Aerie Pharmaceuticals, Inc.
Q4 2014 Earnings Call Transcript

Published: 3 Mar 2015

[Operator:]

Good afternoon, ladies and gentlemen. Thank you for standing by. And welcome to the Aerie Pharmaceuticals’ Year End 2014 Earnings Conference Call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session and instructions will follow at that time. Today’s conference call will be recorded. It is now my pleasure to turn the floor over to Aerie’s Chief Financial Officer, Rich Rubino. Please go ahead, Sir.

[Rich Rubino:]

Thank you, Brandy. Good afternoon and thank you for joining us today. With me today is Vince Anido, our Chairman and Chief Executive 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 press release. Before I turn the call over to Vince, I will address 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 filed our 10-K and proxy on February 27, 2015. They are currently available on our website. Hard copies of the Annual Report and Proxy will be available later this week. Also note that our Shareholder Meeting is scheduled to take place on April 10, 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 press release, which is posted on our website. With that, I will turn the call over to Vince. Vince?

[Vince Anido:]

Thanks, Rich and good afternoon everybody. Thanks for joining us today. As you know and as we’ve talked for quite a while now, we remain focused on building a major ophthalmic pharmaceutical company and today in addition to updating you on the status of our Rhopressa Phase 3 trials in the upcoming Roclatan Phase 3 trials that are scheduled to start sometime around mid-year, I’ll take a few minutes to also address an important new research finding that we announced just about a week or so ago. We are very pleased with the current status of the Rhopressa Phase 3 trials. As you will recall we have a number or registration trials. There was three of them, all comparing Rhopressa to timolol. As a reminder we have selected timolol for a number of different reasons. The entry criteria of intraocular pressure for us just about 20 and below 27 millimeters from Mercury and at that range of pressures, we have shown in a couple of different clinical trials they're as good as latanoprost and historically we also know that timolol has been about 1 millimeter worse than latanoprost. So we think that we're in good position here to prove what we think is necessary here in terms of non-inferiority. Also as a reminder, Rocket 1 is a 90 day efficacy trial only. It is in the U.S. Rocket 2 is the one year safety study but it does have the 90 day interim efficacy readout. And Rocket 3 is just a one year safety study that is being conducted only in Canada. Rocket 1, we announced early in January that we were accelerating our expected Rocket 1 efficacy readout to the middle of next quarter, so may of this year and as the result of very, very rapid enrollment as we’ve said many times there aren’t too many studies being done in the United States for this treatment of glaucoma and we found a very ready audience with a lot of patients which accounted for the past enrollment. It is very important to readout for us. It is rapidly approaching and as I mentioned it’s only a few months away. For Rocket 2 it is on track and we expect to have a readout for the safety portion of Rocket 2 later on this summer sometime in Q3. And for Rocket 3, which is more of a backup safety study that’s being conducted in Canada, it is designed for a number different reasons. One is to familiarize Canada clinicians with Rhopressa and also to help us gather additional data on safety as a way sort of backstopping some of the work we’re doing here in the U.S. and hopefully helping us to accelerate the NDA filing that we expect sometime in the first half of next year. We do expect to have the safety data around the end of this year so that we can file our NDA for Rhopressa with the FDA sometime in the first half of 2016. We also expect to have enough data at that point to pursue filing for regulatory approval in Europe. And moving over to Roclatan, we are well on our in the preparation of our Roclatan Phase 3 clinical trials, which as I mentioned are scheduled to commence sometime in the summer. The Roclatan trial design for Phase 3 at least for the U.S. is expected to be similar to what we show during Phase 2b. You will recall there that the performance result we released in June were exceptional showing the potential for Roclatan to become the most efficacious glaucoma medication on the market. Our current plan is to conduct two Roclatan Phase 3 trials in the U.S. with Rhopressa and latanoprost as competitors. Again in the U.S. we are required to show superiority of the combination versus each individual component. We also expect to conduct this one trial in Europe comparing Roclatan to a widely prescribed fixed dose combination product which we have not selected at this point. This trial design will serve to create awareness for the Aerie product in Europe but also help facilitate our regulatory approvals there and also help us with as many of you know, as a critical component of commercializing Europe which is the providing information for the pricing authorities. The Phase 3 trials in Europe are likely to start sometime after we have commenced our U.S. trials. This is an update. We are scheduled to meet both the FDA, European Authorities in a very near-term to finalize all of our clinical plans. Now turning to the update that I said that I was going to provide in terms of new research that’s coming out of our labs. Our research group collaborating with Duke University and Boston University has an exciting