Relmada Therapeutics Inc (RLMD) 2021 Q1 法說會逐字稿

Good afternoon, ladies and gentlemen, and thank you for standing by. Welcome to the Relmada Therapeutics, Inc. First Quarter 2021 Financial Results Conference Call. (Operator Instructions) Please note, this conference is being recorded.

I will now turn the conference over to your host, Tim McCarthy, with Lifesci Advisors.

Thank you, operator, and thank you all for joining us this afternoon. With me on today's call are Chief Executive Officer, Dr. Sergio Traversa; and Chief Accounting and Compliance Officer, Chuck 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 12, 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, and good afternoon to everyone. I'm pleased to welcome you to Relmada's first quarter 2021 conference call. Today, I will provide an update on the comprehensive development program for the (inaudible) treatment of (inaudible) 1017 and the upcoming milestones.

I will turn the call over to Chuck Ence, our Chief Financial Officer, and (inaudible) recent data that we presented at 3 recent scientific conferences.

With that, I'll begin with an update on RELIANCE that is the ongoing Phase III program (inaudible) consists of (inaudible) from placebo controlled (inaudible) RELIANCE I and RELIANCE II, which includes (inaudible) participants (inaudible). RELIANCE-OLS that stays for long-term open-label safety study that is enrolling both rollover participants from the pivotal studies as well de novo participants. These study are designed to evaluate REL-1017 as an adjunctive treatment for major depressive disorder, MDD, and includes (inaudible) and 25-milligram of REL-1017. Somebody told me that I'm breaking up, so I'll try to switch.

Now it should be better. And I will say, placebo and 25-milligram of REL-1017, and both are on top of standard antidepressant treatment for participants. We have already and successfully tried a minimum of 1 up to 3 antidepressant therapy. The primary endpoint is changing MADRS score at day 20. Key secondary end points include change in MADRS score at day 7 and change in CGIs, the stage 4 severity, the score at day 28. The first Phase III trial, RELIANCE I, continues to enroll as expected, and additional sites are coming online nicely.

In addition, 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 2 trials are expected in the first half of next year.

The reliance long-term open-label safety study is also underway and the rolling participant is 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 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, study. And as we discussed previously, we discontinued the study 120 that was assessing REL-1017 versus oral ketamine as an active control. As part of a preplanned blinded analysis of the initial study completers show that a significant material group of participants did not respond to the active control ketamine, and so most likely, this slight response was due to the poor bioavailability of oral ketamine and this would have resulted in non-concluding findings, so we decided to stop it. And we are now working toward initiating a new ketamine control study, we call it study 126, which we'll use as an active comparator intravenous IV ketamine that has an 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, study 124, is comparing REL-1017 to oxycodone, is progressing as planned, and we continue to expect to complete the study by end of the current quarter. This 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 the Relmada just completed presentation of a total of 9 poster over 3 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, and good afternoon, everyone. Today, we issued a press release announcing our business and financial results for the first quarter ended March 31, 2021, which I will now review. For the first quarter ended March 31, 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 costs associated with the execution of a broader clinical program for REL-1017.

Total general and administrative expense for the quarter ended March 31, 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 31, 2021, we recorded a net loss of approximately $22.2 million or $1.34 per 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 31, 2021, the company had cash, cash equivalents, and short-term investments of approximately $102.7 million compared to $117.1 million on December 31, 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'll proceed. The -- as I mentioned, I'm happy to outline the recent data that we presented in 9 posters across 3 different medical meetings. First at the American Society for Pharmacology and Experimental Therapeutics, and we shared preclinical data that confirm a lack of any neurotoxic feature that potentially link to only lesion. This was totally not a surprise, but it is important because this effect has impacted safety and development of other MBR Blockers like MK-801. And this finding continues to support the consistent safety profile across preclinical and clinical studies.

Next, the Society of Biological Psychiatry, we shared a total 6 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. An insight regarding its binding to an MBR subunit, in particular, the 2D subunit, which appears to explain both the lack of dissociative side effect as well as the rapid and sustained antidepressant effect.

And lastly, we shared the -- at the APA, the American Psychiatric Association, the data from the Phase II study that showed that REL-1017 demonstrated the 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 remained extremely active, and we anticipate multiple key data results 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. And I would also like to extend my sincere thanks to the participant 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 operator, you can go ahead and open the line for questions. Thank you.

(Operator Instructions) Our first question is from Andrew Tsai with Jefferies.

Congrats on all the progress, Sergio and the team. My first question is on the oxycodone study, the data reading out soon. Very clear that all 3 doses need to be stacked versus placebo -- I'm sorry, not placebo but oxy -- sorry, esmethadone and then similar to placebo. But can you describe just how similar esmethadone should be to placebo on the vast liking score because from time to time, I think of a scenario where what happens if esmethadone is showing 60 to 65, for example, just outside of the typical placebo range. How would we interpret that result, I guess?

