Rich Rubino - Chief Financial Officer Vince Anido - Chief Executive Officer Thomas Mitro - President and Chief Operating Officer

Adnan Butt - RBC Capital Markets Annabel Samimy - Stifel Nicolaus Serge Belanger - Needham & Company Caroline Corner - Cantor Fitzgerald Difei Yang - Brean Capital

Thank you, Laurel. Good afternoon and thank you for joining us today.

With me today are Vince Anido, our Chairman and Chief Executive Officer; Tom Mitro, our President and Chief Operating Officer. Today’s call is also being webcast live on our website, investors.aeriepharma.com and it will be available for replay as indicated in our earnings release.

Please note that in a new minutes Vince will be reviewing slides that accompany this call. They were posted on our website shortly after 4 PM Eastern Time today.

Now for forward-looking statements and non-GAAP financial measures. On this call, we will be making certain forward-looking statements, including statements and forecasts regarding our future financial and operating performance, including projected cash burn, the success, timing, and cost of our clinical trials, the clinical effectiveness, commercial launch and potential future sales of our product candidates, the potential of our new research findings as well as other statements related to future events.

These statements are based on the beliefs and expectations of management as of today. Our actual results may differ materially from our expectations.

Investors should read carefully the risks and uncertainties described in our earnings release as well as the risk factors included in our filings with the SEC. We assume no obligation to revise or update forward-looking statements whether as a result of new information, future events or otherwise.

Please note that we expect to filed our 10-K on/or about May 8, 2015. In addition, during this call we will be discussing certain adjusted or non-GAAP financial measures.

For additional disclosures relating to these non-GAAP financial measures, including our reconciliation to the most directly comparable GAAP measures, please see today’s earnings release, which is posted on our website. As a quick financial update for the quarter, first quarter 2015 net loss attributable the common stockholders for the three months ended March 31, 2015 was $17.2 million or $0.70 per share.

The net loss reflects proceeds of $2.9 million for the first quarter 2015 from the sale of the New Jersey State tax benefit which is recorded as a benefit and other income expense net. The net loss also includes non-cash charges for stock-based compensation expense of $2.7 million when excluding the non-cash stock-based compensation expense adjusted operating expenses for R&D and G&A totaled $11.1 million and $5.8 million respectively for the first quarter 2015.

Total adjusted net loss was $14.5 million for the first quarter 2015. The $14.5 million in adjusted net loss were $0.59 per share compares to $4.7 million for the same quarter in 2014.

During the first quarter 2015 we raised $35 million from the issuance and sale of common stock under an aftermarket sales agreement pursuant to a shelf registration statement on Form S3 filed on November 3, 2014 and burned $16.7 million of cash. The first quarter 2015 cash and marketable securities ending balance totaled over $179 million.

With that I'll turn the call over to this Vince.

Thanks, Rich and good afternoon everybody. Thanks for joining us today.

As you know we recently completed our initial or classified three registration trial which we called Rocket 1 and announce the trial didn’t meet its primary efficacy endpoint. As a reminder this is the first time the triple mechanism of action drug has been study for glaucoma, and certainly the first time the drug has been study that treats the trabecular meshwork.

As a result every study provided further inside are uniquely the drug does work. In this study Rocket 1 we have gained far more inside across the spectrum of attributes to this drug and we believe that meaningful potential for both Rhopressa and Roclatan.

Some of the findings validate things we known about a drug since Phase II trials and we will talk about that in just a second. And some of them are really findings that are bit surprising and we'll talk about those as well.

Since the initial release of Rocket 1 results a few weeks ago the team is that a substantial amount of analysis that we believe starts to add meaningful insight into Rhopressa’s performance in that study. Now I want go through the slide deck is up on our website and then when I try to remember to actually tell you what slide number I'm on so that’s you can follow.

I am going to start in Slide 3, just background because there are number folks on the call with perhaps have not story before. Rocket 1 was one of three registration trial so we had in the marketplace over the last year or so it is a 90 day efficacy trial we reported results on April 23 of this year.

We also have Rocket 2 and will be talking about that little bit later Rocket 3 is a safety only study that's been done in Canada and its going to be the supplementing some the work that in some of the information that we get out of Rocket 2. As you know we study these drugs for the treatment of ocular hypertension in glaucoma and it was non-inferiority trial of our drug versus timolol over a 90-day period.

We also looked at the ocular systemic safety of our product over that 90-day period. On Slide 4, gives you just an overview of the trial design, we actually looked at 411 patient randomized over a 36 different clinical sites and we ended up with 370 patients are subjects for the protocol.

The next Slide number 5, we looked at the early terminations and we had little over 10% terminations in the overall trial many of them on Rhopressa and about a third of that on timolol. Most of the protocol violations withdrawal of consent like efficacy, investigator decisions et cetera are pretty balanced between the two drugs on the adverse events.

Many of you have asked about that so that the bottom of the slide we have included the adverse events for Rhopressa that ended up leading too early terminations. As you could see there is only three of them were actually we had – each had two patients and by the why some of these actually the same patient had more than one adverse event that accounted for their early termination, but really it’s just a smattering of different things, there is not general pattern here.

Many of us currently thought that we would see terminations dealing because of hyperemia which is the major adverse event we had reported in Phase II trials, but as you could see only one patient actually withdrew or early terminated because of the hyperemia. As a reminder on Slide 6 are the study endpoints, we looked at mean IOP at the 08:00, 10:00, and 16:00 hours time points during the day and we look at them three times during the 90-day study.