preclinical research that points to Rhopressa potentially being disease modifying. The data we have seen thus far indicates first of all that Rhopressa may be acting as an anti-fibrotic agent on a director meshwork which is a disease tissue in glaucoma. It is a fibrotic process and it calls us as swiftness in the contraction of the disease tissue at least to the elevated intraocular pressure. Our experiments were conducted on human trabecular meshwork cells that were grown on tissue culture plates and then we were able to show the anti-fibrotic effect by blocking something that does cause fibrosis, which is TGF-beta, and by blocking that we were able to show that in fact we are anti-fibrotic. The result of this particular study as well as the next one that I'm going to talk about, they're going to be presented at the AOPT meeting and that’s the Association for Ocular Pharmacology and Therapeutics, which is currently being held in Charleston South Carolina early this week. Next finding in a totally different study relates to the perfusion of the trabecular meshwork outflow tissues. The preclinical research was conducted on human donor eyes with the objective to determine whether Rhopressa can impact increased tissue perfusion thus allowing better flow of eye fluid and associated fluid of nutrients and antioxidants to the trabecular meshwork. The findings here were again very, very impressive, with Rhopressa dosing showing a significantly increase in the percent of trabecular outflow pathway perfused by fluid containing a tracer guide. There is more research being done to further analyze the trabecular meshwork and determine if in fact these effects are consistent with disease modification. And we hope to progress with some additional work that we hope to update you on over the next coming year. You can see not only on our latest corporate slide deck which is February 23, 2015, which is currently on our website, you can actually see some photographs there showing both the anti-fibrotic effect as well as the perfusion findings. In these pictures you will see the Rhopressa effect is being demonstrated. We have also in fact just today have put up the posters that are being shown in the AOPT presentations up on our website. So you can actually see the entire poster there as well. The second bit of study, which is also great news for us, is regards to an early stage molecule which we call AR-13154. It is another molecule, fully owned by Aerie and comes from our library of what is now about 3000 kinase inhibitors. Here we conduct that with this product in that rat study, and it’s very traditional rat study on laser-induced choroidal neovascularization, it’s an early study that’s done with a lot of VEGF inhibitors and alike and it’s basically study where you take rats and you induce these lesions. Then you try to measure how well your drug works by measuring the lesion size and seeing how it decreases over time. This preclinical drug showed a decreased lesion size of about 35% off of their base line, and that compares pretty favorably by a way to EYLEA, which showed about a 23% reduction in lesion size in this particular model. We chose 154 for testing based on its ability to inhibit three different pathways. It is obviously Rho Kinase product. So it does inhibit Rho Kinase. It’s also a JAK inhibitor as well as the PDFGR beta inhibitor. We think the combination of activities here that are all obviously different than just VEGF pathway should reduce the inflammation, the neovascularization and the fibrosis that drives wet age-related macular degeneration. This is a small molecule and there is obviously a quite a bit more work to do. Also here we also got to understand not only how do we get it back into the eye and delivered over a sustained period of time, so looking at various drug delivery systems there, but we also need to understand how this molecule behaves when co-administered with current anti-VEGF treatments. Even with all of these exciting internal discoveries, we continue to explore collaborative opportunities for new ophthalmic products, liberty alternatives and potential new sciences altogether such as cell therapy and gene therapy and we hope over the next 12 months or so we'll be able to update you on the a number of different things that we are doing in that area. Just switching for a minute on our commercialization strategy, as you remember our plan currently remains and that is we're going to sell all these products ourselves in North America. If successful we expect to commercialize in the second half of 2017 for Rhopressa and about a later in Roclatan at least in North America. For Europe we are seeking a regulatory approval on our own. So we’re doing all the development work there for both Rhopressa and Roclatan and may possibly partner or use contract sales organizations we’re building on ourselves in order to conduct the eventual commercialization of both Rhopressa and Roclatan in Europe. Now regarding Japan we exploring the possibility of conducting Japanese clinical trials on our own and we're currently interviewing a number of CROs that have done a quite a bit of work in our space there. But at the same time we’re also talking to Japanese atomic companies not only to develop the product but also obviously to commercialize the products once they're approved. In summary we’re very, very happy with the progress we’ve made so far along with the ophthalmology community. We’re very excited about the prospects for our products and hope to get them on the market as quickly as we possibly can. At this I'd like to turn it over back to Rich for a quick financial overview. Rich?

