Juan Sanchez - IR Sharon Mates - CEO Larry Hineline - CFO Kimberly Vanover - VP Clinical Development Allen Fienberg - VP Business Development Cedric O'Gorman - VP Medical Affairs Ashish Dugar - VP Commercial Development Michael Halstead - SVP & General Counsel.

Seamus Fernandez - Leerink Adnan Butt - RBC Capital Markets Bert Hazlett - Ladenburg Jason Butler - JMP Securities Bill Tanner - Guggenheim Securities.

Good morning, ladies and gentlemen and welcome to the Intra-Cellular Therapies Second Quarter Results Conference Call. At this time, all participants are in a listen only mode [Operator Instructions]. As a reminder, today's conference call is being recorded. I would now like to turn the conference over to your host Dr.

Juan Sanchez, Vice President, Corporate Communications and Investor Relations. Please go ahead..

Thank you, Operator. Good morning and thank you for joining us for today's conference call. Our earnings press release, providing a corporate update and details of the Company's financial results for the quarter ending March 31, 2015 crossed the Wire a short time ago. The press release is available on our Web site at www.intracellulartherapies.com.

Joining me on the call today are Dr. Sharon Mates, Chairman and Chief Executive Officer; Dr. Kimberly Vanover, Vice President of Clinical Development; Larry Hineline, Chief Financial Officer; Dr. Allen Fienberg, Vice President of Business Development, Dr. Cedric O'Gorman, Vice President of Medical Affairs; Dr.

Ashish Dugar, Vice President of Commercial Development; and Michael Halstead, Senior Vice President and General Counsel. As a reminder, during today's call, we will be making certain forward-looking statements.

These statements may include statements regarding among other things, the efficacy, safety and intended utilization of the Company's present candidates, the anticipated conduct and results for future clinical trials, plans regarding regulatory filings, future research and development and possible uses of existing cash and investment resources.

These forward-looking statements are based on current information, assumptions and expectations that are subject to change and involve a number of risk and uncertainties that may cause actual results to differ materially from those contained in the forward-looking statements.

These and other risks are describe in our periodic filings made with the Securities and Exchange Commission, including our Form 10-Q for the quarter ending June 30, 2015, which is expected to be filed with the SEC later today.

You are cautioned not to place undue reliance on these forward-looking statements and the Company disclaims any obligation to update such statements. I will now turn the call over to Sharon..

Thanks, Juan. Good morning everyone and thank you for joining us on the call today. It has been a very busy and productive quarter for ITCI and we are excited to continue the conversation with our investors and the community as we rapidly approach the conclusion of our first Phase 3 clinical trial with ITI-007 in patients with schizophrenia.

I will begin with an overview of our progress this quarter. Kim will then review our ITI-007 clinical development program. Lastly, Larry will review our financial results. After that, we will open the call for questions.

Intra-Cellular Therapies is focused on bringing innovative medicines to patients suffering from neuropsychiatric and neurological diseases. There remains a significant unmet medical need for patients with conditions, such as schizophrenia, biopolar disorder and dementia.

Our mission at ITI is to reduce the burden on these patients and their care givers through the development of innovative treatment options. Our lead product, ITI-007, has unique safety and pharmacological features which allow us to pursue different neuropsychiatric and neurological indications.

Our strategy for ITI-007 is to obtain an approval for the treatment of schizophrenia and to expand the number of indications to include biopolar depression, behavioral disturbances and dementia including Alzheimer’s disease, major depressive disorder and other neuropsychiatric and neurological disorders.

Additionally, we continue our studies to characterize the mechanism of action of ITI-007 to better understand the unique pharmacologic action and resulting differentiated clinical profile.

Our pursuit of each indication for ITI-007 is grounded in strong scientific rationale, the positive safety and efficacy data from our clinical trials, as well as commercial and strategic considerations.

As an example, in the Phase 2 schizophrenia trial, in addition to demonstrating robust antipsychotic efficacy the 60 milligram dose of ITI-007 resulted in robust anti-depressant effect in a pre-specified subgroup analysis of patients with schizophrenia and comorbid depression, contributing to our decision to select biopolar depression as our next indication through which to developed ITI-007.