We looked at them at the end of week two, end of week six and on the 90th day. We also had a number of secondary efficacy endpoints that we were looking at and probably the most significant one as it relates to the trials the fact that we did have in our statistical plan a secondary endpoint for looking at patients and results below 24 millimeters of mercury and we will talk about that in just a second.

As you saw on Slide 7, we did not achieve our non-inferiority to timolol and that was for all patients that were enrolled in the trial below 27 millimeters of mercury. The non-inferiority that we saw was really driven by a number of patients that appear to loose efficacy over time and roughly 20% of the patients on Rhopressa did that.

So we are going to talk a little more about the results that we saw. On Slide 8, as a reminder when we saw the results at below 27 where we did not achieve non-inferiority and then we saw the secondary endpoint at 24 and below where we did meet it and we also gotten a medical superiority at all nine time points.

We started slicing the data by millimeters were we had enough patients so millimeter cuts. So the first cut was below 27 to 26, 26 down to 25 or below 26 down to 25 and so forth.

As you could see from the slide it was only at the upper 1 millimeter range that we did not meet the non-inferiority time point or the endpoint as established by the FDA guidelines. Everywhere else we did it and as we suspected the majority of those and certainly below 24 and 23 we hit all nine time points on a superiority metric.

And so we were very pleased with the results certainly below 26 millimeters of mercury and just wanted to provide this perspective as we go deeper into the data. As we have visited with roughly about 60 different investors over the last week or two and many face-to-face and also many phone calls as well as with the analyst and really had to summarize the questions we are getting into these five bullets.

The first one was dealing with the Rhopressa, intraocular pressure lowering dynamics. What was really happening that caused some variability in the results and people wanted to understand that better, so we are going to address that today.

Many folks wanted to understand exactly what happened at that 1 millimeter cut where we missed the primary endpoint and why were we so successful below that. Obviously folks are interested in what’s going to happen with Rocket 2 which we’ve talked about publicly before getting a readout sometime in Q3 and then we have talked and liked about the need to do another trial in all likelihood, we are calling that Rocket force, so will give you an update on our thinking about that.

And then many of you because a lot of folks out there believe the Roclatan is far more important drug for us than Rhopressa I’ve been wondering about the impact of these results on the future Roclatan so we will address that as well. So as we look at the first full destination of sort of what's been going from the efficacy point of view certainly as we look at week two and then on month three.

I am going to take you back to the chart that we have been showing for below 24 millimeters of mercury. As a reminder this is pre-specified analysis you could see at the top right the number of patients that we had that were in this slice of data that is all patients below 24 millimeters of mercury.

I am going to draw your attention to the extreme left hand column. We haven't spent a whole lot of time talking about this, but I want to emphasize this one for just a second that is the pre-study intraocular pressure.

Patient came into the study and prior to entering the study we are on a prostaglandin and on a alpha blocker or beta blocker everything cetera the pressure was somewhat under control so we put those numbers in there. There also we had a roughly I think around 20%, 25% of the patients were [indiscernible] so we included their entry pressures there because again there are no medications so we can do is put on enter pressure.

So here are enter pressures were somewhere around 80.5 to 19 millimeters from Mercury for the all the patients pre-study we then washed them out they had two qualifying visits this is the first one 8 AM time point so when we do and after that they came back in for a second qualifying visit and so we can establish our baseline at 8 AM 10 AM and 4 PM on the same day disease or that the normal chart there not only for our patient but also for timolol. So this is where it gets fun.

So for us we start looking at that 18.5 millimeters, 19 millimeters pre-study and realize that independent of which IOP cut we took almost every time by significant amount despite all of the ups and downs we saw with the efficacy of our drug we ended up doing better than the pre-study IOP. And so that led us to believe the first of all we are very excited about the fact that we do have a once a day medication here.

And it does control pressure now we just need to understand sort of mechanistically what it's doing and why we had some variability and some of the patients. I pointed to a week two buy far if you look at all the data that we generated we to our drug as far more efficacious not only the timolol but far more efficacious than the drug itself and the other time point.

So we spent a lot of time trying to understand what was happening here because many of you have expressed the concern that perhaps we were losing efficacy and certainly if you draw a line from the 8 AM time points it looks like that line continues to go up, but that we have not seen that before in terms of lost of efficacy so we wanted understand again why did we have this drop and why do we consistently again almost that every IOP cut that we have the same curve occurring. So we spent a lot of time looking at that.

And after we did all of the analysis that we can possibly think of at the end of the day we found something that we think explains what is this event that is occurring in that day 15 timeframe. We had a pre-specified, again pre-specified analysis already built in our statistical plan looking at patient who came into the trial on prostaglandin versus everybody else and reason we did that is because we did see a trend here in the Phase II trials where it appeared that our drug work better when a patient was a prostaglandin.

So we did take those cuts on this Slide number 12 what’s you see here is only those patients who entered the trial where there prior drug was prostaglandin. And as you can see we compared it timolol and in the same conditions by both of them started out by around 21 millimeters from Mercury at baseline on the Meandiurnal and you could see the dramatic drop that our drug cause and day 15 you can also see that four timolol is pretty much flat as a board.