[Rich Rubino:]

Thanks Vince. For the fourth quarter our GAAP net loss attributable to common stockholders for the three months ended December 31, 2014 was $16.5 million or $0.69 per share. The net loss includes non-cash charges for stock-based compensation expense of $2.5 million. When excluding the non-cash stock-based compensation expense, adjusted operating expenses for R&D and G&A totaled $9.3 million and $4.2 million respectively for the fourth quarter 2014. Total adjusted net loss was $14.0 million for the fourth quarter 2014. The $14 million adjusted net loss number or $0.58 per share compares to $5.4 million for the same quarter in 2013. The increase in operating expenses for the 2014 period compared to that of 2013 includes increased clinical and non-clinical research and development expenses and other activities associated with our product pipeline as well as activities to support the growth of our operations. For the full year 2014 we raised $125 million from the Deerfield senior secured convertible debt financing and burned $37.5 million of cash. Our year-end 2014 cash and marketable securities totaled over $158 million. Our cash burn rate is expected to increase in 2015. As you know we expect overlapping Phase 3 trials in 2015 for Rhopressa and Roclatan and we plan to continue to expand our research and operations capabilities. With that, our latest estimate for cash burn for 2015 is approximately $55 million to $60 million. This guidance estimate is based on currently known plans and strategies. These strategies may involve in the course of the year as we continue with our plans to build a major ophthalmic pharmaceutical company. Now I’ll turn the call over to the operator for questions and answers. Brandy?

[Operator:]

Thank you [Operator Instructions] Our first question comes from Adnan Butt from RBC Capital Markets. Your line is now open.

[Adnan Butt:]

I think I’ll start with the preclinical stuff. First, can you foresee at this time how disease modification could be measured? And since the test potential long-term implications, at what time would you expect to actual tissue changes to take place?

[Vince Anido:]

So we do expect that the tissue modification concept is going to play out over maybe a longer period of time than we’re going to see on a 90-day efficacy trials. We’re obviously going to be pretty interested in taking a look at sort of what happens over the 90 day period, because certainly in the trials, in the animal trials that we've conducted it looks like it happens relatively quickly. We just don’t know in many cases how much that tissue really is damaged. And so I think perhaps the more accurate meter reading is going to be as I mentioned we’re going to be taking a look at 12 month safety for these products. That means for example in Rocket 2 we’re going to get the 90-day efficacy trial, all of those patients in that Rocket 2 trial, which is roughly about 690 of them. We’re going to try to hold on to them for a 12 month period. So we’ll have 12 months data on that many patients for each of the arms that we’re looking at. They're once a day, twice a day arms of Rhopressa along with timolol. During the quote safety component of that trial, sort of after the 90 days, we’re going to get those patients back about three times. So instead of what we normally would do for efficacy, where we bring the patients back for an entire day and we take three IOP readings through the day at 8 PM, 10 PM and 4 PM, for the safety component we only bring it back for 8 AM and check for safety. But at the same while they're in there, we will check for efficacy. So that will be our first clue as to how well we’re holding pressure, because as you know in many cases and certainly on [indiscernible] patients, about half of them need a second drug and some of that occurs as early as six months and beyond. And so we may get a meter reading and one sort of metric could be that we don’t need any rescue med after a year’s period. And so that would be kind of interesting finding. And so I think the only way we know so far to measure what we’re trying to measure here, which is improved health is by seeing how well we hold pressure and number two, if we can decrease the number of concomitant meds they are needed. Now all that takes more time. In the meantime we will also work with the FDA, we'll continue to do some additional work in a preclinical stage. We'll then work with the FDA and see we can find some other ways of designing studies that will give us a faster read on how well we're doing versus B2B improvement of function of the trabecular meshwork.

[Adnan Butt:]

Okay. If I can get a follow-up on 13154, I think the poster shows a series of compounds. So was there any specific reason why 154 was picked? And did the company look at it in combination with EYLEA as a well, or not at this time?

