Arena Pharmaceuticals Inc (ARNA) Q3 2020 Earnings Call Transcript

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Arena Pharmaceuticals Inc (NASDAQ:ARNA)
Q3 2020 Earnings Call
Nov 9, 2020, 4:30 p.m. ET

Contents:

  • Prepared Remarks
  • Questions and Answers
  • Call Participants

Prepared Remarks:

Operator

Good day everyone and welcome to Arena Pharmaceuticals Corporate Conference Call. [Operator Instructions]

I will now turn the call over to Pat Malloy, Vice President, Investor Relations and Corporate Communications at Arena. Please go ahead.

Patrick MalloyVice President, Investor Relations and Corporate Communications

Good afternoon everyone and thank you for joining us today. We hope you had a chance to review the press release that we issued this afternoon, announcing both our third quarter 2020 financial results as well as the top line results from our Phase 2b ADVISE trial.

Joining me on today’s call are Amit Munshi, our President and Chief Executive Officer; Laurie Stelzer, our Chief Financial Officer; Dr. Chris Cabell, our Chief Medical Officer and Head of Research and Development; and Rob Lisicki, our Chief Commercial Officer.

Before we begin, I would like to remind you that we’ll be making forward-looking statements that involve risks and uncertainties about our goals, expectations, plans, beliefs, timing of events or future results, including those risks and uncertainties related to our pipeline, financial projections, 2020 financial guidance, and the COVID-19 pandemic and its potential impact on our business. Forward-looking statements involve certain assumptions, risks, and uncertainties that may be beyond our control and could cause actual results to differ materially from these statements. A description of these risks can be found in our earnings press release and our latest SEC disclosure documents. All forward-looking statements are based on information currently available to Arena, and we disclaim any obligation to update these forward-looking statements.

Now, I’d like to turn the call over to Amit. Amit?

Amit D. MunshiDirector, President and Chief Executive Officer

Thanks, Pat, and good afternoon, everyone. I hope you’ve had a chance to review our press release announcing our compelling top line results from the Phase 2b ADVISE trial for etrasimod in atopic dermatitis or AD. This is the first study of an S1P1 modulator, in this indication.

Critically, as we know from our extensive market research, patients and physicians continued to demand a safe and effective oral agent for the treatment of AD. Chris will be going through this trial in greater detail in a few moments, but before he does, I’d like to provide a high level summary of the findings and results of this trial.

The ADVISE trial recurred a moderate patient population with 83% of our participants having a baseline IGA score of three. This is different than population study in recently conducted atopic derm trials with advanced therapies. Importantly, the moderate patient population represents approximately 40% of the entire atopic dermatitis market. Participants in the 2 milligram group show statistically significant improvement compared to placebo at 12 weeks on the vIGA responder criteria, which as you know is the stringent FDA Phase 3 primary endpoint for atopic dermatitis. Etrasimod did not meet the Phase 2 primary endpoint for our present change and easy from baseline at week 12 compared to placebo in the full analysis set.

We are pleased to observe etrasimod’s rapid onset of action, as seen in study of other indications was confirmed in this trial and in this conditions. At week four, participants in the 2 milligram treatment group achieved statistical significance across EASI, EASI-75, and pruritis endpoints. Overall, the 12-week study showed no plateau of effect, and very importantly the safety profile, which Chris will cover in more detail was consistent with previous trials of etrasimod, including low first dose heart rate effects with no titration and no serious adverse events across the groups.

The ADVISE trial was impacted by an unwarranted dose interruption, which generally took place between weeks four and eight in 19% or 9 participants in the etrasimod 2 milligram group. Adjusting for this interruption, the post-hoc Completer Analysis with participants who received full therapeutic exposure of etrasimod 2 milligram showed statistically significant effect on the percentage change in EASI from baseline at week 12 compared to placebo. The analysis of this cohort of participants, who experienced the dose interruption allowed us to visualize what turned out to be an unintended, but serendipitous withdrawal type study design.

This data illustrated a diminishing clinical effect upon withdrawal of etrasimod 2 milligram and a recapture effect upon the resumption of study drug. Across this complete response set, the effect of critical parameters, including vIGA, EASI-75, and pruritis is in the recently approved — in the range of recently approved advanced therapies and therapies currently in latter stages of clinical development.

As we set out to conduct the ADVISE trial, we have three objectives. First, we aim to ensure that etrasimod was safe and well tolerated in atopic dermatitis population. As I mentioned, this is the first S1P1 receptor modulator tested in this indication. Second, we sought to determine whether etrasimod could provide an efficacy signal and a dose response that would inform the decision to move into a Phase 3 program. And finally, we sought to ensure that we would have a profile that would eventually be commercially viable.

We are certain that we have met these objectives and the totality of the data emboldens our conviction to move expeditiously into a Phase 3 registrational program.

In the past 48 hours, we’ve spoken to a number of global thought leaders, who were impressed by the safety and efficacy demonstrated by etrasimod as an oral agent in this ADVISE trial. These global thought leaders were highly supportive of moving forward to a Phase 3 program.

Chris and Rob will be reviewing our top line data and market implications for ADVISE. Following Chris and Rob, I’ll provide some key program updates and then Laurie will provide an overview of the third quarter financial performance. And then following our prepared remarks, as always, we will hold a Q&- session.

So with that, I’m going to go ahead and hand the call over to Chris.

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Thanks, Amit, and good afternoon, everyone. Today, I’m pleased to take you through the top line data from the ADVISE trial, a Phase 2b placebo-controlled, dose finding trial to assess the safety and efficacy of etrasimod in patients with moderate to severe atopic dermatitis.

In ADVISE, we enrolled 140 participants across the U.S., Canada and Australia. The efficacy measures for this trial included the percent change in the Eczema area and Severity Index or EASI from baseline to week 12, the proportion of participants achieving EASI-75 from baseline to week 12, the proportion of participants achieving the validated Investigator Global Assessment or vIGA of zero or one and a reduction from baseline greater than equal to two at week 12 and the percentage change in peak pruritis.

Inclusion criteria for this study were as follows, male and female participants between the ages of 18 and 70 years of age, with baseline atopic dermatitis scores of EASI greater than equal to 16, IGA greater than equal to three and body surface area or BSA involvement of greater than or equal to 10%.

Patients were screened over a four-week period and then randomized in a one-to-one to one fashion between placebo, 1 milligram etrasimod and 2 milligrams of etrasimod. A four-week screening was followed by 12-week double-blinded treatment period. After completing the 12-week period, study drug was discontinued for a four-week safety follow-up. All participants, completing the four-week follow-up period were eligible to enter a 52-week open-label extension evaluating 2 milligrams of etrasimod followed by a final four-week safety follow up.

The data discussed today will only include efficacy through week 12 and then safety through week 16.