You also see that our drug continued to come up a little bit so and then levels off at around 16 millimeters almost 17 millimeters from Mercury so a little bit below what we saw the timolol. So we think that what we’re seeing here and is consistent with what we have seen in other studies and Phase II trials is there appears to be tremendous synergistic effect between our drug and prostaglandins and you we think that what is happening here it is not that there's still prostaglandin's in the system because these patients were washed out for a least four weeks.

We think that the prostaglandin therapy in these patients basically sets the outflow mechanisms and in both the primary drain the trabecular meshwork goes well to secondary drain I think it sets them up and oversight them in just washing it out doesn't get rid of that sort of it almost preps the waiting for something else to hit it and so when we introduced our drug to these patients we see an almost immediate just a very solid bottoming out of the pressure. And we see that over time that sort of setup that is occurring in a prostaglandin patients had to diminish a little bit is still a little bit there when we look at that the end of week six for the day 43 and so by the day 90 is pretty well gone.

And so we can stabilize the reason were convinced that this is exactly what is happening this is due to prostaglandin patients who were on the patients were on prostaglandin prior to coming into the trial is when you look at Slide 13. This is the same kind of data, but only looking at patients were not prostaglandins so these are patients who were on beta blocker, alpha blockers, combigan are some combinations et cetera.

And as you can see here we still have the same dynamics in the sense that they were started out about 21 millimeters from Mercury you see that both for us and for timolol the board so it doesn't have that variation that we see are the proceed variation we see in the efficacy. So if you toggle back and forth between Slides 12 and 13 you begin to understand sort of the importance of this.

As I said earlier this is the first time we studied a drug that actually treats trabecular meshwork in this many patients and certainly one that has two other mechanisms on the top of that. And so this is the first time where we've been actually able to show that we have this unique synergistic effect with prostaglandins that is not present with timolol and we don't think it's present with any other drug because as we’ve searched literature and we don't find that internally as we look at the – at the result of various clinical trials we don't see that.

And so the other thing that I want to point out as if you take a look at day 90, which is the dark blue line for us you see that on prostaglandins we ended up with a pressure of 16.7 millimeters. And if you look at the next one on the non-PGA patient it was 17.1.

So again we’re very, very pleased with how low these pressures got. Even though the patients were all below 24 millimeters of mercury, but we think that this affect that is the prostaglandin effect and synergistic effect that Rhopressa has with prostaglandin is what is causing this appearance of loss of efficacy over time.

And the fact is when you look at day 90 these patients intraocular pressures are very well controlled. I do want to point out that this happens across all time points and so I did take Thursday to end here for the first time on the next time point out which is below 25 millimeters of mercury against you see the same dynamics if you look at the pre-study IOP here they were a little over 19 millimeters.

And you see how well we kept it down, and then we kept it down well below that throughout the time on this trial, you see again the day 15 effect which again we believe is driven by prostaglandins and again it gets a little bit washed out if you will or dissipate over the other time period of the study. Next slide 15 just basically gives you the actual numbers we want to make sure that everybody had the same dataset with the on the below 25 that we gave you earlier and prior slides in – for the group below 24.

But again it just shows a consistency of the effect. Slide 16 again the same two data cuts below 25 millimeters of mercury those patients on prostaglandin had a dramatic drop in their intraocular pressure if prostaglandins were again loaded in or that was their prestudy drug.

Again you don't see any effect or any synergistic effect between timolol prostaglandin, but sure do see in between our drug and prostaglandins. Likewise, next slide which is Slide 17 when they’re taken off, when they don't have prostaglandin on board so again they are alpha blockers, beta blockers et cetera.

You see that the pressures are relatively flat, you see some ups and downs in all the studies and so these are pretty much within the noise levels of all the studies. So again we’re very, very pleased with these findings, we do think it explains the mechanism of the drug and why we’re seeing this perceived loss of efficacy.

But in fact we think is just a dramatic synergistic effect between Rhopressa and prostaglandins and so we think as data proves it. As a reminder on Slide 18 this is the summary it is this was prospectively defined analysis we had seen this before if you go from the first bullet to the last bullet, you will see that we had identified this in a Phase II trial as part of a retrospective analysis where we did see some signs there.

All we thought was that sign or that signal that we were picking up was going to help us in Roclatan because again we were looking at combining Rhopressa with a prostaglandin. But we didn't realize how big of a deal this was in terms of the IOP drop until we saw, so it matched with a drug that doesn't have a synergistic effect with prostaglandin I mean timolol.

And we saw how dramatic of a difference in terms of efficacy that occurs. And so as a result we do believe that the PGA effect is lost over time it does create a false impression that Rhopressa losses efficacy over time.

We do believe that based on this information in comparison to the non-prostaglandin patients, we do have the synergy here against a synergy not seen in any other drug ever before. So I think this is a unique thing for us that again bodes very, very well not only for Rhopressa in terms of adjunctive use as a standalone when prostaglandins already loaded onto the patient, but also in combination when we study Roclatan.

So the next thing that I’m going to address is sort of what happened at about one millimeter so from 26 to below 27 millimeters of mercury as you know we had an awful lot of noise in that data, unlike so we spent a lot of time trying to understand that. As a reminder on Slide 20 the majority of drifters were in fact that upper 1 millimeter cut where we had 18 of them in fact on Rhopressa arm a little over 40% of the patients were - they were enrolled just this 1 millimeter cut were actually what we consider drifters.