Andrew, look, the -- it's a key question, so oxycodone 40 milligrams, it is what we use as a comparator, it's not a very high dose, but it's high enough. That is clearly likable type patients or people, participants that like to take narcotic as a recreational drug abuse. It is a CNS drug. You may expect, we may expect, that it's not placebo, right? You're taking benzodiazepine, you take a sleeping pill, it's not placebo. You feel something. And if this feeling will be pleasant or not, it's 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 likeability at all. If you really take in Phase I, if you take a high dose like 150 milligrams, and some patients experience nausea, so that is not a very pleasant feeling.

So to answer directly your question, we -- the most important is to differentiate all 3 doses of esmethadone from 40 milligram of oxycodone. We don't expect to be very different from placebo, but also does not require that we are similar to placebo. So I would focus everybody's attention to oxycodone. Placebo is there just because we have something to compare. But it -- we are not comparing esmethadone to placebo. I hope I answered your question.

Yes, that's very clear. So my follow-up question is, let's just say, data is clearly positive, completely clean. Would it be then be fair for investors to assume that the second abuse liability study versus ketamine is pretty much derisked? Because you would have seen data on, for example, dissociation, hallucination from the oxycodone study.

The straight answer is yes. The -- I would say that I'm an old pharmacist and I always say that drugs tend not to change the way they work in -- over time. So we don't see anything that would show any dissociative or any hallucination or anything that would be like ketamine or like NMDA toxic effect. There is no guarantee. I mean, it's not 100% guaranteed, but it's unlikely that in a different study, that will show up as very different from what we see so far. So yes, the answer is yes. We do believe that there is a derisking component when we will see the oxycodone data.

Our next question is from Joon Lee with Truist.

I believe the DEA is on record saying that dexamethasone is -- lacks addiction like OD. What's the basis for that for DEA making that claim? And is that based on a specific study and if so, what doses were used? And related to that, are you aware of DEA making similar claims about esketamine as compared to ketamine?

Thanks for the question. Yes, we actually asked the same question to the DEA, where the data that based the statement that esmethadone is exempt from abuse risk and respiratory depression. And they did not do any proprietary study that is not published. They base their statement and their opinion on what is available. And there is quite a bit of literature available, including the Phase I that Relmada did with the single dose and multiple dose of esmethadone. So they look at whatever is available and they drew their conclusion. So 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 and is a lower dose of racemic ketamine. I mean, technically, pharmacologically, there is no difference between esketamine and racemic ketamine. So it's pretty much the same thing, just differing dose. So I would be surprised if the DEA would schedule esketamine in a different way than racemic ketamine. And the Johnson & Johnson with provided the -- performed the abuse study comparing nasal esketamine spray versus intravenous ketamine and pretty much, they are the same thing. So there was no real difference. So esketamine is pretty much -- will remain the same schedule as racemic ketamine.

With that said, maybe I can add 1 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. And the reason being that the major worry of the FDA is not really just the abuse potential, it's the safety. And while narcotic, opioid, oxycodone, purpose, whatever is like a mu-opioid agonist has that dangerous side effect that is respiratory, the pressure that we have not seen with esmethadone.

Ketamine and esketamine, they don't do any respiratory depression. That's why they use in kids and they use as an anesthetic because they are very safe. So that's the reason that they are in Schedule III, not because they are less abusable than narcotics. You get less high with ketamine or esketamine, but because really, they are not very dangerous in terms of overdosing. So I hope that helps.

Yes, and just 1 more thing. You -- there was a preplanned interim for the HAP study using ketamine, which led to sort of a very premature termination because of the lack of effect there. It's similar, in turn, look what's done for the study using oxycodone? And was there anything out of the ordinary that you saw on a blinded basis in that setting? Or did oxycodone behave as it should, based on historic data in terms of inducing 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. So 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. So unfortunately, it will not help much. I believe it would be like probably end of May or early June. And the last patient is supposed to be out before the end of June. So the -- we won't be able to do much in terms of taking action like we did with ketamine.

With that said, ketamine, especially oral ketamine, has a history of not being -- like biovailability is very valuable and not being very likable in terms of like abuse potential. While oxycodone 40 milligrams is not a very high dose, but definitely, it is much more likable than oral ketamine 100 milligram. So 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 have to -- they are tested and they have to recognize and like the control. While ketamine, the percent of patients that we are excluding from that qualification was over 50%. In the oxycodone study in qualification, the percent of people that or participants that they like the control, that was 40-milligram oxycodon was very high, was close to 100%, so. that we feel more comfortable about this study. Clearly, oxycodone is a much more easier control than ketamine.