We will now turn to demographics and baseline characteristics. As you can see from this table, the treatment arms were well balanced. The overall population was more moderate than severe with 83% of participants having an IGA score of three at baseline.

From a safety perspective, etrasimod was shown to be well tolerated with a strong safety profile, similar to that seen in previous studies with most of the adverse events classified as mild. We monitor specific adverse events of special interest or AESI for the S1P receptor modulator class and etrasimod in general. As you can see from the data shown here, there were no AESIs of concern in the ADVISE trial. Specifically, there were no cases of macular edema. There was one case of dyspnea in the placebo group, as well as one case in the 2 milligram etrasimod group. There were no AEs related to heart rates or cardiac conduction. There were two participants with non-disseminated herpes zoster or shingles, and both of these were in the placebo group.

In terms of AESIs for the broader immune modulator classes, there were no reports of conjunctivitis, acne, venous thromboembolic events, and no opportunistic or serious infections. Overall, the safety profile of etrasimod was favorable and as expected in the ADVISE trial.

In taking a look at the etrasimod impact on heart rate, we observed a placebo-corrected maximum mean heart rate change from baseline at two hours. In the 1 milligram group, there was a decrease of 1.5 beats per minute and a decrease of 6.7 beats per minute in the 2 milligram group. These single digit heart rate changes were not associated with any blood pressure changes or symptoms.

After the first dose, the heart rate differences across the three groups came together by week one, and we’re near identical from weeks two through 12, similar to previous observations. One participant in the 2 milligram etrasimod group had a transient second degree AV block type 1 which was self limited and asymptomatic. The participants went on to further etrasimod dosing without any cardiac changes or symptoms. These events have been very rare in our clinical trials and have been clinically insignificant.

As is well characterized, lymphocyte reduction is an expected and on target effect of a etrasimod. It is through this process that etrasimod effects inflammatory disease and potentially provides clinical benefit. In the ADVISE study, there was a maximum reduction in the peripheral lymphocyte count in the 2 milligram group of 43.6% at week two, which was consistent with our previous studies evaluating etrasimod. Between weeks four and eight, as noted in the yellow box, there was an unanticipated increase in lymphocyte count with a gradual reduction in lymphocytes from weeks 8 to 12. This unanticipated finding led to further analyzes.

As previously mentioned, lymphocyte reduction is an expected on target effect of etrasimod. As per protocol, study drug could be interrupted if the lymphocyte count decreased to CTCAE criteria Grade 4 which is less than 200 lymphocytes per microliter. During the study, starting around week four, a small number of investigators with a cluster at a single site discontinued the study drug in nine participants, because of lymphocyte counts only meeting CTCAE criteria Grade 3. As you would expect and consistent with etrasimod’s mechanism of action, these nine effective participants were all receiving 2 milligrams of etrasimod representing 19% of the total 2 milligram population.

Importantly, these participants evidenced no other clinical symptoms or adverse events that would have warranted stopping the study drug. Notably, the study protocol did not specify study drug discontinuation for these levels of lymphocyte reduction. These actions were taken by the investigator, the investigators without timely awareness by Arena’s study personnel, because the company was blinded to lab values, like lymphocytes, that would indicate which patients were taking active drug.

As seen in the lower red line, there was a rapid rebound in lymphocyte counts between weeks four and 8 in this group of nine participants. In the majority, study drug was resumed by week eight with subsequent decreases and lymphocyte count between weeks eight and 12.

As will be discussed in subsequent slides, it is clear from reviewing the data from this group of participants that stopping etrasimod led to a clinical rebound or worsening of atopic dermatitis and restarting etrasimod resulted in the resumption of clinical benefit.

Turning to our discontinuation, it was clearly unwarranted and in fact was directly counter to the clinical benefit that participants were receiving. We plan to incorporate this important learning and apply it to the Phase 3 program to avoid unnecessary study drug discontinuations.

Now, let’s take a look at the efficacy results. In the primary endpoint analysis of the percent change in EASI from baseline to week 12, the overall response rate was 57.3% [Phonetic] in the 2 milligram group, which was not statistically significant. Of note, in this moderate patient population, there was a relatively high placebo rate.

In the analysis of the FDA regulatory endpoint of the proportion of participants achieving IGA success, defined as IGA 0 or 1, with a greater than or equal to 2 point improvement from baseline, 29.8% of participants achieved IGA success versus 13% in the placebo group, which was a change of 16.8% and was statistically significant. IGA success criteria is the more stringent and more conservative endpoint when compared to EASI. Even though the study was not powered for IGA, there was a significant difference.

In the analysis of the proportion of participants achieving at least a 75% reduction EASI from baseline, 38.3% of the 2 milligram etrasimod group achieved EASI-75 versus 26.1% in the placebo group, which was not significant.

To understand the impact of etrasimod treatment over time, we analyze the EASI change from baseline at each clinic visit through week 12. EASI improved in all three groups through 12 weeks. In the etrasimod 2 milligram group, the EASI improvement was statistically different from placebo at week 4. In this group between weeks four and six, the treatment effect plateaued with recovery of treatment effect from weeks eight to 12. The trajectory of improvement did not return to the same level seen through week four.

This observation was similar to the lymphocyte changes previously reviewed, where there is an increase in lymphocyte count beginning at week four due to the 19% of participants that had treatment interruption in the 2 milligram group. From a mechanistic standpoint, this observation is important, because it shows that with treatment withdrawal, efficacy is lost, and we’re treatment reinitiation, there is a recovery of treatment effect.

Similarly, we analyze IGA and EASI-75 over time. For both of these assessments, it is notable that in the 2 milligram group, there was a change in the trajectory of treatment effect between weeks four and eight with recovery after week eight. In the 2 milligram group, the difference from placebo was significant for IGA at the week 12 time point. For EASI-75, similar to percent change in EASI over time, the difference from placebo was significant at week 4. Notably, we did not see a plateau effect between weeks eight and 12.

From our experience in UC, we have seen continued improvement in efficacy over time in our completed trials. Based on the trajectory of the response from weeks eight to 12, we would expect continued improvements in IGA and EASI. And we will take us into consideration in our Phase 3 planning, which will likely be 16-week studies.

In a similar fashion, looking at the pruritis changes over time, there was an early and significant effect through week six, with continued improvement through week 12. To further understand the impact of the treatment interruptions, we analyzed the key outcome variables in the 2 milligram etrasimod group that received complete therapeutic exposure, which was 38 participants. For the percent change in EASI over time, there is clear and early separation in the 2 milligram group versus placebo, which was significant at four weeks and continued to show separation after week 12, which was also statistically significant.