In the second quarter of 2015, we achieved important milestones in both schizophrenia and biopolar depression. As we announced in our press release this morning, clinical conduct in the first Phase 3 trial has been completed and we expect to announce top line results late in the third quarter or early in the fourth quarter of this year.

Additionally, we initiated patient enrollment in our second Phase 3 schizophrenia study. Recently, following communication with the FDA, we announced our plans for the Phase 3 program for the treatment of depressive episodes associated with biopolar disorder, otherwise known as biopolar depression.

This program allows us to seek an indication in bipolar depression both as monotherapy and adjunctive therapy with one trial for each of these treatments strategies. This means we have now advanced ITI-007 in to multiple late stage programs, an exciting development for the company.

We also plan to advance ITI-007 into yet another late stage development program later this year to address the behavioral disturbances seeing in patients with dementia including Alzheimer's disease. We have an ongoing positron emission tomography or PET study in patients receiving ITI-007.

The main objective of the study is to increase our knowledge of the mechanism of action of ITI-007. To accomplish this we are assessing the stratial [ph] occupancy of D2 receptors in the brain of patients with schizophrenia at the effective 60 milligram dose.

In this study patients are washed off their medication and treated with ITI-007 for two weeks. We expect results from this study later this year. We believe ITI-007 represents a first-in-class new chemical entity for the treatment of schizophrenia and other neuropsychiatric and neurological disorders.

ITI-007 has a unique pharmacological profile acting on the serotonergic, dopaminergic pathways and downstream by the D1 receptor also has glutamatergic effect. We have demonstrated ITI-007 is safe, well tolerated and effective at 60 milligramns.

As pre-synaptic partial agonist and post-synaptic antagonist at the D2 receptor ITI-007 may achieve antipsychotic efficacy at D2 receptor occupancy levels lower than that seen with most antipsychotic other than Clozapine arguably the most efficacious antipsychotic.

Our Phase 3 program in schizophrenia is evaluating ITI-007 at doses of 20 milligrams through 60 milligrams which we believe will be effective with an unprecedented safety profile and without the motoric and metabolic side effects associated with other antipsychotics.

We continue to make progress in several other programs including ITI-007 for the treatment of major depressive disorder our ITI-007 long acting injectable program and our PDE inhibitor program. Turning to our financials, at June 30, 2015 we had cash and investments totaling $204 million.

We believe that our financial position is strong and we continue to move forward with our development programs. Lastly we continue to strengthen our organization as we announced earlier this week Dr. Ashish Dugar has joined us as Vice President of Commercial Development and he is in attendance on the call today. I will now turn the call over to Kim..

Thanks Sharon. My remarks will focus primarily on our most advanced program, ITI-007 for the treatment of schizophrenia. This Phase 3 program includes two randomized double blind placebo control clinical trials in patients with acutely exacerbated episode of schizophrenia.

The primary measure is changed from base line on the positive and negative syndrome scale PANS total score. Additional measures along with safety and tolerability include the sub sales on PANS and other measures that may highlight the differentiating features of ITI-007 among anti-psychiatric drug.

The first clinical trial which we call 301 is evaluating 40 milligrams and 60 milligram of ITI-007 compared to placebo after four weeks of once daily treatment. This trial has been fully enrolled with 450 patients randomized.

The second Phase 3 trial or 302 trial is evaluating 60 milligrams and 20 milligrams of ITI-007 compared to placebo after six weeks of once daily treatment with risperidone as an active control. We planned to randomized approximately 580 patients in this trial.

As Sharon mentioned we look forward to announcing the results of the first Phase 3 trial late in the third quarter or early in the fourth quarter of this year. The second Phase 3 trial is ongoing and proceeding well with data anticipated in mid-2016.

While most of the existing antipsychotics have demonstrated sufficient efficacy in treating the positive symptom because of the associated metabolic and motoric side effects patients often do not stay on their medications.

In addition these approved medications have limitations in their ability to treat the negative and depressive symptoms or to improve social interactions. We believe the profile of ITI-007 represent a differentiated treatment alternative for patients with schizophrenia.

We further believe ITI-007’s profile will translate clinically to better medication adherence and improved clinical outcomes without the high cost associated with management of metabolic cardiovascular and motoric side effect. We believe ITI-007’s clinical profile extends beyond safely controlling acute symptomatology.