[Vince Anido:]

Let me do it backward. So we have not yet looked at EYLEA. That’s certainly the next step that we are going to do. The first one was just simply measuring to see whether we got the efficacy there. So then obvious next step is do concomitant therapy with EYLEA and lucentis and the like, just like a number of other PDGFR beta drugs have done. Relative to why we picked it, we took a look at handfuls of products and we -- if you can imagine laying out all 3000 molecules in the buckets of similar structures and looked at things that had different levels of activity and you sort of see it in our corporate slide deck, you will see that there is a quite a few products and some of them had some activity and some had limited activity in terms of various different mechanisms. And then we found one meaning 154 that actually hit all of the different pathways that we could think of that one would want to hit to be used for wet AMD. And so that’s how we came up with picking 154 while we did test a whole bunch of different structures. We did get some structures. There were dithro [ph] kinase JAKs, other ones that hit some other pathways of interest but this one was the most potent in hitting the three pathways we were most interested in. Then we tested various concentrations. The nice thing about it as we still have some additional chemistry effort in the Company. So if we need to tweak this particular molecule, we certainly have the capabilities of doing that. But that’s how we ended up picking it.

[Adnan Butt:]

How far is something like this potentially from the clinic or an animal model?

[Vince Anido:]

We will be talking beyond the animal model. So we think that we have got maybe another year's worth of work or so in order to get this into I&D, so we can put it in humans. And so depending on also -- because the chemical structure is so close to Rhopressa, there's about a couple of methyl groups different in the structure, we may or may not have to do a huge amount of incremental tox work before the FDA will allow us to put it in humans, although this will obviously be the first time we inject it intravitreally So we need to talk to them and show them the result so far and see what the path forward is, but if you use Rhopressa as a guide from the time that we came to the same point, to the time we had it in humans, it was about 16 to 18 months maybe.

[Operator:]

Our next question comes from the line of Annabel Samimy from Stifel. Your line is now open.

[Annabel Samimy:]

I had some more questions along the same lines as Adnan. Just with regard to the various metrics you saw in the animal model, how rapidly did you did the sex become known? And it seems like you might have to wait sometime before you see any impacts in human. So is there anything in this preclinical data that might resonate early on with physicians if they see this as they'll be able to connect right away that there might be some kind of disease modifying aspect of it, and that Roclatan and Rhopressa are actually yet more differentiated than they were initially thought to be.

[Vince Anido:]

We do think that the differentiation is building, right. So there's no other drugs that have done these two things that we're talking about in terms of being able to protect the trabecular meshwork and then also enhance the perfusion. And so we think that the incremental differentiation is started. An obvious next step for us to do is take, and again we have determined which animal model works best, but being able to control the -- I've got no other way to put it -- control the disruption of part of the trabecular meshwork and then introduce our drug and see over time how long it takes for it to come back. Because here we were taking absolutes and just trying to see whether we had the activity. The next step is just to see whether in a damaged trabecular meshwork in a living subject meaning an animal, that we can actually re-grow it, and that will give us a much better feel for how long it takes to re-grow. But again I think this is great first step because we're the first ones to be able to show this.

[Annabel Samimy:]

And can you just clarify on the catalyst? You mentioned Rocket 2 was -- the safety was going to read out mid-2015. I thought it was just a 90 day component or readout 2015?

[Vince Anido:]

So the readouts for this year will be -- as we mentioned Rocket 1, it’s in the May timeframe. That's efficacy only. Rocket 2 efficacy only will be in Q3. So still sort of in summer. And the safety for Rocket 2 will be in Q4. Now to be perfectly clear, we will provide both the Rocket 1 and Rocket -- whatever safety information we get for the first 90 days. So we will show that. But the full safety that we’re looking for, which is the requirement for NDA filing which is a 100 patients on drug for 12 months, we’re not going to have that till the end of this calendar year.

[Operator:]

Thank you. Our next question comes from Corey Davis from Canaccord Genuity. Your line is open.

[Corey Davis:]

So as I was going back over these ACT endpoints for Rocket 1 and Rocket 2 and realizing that there is actually 14 different time points that you have to hit right now, the nine and then five out of nine, is there any grey area where you might miss one of those by a tiny bit or is it really the case that say in one of the first nine time points you are worse than timolol by 1.6 millimeters of mercury and the whole trial would be a failure or, again is there any great area?

[Vince Anido:]

Hi Corey, Vince. So just to be clear, so there are nine time points, and what you are referring to and five of them being within a millimeter that is embedded in the nine. So it’s five out of those nine. We have to be within a millimeter. And then the other four we can be 1.5 millimeter worse than timolol. So the answer to your question is, if you look historically a number of products that have been approved have been approved on data that was less than perfect. The latest one was Simbrinza where there they -- I’m sorry, the latest drug that was accomplished [ph]. So the latest drugs that we have were -- there was Lumigan. And in Lumigan they did not reach all of their time points. They were just barely off on some but they were able to get approval on sort of the history and the sum of all the parts if you will, all the data that was available. So the FDA always has a little bit of leeway on some of these kinds of things. It is also depends on sort of what happened at that one particular time point. As we saw on the Roclatan, when we were looking at some of the time points, Roclatan and latanoprost actually had a screwy [ph] result on the 4 PM time point on the very last day of the trial relative to what we had seen in the past. And so that was sort of an unexpected one. So if something like that would happen, certainly we think it all depends on how well the rest of the study or the results were.