And on top of the slide you could see that we consider drifters anybody who had a greater than a 3 millimeter increase in intraocular pressure from week two all way up to month three. Putting up slide the next Slide 21, which is the IOP below 27 millimeters of mercury again just put it in perspective again you can see that was not as good as some of the other slides in terms of how well we did in controlling pressure then in all these points we were still below the entry of the pre-study IOP's that this - the patients entered this study with.

So we saw some pretty good efficacy again we saw the day 15 effect that I've already talked about remember a lot of these patients were on our prostaglandin therapy in fact if you look at the entire trial well over 50% of the patients were on prostaglandins and that’s not real surprise that’s what we see out in marketplace. Not surprisingly we remove the drifters, those who didn't respond we get pretty good efficacy here and pretty good just a straight line across the 8 AM time points and so again our focus here was understanding why we got 18 out of our 36 drifters in this particular slice of date.

And what we found was is as following which is Slide 23. We found that on average those patients who drifted were about 1 millimeter higher in pressure than the patients who didn’t drift.

We also saw that the duration of their disease that is the time from diagnoses either for ocular hypertension or glaucoma was about three years longer on average and some of them extended well beyond that. The other interesting finding we didn’t put it up on slide, but it was a pretty interesting from my perspective is you saw that the drifters had been changed - had a change in their therapy more recently that all the non-drifters prior to entering the trial.

So we thought that was an interesting part of finding and again when we see based on that bit of an information that I just shared is potentially one difference between the drifters and a non-drifters is that maybe they had more severely diseased trabecular meshwork and if our drug works on a trabecular meshwork it’s a primary mechanism of action perhaps we don't get the efficacy in some of these kinds of patients. But what’s surprising is how variables are intraocular pressure was we started looking at each patient individually because we only had 18 of them so we could do that pretty easily.

What we noticed is that over a half of them actually had fairly significant drops in pressure inside the day-15 and then it vary after that. Some went up and actually some went up and really hard I mean they went up three, four, five millimeters and then they came back down and so there is an awful lot of variability here that we saw.

The other thing that we saw and because we done a number of different studies and some of these sites are repeat sites for us, we were able using the analytical tool that we have to obviously on a friendly basis be able to identify a number of patients who had participated in some of our prior Phase II studies that were also part of our Rocket 1 studies and so I am going to show you some data that we were able to collect on those patients just to show you how variables some of these higher pressures could be. And interesting finding force was that of about two thirds of the total drifters came from five clinical sites to represent really only about 20% of all patients enrolled.

So as you can imagine we are going to be spending an awful lot of time and those sites trying to understand why there is so much variability there [indiscernible] and not others. We did and we talked about this before, we actually got everybody’s bottles back and what we found was the retired non-compliance rate about 28% on the drifters versus about 13% for the non-drifters and so I’ll walk you through some of that data.

And we did have a slight discrepancy on the PGA use, we had slightly higher PGA use in these higher IOP patient. That's not surprising when you look at the market overall, but in terms of our study it’s 66% for the drifters versus 50% for the overall patient population.

Next study, Slide 24 – next slide 24 is basically talk to you about the data that we have about patients you participated in number of our trials. We had a total of 71 patients in Rocket 1 who had been prior patient in one of two Phase II studies that we did.

Some patient actually responded them actually were involved in two of those trials and some just in one or the other, but as you could and this talks to the variability of the IOP measurement systems level. For Rocket 1 they came in at 8 AM on average about 24 millimeters of mercury was really in pressure they get in the prior study.

So again with the matching that we’re able to do with our tool with you see that they came in somewhere between 26 and 27 millimeters of mercury. So when you have a 2 to 3 millimeters of mercury swing and then you are showing a patient that is sort of moving around in their IOP throughout the weeks of the study you are not really sure here which of these IOP is true and which ones we really should be comparing ourselves against and so it does show some fault in the upper end of this trial, and certainly we think that there is ways of fixing that as we move forward in additional trials.

The next Slide I am showing you a little bit about the compliance here we talked about those patients who only missed their evening dose and the importance of that is whenever a patient enter the randomized they got a kit, each kit contained two bottles – AM and PM and the patient who didn’t make any difference whether they were on timolol or whether they were on our drug. If they are on timolol both bottles were active and our drug only the evening does was active and the morning dose was placebo.

And so that's why we focused on those who miss more than 35% of the evening dose and there's what you see that the difference is non-compliance, we had 13% for the non-drifters versus more than double that for the drifters. And the importance of this as it relates to when the patient show up.

Our drug if you take it night by the time you get up in the morning and you come into the doctor's office you can see a little bit redeye. But if you take a drug holiday so if take it 15 days let say and you get great results and say well in don’t you need take this drug every night in fact I don’t like the fact that gives me a little bit redeye as they use the morning dose because that's really just placebo because it doesn't make my eyes red.

Well if they realized the next day they're going to go in to see the doctor they may take their night dose again so they show up in a morning and have a little but a redeye the doctors and to be concerned because these aware that hyperemia is a hallmark sign for our drug. So you think okay compliant patient et cetera.

But it's not getting impact the intraocular pressure one takes the drug holiday off of our drug and goes back on that eighth two or three doses – two or three night doses for the kit bag in the high gear. So this is something that we think is playing out here and certainly account for some of the variability that we saw.

So the overall as we look at Rocket 1 observation we think that the right thing to do is focus on those patients that are either below 24 below 25 millimeters from Mercury, clearly we had some great efficacy results here especially as related to those patients who were on pre-study prostaglandins and we saw that as we compared those to those who had no prostaglandin therapy or something else we had great results. We do think that the prior PJ users and residual PJ effect does enhance the Rhopressa IOP lowering creating a false depression and loss Rhopressa efficacy.