We analyze the proportion of participants achieving IGA and EASI-75 response at week 12, excluding those participants with those interruption. For IGA there was a 23.8% improvement versus placebo, which was statistically significant. Of note, as you remember in the full analysis set previously presented, there is a greater than two-fold improvement in IGA at week 12. And when analyzed for the group, they had the full treatment exposure, there was nearly three-fold improvement in IGA at week 12. For EASI-75, there was a numeric 16 point improvement over baseline.

In a similar fashion, looking at the pruritis changes over time, the etrasimod treatment group, when compared to placebo was statistically significant from weeks two through eight.

I will now hand it off to Rob to provide some commercial context. Rob, over to you.

Robert LisickiExecutive Vice President and Chief Commercial Officer

Thanks very much, Chris, and good afternoon to everyone. You should be seeing a slide that is titled cross trial comparisons. Just a few comments to share and some of the different data that you may see from these Phase 2 results. Just to be clear, this is an indirect cross trial comparison of select Phase 2 studies in atopic dermatitis. These studies have been conducted at different times and they have different protocols as well, but in part it demonstrates the heterogeneity of both study design in the baseline patient demographics across these studies.

It’s also notable that both the etrasimod and baricitinib [Phonetic] studies were 12 weeks. All of the other studies were 16 weeks of drug exposure for patients. In addition to that the baricitinib study included topical corticosteroids. What’s particularly of note in this data is, the etrasimod baseline IGA score, which clearly demonstrates that this was largely a moderate group of patients, that becomes meaningful because moderate patients as a group in the U.S. represent roughly 65% of the moderate to severe total patient opportunity.

If you can advance the next slide for me, please? So, we will look at one particular — when we look at one particular endpoint, atopic dermatitis competitive landscape, the endpoint that we’re choosing here the IGA 01, as it’s a Phase 3 primary endpoint, and again, just as a reminder etrasimod in adverse fitment reflects 12 weeks of exposure, other agents have 16 weeks of exposure. Baricitinib included topical corticosteroids. So while understanding and appreciating that there are always limitations of indirect comparisons, we do note that etrasimod demonstrated a statistically significant effect in ADVISE. And as you can see in the blue box that is surrounded by the bars we’ve highlighted, that effect size for etrasimod is in our opinion commercially attractive delta of 24%. While indirect, the effect size for etrasimod observed in the study demonstrates a result that is largely in line with other studies agents and Phase 2 studies.

Now, I’d like to hand the call back to Amit, who will provide a summary and key program update.

Amit D. MunshiDirector, President and Chief Executive Officer

Thanks, Rob. As you’ve seen by the totality of the data, an oral once-daily etrasimod represents a novel therapeutic option for patients with moderate to severe atopic dermatitis. The ADVISE trial despite unnecessary interruptions in dosing of a subset of etrasimod 2 milligram participants showed consistent in early effect of treatment, and very importantly etrasimod met the IGA responder criteria, the stringent FDA Phase 3 primary endpoint.

Overall, etrasimod demonstrated rapid onset of action illustrated by patients in the 2 milligram group achieving statistical significance in pruritis, EASI and EASI-75 at week four, and in the post-hoc Completer Analysis, patients who received a full therapeutic exposure throughout the study achieved statistical significance in EASI base changed from baseline at week 12, multiple time points in pruritis and further improvements on IGA from baseline compared to placebo.

Participants with dosing interruptions as Chris pointed out, experienced disease recurrence, but recaptured response upon restatement of treatment. Safety profile remains commensurate with previous trials, and overall the efficacy and safety profile, a potentially strong competitive profile and rationale to advance to a Phase 3 program.

As you can see, we’re excited about the ADVISE data and we’ll be happy to address questions relative to the full data set during the question-and-answer session. But before we get there, I would like to walk you through key updates on other core programs.

Despite the COIVD-19 pandemic, Arena continues to make strong progress on all fronts, clinical, operational and financial. Over the quarter, we have reached several clinical development milestones across our programs. Let’s go with etrasimod GI franchise, in September, we announced the first subject dose in the ELEVATE UC study, UC 12 study, the second of two pivotal trials within the ELEVATE — within the Phase 3 ELEVATE ulcerative colitis program.

The ELEVATE UC 52 study remains on track to complete enrollment by the end of this year, with the expected completion of the 52-week treatment period by the end of 2021, and top line data shortly thereafter. UC 12 continues to make strong progress and we expect data in the same time frame. As you might expect, we’ll continue to monitor the impact of the COVID-19 resurgence on study enrollment for both UC 52 and UC 12.

For both of our studies in the ELEVATE UC program, it has been our plan to study a contemporary patient population, and as such we chose not to pre-specify or limit the mix of patients in our protocol. We continue to monitor the distribution of patients closely and we currently expect the patient distribution to be approximately 70% naive and 30% previously treated with advanced therapies. Importantly, by letting the patient mix evolve with contemporary treatment patterns, we may be learning about where etrasimod might eventually be used in the marketplace.

In September, we announced a new trial GLADIATOR UC to evaluate etrasimod in a less severe patient population than ELEVATE UC program. GLADIATOR UC’s design involve more moderate patients as defined by modified Mayo score four to six, but those who have an endoscopic score greater or equal to one, as well as patients who screen failed ELEVATE UC. The GLADIATOR study addresses a broad unmet need for patients that are sub-optimal controlled via failed conventional therapies, but a resistance of risk benefit profiles current biologics or JAK inhibitors.

Our etrasimod dermatology franchise continues to advance. In addition to the progress the ADVISE trial, in September, we announced our first patient dose in the Phase 2 trial evaluating etrasimod in alopecia areata. As a reminder, this is a Phase 2 multicenter, randomized, placebo-controlled trial that will assess the safety and efficacy of once-daily etrasimod 2 milligrams, in subjects with moderate-to-severe alopecia areata.

In all of these trials, we will continue to monitor for discontinuations based on the lessons learned from the ADVISE trial. To date, we have not seen any similar type of issues in ELEVATE 52 or 12.

Moving onto olorinab. As a reminder, olorinab is our investigational, oral highly selective full agonist with a cannabinoid type 2 receptor for the potential treatment of visceral pain and a broad range of GI conditions. In October, we announced, we have completed full enrollment in the CAPTIVATE trial, evaluating three doses of olorinab for abdominal pain in both IBS-C and D. We expect top line data for CAPTIVATE to read out in mid-Q1 2021.

I’m also pleased to announce that our cardiovascular franchise continues to progress. APD418, oru selected beta-3 antagonist and cardiac myotrope in development for treatment of acute heart failure reached completion of the Phase 1 safety study. APD418 it was generally safe and well tolerated, and we’re in a Phase 2 planning process. We will also be unveiling a second clinical stage cardiovascular asset before the end of the year.