Our next question is from Yatin Suneja with Guggenheim Partners.

Just a couple on the HAP side, or human abuse liability study. So I think, Sergio, 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 strategic difference versus oxy and ketamine, do we know you're not going to get the same level of scheduling?

And then 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? So that's the first question. I do have another follow-up.

Thanks, Yatin. Yes, so let me answer the question a little bit more expanded way to be very clear. So the scheduling is determined by a process that involves the CSS, that is the Controlled Substance Staff, that is abuse part of the FDA. The CSS advised the FDA, then the FDA kind of give recommendation to the DEA and the DEA makes the final conclusion. All this happened after approval. The DEA has 90 days after approval to determine the scheduling.

As scheduling is based on a -- and it's called a factor analysis, that includes the pharmacology, the mechanism of action, the receptor affinity, the danger, how dangerous is the drug, and includes the likability, how much potential abuser like the drug. Clearly, the likability, it is a key factor, as well as safety, right? If you show safety, like ketamine, then the FDA clearly looks at things in a different way.

So to answer directly your question, if we -- the data that we will see and hopefully, that we hope we will see, they are statistically different from oxycodone, all 3 doses of esmethadone, we cannot say, so like this is an FDA and DEA decision, we cannot say with 100% certainty. But it's going to be extremely unlikely that it will be the same schedule of Schedule II. I mean, it could be higher schedule than 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 milligrams. That I would be extremely surprised is that, that would happen.

That's also with the old body of data that are already available, that show like a very high safety profile, and there is no respiratory depression. The most frequent or the most like the -- dose limit in toxicity is nausea, and so that makes us pretty comfortable that if we show these results, it's not going to be scheduled, too.

And to the second part of your question, what kind what schedule we would be happy with, well dextromethorphan is sold behind the counter. There's not even a prescription. Now we definitely do not expect 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. But the benzodiazepine and sleeping pills, they are Schedule IV, V. If you ask me directly, and this is not a guidance of what the scheduling of esmethadone will be. But I would say, Schedule IV, V is pretty much the same as non schedule. Schedule III is very benign, and there is many drugs that are Schedule III, and they are prescribed very widely.

So I would -- 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, we cannot hide that.

Then 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?

Yes. Yes. The -- so 2 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. So we are in process with the 2 Phase III as add-on therapy. And so 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. So the FDA was okay with the add on therapy. We do believe that they are okay with the monotherapy as well.

The data -- well, yes, the patient population for monotherapy is much larger than about, I would say, at least 2x to 3x, the patient population or add on therapy. So recruitment is -- we've been guided to like 6, 7 months recruitment and we are planning to start before the end of this quarter, that is, over the next 2, 3, 4 weeks. So we should be on time to get it done by year-end. And we're always a little cautious in terms of top line because it's always -- it takes some time to print data and the statistical analysis. And year-end, it comes around Christmas. So I'm sure you don't want to have to write a note on Relmada on December 24. That would not be, so -- yes, but it should be done around year-end.

The result is taking work. And I don't know if it's going to be virtual or enforcement. It's always (inaudible). It's usually a nice stage if we have some good data to share. But we haven't even started. So I don't want to give you any particular guidance. It's too far away to give you something specific. Soon to be around there.

Our next question is from Salveen Richter with Goldman Sachs.

This is Sonia on for Salveen. So 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, yes, that's a very good question. The straight answer is no. The -- we -- the overall idea is to mimic as much as possible the overall like standard population. So we don't want to preselect. And we should have to stratify. We discussed it, but we should have had to stratify the patients based on how long they have been affected by depression and was the next work, but the FDA likes to see like real world studies. So we prefer to do it in a standard way without stratifying. So we will enroll patients that have depression for 20 years and patients that have depression for like 2 months. So that's straight answer is no. There was no impact from this data.

The way we read these data that have been imported for 1 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 did -- I was involved in the development of Prozac for quite a bit of years, for 5 or 6 years.

And the SSRI, they are traditional antidepressants. They tend to be more -- they are symptomatic, right? They treat the symptom of depression. And if you -- 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 in esmethadone, that the neuroplastic effect is more evident, especially this patient was treated for a week, right. So if you have been depressed for 25 years and you get treated for a week, it's unlikely you see like a drastic effect that you actually have seen in patients that are depressed for a shorter time.

So most likely in patients that have been depressed for a long time, it's going to take a little bit more longer treatment. And so that's -- we probably -- we may see something in Phase III.