And certainly we think that the drug here is a clear once day drug and that the we are very, very excited about looking forward. We think the potential synergistic effect of prostaglandin so along with Rhopressa is a major positive not only for Rhopressa but certainly speaks very highly and goods great hope for Roclatan.

So with that I am going to switch gears and talk merely about Rocket 2 we do have FDA meeting that we’re trying to schedule right now and we’re trying to get the IOP range lowered for the primary efficacy endpoint either 24 below 25. There is president with entomology for doing this before locking the database and so was IOP 10 which is a [Santan/Merck] drug for glaucoma which is approved in February 12 is the major indicator for this and nice thing about this is.

That in their summary basis of approval you could see that the FDA actually recommended to them that they actually switch to a different endpoint prior to locking the database. And so we think there is present for us to be able to do this.

Now the outcome for our switching is not only dependent on the FDA discussion we want to make sure and we’re talking to the analyst about statistician make sure we have enough power either below 24 below 25 in order to proceed with making that are the range for our primary efficacy endpoint. As many of you know who understands statistics the various ways of looking at statistical analysis here our preferred methodology is looking at hierarchical approach where we look at QD first and then BID comparing that timolol.

As opposed to doing them sorted both in parallel taken [indiscernible] correction for the analysis and like. We do think that the both below 24 below 25 we are powered appropriately for the hierarchical approach however what we’re going to do is hold off on our final decision as to whether working enroll additional patient in the Rocket 2 until we a little bit more clarity from the FDA about switching the endpoints because they may not be necessary for us to switch endpoints, I am sorry the switch statistical methods or pick a statistical method if the FDA agrees to the lower endpoint.

So again we feel pretty comfortable with the data that we have we feel comfortable with the president about switching endpoints and so we hope the two I mean with the agency relatively soon we have already talked and trying to move the agenda around the one of our prescheduled meetings that we have on the upcoming months and so we do expect that this information will be completed over the next couple months or so. As a result assuming that that we don't need to increase enrollment and for Rocket 2 we continue to expect that the efficacy resolve read out to be some timing in Q3 and if we do have to increase enrollment we don't think it's going to delay is by more than roughly a few months and so we do expect that will have - worse case will have data on Rocket 2 before the end of the calendar year.

Now as I've mentioned before regardless of which scenario we look at. We do expect that we are going to need another clinical trial for Rhopressa so we are planning on Rocket 4.

So for example if we are successful in moving the efficacy for the primary efficacy endpoint on Rocket 2 to a lower baseline will then have and we hit that will have an efficacious clinical trial in Rocket 2 we will have supportive clinical trial in Rocket 1 with a secondary endpoint below 24 and we think it's enough to go ahead and file. However we want to make sure that and I'm perfectly willing to bet it will just get in some notices as well of final approval will be a based on the review of the data and so what we want to do is go ahead and for about $10 million or $12 million go ahead and start Rocket 4 as soon as we can we think we can be in the marketplace by Q3 of this year the primary endpoint will be the same it will be non-inferiority timolol across nine time points looking at day 90 baseline of either below 24 below 25 depending on discussions with the FDA but will also look at bunch of the secondary endpoints light and looking at a higher IOP range in below 27 or so.

And potentially making it not only a third 90 day for primary efficacy but looking potentially at six-month efficacy as a secondary endpoints as well. We do expect to Rhopressa NDA in the first half of 2016 yes we don’t need additional patients are Rocket 2 or again if we don't need to wait for Rocket 4 results.

If we have to wait for one of the other we do expect and that the NDA would be filed sometime towards the end of 2016. Now last but not least before I turn it over for questions on Roclatan we do think that the news that we have today that we share with you earlier about this great synergistic effect that we have with prostaglandin the Rhopressa ahead of prostaglandin is incredible news for Roclatan as you know we were planning three registration trials two of them here in the U.S.

and one in Europe I was called Mercury series. Our plans right now are that we are going goes fastest as we can and start enrolling Mercury 1 sometime in Q3 of this year.

We are still looking at some of the data out of Rocket 1 and going back into Roclatan Phase II study to make sure that we have the right IOP range for this particular trial again I think you think about a dumbbell words got two and that are equally balanced I really think we need that enroll patients of the upper end of the ranges as well as the lower end of the range. So we may end up having to stratify enrollment above and below some midpoint.

The trial design there will be superiority of Roclatan versus each individual component. Again as soon as we are able to free up clinical site will immediately after that start enrolling I am sorry Mercury 2 and begin the European trials as well.

So in summary we think we've been able to show a lot of brand-new data then we think we've answered a lot of the questions we set out the answer for you that came out over from the feedback we've gotten over the last couple weeks. So with that I am going to turn it over to the operator for Q&A.

Thanks for taking the question and for the details. Let me start with the couple, first in terms of the prostaglandin analysis that you will seen – that seems to happen to need and then kind of – is that is there mechanistic explanation for that and then which ask the publisher had what for prostaglandin what the resolute time and after patients come of with that.

We don’t think that I can’t remember exact half-life-we don’t take its much more than 24 hours or so. Again we seen the data in fact that are own clinical trials where you know after you quit taking latanoprost as an example after about 36 hours or so the IOP start rising again and I suspect that you see that continue to raise I don't think the effect here that we see in day 15 and sort of trickling in today day 43 is really that there is any latanoprost left in the system.

