is there just because to have something to compare. We are not comparing esmethadone to placebo. Right. I hope I answered your question there. Oh, yeah. That's very clear. Yeah, thank you. Yeah, very good. My follow-up question is, let's just say data is clearly positive, completely clean. Would it then be fair for investors to assume that the second abuse liability study versus ketamine is pretty much de-risked because you would have seen data on, for example, dissociation, hallucination from the oxycodone study? The straight answer, yes. I would say that I'm an old pharmacist and I always say that drugs tend not to change the way they work over time. If we don't see anything that would show any dissociative or any hallucination or anything that would be like ketamine or like an NMDA toxic effect, there is no guarantee. I mean, it's not 100% guaranteed, but it's unlikely that in a different study will show up as very different from what we see so far. Yes, the answer is yes. We do believe that there is a de-risking component when we will see the oxycodone data. Perfect. Thank you, Sergio. Thank you, Andrew. Our next question is from Joon Lee with Truist. Hi. Thanks for taking our questions. I believe the DEA is on record saying that dextromethorphan lacks addiction liability. What's the basis for that, for DEA making that claim? Is that based on any specific study? If so, what doses were used? Related to that, are you aware of DEA making similar claims about esketamine as compared to ketamine? Thank you. Hey, Joon. Good afternoon. Thanks for the question. We actually asked the same question to the DEA, where the data that they based the statement that esmethadone is exempt from abuse risk and respiratory depression. They did not do any proprietary study that is not published. They based their statement and their opinion on what is available. There is quite a bit of literature available, including the phase I that Relmada did with the single dose and multiple dose of esmethadone. They look at whatever is available. They draw the conclusion. That's pretty much how they did it. The comments on esketamine. Well, esketamine, look, esketamine has been on the market for quite a bit of time in few European countries as an anesthetic to replace ketamine. It is a lower dose of racemic ketamine. Technically, pharmacologically, there is no difference between esketamine and racemic ketamine. It's pretty much the same thing, just different dose. I would be surprised if the DEA would schedule esketamine in a different way than racemic ketamine. Johnson & Johnson, which SPRAVATO, they performed the abuse study comparing nasal esketamine SPRAVATO versus intravenous ketamine, and pretty much, they were the same thing. There was no real difference. Esketamine will remain the same schedule as racemic ketamine. With that said, maybe I can add one thing that ketamine and esketamine, they are both Schedule III. That is very different from Schedule II, and there is probably more difference between Schedule II and III than any other scheduling between III, IV, and V. The reason being that the major worry of the FDA is not really just the abuse potential, is the safety. While narcotic, opioid, oxycodone, Percocet, whatever is like a mu-opioid agonist, has that dangerous side effect that is respiratory depression that we have not seen with the esmethadone. Ketamine and esketamine, they don't do any respiratory depression. That's why they're used in kids, and they're used as an anesthetic because they are very safe. That's the reason that they are in Schedule III, not because they're less abusable than narcotic or you get less high with ketamine or esketamine, but because really, they are not very dangerous in terms of overdosing. Hope that helps. Yeah. Just one more thing. There was a preplanned interim for the HAP study using ketamine, which led to sort of study premature termination because of the lack of effect there. A similar interim look was done for the study using oxycodone. Was there anything out of the ordinary that you saw on a blinded basis in that study, or did oxycodone behave as it should based on historic data in terms of eliciting the likability? Yes. No, that's a great question. The oxycodone study is going much faster than the ketamine because there is a lot more subject that like to abuse opioids than they like to abuse ketamine-like product. We will have the blinded, as what I would call it, like quality control, but it's going to be very close to the end of the study. Fortunately or unfortunately, it will not help much. I believe it will be probably end of May or early June. The last patient is supposed to be out before the end of June. We won't be able to do much in term of taking action like we did with ketamine. With that said, ketamine, especially oral ketamine, has a history of not being, like bioavailability is very variable and not being very likable in term of abuse potential. Oxycodone 40 mg is not a very high dose, but definitely it is much more likable than oral ketamine 100 mg. We do believe that it's going to be unlikely that we will see what we saw with the ketamine study. We have seen in the qualification period where you select the participants. They are tested, and they have to recognize and like the control. Ketamine, the percent of patients that were excluded from the qualification was over 50%, in the oxycodone study, in qualification, the