And finally, at the end of October, we announced the successful spin-off of our neurology franchise with the inception of Longboard Pharmaceuticals, which we expect will unlock the value of these important programs. I’d like to take this opportunity to congratulate Kevin Lind and wish him the best of luck in leading this important endeavor. Importantly, Arena shareholders will participate in the value of these assets, Arena’s ownership in the entity, as well as future royalty streams on the specific programs.

So with that, I’ll pass the call to Laurie to review our financial results for the quarter. Laurie?

Laurie Stelzerxecutive Vice President and Chief Financial Officer

Thank you, Amit, and good afternoon, everyone. I will provide a brief review of our third quarter 2020 financial results, but for more details regarding our results, please refer to our earnings press release from earlier today and our 10-Q.

Revenues for the third quarter were $20,000 compared to $1.4 million in the third quarter of 2019. Research and development expenses for the third quarter totaled $79.8 million compared to $60.3 million in the same period in 2019. This increase was primarily driven by advancement of our clinical trial programs as well as an increase in personnel expenses as we staff to support our program growth.

General and administrative expenses for the third quarter totaled $19 million compared to $20.4 million in the same period in 2019.

Net loss for the third quarter was $97.4 million, compared to net loss of $72.9 million for the same period in the prior year. Basic and diluted net loss per share for the third quarter was $1.69, compared to basic and diluted net loss per share of $1.46 for the same period in 2019.

And as of September 30, 2020, cash, cash equivalents and marketable securities balance were approximately $1.2 billion, compared to $1.3 billion at June 30, 2020.

Arena continued to achieve clinical development and operational milestones, while reducing operating expenses through enhanced clinical trial efficiencies and focusing on optimizing our spend. As a result, our guidance range for operating cash burn for the full-year 2020 is expected to be $345 million to $355 million, which is down from our previous guidance of $400 million to $430 million.

That concludes our prepared remarks. So, now I’d like to open up the call for a brief question-and-answer session. Operator, please open up the lines, and we’ll take our first question.

Questions and Answers:

Operator

Sure. [Operator Instructions] Our first question comes from the line of Jason Gerberry with Bank of America. Your line is now open.

Jason GerberryBank of America Merrill Lynch — Analyst

Hi, thank you for taking my questions. So I guess, I just wanted to follow-up with my first question, just the commentary around the, not seeing, I guess the risk of those modification in the UC, the Phase 3 UC trials, given it sounded like there wasn’t a lot of visibility given the blinded nature of ADVISE. So just curious what gives you guys confidence that there wouldn’t be a risk of dose modification in the Phase 3 UC trials? And then how are you guys thinking about Phase 3 atopic derm study start time? Would you could think about commencing a Phase 3 during COVID-19 surge? Would you wait for the situation to stabilize? Just sort of curious how you think about mitigating this risk in a Phase 2 trial setting. Thanks.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, Jason, so just going back to [Indecipherable] we’ve not had any discontinuations due to Grade 3 leukopenia, going back to the Phase 2 study and looking forward into, and so we know a lot of the gastroenterology community and how they think about it. I think the real lesson here is, there is a subsequent dermatologists that are — that require more education, that are just included, they are just a more cautious. And so this, we think this is much more of a dermatology specific thing that we’re going to have to be mindful as the go to Phase 3. So let me ask Chris to lend in more color.

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

No, I think you’ve got it. I would just to say in the ELEVATE trial, we haven’t seen any discontinuations relative lymphopenia. And so we kind of, we’ve been looking at that as we go. Again the issue here in these trials is that, we’re blinded to lymphocyte count, obviously because that was unblinded study to us, and so we have to wait till these things show up and the electronic data capture record. And so, we are confident in the UC program, how things are moving.

Amit D. MunshiDirector, President and Chief Executive Officer

So again, it really comes back to the different specialty, Jason, and how they view the specific types of agents and conservatism in general. We’ve got a lot more extensive safety experience in the gastroenterology community. We haven’t seen any concerns from that side of the fence.

In terms of starting a atopic derm, it’s going to take us a while anyway to design the studies, work with external experts. It will be a global study and naturally we will want to have a conversation with the various regulatory agencies. So, we’ll proceed along at the most expeditious path we can, and then we’ll take a look at the external landscape and see if it’s prudent to start a study in that setting depending on where we are on the pandemic. So I think will continue our preparation, and then we’ll make that decision as we get close to initiating the trial. Just, lot of uncertainty externally.

Jason GerberryBank of America Merrill Lynch — Analyst

Yeah, if I could ask a follow-up, how do you try to mitigate this in the Phase 3 setting? Is it all about site selection to try to avoid having investigators you might be more cautious and — do they kind of this sort of thing? I imagine that you have to allow the physician have the discretion to dose modify in the Phase 3 trial. Just sort of curious how you navigate that?

Amit D. MunshiDirector, President and Chief Executive Officer

All right. I think the first thing is, when you’re entering into these areas with a novel mechanism of action and if you looked at most products that have entered novel MOAs in dermatology setting, there is a finite subset of investigators who will engage and will have a broader access to more experienced clinical trial sites as we got a Phase 3, for sure. The other, the burden on us is really on the education side, on the mechanism of action, and we’ll be paying particular attention to that as we go into Phase 3.

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Going to the other comment, just focusing on safety, we have established, I think in this trial, in dermatologic patients that the profile continues to be very consistent across all of our experiences, relative to the safety piece and that’s really critical. And then just continuing to educate dermatologists around the lymphopenia and how that plays into efficacy while also being safe.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, one of the thing that’s really interesting here is, even with Grade 3 and even Grade 4, we’re not seeing the serious and opportunistic infections that you see other oral agents, and just being able to communicate that we’re maintaining immuno surveillance, even though we’re reducing T lymphocytes will be an important part of the education as we move to Phase 3.

Jason GerberryBank of America Merrill Lynch — Analyst

Got it. Thank you.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, thanks, Jason.

Operator

And our next question comes from the line of Alethia Young with Cantor. Your line is now open.

Alethia YoungCantor Fitzgerald — Analyst

Hey, guys. Thanks for taking my questions and thanks for all the details today. Maybe two for me. One, I think I might know the answer, but I just wonder, is there any kind of additional sensitivity with derms, just in might of being in a COVID environment and lowering lymphocytes, or is this kind of their default position? And then can you just talk a little bit about, the measurement of the vIGA versus the EASI-75, being able to achieve the measure in one endpoint versus the other? Just kind of how to think about those endpoints and the differentials in those? Thanks.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, let me take the first one, and the second one off on the endpoints to Chris. It’s difficult to tell whether it was COVID sensitivity or not COVID sensitivity, and we just don’t have that line of sight. As Chris mentioned, it was a cluster of patients in a single clinical site that had most of the effect here. So, there is definitely additional sensitivity on the side of the dermatologists. And we’ll just have to spend more time making sure that we’re getting to more experienced clinical sites and we did the job on the front-end education here with these clinical sites.