ITI-007 has shown differentiated improvements on negative symptom, depression symptoms and pro social behavior. Our ITI-007 Phase 3 program will continue to capture these and other secondary end points. I would like to move on to discuss a few details from the biopolar depression program.

Following communications with the FDA we recently announced that we are proceeding with the ITI-007 Phase 3 clinical program in biopolar depression. This program consists of two Phase 3 multicenter randomized double blind placebo controlled clinical trials.

The first Phase 3 study which we call the 401 study, will evaluate ITI-007 as a monotherapy and the second Phase 3 study which we call the 402 study will evaluate ITI-007 as an adjunctive therapy with lithium or valproate [ph] in order to seek approval for indications as both monotherapy and adjunctive therapy in biopolar depression.

We plan to commence these studies later this year. Lastly, we will update you further on our program for the treatment of behavioral disturbances in dementia later this year. I’ll now turn the call to Larry who will review the financial results for the second quarter..

Thanks, Kim. I will be reviewing our financial results for the quarter ending June 30, 2015, and provide an overview of our expectations for the use of our cash and investments. The net loss for the second quarter of 2015 was $21.5 million compared with a net loss of $4.5 million for the second quarter of 2014.

Basic and diluted net loss was $0.61 per share for the second quarter of 2015 compared to a basic and diluted net loss of $0.15 per share for the same period in 2014. R&D expenses for the second quarter of 2015 were $17.8 million compared to $2.7 million for the second quarter of 2014.

The increase in R&D cost year-over-year is primarily due to cost associated with the Phase 3 clinical development program for ITI-007 in schizophrenia which was initiated in late 2014. G&A expenses were $4 million for the second quarter of 2015 compared to $2.1 million for the same period in 2014.

The increase in G&A expenses is primarily the result of higher stock based compensation expense and to a lesser extent salaries and professional fees and cost due to the activities associated with being a public Company. Cash and investments totaled $204 million as of June 30, 2015 compared to $129.6 million at December 31, 2014.

On March 11 2015, the Company completed an underwritten public offering of its common stock for gross proceeds of approximately $130 million and net proceeds of approximately $121.8 million.

We expect that existing cash and investments will be dedicated primarily to the ITI-007 program, including clinical trials of ITI-007 in schizophrenia, biopolar disorder, behavioral disturbances in dementia, depressive disorders and related clinical and non-clinical activities, including manufacturing.

To a lesser extent, funds will be used for other clinical and preclinical program including the Company’s phosphodiesterase PDE development activities.

With that operator, could you please open the line for questions?.

[Operator Instructions] And our first question comes from the line of Seamus Fernandez of Leerink. Your line is open..

So maybe first off Sharon, can you just update us on little bit closer to the timing of the first trial read out. As we look at when the trial completed, it looks like we’re getting very-very close to what will be the primary analysis. So that would be helpful.

Second question is in terms of what you hope to communicate with regard to the top line results, can you help us understand what is essential in that communication? And then lastly, can you just help us wrap our hands around a little bit the difference between the -- the overall ITT randomized patient population? And what is the evaluable patient population in these studies typically, as well as what we saw in the Phase 2?.

Hopefully I’ll remember all your questions. So, for readout, yes we’re very excited that we have completed clinical conduct and we are anticipating that we will have the top line readout late in the third quarter or early in the fourth quarter. At that time, we will communicate to you the top line data.

Certainly, we will have the primary efficacy endpoints and we will have some of the secondary endpoints as well at that time.

If you like to add anything to that Kim?.

So, similar to our Phase 2 trial, we’ll be looking at the PANS subscale as secondary outcome measures including the positive symptoms and the negative symptoms, we’ll be looking at the symptoms as depression, the pro social effect and the clinical global impression of the severity of illness..

So and then your third question is difference between randomized patients and an Intent To Treat or what studies are now calling efficacy, they are actually moving away from the term ITT. In our study in the Phase 2 we had 335 patients who were randomized, that means they are putting one of the group.

Okay, in the end we had 311 subjects in the what we called ITT population, in was schizophrenia studies to be included and then efficacy analysis patients must have received at least one dose of drug and have a valid base line and post dose PANS assessment.