The understanding and the learning from this data is that -- that is confirmed, is a confirmation that antagonist or esmethadone, they have a different mechanism and they do something different to patient with depression. So it's -- 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.

(Operator Instructions) Our question is from Jay Olson with Oppenheimer.

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 agonist versus -- sorry, an NMDA antagonist versus a GABAA PAM, and what you think would motivate MDD patients to prefer esmethadone versus (inaudible)?

You only ask me to ask questions. The -- well, there is quite a bit of differences between the allosteric modulator and the GABAA modulator like Sage and Praxis, then NMDA channel blockers like esmethadone, so 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. So probably, mechanistically, they're very different.

In terms of activity, probably, I mean, I know what is available publicly from Sage and from Praxis, but they tend to have a -- they are rather fast acting, but they tend to like have a shorter-term efficacy profile. So they are more suitable and that's what Sage is claiming, and they definitely know a lot more than I do. But they're more suitable for episodic short-term treatment of depression, and we do believe there is a market for that.

So it's a very large market. So there is enough space for drug with different profiles. So they're quite a bit different. The bottom line is that there's very little correlation between the 2 different mechanisms of action, different clinical profile. We hope they all work.

Likewise. And 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?

Yes. So the -- unfortunately, virtual is not the same thing that you sit there and to hear is like the whole talking and the right, the direct comments when they see the poster. So there is a little bit of guessing here, but the feedback was definitely positive. And it looks like, based on data, esmethadone is talking to differentiate not only from racemic methadone. Look, the fact that esmethadone is different from an opioid, it's very clear to me and I can see all the data, you've seen them as well.

And also in terms of like the other NMDA antagonist, right, because the question that I've been -- we have been asked, and we asked ourselves is why esmethadone, even at very high doses, forget narcotic effect, that is not there, but even the hallucination and dissociation, the ketamine-like effect is not there, even at doses that patients or healthy volunteer, they cannot tolerate. And that one was one of the angle that was came up from this study, right? There is a mechanism, I don't want to go too much in detail on an earnings call, but the specific activity for the subunit 2D of the NMDA receptor, unlike ketamine that seems more -- works on the 2D, but it also is -- has affinity for the A and B. They are more related with the physiological activity of the NMDA system and the glutamate. And that could explain or should explain the fact that esmethadone does not have this dissociative hallucination effect even at high doses.

So it seems that the differentiation process is moving ahead rather successfully. We are learning, too, right? It's not -- we saw the clinical also. So we are looking of the reason that the clinical profile looks like that. And we made good progress in really understanding how esmethadone works, and it's fascinating.

Our next question is from Marc Goodman with SVB Leerink.

This is Rudy on call for Marc. So can you provide more color on the enrollment of the RELIANCE trials? Are you still targeting 55 sites for each study. And how should we think about the COVID impact on the clinical conduct of these trials as the pandemic condition continues to improve?

Thank you, Rudy, and my regards to Marc. The -- well, let me start with the COVID impact. In terms of enrollment, we have not seen, especially now with the vaccine and we have not seen really any impact of -- that would slow the enrollment. And if any, clearly, you can read that everywhere. I mean, 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, but also the old economic situation and the old everything that we know enough about.

So -- no, there has been no impact from the COVID situation on enrollment. It's a bit early to like give exact guidance on how we are going. We started like 3 months ago in December, January, to enroll the first one. And then recently, a few weeks ago, we started to enroll the second one. So it's moving. The sites are -- most of the sites are already in place for the -- definitely for the RELIANCE I. RELIANCE II is coming very fast. So we learned from the first one. So we've been a lot more efficient in activating sites and starting to enroll patients. So so far, so good. We don't really expect any major impact barring catastrophic event that are not predictable, but COVID definitely is not an issue.

Cool, cool. That's very helpful. I also have a quick question for SG&A. I think there was an increase in stock-based compensation in 1Q. So should we expect similar levels of spending for the remainder of the year? Or is this more of a onetime payment?

Yes. I do believe that this is a question that Chuck can answer.

Yes, 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. But 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.

We have a follow-up question from Joon Lee with Truist. Mr. Lee?

Sorry, I was on mute. Sorry. 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. So for the HAP study using OxyContin as an active comparator, those subjects are experienced in oxycontin or oxycodone or 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 it's not a highly abusable opioid for a variety of reasons, 2 in particular. One, is that it has a long half-life, so you don't have the pick that you have with oxycodone or immediate release. That's what the drug abuse or the recreation, 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 it really does not have any -- we do believe that does not have any narcotic effect. So it's not something that even recreational drug abuser they like a lot.

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. So 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 catalysts 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 the day. Thank you.

This concludes today's conference. Thank you for your participation. You may disconnect your lines at this time.