So, Chris you want to take vIGA versus EASI?

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Sure. I think one of the key observations here is that there was a high placebo rate on the EASI side, but not on IGA. It’s not entirely surprising kind of on a couple of levels, one is that, the placebo rate and EASI tends to be higher in moderate AD, and we had a fairly high moderate population in this particular study. And that the other observation is that the placebo rate in EASI, in particular, has been higher in Phase 2 studies when you a novel MOA. So kind of two things going on there, but again not high on the IGA side.

And that’s also not surprising, IGA is more conservative, more stringent and importantly, it’s the FDA regulatory endpoint. And so it is going to be the IGA treatment effect, which is going to be driving our design and sample size calculations. And so feel good about what happened on the IGA side.

Amit D. MunshiDirector, President and Chief Executive Officer

Alethia, did we answer all your questions?

Alethia YoungCantor Fitzgerald — Analyst

Yes, that was very helpful, thank you.

Amit D. MunshiDirector, President and Chief Executive Officer

Great, thank you. Really appreciate it.

Operator

And our next question comes from the line of Martin Auster with Credit Suisse. Your line is now open.

Thomas DealCredit Suisse — Analyst

Yeah. Hi, everyone. It’s Thomas on for Marty. Thanks for taking the questions. I guess two on the topic derm here. Maybe first, in these 19% of patients, who had dosing interruptions. Can you clarify how those patients were handled in the full primary statistical analysis? Was that kind of the last observation carry forward or was there some other handling there? And I’m curious if you can contextualize kind of this fast onset of action, you hit some key endpoints, start saying, at week four. Can you put that in context, kind of relative to other agents and AV and how meaningful that might be clinically? Thanks.

Amit D. MunshiDirector, President and Chief Executive Officer

Sure. Let me have Chris take the first part of that, which is the statistical for the full analysis set.

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

So on the full analysis set, those nine participants or 19% were not handled any differently than any other subject in the trial. So we had two different analysis methodologies that we applied across the trial, whether it was imputation or not. And so they weren’t handled any different. So the only subject that we’re missing, say the week 12 data, and that didn’t — that was not dependent on whether they missed any doses or not. So they are handled exactly the same as the rest of the population.

Amit D. MunshiDirector, President and Chief Executive Officer

The second part of your question, Thomas, on the fast onset of action. I think the real key here is that, fast onset of action, combined with the safety profile, and I’ll ask Rob Lisicki to provide some commentary on what we know what the marketplace and how those things, we think are going to be important competitively. Rob?

Robert LisickiExecutive Vice President and Chief Commercial Officer

Yeah. Thanks, Amit, and hi, Marty. Certainly physicians want drugs that work as quickly as possible for these patients. But it is a chronic illness. So the long-term profile of an agent, is really important. So one of those components is going to be efficacy, but the two others will be long-term exposure and any safety disadvantages that an agent may potentially provide. And then the second is the relative use of use of the agent. Injection therapy is challenging for patients, JAKs are likely to have recurrent monitoring and AD. So when you think of the totality of those three attributes, efficacy, safety and ease of use, etrasimod has we think a really attractive profile. Specifically to your question, you see most of these studies start to separate by two weeks. So, you do see statistical significance for some of the key endpoints. In some studies, they measure it as soon as two days. And we think that in an acute situation, that’s probably a valuable endpoint to have. I think a little bit less so in a chronic situation or chronic administration for patients.

Amit D. MunshiDirector, President and Chief Executive Officer

Does that answer your question?

Thomas DealCredit Suisse — Analyst

Yeah, that’s helpful. Thank you.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, thanks, Thomas.

Operator

And our next question comes from the line of Kennen MacKay with RBC Capital. Your line is now open.

Kennen MacKayRBC Capital Markets — Analyst

Hi, thanks for taking the question. Wondering if there is anything in terms of efficacy or safety profile that we can derive from the 1 milligram etrasimod group, given these patients did stay on therapy across the entirety of the study. Just again, thinking about that group, what stands out mostly on the team about the the efficacy or safety profile? Thanks.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah. So, I think what’s interesting about the 1 milligram, especially as we look at the Completer Analysis of patients who received the full threshold in terms of 2 milligrams is that, we see a nice dose response across all, two looks better than one, across most of those metrics. It could be interrupted patients on two — makes the curves look a little bit strange, but we do believe that two is better than one. Encouragingly for us two was sufficiently safe and it really just begs the question whether, we pushed two and three in the next stage of our of our valuation. So while one looks interesting and there may be a wall [Phonetic] for one in terms of chronic therapy, at some future point in time, in terms of these 12-week, 16-week conduction trials, we’d be looking for two and potentially even thinking by three, and again we’ll have data this year in patients in the Crohn’s setting for the 3 milligram, which allows to — just a little bit more informed about where we can go with that version. The final point I’ll bring up is, both on 2 milligram and 3 milligram, as you know, we have the etrasimod CR profile, so we’ll be exploring those this year too. So gives us lots of options to think about optimizing dose for these patients over a longer period of time.

Kennen MacKayRBC Capital Markets — Analyst

Got it. Thank you.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah. Thanks, Ken.

Operator

And our next question comes from the line of Jessica Fye with JP Morgan. Your line is now open.

Jessica FyeJP Morgan — Analyst

Hey, guys. Thanks for taking my question. I’m curious, if you’re going to try to include more IGA for post patients in the Phase 3. And if so, is that focus all about how the admittedly small subgroup of more severe patients did in this trial relative to placebo, obviously?

Amit D. MunshiDirector, President and Chief Executive Officer

So, I’ll take the first part and let Chris answer the second one. The IGA for patient, in the Phase 3 program, we’ll be looking for a little better stratification and understanding a little bit more about the IGA 3 and 4. One thing, we are encouraged with is to see this type of IGA response in moderate patients, it’s actually quite substantial. And if you look at the IGA scores across all the competitive programs and the magnitude of effect, it’s all been in more severe patients or more severe patient groups than that. So the modern patient population is the more substantial, a numerical patient opportunity and being able to demonstrate that change, is important to us. So we’ll have to balance that with the more severe or more serious patients. We know that the JAK inhibitors from our market research will be really reserved for later in the duration of the disease or severity disease. We know that [Indecipherable] predominantly used in more severe patients, that really need that moderate population available for, in terms of market opportunity. So we’ll have to balance those two things out, — subset of IGA 4.

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Well, not a lot to say there yet. We just have the top line data and certainly we’re going to be looking at various subsets of patient populations and doing some sensitivity analysis to tease that out a little bit. The IGA 4 will be somewhat limited in terms of the conclusiveness of those analysis, just because we had relatively a small number of patients in that — in those groups.

Jessica FyeJP Morgan — Analyst

Okay. Thank you.