Some studies call this the ITT or modified ITT analysis other studies call this and efficacy analysis, but all studies have a criteria of receiving one dose and have a valid baseline and valid post assessment in our study 24 patients did not meet this criteria. In all studies there is a certain number of patients that don’t meet the criteria.

All of these patients are included in your safety analysis expect for in our study one patient who was randomized but withdrew before -- they withdrew consent, before receiving any study drug. So the efficacy analysis contains 334 patients but our -- the safety analysis has 334 patients and the ITT or efficacy analysis included 311 patients.

An efficacy analysis on your ITT or your efficacy patient population uses a mixed effect model repeated measure or MMRA for handling missing data and this is the current standard approach to assess efficacy in a patient population.

And there are several recent examples of this but latest being the [indiscernible] result analysis which was coral [ph] at all in 2015 and came it all in 2015 as well. I hope that answers your questions..

That's perfect, yes. Thank you so much. And then just as a follow up on the secondary analysis.

Can you help me just understand a little bit the PANS analysis camp, as we look at the subscales would that be in the overall patient population or is it subset of patients on the subscale that would be evaluated with those sort of negative symptoms would be the analysis, sort of similar to what we saw in the Phase 2 or will we get or with the secondary analysis basically be the overall PANS for in the overall patient side?.

Right. I think you can anticipate that it will be similar to the way that we conducted the Phase 2 data so as a reminder in the study for acute schizophrenia that we screen for patients that are required to have the positive symptom. .

So to get in to the study you need to have those hallucinations and dilutions..

That's right.

And then we anticipate that a subset of those patients will have also the prominent negative symptom and so we can look at the negative symptom both in the overall population but are particularly interested in the pre-specified population of those patients who have to meet the criteria of having the prominent negative symptom as they find in similar with the depression analysis those patients who come in with depression and see whether those improve..

Thank you. Our next question comes from the line of Adnan Butt of RBC Capital Markets. Your line is open..

Couple of questions here.

First could you remind me if the first Phase 3 that's reading out, does it have a positive control and if not will we still be able to discern safety differences, so favoring the 007 potentially and then in terms of an effect size should the Phase 2 be a guide as to what kind of an effect size we should look for?.

So I'll address the whether or not the first Phase 3 has a positive control of this Shanghai, Adnan. So the first Phase 3 is a four week study and it does not have a positive control, it has two doses of ITI-007 and placebo.

We already had a positive control and a four week study before so we didn’t believe that it was necessary to have one again and then as to the effect size, our effect size and our Phase 2 study was 0.4, which is really a quite a robust effect size for studies done in North America and we have modeled the Phase 3 at a similar effect size..

And in terms safety differences being able to see that?.

So as you know where you are -- in this study the answer is we can’t compare it to anything other than placebo and we certainly will be comparing it to placebo, which is very important.

We have the first four week study where we also have the data from risperidone and we will have the second Phase 3 study where we also will have a positive control with risperidone. So we are increasing our data base from those studies..

Yes, I will just add that from our Phase 2 study you may remember that 60 milligram dose of ITI-007 in terms of any treatment emerging adverse events there was no difference between 60 milligrams of ITI-007 and placebo and we think that’s pretty powerful of comparison to look at as being similar to placebo..

Okay, thanks. And if I can get a follow up in terms of the recently announced bipolar depression study, since it’s one trial each for mono-therapy and adjunctive, what’s the FDA thinking there in terms of approval or indication? And then how does the 007 fit into this treatment paradigm which you can give some color there? Thanks. .

This is Cedric here. Well, in terms of bipolar depression it’s a very important disorder to go after. Currently bipolar disorder effects almost 6 million adults in America or like 2.6% of the U.S. population 18 and older, and they are National Institute of Mental Health statics.

Bipolar depression is the most predominate clinical presentation, the episodes occur most often, they’re associated with a work prognosis, suicide risk is higher in bipolar depression as our cost and hospitalizations due to cardiovascular and metabolic disorders. And despite all this there are very few FDA treatment options available.

So in terms of why we think ITI would be special, I think both mechanistically would serotonin re-uptake inhibition of the 5-HT2A antagonism coupled with the robust anti-depression effect we’ve seen in Phase 2, we feel that ITI-007 would be a particularly good choice as a drug to treat bipolar depression..

And the unique dopamine blockade..

