Good afternoon, ladies and gentlemen, and thank you for standing by. Welcome to the RAYMADA Therapeutics Incorporated 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. 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, Doctor. Sergio Traverza and Chief Accounting and Compliance Officer, Chuck Ents. This afternoon, Rob Nada issued a news release providing a business update and announcing financial results for the Q1 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, Ramada'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 Brahma's press release issued today and the company's SEC filings, including in the annual report on Form 10 ks 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. Ramada 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, Ian, and good afternoon to everyone. I'm pleased to welcome you to Ramada's Q1 2021 conference call. On today's call, I will provide an update on the comprehensive development program for the lymphocytes of the treatment of the trident we have 10/17 and the upcoming milestones. I will turn the call over to
Paquette, our Chief
Accounting and Finance Officer and we'll be standing today for our technical guidance and for review of the scenarios by the stiff overview of the 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 3 program consists of placebo controlled pivotal studies for HIF-one and RELIAN-three. Which includes 64 participants per study of Reliance OLS that stands for long term open label safety study that is enrolling both rollover participants from the TiVo studies as well as de novo participants. These studies are designed to evaluate REL 10/17 as an adjunctive treatment for major depressive disorder, NPD, and includes smart and 25 milligram oral1017. I just got somebody told me that I'm breaking up, so I'll try to switch.
Now it should be better. And I was saying placebo and 25 milligram of rel1017 and both are on top of standard antidepressant treatment for participants. We have already unsuccessfully tried a minimum of 1 up to 3 antidepressant therapy. The primary endpoint is change in MADRAS score at day 28. Key secondary endpoints include change in MADRS score at day 7 and change in CGIS, the stage for severity, at the score at day 28.
The first Phase 3 trial, RELIANCE 1, continues to enroll as expected and additional sites are coming online nicely. In addition, we recently began enrolling participants into the 2nd Phase III trial, RELIANCE II, which is a MIRROR study of RELIANCE 1. Top line data from these two 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 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 part of the NDA filing package. We remain on track to initiate the study, evaluating the use of our rel=ten seventeen 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 studies. And as we discussed previously, we discontinued the Study 120 that was assessing versus oral ketamine as an active control. As part of a preplanned blinded analysis of the initial study completers showed that a significant material group of participant did not respond to the active control ketamine. And so most likely, this LICA response was due to the poor bioavailability of oral ketamine. And this would have resulted in nonconcluding findings, so we decided to stop it.
And we are now working toward initiating a new ketamine controlled 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=ten seventeen to oxycodone. It's progressing as planned and we continue to expect to complete the study by end of the current quarter.
This hep study, the standard component of the NDA submission for many CNS drugs and will inform the assessment of rel=ten seventeen for the scheduling. The UP studies also represent an important opportunity to add to the existing very strong body of literature that clearly differentiates rel=ten seventeen from the parent drug, racemimethodone and any potential perceived association with opioid effect or distortionative symptoms. I'm also happy to share that Remada just completed presentation of a total of 9 posters over 3 different scientific congresses. I will provide a brief overview of the data for RETA1017 that we presented. However, before I do that, I will turn the call over to Chuck for his review of the financial.
Chuck? Thank you, Sergio,
and good afternoon, everyone. Today, we issued a press release announcing our business and financial results for the Q1 ended March 31, 2021, which I will now review. For the Q1 ended March 31, 2021, total research and development expense was approximately $14,000,000 as compared to $4,500,000 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-ten seventeen. Total general and administrative expense for the quarter ended March 31, 2021 was approximately $8,400,000 as compared to $5,500,000 for the comparable period of 2020.
The increase was primarily due to an increase in stock based compensation. For the Q1 ended March 31, 2021, we recorded a net loss of approximately $22,200,000 or $1.34 per basic and diluted share compared to a net loss of $10,700,000 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 $102,700,000 compared to $117,100,000 on December 31, 2020. We continue to expect that this strong cash position will support us through at least the multiple beta readouts we anticipate through the first half of twenty twenty two. I will now hand the call back to Sergio for further remarks on the most recent progress.
Sergio?
Thank you, Chuck. I'll proceed it. 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 share preclinical data that confirmed lack of any neurotoxic feature that potentially linked to only lesion. This was totally not a surprise, but it is important because this effect has impacted safety and development of other MDR blockers like MKH-eight zero one and these findings continue to support a consistent safety profile across preclinical and clinical studies.
Next, the Society of Biological Psychiatry, we share a total of 6 posters that outline new work to understand the underlying mechanism of REL1017. What we find was very interesting and included additional support for a role in neural plasticity and insight regarding its binding to an MDR subunits, in particular the 2 d 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 RAS1017 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 RAD1017 development program remains 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 and D effort, and we have cash to support us through this expected data point. As always, I'm grateful to the Remada 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 participants and clinical partners involved in the rel=ten seventeen clinical trials for the 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 and congrats on all the progress our JON team. My first question is on the oxycodone study, the data reading out soon. Very clear that all three doses need to be stat sig versus placebo. I'm sorry, not placebo, but oxy sorry, esmethadone and it's similar to placebo.