Amit D. MunshiDirector, President and Chief Executive Officer

Thanks, Jess. Appreciate it.

Operator

And our next question comes from the line of Jason Butler with JMP Securities. Your line is now open.

Jason ButlerJMP Securities — Analyst

Great. Thanks for taking the questions. First one, just on placebo rate, I think you’ve mentioned before the higher placebo effects for [Technical Issues] Phase 2 trials. Why is that? And how do you think about managing placebo effect in a Phase 3 study? And then for the sites where you have the dose interruptions, was there any other notable findings from the data at those sites, for example, in the placebo arm. And just to clarify, were the placebo patients and other data for the 1 milligram from those sites included in the Completer Analysis? Thanks.

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

So, I think three questions there. If I got it right. So, in terms of thinking through placebo rates for the Phase 3 trial, and why are they higher in studies where you have a novel mechanism. So we don’t really know the answer. So just a conjecture would be that when you have a novel mechanism of action in a particular disease and in here, atopic dermatitis in general, the types of investigators that participate in the studies may be fundamentally different than the types of investors that that participate in the larger studies, once you already have an efficacy signal. And so it may be that those sites that participate early aren’t as experienced in clinical trials and may not be able to consistently perform some of these more detailed measurements, and EASI is a much more detailed kind of intensive from an experience perspective, measurement. And so we see in lots of studies in Phase 2 trials, where you have a novel mechanism, that the placebo rates, particularly related to EASI are higher. We’re not really concerned about that, because again we are going to be focusing on IGA as our main endpoint, and that’s going to be critical in the Phase 3 trial. So, we’ll have to work through that. We do think that site distribution from an experience standpoint will be different in Phase 3 trial relative to Phase 2.

Your last question had to do with how we analyzed placebo at the sites, where there was study discontinuation, if I got that right. And we just need have to analyze them like every other we did. There was nothing else on the data that was particularly of concern at those slides. Again, there was one site, where there is a cluster of drug interruptions and the rest was scattered across a couple of others. And so there is nothing else in the data that led us to concern. We did not exclude other patients from those sites from the analysis.

Jason ButlerJMP Securities — Analyst

Okay, great. Thanks for taking my questions.

Amit D. MunshiDirector, President and Chief Executive Officer

Thanks, Jason.

Operator

And our next question comes from the line of Yatin Suneja with Guggenheim. Your line is now open.

Yatin SunejaGuggenheim Securities, LLC — Analyst

Hey, guys. Thank you for taking my question. So two from me. With regard to the lymphocyte count reduction, I think it was about 40%, 45% in the study. Can you remind us what you saw in OASIS and the healthy volunteer study that you’ve done? Any reason for a difference here? And then, I have a follow-up.

Amit D. MunshiDirector, President and Chief Executive Officer

No, so, looks just like always is, really not much different.

Yatin SunejaGuggenheim Securities, LLC — Analyst

Okay. And then with regard to the Phase 3, I think you’re saying it will be a 16-week study. Can you maybe point us to data that gets you, sort of, conviction to capture additional efficacy at week 16? And the reason I ask is that, because if you look at the data and I’m just focusing on the Completer, across all endpoints, it doesn’t seem like there is a separation or there is a continued separation, there are some endpoints that fixed assets have been — time point, but then, not significant that’s certain. Why is that the case? What is the data that gives you confidence on the 16-week is going to be better?

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah. I’ll answer that with sort of a broader response, and then Chris can talk about specifics. As we’ve seen with the etrasimod Phase 2 in open label patients continue to improve over time. And we will be continue to see effective — one of the challenges in this Completer response and because we — the sample size gets smaller, it’s difficult to interpret, but we do see continued response, continued improvement in response in patients from the OASIS work in the open label. So there is no reason to think it would be otherwise in this patient population. Chris?

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Yeah, I think that’s exactly right, Amit. And we didn’t, obviously, it’s a brief presentation, we didn’t show you all of the graphs, but if you go back and review the graphs, particularly looking at IGA response in the full analysis set, there continues to be separation of IGA from placebo in that group, even though 20% of the patient population had inadequate therapeutic exposure. And so from our experience with etrasimod, from OASIS, in particular, we know that there continues to be therapeutic benefit derived over time. And so we will have to do some modeling to look out to week 16, but we believe this in our previous experience and from the data that we see here that it is likely that you would see continued separation of the curves, particularly related to things like IGA, but also EASI, and that the overall treatment effect would be significantly higher at week 16. The other piece is going to come into plan in our planning, which we’re not at liberty to discuss yet, because the data aren’t cleaned and locked, is that we will have open label extension data in this trial going out to be — we will be able to look at that data to get a sense of what happens with continued etrasimod exposure, obviously, it’s open label, so we’ll have to take that caveat into account as we plan. But there will be significant long-term exposure data that will help us in our planning for Phase 3.

Amit D. MunshiDirector, President and Chief Executive Officer

Rob, anything to add from the commercial side in terms of 12 versus 16?

Robert LisickiExecutive Vice President and Chief Commercial Officer

Yeah, two things. The first, if you look at the slope of the curve to Chris’s point, you see what appears to be improving separation between the two in the placebo. Secondly, and I think probably, more importantly, is when you look at the Phase 3 programs across studies, they are 16-week studies. So we provide a fair comparison to other readouts for other agents that are either in market or in development.

Yatin SunejaGuggenheim Securities, LLC — Analyst

Got it. Thank you very much.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, thanks, Yatin. Appreciate it.

Operator

And our next question comes from the line of Joel Beatty with Citi. Your line is now open.

Joel BeattyCiti Investment Research — Analyst

Hi, thanks for taking the questions. The first one is, for Phase 3, would enrolling a somewhat larger percentage of more severe patients, is something that might have the potential to show a larger gap between treatment and placebo? And then second question is, with this data that’s in hand, they have today, what’s the outlook for expanding the study of etrasimod to other dermatitis indications?

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, so, Joel, I think on your first question, the answer is absolutely, we’ll be looking at modeling that out and looking at that mix of patients. And it’s a little early for us to think about other dermatitis indications. I think we need to fully digest this, begin to plan our Phase 3 programs here. But we will be looking toward our EOE data, and our EOE study, which we continue to hope to start this year, COVID dependent. And then over time, as those data readout become more robust and as Chris mentioned, we see more of the open label data, we’ll start thinking about other areas that overlap with these conditions. We tend not the jump from dermatitis to dermatitis, I think we tend to try to follow the biology. We mentioned the bidirectionality of UC to atopic derm. We know atopic derm and EOE have bidirectionality to other conditions, and that’s sort of how we will approach it. But as the data fairly freshen, we’ve got little work to do to get Phase 3 ready, that’s going to be our near-term priority.

Joel BeattyCiti Investment Research — Analyst

Great, thank you.