percent of people or participants that they liked the control that was 40 mg oxycodone was very high, was close to the 100%. We feel more comfortable about this study. Clearly, oxycodone is a much more easier control than ketamine. Great. Looking forward to the data and thanks for taking our questions. Likewise. Thank you, Joon. Our next question is from Yatin Suneja with Guggenheim Partners. Hey, guys. Thank you for taking my question. Just a couple on the HAP side or human a buse liability study. I think, Sergio Traversa, you were just talking about the scheduling. Can you maybe help us understand how each of these studies help you from scheduling perspective? If you show a statistic difference versus oxy and ketamine, do we know you're not going to get the same level of scheduling? The other part of the question is what type of scheduling would you be okay with? Do you expect some form of scheduling with -1017? That's the first question. I do have another follow-up. Thanks, Yatin. Let me answer the question a little bit more expanded way to be very clear. The scheduling is determined by a process that involves the CSS, that is the Controlled Substances Staff that is a piece or part of the FDA. The CSS advises the FDA, the FDA gives recommendations to the DEA, the DEA makes the final conclusion. All this happens after approval. The DEA has 90 days after approval to determine the scheduling. Scheduling is based on a, it's called a factor analysis that includes the pharmacology, the mechanism of action, the receptor affinity, the danger, how dangerous is the drug, includes the likability, how much potential abusers like the drug. Clearly, the likability is a key factor, as well as safety, right. If you show safety by ketamine, then the FDA clearly looks at things in a different way. To answer directly your question, if the data that we will see and hopefully that we hope we will see, they are statistically different from oxycodone, all three doses of esmethadone, we cannot say, so this is an FDA and DEA decision. We cannot give you the 100% certainty, but it's going to be extremely unlikely that it will be the same schedule of a Schedule II. Could be higher schedule, then it will depend on what the ketamine study will show, but definitely being Schedule II, when you see a total statistically different score from oxycodone 40 mg, that I would be extremely surprised if that would happen. That also with the whole body of data that are already available that show a very high safety profile, and there is no respiratory depression. The most frequent or the most, the dose-limiting toxicity is nausea. That makes us pretty comfortable that if we show these results, it's not going to be Schedule II. To the second part of your question, what schedule we will be happy with. Dextromethorphan is behind the counters. There's not even a prescription. We definitely do not expect as esmethadone first because it's a new chemical entity, and it's very unlikely, it's impossible. It's not going to be an over-the-counter or anything like that. The benzodiazepine and the sleeping pills and they are Schedule IV or V. If you ask me directly, this is not a guidance of what the scheduling of esmethadone will be. I would say Schedule IV or V is pretty much the same as a non-schedule. Schedule III is very benign. There is many drugs that are Schedule III, and they're prescribed very widely. Got it. Let me answer your question directly. I would be happy with Schedule III and above. I don't think commercially it would make any difference. Schedule II would be an issue. Got it. We cannot hide that. Yeah. Very helpful. The other question I have is on the monotherapy study. Can you maybe help us understand a little bit more in detail any particular feedback you got from the FDA, the type of patient you're going to enroll, any standard medication that is allowed? It seems like you are guiding for completion of the study this year. Do you mean the data will become available this year, or just maybe provide some color there? Thanks. Yes. Two parts, right? The feedback from the FDA, I'm not sure I'm allowed to say anything, but let me try to phrase it in a nice way. The monotherapy protocol is very similar to the RELIANCE I and II to the add-on therapy. The only difference is the patient population. They are not taking any treatment, while the other one, they are taking a treatment. We are in process or with the two phase III as add-on therapy, let's put it in this way. We don't expect that there is anything that is particularly worrisome about the monotherapy. It's the same thing. The FDA was okay with the add-on therapy. We do believe that they are okay with the monotherapy as well. I hope I answered you in some way. Thank you. Yeah. Thank you. The data, well, yes, the patient population for monotherapy is much larger than about, I would say, at least 2x-3x the patient population for add-on therapy. Recruitment is, we've been guided to six,seven months recruitment, and we are planning to start before the end of this quarter. That is over the next two, three, four weeks. We should be on time to get it done by year-end. We are always a little cautious in term of top line because it takes some time to print data and the statistical analysis, and year-end, it comes around Christmas. I'm sure you don't want to have to write a note on Relmada on December 24th. That would not be so. Yes, but it