But can you describe just how similar esmethadone should be to placebo on the VAS 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? Thanks.
Thank you, Andrew. Good afternoon and thanks for the question. Well, look, it's a key question. So oxycodone 40 milligrams, 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.
In the CNS drug, you may expect that it's not placebo, right? You take Benzodiazepine or 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 likability 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 very pleasant feeling. So to answer directly your question, we the most important is to differentiate all three doses of esmethadone from 40 milligrams of oxycodone. We don't expect to be very different from placebo, but also it does not require that we are similar to placebo.
So I would focus everybody's attention to the oxycodone. Placebo is there just because we have something to compare, but it's not we are not comparing s methadone to placebo.
Right.
Hope I answered your question there. Yes. That's very clear.
Yes, thank you. Yes, very good. And 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 an NMDA toxic effect, there is no guarantee. I mean, it's not 100% guaranteed, but it's unlikely that in a different study, we'll show up as a 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.
Perfect. Thank you, Sergio.
Thank you, Andrea.
Our next question is from Joon Lee with Chooist.
Hi. Thanks for taking our questions. I believe the DEA is on record saying that dextromethrone
is the last addiction liability. 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? Thank you.
Hey, Jun. Good afternoon. Thanks for the question. Yes, we actually we asked the same question to the DA where they the data that they base 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 based their statement and their opinion on what is available. And there is quite a bit of lead transfer available, including the Phase I that Ramada did with the single dose and multiple dose of esmetadine. So they look at whatever is available and they draw a conclusion. So that's pretty much how they did it. The comments on esketamine, well, esketamine, look, esketamine, it is 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.
Technically, pharmacologically, there is no difference between esketamine and racemic ketamine. So it's pretty much the same thing, just different dose. So I would be surprised if the DA would schedule esketamine in a different way than racemic ketamine. And the Johnson and Johnson, which provided they performed the abuse study comparing nasal esketamine SPRAVATO versus intravenous ketamine and pretty much they are the same thing. So there was no real difference.
Esketamine is pretty much will remain the same schedule as rocemic 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 different between Schedule 23 than any other scheduling between 3, 45. 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, Percocet, whatever is like a more opioid agonist as that dangerous side effect that is respiratory depression that we have not seen with the esmetadone. 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 Arcadia. They 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 one more thing. There was a preplanned intern for the HAP study using Ketamine, which led to sort of a steady premature termination because of the lack of effect there. It's similar in turn look was 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 OxyContin behave as it should based on historic data in terms of eliciting the likability?
Yes. 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, whatever call it, like quality control, but it's going to be very close to the end of the study. So unfortunately or unfortunately, it will not help much.
I believe it will be like probably end of May or early June, and the last patient is supposed to be out before the end of June. So 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 terms of like abuse potential, while oxycodone, 40 milligram 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 were excluded from the qualification was over 50%. The in the oxycodone study in qualification, the percent of people that are participants that they like the control that was 40 milligram oxycodone was very high, was close to the 100%. So that we feel more comfortable about this study. Clearly, oxycodone is a much more easier control than ketamine.
Great. Looking forward to data and thanks for taking our questions.
Likewise. Thank you, John.
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 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 static 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 10/17? So that's the first question. I do have another follow-up.
Thank you. Yes, I think. Yes, so let me ask you the question a little bit more expanded way to be very clear. So the scheduling is determined by a process that involve the CFS that is the controlled substance stuff that is a piece of part of the FDA. The CFS advises 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. The scheduling is based on a it's called a factor analysis that includes the pharmacology, the mechanism of action, the receptor affinity, the danger, I mean, 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 has clearly looked 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 three doses of s methadone. We cannot say for like this is an FDA NDA decision. We cannot give you the 100% certainty. But it's going to be extremely unlikely that it will be the same schedule of Schedule 2.
I mean, it could be higher schedule, then it will depend on what the ketamine study will show. But definitely being scheduled to when you see a total statistically different score from oxycodone 40 milligrams that I would be extremely surprised if that would happen. That's also with the whole 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 limiting toxicity is nausea. And so that makes us pretty comfortable that if we show these results, it's not going to be scheduled to.
And to the second part of your question, what kind of what schedule we will be happy with? Well, dexamethorphan is behind the counter. So it's not even a prescription. Now we definitely do not expect as methadone 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 of anything like that. But the bandodiazepine and sleeping pills and they are scheduled 4, 5. If you ask me directly and this is not the guidance of what the scheduling of esmetadolone will be, but I would say Schedule IV or V is pretty much the same as non schedule. Schedule III is very benign and there is many drugs that are Schedule 3 and they are prescribed very widely. Got it.