Amit D. MunshiDirector, President and Chief Executive Officer

Thank you, Joel.

Operator

And our next question comes from the line of Joseph Schwartz with SVB Leerink. Your line is now open.

Joseph SchwartzSVB Leerink — Analyst

Hi, thanks very much. I was wondering if you could talk about the reasons for the relatively moderate patients being enrolled in ADVISE and whether you’re confident that you can control that in Phase 3 for AD?

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, Joe, one of the things that happens, Joe, is that the number of sites that are open to new mechanisms of actions — for the first time are relatively limited and those sites tend to have moderate patients. There is more comfort with patients who are less sick in general. So now that we’ve got a strong safety database, we’ve shown evidence of how that — is effectively part of the study, we think we’ll be able to address a broader set of clinical sites, more experienced sites, sites that have both moderate and severe patients with larger practices. Again to Chris’s point, we’re also more experienced on the EV side. So, we didn’t step in the right direction, yet the clinical signal is clearly provocative from our point of view and warrants moving forward. That was consistent with the conversations we had with the experts we spoke to. So this will all be a matter of just being able to get out and educate folks on the MOA, the safety profile, which we’re incredibly encouraged with. And we think that will give us access to a much broader range of sites and more experienced investigators.

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Yeah, and if I can just ask one quick comment to that, the opinion is supported by what you see in the Phase 2 versus the Phase 3 studies. If you look at the Phase 2 studies across AD, you see this, as I mentioned a lot of heterogeneity, but you also see in some cases lower rates of four’s, uPA, for example and their Phase 2 study for their high dose arm, 26% of patients were in IGA 4. So it’s higher than the number we saw in etrasimod, but again it’s not significantly higher.

Joseph SchwartzSVB Leerink — Analyst

That’s interesting. Okay. And then what work will you be doing to determine the best dose or doses to take forward? What information do you have that you can analyze to make that decision?

Amit D. MunshiDirector, President and Chief Executive Officer

Sure. Let me start and then we’ll have Chris comment further. But we know the 2 milligram is active here. It was active in the UC study. We know the corresponding, one of the thing that’s really interesting here is to look at the pharmacodynamics of the lymphocytes, both the drop to four weeks, the recovery with the nine patients who had the interruption, and then again resumption of leukocyte decline. And then watch that the clinical response actually mirrors that, right. So, you really have a really nice PD marker with the leukocyte counts dropping, really look the shapes look very quite identical. So that gives us reason to understand the 2 milligrams is active. We saw that exact same phenomenon in US study. We’re seeing the exact same phenomenon here. So whether we push up in dose of 3 milligrams, that’s something that we’ll have to discuss, as I mentioned, we’re thinking about it. We have to began thinking about this week, whether we have to push the dose, a little bit. These are in general, healthier patients. Then you would see for example in Crohn’s. And we think our 3 milligram, we have a broad therapeutic index with this compound, there might be something worthwhile look at it. So we’ll keep you guys updated. We have a lot of work to do on that, but two is definitely our — we think is our sweet spot.

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Yeah, the only thing to add into that, is that, because it’s a relatively small Phase 2 study, we do have intensive pharmacokinetic data to look at. So it’s going to take a little bit of time, but we will look at that PK data relative to lymphocytes, relative to kind of clinical efficacy, relative to other biomarkers and it’s that totality of data that we’ll use to think through dosing.

Joseph SchwartzSVB Leerink — Analyst

Okay. And then if I could just ask a housekeeping question, how actually, is it, do you think that ELEVATE UC 52 and 12 data might flip into early ’22?

Amit D. MunshiDirector, President and Chief Executive Officer

I’m sorry, would flip to early ’22, Joe? Is that what your question was?

Joseph SchwartzSVB Leerink — Analyst

Yeah, it seemed like in your press release you noted that the data collection would be in late ’21, but I just didn’t know if the data itself, if we should expect it to be reported in 2021 as well?

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, we haven’t completed enrollment in UC 52. We think it will be by the end of the year, some of that is COVID dependent, but we do think it will be by the end of the year. Then you go into 52 weeks of treatment that takes us to the end of next year. So we’ll have data shortly thereafter. It’s really hard to tell right now. As you know that the end of the study, when you begin to close screening, you get a bolus of patients in, the speed of those patients, the ongoing pandemic, and the second wave a pandemic in Europe, for example, and here in the US, those — all these things that impacted. So we’re watching that carefully. Right now we feel — complete enrollment before the end of the year, and I can tell you it’s November, December, when that’s going to be. And then it will take 52 weeks, which would push the data read into early 2022, and that we’ll just have to watch that over the next month or two.

Joseph SchwartzSVB Leerink — Analyst

Makes sense. Thanks for the color.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah. Thank you, Joe. Appreciate it.

Operator

And our next question comes from the line of Jim Birchenough with Wells Fargo. Your line is now open.

Jim BirchenoughWells Fargo — Analyst

Hey guys, thanks for taking the question and for all the details. Just a couple for me. I guess one, I might have missed it, but in the patients that didn’t discontinue, the 81% at the 2 milligram dose that didn’t discontinue, what was their easy 75 improvement versus placebo? And I guess the second part is how do you benchmark that against the more moderate population for the things — JAK inhibitors?

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, so let me just pull that slide here, and show [Indecipherable] the…

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Just one comment. It’s not that they discontinued, there was dose interruption.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah.

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Just to make that right clarification, and then go ahead, Amit.

Amit D. MunshiDirector, President and Chief Executive Officer

So the EASI-75, we saw about a 16 delta which Rob, you want to put that into some commercial context of competitive products?

Robert LisickiExecutive Vice President and Chief Commercial Officer

Yeah. So that would be a delta, that is in the range of baricitinib on the EASI-75 delta. So it’s a little bit tough with baricitinib, because their study included topical corticosteroids. So if you look at those, that didn’t — were roughly in that same range. If you look at the IGA score, it’s in the range of low dose JAK’s, the delta. It’s pretty much on top of lebrikizumab, IL-13, and it’s slightly — a little bit south of dupilumab. So the IGA was a really strong read through. And the EASI-75 delta that is in the neighborhood of baricitinib.

Jim BirchenoughWells Fargo — Analyst

And then just on the pharmacodynamic effects, I can’t remember if you took biopsies or if you could look at this in the blood, but TH1, TH2, TH17, cytokine responses, and do you have any sense of either how the patient population still between TH1, TH2 and TH17 and would do you expect to collect some data on how you impacted the different cytokines?

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, we do have a lot of that type of data. It will be a while before we can analyze and share that with you. But we’ll do that over time. Again this is top line data, almost real time. So we will definitely take a look that. We’re as curious as you are.