should be done around the year-end. Got it. Very helpful. Yeah. There is always JPMorgan work and I don't know if it's going to be virtual or in-person, but there's always JPMorgan work in general. It's usually a nice stage if we have some good data to share. We haven't even started, so I don't want to give you any particular guidance. It is too far away to give you something specific. It's going to be around there. Thank you. Our next question is from Salveen Richter with Goldman Sachs. Hi. Thanks so much for taking our questions. This is Sonia on for Salveen. At APA, you presented some data on REL-1017, where the effect was a function of percent life years since onset of MDD. Just wondering if those findings will influence the design of your monotherapy trial at all. Thank you, Sonia. Yeah, that's a very good question. The straight answer is no. The overall idea is to mimic as much as possible the overall standard population. We don't want to pre-select and we should have to stratify. We discussed it, we should have had to stratify the patients based on how long they have been affected by depression. It was an extra work, the FDA likes to see real-world studies. We prefer to just do it in a standard way without stratifying. We will enroll patients that have depression for 20 years and patients that have depression for two months. The straight answer is no. There was no impact from this data. The way we read this data, they've been important for one specific reason. The NMDA antagonist, like esmethadone, they have this feature. They are neuroplastic, so they increase the functionality and the number of synapses in the brain, the communication between brain cell. That is very different from SSRI. You may remember, I was involved in the development of Prozac for quite a bit of years, for five or six years. SSRIs, SNRIs, the old traditional antidepressants, they are symptomatic, right? They treat the symptom of depression. If you stratify the patient from long-term depressed patient and short-term depressed patient, you don't see any difference with traditional antidepressant because they don't have really a neuroplastic effect. Unlike what we have seen as esmethadone that the neuroplastic effect is more evident, especially these patients were treated for a week, right? If you have been depressed for 25 years and you get treated for a week, it's unlikely you see a drastic effect that you actually have seen in patients that were depressed for a shorter time. Most likely in patients that have been depressed for a long time, it's going to take a little bit more longer treatment. We may see something in phase III. The understanding and the learning from this data is that it's confirmed. There's a confirmation that the NMDA antagonist or esmethadone, they have a different mechanism and they do something different to patients with depression. I would say, in quotes and very carefully, that we are looking more at disease-modifying effect instead of being asymptomatic. I hope that helps. Thank you. Once again, if you have a question, please press star one. Our next question is from Jay Olson with Oppenheimer. Oh, hey, Sergio. Thank you for taking the questions and congrats on all the progress. Since Sage has an important catalyst coming up with data from their MDD study, can you just talk about what some of the differentiating features are for an NMDA antagonist versus a GABA PAM, and what you think would motivate MDD patients to prefer esmethadone versus [our own]? Thank you. Thank you, Jay. You only ask me tough questions. There is quite a bit of differences between the allosteric modulator and the GABA modulator like Sage and Praxis than NMDA channel blockers like esmethadone. The mechanism is totally different. Although ultimately, at the end, we do believe that also the GABA modulator, they may have some influence on the NMDA process and activity, but it comes from a different angle, and quite a bit the opposite angle. Probably mechanistically, they're very different. In term of activity, probably, I know what is available publicly from Sage and from Praxis, but they are rather fast-acting, but they tend to have a shorter-term efficacy profile. They are more suitable, and that's what Sage is claiming, and they definitely know a lot more than I do. They're more suitable for a episodic short-term treatment of depression, and we do believe there is a market for that too. It's a very large market, so there is enough space for drug with different profiles. Yeah. They're quite a bit different. The bottom line is that there is very little correlation between the two. Different mechanisms of action, different clinical profile. Excellent. We hope they all work. Likewise. Thank you for that. I guess since you had a number of posters that you presented at recent medical meetings, can you just talk about any feedback that you got from physicians and KOLs at those conferences? Yeah. Unfortunately, virtual is not the same thing that you sit there and to hear the whole talking and the direct comments when they see the poster. There is a little bit of guessing here, but the feedback was definitely positive. It looks like, based on data, esmethadone is starting to differentiate, not only from racemic methadone. Look, the fact that esmethadone is different from an opioid is very clear to me. You see all the data. You have seen them as well. In terms of the other NMDA