[Corey Davis:]

That’s kind of where I was going with this. What are the chances, and I know impossible to predict but timolol just doesn’t behave as you’d expect it to based on history. All of the studies that you cite, how old were they in saying that it’s consistently 1 millimeter mercury worse than latanoprost. So there's very old studies and has the standard of care changed to a point where it might not behave like it has historically.

[Vince Anido:]

Well, this has nothing to do with the standard of care because timolol always been dosed twice a day. So that’s really what we’re comparing it to and that’s a sum total of all the studies that have been done timolol and then compare to that due to some studies of those, -- of the results for latanoprost when you just plot those out. That’s the graph that you see. There is a lot of variability within those results but when you plot it out your average amount, that’s when you get the one millimeter difference between the two. Could we have inherent time points? Sure. Do we that there's going to be consistent we'll see [ph] in that, meaning that we’re going to see nine time points sort of that, that's sort of doubtful. I think what gives us a lot of comfort is that when we looked at the Roclatan results and then compared Rhopressa to latanoprost, and that was done not by controlling pressure. We took on all comers. In that clinical trial pressures between 22 and 36. There we were able to show that we were not inferior to latanoprost, which was sort of a better result than what we got Rhopressa’s own Phase 2 trials. And so we think that delta here could be anywhere from -- we think we should be about 0.5 millimeter to 1 millimeter better than timolol at the time point, certainly to the pressures that we’re studying. But yet we can be anywhere from 1 to 1.5 millimeters worse. So it gives us a pretty broad range here to -- and still be okay.

[Corey Davis:]

Right. And last question would be on a blinded basis if you look at the dropout rate, and if so, was it within what you’d expect for these trials.

[Vince Anido:]

Yes, so far. Rocket 2 is the one that we have the most data on because that’s the one is fully enrolled and didn’t see any major surprises on that one.

[Corey Davis:]

In Rocket 1?

[Vince Anido:]

Rocket 1, yes, I’m sorry.

[Corey Davis:]

Okay.

[Vince Anido:]

And in Rocket 2 I would expect that there you have both once a day and twice a dose versus timolol. If we see anything at all you would expect to see greater degree of redness as an adverse event in Rocket 2, because they'll be taking our drug twice a day. So they'll get a morning dose and their eyes will be red in the morning for a big chunk of the patients. And so that it all depends on how that adverse event plays out. So we should see a difference but it should be related to that arm. So we don’t have that full enrolled yet. So it’s hard to predict.

[Operator:]

And our next question comes from Elliot Wilbur from Needham & Company. Your line is now open.

[Unidentified Analyst:]

This is Nicole [indiscernible] of Elliot Wilbur. I just have a quick question here. Assuming the Rhopressa Phase 3 trial is successful, what would be the remaining risk for Roclatan in Phase 3?

[Vince Anido:]

I am sorry, you broke up for just second for me. Could you repeat the question?

[Unidentified Analyst:]

Assuming the Rhopressa Phase 3 trial is successful, what would be the remaining risks for Roclatan in Phase 3?

[Vince Anido:]

That’s a good question. So from an efficacy point of view, with Roclatan we do expect that if we have successful Rhopressa trials that all that's going to do is shore up our belief that we'll have a better metric in terms of the IOP drop for Rhopressa alone. Certainly as we looked at the Roclatan Phase 2 trials, it was pretty clear difference between Roclatan and Rhopressa, and same way with Roclatan versus latanoprost. So it certainly will be continue to be encouraging us to believe that Roclatan should beat both latanoprost and Rhopressa in a combo trial. So really the only thing that's left at that point to think about is what’s the final adverse event rate going to be. We reported that we saw in Rhopressa alone about a -- the only adverse event of note was the hyperemia and that was about 20% to 30% on Rhopressa alone, and it was close to 40% on Roclatan. So we expect that, that will be -- then the only wild card is will the redness come out in the Phase 3 trial just like at the same percent as it did in their Phase 2s.