Jim BirchenoughWells Fargo — Analyst

Just maybe just one final question. Just I recognize that a Grade 1 AV block in a single patient isn’t a big deal, but just to contextualize that with what we’ve seen from ponesimod [Phonetic], maybe just for proper context.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah, so, Chris, do you want to take that?

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Yeah, so we continue to observe very low rates of any cardiac issues relative to other S1P modulators in the class ponesimod and ozanimod. We have nearly 1,000 patient exposures and have seen a very low rates of cardiac conduction issues. In fact, it’s actually lower than what you see in epidemiologic studies of healthy volunteers. So feels very good about the cardiac safety profile.

Amit D. MunshiDirector, President and Chief Executive Officer

And again remember, we have no titration. Ozanimod are double digit heart rate — placebo adjusted after day eight, then we’re talking about placebo adjusted in that six beats range within no titration, within the substantially different, also recall that ozanimod had multiple cases, sign of atrial — going back to their Phase 1 studies. And again, we haven’t seen any evidence of anything remotely that severe.

Jim BirchenoughWells Fargo — Analyst

Great. Thanks for you taking the questions.

Amit D. MunshiDirector, President and Chief Executive Officer

Thank you.

Operator

And our next question comes from the line of Alan Carr with Needham & Company. Your line is now open.

JoeyNeedham & Company — Analyst

Hi, this is Joey on for Alan. Thanks for taking our questions. Just a quick one, can you discuss how many patients entered the to make 2 mg open label expansion? Thanks.

Amit D. MunshiDirector, President and Chief Executive Officer

We haven’t disclosed that. I’m not sure the data has been cleaned at this point. So as soon as we have stated on the open label, we’ll share it with you. Again this was designed be top line on the first 12 weeks of efficacy and the 16 weeks of safety. But as soon as we see the data and we can digest it, we look forward to sharing that with you.

JoeyNeedham & Company — Analyst

Great, thanks.

Amit D. MunshiDirector, President and Chief Executive Officer

Thank you, Joe.

Operator

And our last question comes from the line of Patrick Trucchio with HC Wainwright. Your line is now open.

Patrick TrucchioH.C. Wainwright & Co. — Analyst

Thanks. Good afternoon. Just a few follow-ups for me. Just the first one, is there a possibility of an increased level of ongoing monitoring by derms, post the potential approval? And how should we think about that possibility from either regulatory or clinical perspective compared to some of these other novel compounds like the JAK inhibitors? And then secondly, how could this the ADVISE data demonstrating the quick rebound in lymphocytes upon dose interruption, how can that factor into the Phase 3 program and the potential label for etrasimod, in [Indecipherable], if approved.

Amit D. MunshiDirector, President and Chief Executive Officer

Yeah. So just to give you a little bit of context, Rob, can you talk about the competitive label profiles, as it will link the monitoring, ongoing monitoring, early monitoring [Indecipherable]?

Robert LisickiExecutive Vice President and Chief Commercial Officer

Yeah, and I’m happy to do it. So we’ll talk about the JAK, specifically. So all of the JAKs, I know everyone knows, this carry box warnings for malignancy opportunistic serious infections, TB and VTE, but they also carry monitoring that can be rather onerous, particularly for dermatologists, when bulk baricitinib [Phonetic] is an example. All the patients have to have baseline labs, which is normal and typical for any of these treatments in any of these patients. But by label they recommended to test those patients every 12 weeks for lymphopenia, neutropenia, hemoglobin changes, changes to LFTs and changes to lipids as well. So you can imagine that creates a lot of work for an office tracking down those patients.

If you look at the S1Ps that are approved, different category right, and MS baseline labs are normal and required for all of those patients. But there is no recommendation for ongoing monitoring for S1Ps. We think that’s going to be an important difference in the market. We think that makes the molecule more attractive to physicians and to patients as well, and it’s something that would be advantageous relative to a JAK inhibitor.

Amit D. MunshiDirector, President and Chief Executive Officer

I’ll just said, broad hematologic changes, which are directly corresponding to serious opportunistic infections that’s just not what we have seen with the etrasimod in S1P modulation. Decreases in lymphocytes are an on target activity, but they don’t correspond to severe opportunistic infections. So, there is no real pressing need to monitor it on an ongoing basis. In a clinical program you do that. We do that in the GI space and, of course, we don’t see the discontinuations, we don’t see the discomfort there, because we’re not seeing the infections. And now that we have this data, now that we can confidently speak to clinical trial sites, about the fact that the drug is safe, it’s effective, we think that will go a long way toward building the Phase 3 program and making sure we have a strong competitive label.

Robert LisickiExecutive Vice President and Chief Commercial Officer

Yeah, the other one I forgot to mention and I apologize is, herpes zoster, you heard Chris mention that there were two cases in the placebo arm. One of the challenges that the JAKs have, particularly in these AD studies is, high-end balances, high rates of herpes zoster, sometimes five to ten-fold higher, which can be disseminated, quite challenging for patients and for physicians as well. So not seeing that, and albeit a small Phase 2 study is encouraging.

Patrick TrucchioH.C. Wainwright & Co. — Analyst

That’s helpful. Thank you very much.

Operator

And there are no further questions. I will now turn the call back over to Amit Munshi for closing remarks.

Amit D. MunshiDirector, President and Chief Executive Officer

Great, thank you. I want to start by thanking our team internally for the tremendous effort across the entire pipeline this quarter and the tremendous commitment while we all work remotely and work from home and deal with lots of external environment-related issues. I also want to take this opportunity to thank the investigators involved in this trial, the patients and all the people involved in executing this program. We learned a lot through this program. We are incredibly excited to move to Phase 3 and we look forward to sharing details of our future plans with you on upcoming calls. So, thank you again everybody and stay safe.

Operator

[Operator Closing Remarks]

Duration: 70 minutes

Call participants:

Patrick MalloyVice President, Investor Relations and Corporate Communications

Amit D. MunshiDirector, President and Chief Executive Officer

Chris CabellExecutive Vice President, Head of Research and Development, and Chief Medical Officer

Robert LisickiExecutive Vice President and Chief Commercial Officer

Laurie Stelzerxecutive Vice President and Chief Financial Officer

Jason GerberryBank of America Merrill Lynch — Analyst

Alethia YoungCantor Fitzgerald — Analyst

Thomas DealCredit Suisse — Analyst

Kennen MacKayRBC Capital Markets — Analyst

Jessica FyeJP Morgan — Analyst

Jason ButlerJMP Securities — Analyst

Yatin SunejaGuggenheim Securities, LLC — Analyst

Joel BeattyCiti Investment Research — Analyst

Joseph SchwartzSVB Leerink — Analyst

Jim BirchenoughWells Fargo — Analyst

JoeyNeedham & Company — Analyst

Patrick TrucchioH.C. Wainwright & Co. — Analyst

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