antagonists, right? The question that we have been asked and we ask ourselves is that why has methadone, even at very high doses, forget narcotic effect, that is not there. Even the hallucination and dissociation, the ketamine-like effect is not there, even at doses that patients or healthy volunteers, they cannot tolerate. That one was one of the angle that came up from this study, right. There is a mechanism, I don't want to go too much in detail of an earnings call, but the specific activity for the subunit GluN2D of the NMDA receptor, unlike ketamine, that it works on the GluN2D, but it also has affinity for the A and B. They are more related with the physiological activity of the NMDA system and the glutamate. That could explain, or should explain, the fact that esmethadone does not have this dissociative and hallucination effect, even at high doses. It seems that the differentiation process is moving ahead rather successfully. We are learning, too, right. We saw the clinical. We are looking of the reason that the clinical profile looks like that. We make good progress in really understanding how esmethadone works. It's fascinating. Excellent. Super helpful. Thank you for taking the questions. Likewise. Jay. Our next question is from Marc Goodman with SVB Leerink. Hi, this is Julian Kao from Marc. Thanks for taking my question. Can you provide more color on the enrollment of the RELIANCE trials? Are you still targeting 55 sites for each study? How should we think about the COVID impact on the clinical conduct of these trials as the pandemic condition continues to improve? Thank you. Thank you, Julian. My regards to Marc. Well, let me start with the COVID impact. In terms of enrollment, we have not seen, especially now with the vaccine, we have not seen really any impact that would slow the enrollment. If any, clearly you can read that everywhere. There's been an increase in patients affected by depression following the COVID situation. People have COVID and have consequences with depression related to the aftermath of the virus, also, the whole economic situation and everything that we know enough about it. No, there has been no impact from the COVID situation on the enrollment. It's a bit early to give exact guidance on how we are going. We started three months ago in December, January, to enroll the first one, recently, a few weeks ago, we start to enroll the second one. It's moving. Most of the sites is already in place definitely for the RELIANCE I. RELIANCE II is coming very fast. We learn from the first one. We've been a lot more efficient in activating sites and starting to enroll patients. So far, so good. We don't really expect any major impact, barring catastrophic event that are not predictable. The COVID definitely is not an issue. Of course. That's very helpful. Right. I also have a quick question for SG&A. I think there was an increase in stock-based compensation in 1Q. Should we expect similar levels of spending for the remainder of the year, or is this more of a one-time payment? Yeah, I do believe that this is a question that Chuck can answer. Yes. Charles, you there? Yes, I am. Yeah, we've had a few fluctuations in stock-based compensation based on either folks leaving the company and their stock options being brought back in-house. The stock-based compensation expense that you saw in Q1 of this year is a reasonable trend that you can expect throughout the next few quarters. Got it. Yeah, that's very helpful. Thanks for taking my question. We have a follow-up question from Joon with Truist. Mr. Lee? Sorry, I was on mute. Sorry. Thanks for taking our follow-up question. Per FDA guidance, the HAP study should be conducted in experienced recreational users with recent history in the same general pharmaceutical class or pharmacological class. For the HAP study using OxyContin as an active comparator, those subjects are experienced in OxyContin or oxycodone on that class, not necessarily methadone. Is that a fair assumption? Yes, it is a fair assumption. Look, methadone is used widely as a replacement for maintenance but is not a highly abusable opioid for a variety of reasons. Two in particular. One is that it's a long half-life, so you don't have the peak that you have with the oxycodone or immediate release. That's what the drug abuser or the recreational, they want the high, right? If you have a slow onset, it's not something they like in particular. The second one is that racemic methadone, part of racemic methadone, is dextromethadone, and dextromethadone is an NMDA, and we do believe that does not have any narcotic effect. It's not something that even recreational drug abusers, they like a lot. All right. Very helpful. Thank you. You're welcome. Ladies and gentlemen, we have reached the end of the question and answer session, and I would like to turn the call back to Dr. Traversa for closing remarks. Thank you, operator. Thank you all for joining on the call today, and we are very pleased to share the recent progress with you as the REL-1017 clinical development program continues to advance. We are excited about the important catalyst ahead of us, and we'll keep you updated on clinical readouts and activities throughout the remainder of 2021. Thank you again all for joining us on the call and enjoy the rest of your day. Thank you. This concludes today's conference. Thank you for your participation. You may disconnect your lines at this time.