[Operator:]

And our next question comes from Caroline Corner from Cantor Fitzgerald. Your line is now open.

[Caroline Corner:]

So my question is around the pipeline. You had mentioned that you have 3000 kinase inhibitors in your library right now. Obviously you're making some progress preclinically with several compounds. That all sounds really great. As you're moving now to become a major ophthalmology company and making progress along those lines, and you've said previously that you want to approach multiple large end markets. Should we expect you look externally for candidates as well and perhaps for some candidates that are already in the clinic or a little bit further along than the ones you're developing inside?

[Vince Anido:]

I think we do expect that we'll kick in -- our business development activities are already pretty robust in terms of not only out licensing, but also in licensing, and we certainly have made an awful lot of progress and have been talking to a number of different companies. We do expect that with some of the changes that we've seen in ophthalmology, there is going to be some pipeline products that become available and we certainly will take pretty hard look at those as soon as there is an indication of interest by some of the companies who jettison their pipeline products and see we can find something that’s a little later on. And that could move us into the marketplace faster than some of these preclinical candidates that we're looking at. As I mentioned earlier, we're also looking at some gene therapy ideas as well as some cell therapy ideas to supplement some of the other work that we're going to be looking at right now. So we hope that we'll be successful and certainly it won’t be for lack of trying. It’s just a function of being able to identify and grab them as quickly as we possibly can. Our intent is to build out a pretty good pipeline prior and have products that are in the clinic by the time we launch Rhopressa and Roclatan. And if we can have the mix of both internally developed and externally developed products, that'd be the best of all worlds.

[Caroline Corner:]

My other question, not to get too acute about the timelines, but you have been saying that Roclatan as a commercial product is about a year behind Rhopressa. Rhopressa started in June of 2014 and then you're saying Roclatan is third quarter. Now I'd assume there is a bit of a learning curve and enrollment would probably go bit faster with Roclatan. Are we still seeing that about a year part in your timelines for commercial launch?

[Vince Anido:]

Yes, I think the clinical guys would get really upset if I started to shorten up their timelines at this point before they've even started the trials. And so I think the yes, it still has to be about a year because the sheer number of what we're looking at, we are going to have two -- in Roclatan in the U.S. we're prepared to do two superiority trials, and they have to be -- we have to pick specific sites for each side but they will be called, for the first study and the second study, we may have to split the U.S. in half, either go south or east, west and do it that way. So it would be a little bit more complexity from that point of view. And we need to make sure as we do the powering because we need safety as well, we could end up needing 700 patients per different set of trials. So that’s an awful lot of patients to enroll. So I think at this point we want to be just little bit cautious about that, about forecasting that we’re going to be doing that any faster than we plan.

[Caroline Corner:]

Okay. And then just a quick one for Rich, please. The SG&A line came in a little bit higher than I think some of us have been expecting in particular, and I know you’ve got a lot of clinical work going on, but can you talk us through a little bit about what the spend is that’s affecting that SG&A line please.

[Rich Rubino:]

Well, a slight uptake in the fourth quarter is the usual stuff we see in the fourth quarter which would include audit fees, legal fees and we are continuing to grow the business of course. At the end of the day for the year full year 2014 G&A came in pretty much where I expected, where I had guided, about 30% of the total adjusted expense, and I would expect that to be the case again next year, 2015.

[Operator:]

Thank you. I will now turn the call back over to Dr. Vince Anido, Chairman and Chief Executive Officer for any final remarks.

[Vince Anido:]

Thank you for attending our call. Obviously we’re very, very pleased with the progress that we're making and we certainly have been surprised by acceleration of our clinical trials and also by the good luck we continue to have in identifying preclinical candidates, and finding ways to further differentiating not only our products but also finding other molecules within our library with which to grow our business. We do believe that we’re in somewhat unique position, just came from the American Glaucoma Society meeting, and I have to tell you that I’m obviously biased that we thought that we made a great impression there. This is the first time we’ve been able to and match to attend the meeting and we think that we’re enhancing the awareness and the visibility of our Company to not only the glaucoma specialist but also the ophthalmology group overall, and we’re pleased with the progress and we hope to be able to continue showing that progress. Just as a reminder we do expect readout for the Rhopressa Rocket 1 study in May. And so hopefully we look forward to talking to you then. Thank you and have a great day.

[Operator:]

Ladies and gentlemen, thank you for participating in today’s conference. This does conclude the program. You may all disconnect. Everyone have a great day.