I think that was happening is long-term latanoprost use actually somehow or other activate these outflow mechanisms and that maybe that the ciliary tissues et cetera. And basically provide to setup for another outflow drug like ours.

And so again I don't think it's of latanoprost because I know if you take a look at the FDA guidance for washout it is a four weeks the majority of the studies that look at prostaglandins is being in their they do wash them out for four weeks we saw a couple of the wash them out for a six most extremely saw with European publication and recommended eight weeks. But we just don't think that it's the half-life it's keep latanoprost is too short to worry about, but I think it's just simply that the tissue that were talking about in terms of outflow is somehow or other setup for another outflow drug and so we’re obviously going to be spending a lot more time because there perhaps what this indicates is that you know maybe that there are something that we haven't figured out yet relative to may be our ability if the tissue is sort of set up to activate a little bit more of the [UV-Vis] for example.

But certainly what we’re really focused on here is that we do have the synergism and that we certainly saw that in the Roclatan Phase II data when we have both of them on board because we got results that we hadn't seen before with any combination with prostaglandins. And so, but again I don't think this is latanoprost or prostaglandin hanging out is just the tissue is set up for.

Okay, Vince and I think you said it’s versus the – just for prostaglandin versus non-prostaglandin, not for the individual different process?

I'm sorry, ask your question because you…

Was the comparison just sort of prostaglandin versus non-prostaglandin or you look that data blockers Carbonic Anhydrase Inhibitor 53 as well.

We lump sum them all in the prostaglandins and then all others plus naïve patients.

Okay, and a follow-up on Rocket2 - have you heard a chance to look to see what’s based on IOPs order in for patients in that study at this time and what’s the thinking behind the side in less than 25 or less than 24. And you’d let us know when the FDA gives you final from that design change?

That’s it.

The answer to your last question is yes we will, as soon as we get an agreement with the FDA not only in terms of the final IOP, but also statistics plan et cetera – or at least the statistic guidelines et cetera that we’re going to using, we’ll certainly let you know the idea of using below 24, below 25 is because we think the data is generally the same. The action of our drug relative to timolol was basically the same exact same characteristics there.

And so we think that the FDA may want to take a look at it and obviously they will have an opinion about how low we should go or whether we should go up a little bit. So we want to just be flexible and we don't want you and investors to be surprised if instead of 24, below 24 we end up picking below 25.

Okay, Vince. And then have you had that chance to look at enrollment in Rocket2.

We have. And so Rocket2 is still treating patients and so what we don't have, we have some estimates, we have some forecast in terms of things like the dropout rate and things like that we can look at anything by per arm.

We can look it only in aggregate, and so we have some idea in terms of sort of how things are coming in, but it’s just aggregate we don't know how it breaks out by any one individual arm. And so we think we’re okay from an IOP point of view as I mentioned.

We think we are okay from a powering point of view if the FDA agrees with us and we can use the hierarchical approach versus using a [Bonferroni] corrected one. And so but again it all depends on the final discussions with the FDA and so that's why from our perspective we think the right thing to do is to be prepared to add more patients, we think we can do that in a very, very short period of time, so that you know worst-case we’re delayed in reading out Rocket2 if we have to add more patients the readout will only be delayed by a few months.

Okay, thanks.

Yes, sir.

Hi, so thanks for all the explanations. Just while on the topic of Rocket2 and what you can look at right now.

So you mention that you feel that you have enough patients to be appropriately empowered I guess for that 24, 25 population. But you said that you don’t have information on the arms.

So how will you know if you have the right powering for the 2D arm? I guess I am a little confused how you get all this information?

Well you haven’t made some educated guesses about the data right, so for example we know what the general dropout rate is. And so the easy one is you just average out by arm and you sort of figured it that out.

So that’s relatively conservative because we think and we’ve said this before. So it's not new news, we think that the Rocket2’s BID arm is going to have more hyperemia so it wouldn’t surprise us.

That we have more dropout rates, we already know so but our dropout rate was in Rocket1. So we could assume that any deviation or changes between Rocket1 and Rocket2 are primarily driven by the BID arms.

We can make those kinds of inferences but again at the end of the day it's - we can't really look at that data or all we can do is make sure we have enough power to withstand shift in any one of the arm. And enrolling up patients we can withstand those shifts.

And so that’s why.

Sorry, go ahead.

No, that’s right. That’s why we’re looking enrolling more.

Okay. And when did you have a timeline when you are speaking to FDA?

We do it will be over the next couple of months, it will be a series of discussions, we've already started talking to them. We send them data, we’re going to send them some more data based on what you saw today.

And so that will just generate the discussions we have multiple meetings already on the schedule for either Rhopressa or Roclatan with the FDA. We’re just trying to find the best one in order to slide in significant discussion with them about switching the range for the primary endpoint of Rocket2.

Okay.

So we don’t have a firm day yet and we won’t release anything like that I’ll give you the final answer, but we won’t tell you when that date is.

Okay, so going back to the whole PGA effect that you are talking about, so if you have this benefit initially and then this benefit kind of goes away by three months. So what does this mean clinically for you?

All right so you end up with the drug that seems to be generally in line with timolol, so is there some clinical benefit that these patients would have getting that initial PGA response and then seeing a washout over time. So I’m just trying to understand the meaning of this?