So I would let me answer your question directly. I would be happy with Schedule 3 and above. I don't think commercial it would make any difference. Schedule 2 would be an issue. We cannot hide that.
Yes. Very helpful. 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? Thanks.
Yes. So two parts, right. The feedback from the FDA, and 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 RELIANANCE 1 and 2 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 or with the 2 Phase 3 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. I hope I answer you in some way.
Thank you. Yes. Thank you.
The data well, yes, the patient population for monotherapy is much larger than about, I would say, at least 2 to 3 times 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 clean the 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 Remada on December 24. That would not be so. So yes, but it should be done around year end.
Got it. Very helpful.
Yes. There is always taking work and I don't know if it's going to be virtual or in personal. It's always jumping working in January. 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. 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. So at APA, you presented some data on RAL1017 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 overall idea is to mimic as much as possible the overall like standard population. So we don't want to pre select 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 award, but the FDA likes to see like real world studies. So we prefer to just 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 the straight answer is no. There was no impact from this data.
The way we read these data, they have been important for one specific reason. The NMDA antagonist like hesmetadone, 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 SSRI, the CENRI, the old traditional antidepressants, they tend to be more they are symptomatic, right? They treat the symptom of depression. And if you satisfy 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 methadone 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 get treated for a week, it's unlikely you see like a drastic effect that you actually have seen in patients that were 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 the Phase III. The understanding and the learning from this data is that it's confirmed is a confirmation that NMEDI antagonist or asmethidine, they have a different mechanism and they do something different to patients 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.
Thank you.
Our next question is from Jay Olson with Oppenheimer.
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 agonist versus sorry an NMDA antagonist versus a gabap And what you think would motivate MDD patients to prefer ezmethadone versus oranolone? Thank you.
Thank you, Jay. You only ask me tough questions. Well, there is quite a bit of differences between the allosteric modulator and the GABA modulator like Sage and Praxis than NMNDA 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 NMNDA 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 term 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 this is that's what Sage is claiming and they're definitely 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 too.
So it's a very large market. So there is enough space for drug with different profiles. So yes, so they are quite a bit different. The bottom line is that there is very little correlation between the 2 different mechanisms of action, different clinical profile.
We hope they all work.
Likewise. And 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?
Yes. So the right. The unfortunately, virtual is not the same thing that you sit there and to hear is like the whole talking and the direct comments when they see the poster. So there is a little bit of guessing here, but the feedback was definitely positive. And then the it looks like based on data, as methadone is starting to differentiate, not only from proximic Methadone.
Look, the fact that this methadone is different from an opioid is very clear to me. I mean, you see all the data. You have seen them as well. And also in term of like the other NMDA antagonist, right? Because the question that I've been we have been asked and we asked ourselves is that why has methadone 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 are healthy volunteer they cannot tolerate. And that one is was one of the angle that was came up from the study, right? There is a mechanism, I want to go too much in detail in the earnings call, but the specific activity for the subunit 2 d of the NMNDA receptor unlike ketamine that it seems more it works on the 2 d, but it also has affinity for the A and B. They are more related with the physiological activity of the NMNDA system and the glutamate. And that could explain or should explain the fact that esmethelone 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, so we are looking of the reason that the clinical profile looks like that. And we made good progress in really understanding how its net doesn't work, and it's fascinating.
Excellent. It's super helpful. Thank you for taking the questions.
Likewise, Jay.
Our next question is from Marc Goodman with SVB Leerink.
Hi, this is Yuri on call for Marc. Thanks for taking my question. So can you provide more color on the enrollment of the RELINE 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.
Thank you, Julian. And my regards to Mark, the well, let me start with the COVID impact. In term of enrollment, we have not seen, especially now with the vaccine and we have not seen really any impact of the that would slow the enrollment? And if any, then 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 the depression related to the aftermath of the virus, but also the old economic situation and the old everything that we know enough about it. So the no, there has been no impact from the COVID situation on the roll. 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 is moving. The sites are most of the sites are already in place for the but definitely for the Reliance 1. Reliance 2 is coming very fast. So we learn from the first one. So we've been a lot more efficient in activating sites and starting to enroll patients.
So far so good. And we don't really expect any major impact barring catastrophic events that are not predictable. But the COVID definitely is not. It's not an issue. Okay.
That's very helpful. So I also have a quick question for SG and 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. Chuck, you're ready.
Yes, I am. 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.
Got it. Yes, that's very helpful. Thanks for taking my question.
We have a follow-up question from Zhu Li with Truist. Mr. Li?
Sorry, I was on mute, sorry. And 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. So for the half study using OxyContin as an active comparator, those subjects are experienced in oxycodone or oxycodone on that class, not necessarily methadone. Is that a fair assumption?
Or is it 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's a long half life, so you don't have the peak 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 Doctor. 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=ten seventeen 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 the day. Thank you.
This concludes today's conference. Thank you for your participation. You may disconnect your lines at this time.