Okay, that’s fair. So what this indicates is the following almost every patient in the United States today that has glaucoma, Rocket or hypertension has prostaglandin as primary therapy.

With this data show is that even when there is no prostaglandin on board that are just remnants of the fact that leads like an imprint that it was there. Our drug is very synergistic, so what that does with the data show is that we can then safely conclude that when a prostaglandin is on board that we do have a synergistic effect so you'll see better efficacy either additive when you have a prostaglandin patient and you add Rhopressa to it and you should see better effect there than what you currently see when you add either alphagan or whether you add timolol or any other additive drug and then also it should be beneficial when you had put them both in one bottle and you have latanoprost plus Rhopressa and Roclatan and then you put that in your eyes to see a fairly dramatic improvement over and above anything that's available today.

So that’s the clinical implication.

Okay, so this would bode well nimbly before Roclatan.

And it does bodes very, very well for Roclatan, but don't discount the fact that what this shows to for the doctors out there is that the incremental benefit they are going to get on the prostaglandin patients if they add rhopressa.

Okay and then just on the theory of the PGA timing on this meshwork are the drainer system. Have you pass this by anyone in your scientific advisory board or any of these physicians that they could validate that there is some kind of mechanistic timing going on?

Yes, so our CSO has actually talked to a number of trabecular meshwork people and the like and so do we think that there are certainly sort of some scientific rationale for this. The real issue is that there's never been a drug is been able to do this with prostaglandins and so a lot of them are looking at this thing and saying Bob never seen this before.

And it's not surprising because again when you look at the data cuts that we saw versus us versus timolol on prostaglandin patient you just didn't see this synergistic effect. And so this is one of those things that I mentioned earlier when we’re talking about a brand-new mechanism.

Folks are setting sort of scratching their heads saying that I've never seen that before, but it is real when you cut the data. So I would digging into sort of the hard-core science to really come up with sort of what could be happening here, but the data not only here, but also in our Phase II and it was hidden because we are using latanoprost as our comparator, but it was there.

Okay, and if I can just ask one more question so you gave us some pretty decent explanations about the drifter characteristics. So I guess what I’m wondering is when you enroll a glaucoma trial are these characteristics that you can end up controlling for any and I mean doesn’t everyone sort of conducted trials in the same way and have these other trials had this level of drifters in their population relative to what you’ve seen and how do you control for that in the next trial I guess.

So there are drifters for both timolol as well as latanoprost and you see timolol in the 5% to 10% range in drifters and sort of you see latanoprost in the 5% to 6% range or so. So you do see them and I think the biggest issue that we face in this trial as was explained to us by our SAB is that this is the first trial anybody can remember were the upper limit of IOP's were kept.

Typically they are open-ended or if they are kept they are up to 36 and just not very many patients up there. So the effect that we saw that I showed in the slide of some patients who got into the study with what appeared to be precious about 24, but in prior studies they were up to 26 and 27 you just don't see that if you're upper end is 36 because there is just not that many more patients.

And so we think some of the discrepancy that we see here is that, we think that we should be able to figure out whether there is things that we can do for these patients in terms of the compliance because again as we dig into the date on these five sites we can get in pretty quickly and pretty deep and see if there are things that we can do from a compliance point of view. We did not try to in any way control for compliance, we didn't do any patient calls, we didn't do any reminders, we didn’t give them anything that you can, so we can be bad among their cell phones and remind them that it was time to take their meds.

And so but I guarantee you and Rocket for we will

Is that done another trial?

In ophthalmics not so much but certainly everywhere else it's been done.

Okay, thanks, I will get back in the queue.

Yes, ma’am.

Hey, good afternoon just a couple questions. First on the PGA synergistic effects you saw I guess in Rocket1 from the data you showed that almost half the patients were on prior PG treatments.

Do you expect the same amount of patients in Rocket2 to become an half PGA?

That's a great question. Because, the half the patient being on PGA is sort of consistent with what we see on the prescription activity.

So yes, we think that that makes all that sense in the world that we would expect to see roughly half of the patients in Rocket2 and then again in Rocket4 we conducted to be former PGA patients

Okay, so in Rocket4 you plan on enhancing this synergy and doing all patients come in off PGA?

No I will be controlling for that because the FDA really wants to see how this works across all patients, but certainly you can imagine that just like we did in this trial we will have a separate pre-specified analysis of that data showing again the PJA versus the all other category.

Okay. And then just I guess a follow-up on the prior drifting question, you showed there is a lot of variability in terms of the response some go up, some go down.

Is there really a way to do screen for these drifters beyond just the compliance?

So, some of the data that I showed you would indicate that some of these patients got into the trial well above the 27 millimeters of mercury that we said they had to be, some of them are 28, 29 or so. So when we think about some of those patients quote drifting they could have a 2 to 3 millimeter drop simply because on the one day they came in to get tested or the two days they came in to get tested for our study, they happen to be pretty relaxed and their pressures were lower.

And so what we call drift is really to start drug working but of their real baseline not also the baseline that they came into this study's with. So one way to control for that is really the only way we could do it, is we could enter a trial where we have a higher IOP in the upper end say 30.

And so we enroll all patients all the way up to 30 we stratify sort of between 30 and 20, so you know we get as many patients about 25 and below 25. But then for the analysis I don’t look at 30 at all I only look at say 28 and below because that way I've eliminated sort of the upper-end problem that it got created here because there are so many patients about 27 - that we just got you know quite a few of them actually came into the trial.

Of the 71 patients that I talked about in that one slide that had been in our prior studies before 30 of them were on the Rhopressa of Rocket1 and 13 of them were drifters. So we think it does show that - there's something going on there that we think we can eliminate by just changing the protocol.

Okay, thank you.

Yes, sir.

Hi, guys thanks for taking my call. Can you hear me okay.

Yes, ma’am.

Yes. So just think about Rocket4 understand why you’re putting that trial in place.

My question on Rocket4 is if you’re doing that secondary endpoints with a potential six-month efficacy endpoint and I understand why you want to do that as far as demonstrating how the drug works? Is there a risk there that that’s actually going to make the Rhopressa approval process that much longer at the FDA someone else back say’s we do want that Rocket4 data rolled in for approval

I think its great question, Caroline. If you think about the timing here look at this way.

So we’re starting planning for Rocket4 right now, we’ll start enrolling sometime in Q3 which means by Q3 of next year it will be completed. If Rocket2 we’re able to change the range for the primary to a lower one and it hits, we then can go ahead and file in the first half of 2016 with Rocket2 lower range with the secondary efficacy point that we achieved in Rocket1.

And then by the time the FDA's is looking all the stuff we will have completed and reported out Rocket4. So we'll have that available in case they require that that we submit more data.

Okay. Very good that’s helpful.

And then just looking at these drugs in big picture and it’s definitely really interesting that synergistic effect that you’ve elucidated from the data, so assuming the FDA as you look at Rocket 2 from 20 to 24, 20 to 25 and you are successful with that, Rocket 4 is successful and then you get Rhopressa approved and then you have Roclatan, Roclatan gets approved and say we are now in 2019. Can you just walk me through how these drugs sit in the clinical treatment paradigm, so who is prescribing which drug Vin?

Well I think it falls right into what we've been saying since day-one, we think that Roclatan for those patients with a broader range of IOPs typically on the higher end, perhaps it had severe damage to the optic nerve and significant loss to vision where the doctor says I'm not messing around I got to get this pressure down as well as I can get it I need the biggest gun that I possibly can get, you are the biggest ball that I can possibly shoot. I think that makes most sense.

For Rhopressa we think that we will get a huge chunk especially with this data, we think we will get a huge chunk of the additive market and so if timolol today has something like 30%, 40% of the prescription market for additive therapy and here we can show this tremendous synergistic effect with prostaglandin and the timolol doesn't have. You got to believe we’ll do as well as that, so you're looking at 5, 6 million prescriptions and so we think that additive therapy for Rhopressa especially for those patients who maybe on one of the other prostaglandins, whether it's Lumigan or whether it's Roclatan I think it makes all the sense in the world.

And also I still believe that we are going to get fair bit of use for those patients who have light colored eyes or on the lower IRP side that just simply don't want to mess with the potential permanent cosmetic changes to prostaglandin.

All right, very good. Well, thank you for walking us through all this data.

I really appreciate it.

Yes ma’am.

Hi, good afternoon thanks for taking my question. Just a couple with regard to Rocket 2, if we go back to Rocket 2 for a moment and that does imply well I guess is there anything you can do to improve compliance at this point?

Rocket 2, unfortunately we can’t do much of Rocket 2 because a lot of the patients have already been completed, we do have - we announced I think it was about a month or so ago that we had enrolled our last patient so really we're in our last group of patients that are just trudging through the 90-day period and which by the way we think it will be over by the end of June. And so there is very little we can do for the compliance stuff now.

We think that because again if you look at Rocket 1 the way it breaks down for the drifters and the correlation between drifters and non-compliance. We think the fact that if we can lower the pressure, the range of pressures to either 25 or below or 24 and below that we think that will get rid of a lot of the variability because we won’t be dealing with the top end variability and so that's we can do this study too far down the road.

Yes, but certainly Roclatan and Rocket 4 we can make changes there.

Yes, it makes sense. So moving on to I think somewhere in the presentation you mentioned there was three sites, yes I think three sites where you see the most drifters?

It was actually 5 sites.

Five sites, okay. Is it possible, is it part of your discussion with FDA that potentially without even looking at the data to excludes these 5 sites?

We know that not all five sites were participating in both Rocket 1 and Rocket 2. I believe that maybe there was 3 sites were actually common to both Rocket 1 and Rocket 2, but I’m doing that one by memory and so it’s either two or three that were for both, but it's little too late to do that all we could do is again do what I just said which is – if we can move the range down to 25 and below or 24 and below we are starting to get rid of a huge chunk of what we believe to be our problem.

Yes, thanks. That’s very helpful.

End of Q&A

Thank you and hopefully we’ve answered many of your questions regarding the result of Rocket 1 and the path forward whether it's Rocket 2 or Rocket 4 or Roclatan as we continue to analyze the results of Rocket 1 and target some of the milestones we set for ourselves relative to FDA communications and moving forward with a clinical trials that we’ve talked about. We’ll continue to keep you inform.

Our next opportunity to provide you with additional updates and perhaps even more data that we are able to generate from the trial. We’ll be participating in the Jefferies Healthcare Conference on June 3.

I want to thank all of you for taking the last hour or so to spend it with us and again we are very, very pleased with the findings here especially this great synergistic effect that we have with prostaglandin because I think it bodes very, very well for the future both Rhopressa as well as Roclatan. Thank you and have good evening.