Absolutely. And in terms of the thinking, I think you asked about the regulatory thinking there is precedence here that doing one trial as an adjunctive to let [indiscernible], plus one trial as a monotherapy has at least precedential or achieving both indications..

Thank you. Our next question comes from the line of Bert Hazlett of Ladenburg. Your line is open..

Sharon and other, as you considered the 301 study that has just completed enrollment, could you talk a little bit about what you learned from the Phase 2 that was able to inform you for design of this study that in terms of patients, in terms of structure, in terms of design.

Again there have been some advancements in the conduct of clinical trials in CNS and if you could discuss some of the additional bells and whistles that you’ve included in the study that would be helpful.

And then secondly I am going to ask it’s upfront, but could you just remind us of the strategy for 007 for EU and the rest of the world in terms of its development in general terms? Thank you..

Great. So, maybe Kim you want to take the first part..

Sure. So we designed our Phase 3 program on schizophrenia very similar to our Phase 2 trial. We’re including the same patient population and using the same primary end point change from base line on the total PAN. In Phase 2 we did include certain design features that we believe helped us to decrease the variability and increase our signal detection.

For example we ensure that patients have the right diagnosis and the appropriate severity of illness at baseline and then we included potential ratings on the PAN. So we’ve carried these design features through to our Phase 3 program. So we hope that we have a good signal detection in these studies as well.

And maybe Sharon wants to address the strategy for the EU..

Thank you. So all of our studies have been conducted under ICH compliance. So all of our studies will be both for the U.S. and ex-U.S.

in terms of the marketing in the EU, I think we’re still putting that strategy together, but we will -- we think that there are certain countries that we can be marketing on our own in and certain countries that we would have partnerships with others be in..

Thank you. Our next question comes from the line of Ritu [indiscernible] of Cowen & Co. Your line is open..

Sharon, you mentioned that the 0.4 was in line with expectations on the overall PANS score from the current Phase 3 study.

Can you address what you might expect on the negative symptoms side, specifically that subscale and what’s the meaningful change on the negative symptoms on scale and also if you could review for us the pattern of the study, now that you’ve probably nailed down the statistical analysis for them..

Sorry Ritu, we couldn’t understand the second part of that question, also if we could help review the powering of the study?.

No [multiple speakers] the statistical analysis plan..

So, first, we can talk about the effect size of 0.4 and maybe just taking a step back as making sure everybody understands what an effect size is and that’s a standardized mean difference or in other words the magnitude of the effect of drug minus your effect of placebo is divided by the standard deviation.

And this is a way to standardize differences of the way to compare cross study. In our Phase 2 trial we demonstrated the antipsychotic effects of 0.4 for both 60 milligrams of ITI-007 and for our active control risperidone.

This does represent a clinically meaningful improvement and is in the range of approved antipsychotic drugs, there is a number of publications that support this.

There is KAYN [ph] and colleagues in 2012 and [indiscernible] and colleagues published papers in 2006 and 2013 that address the effects size that I think help to put the recent studies and the studies that were conducted in North America that these dose effect size does fall in line with our expectation.

And we have powered our Phase 3 program to 90% so we’ll have more subject as we’ve said in our Phase 3 studies than we had in our Phase 2 studies that reflect the higher powering..

But what about the negative symptoms in the subgroup?.

So on the negative symptoms in the subgroup of patients where they had prominent negative symptoms at base lines, we have an effect size of between 0.3 and 0.4 and this is with negative symptoms they generally take long -- they’re not as responsive to the current treatments and sometimes they take longer to respond.

So, that I think this is a clinically meaningful improvement. It’s certainly better than what we saw with risperidone in side tested side by side where risperidone did not improve the negative symptoms and 60 milligram did in this patient population..

And we’ll continue to monitor this in the Phase 3 program as well..

Right..

So how low was an effect would still be meaningful just on the negative symptoms? Like would a 0.2 would be clinically meaningful, or the 0.1 be clinically meaningful?.

I think that’s hard to say. I mean typically an effect size of better than 0.3 is considered to be a clinically meaningful or so..

But that’s a good sort of rollup from..

And a quick follow up, Kim and Sharon you mentioned some of the other secondary endpoints that might be released in some global impression -- depression -- global impressions anti-depression symptoms.

Are those non-PANS secondary endpoints? What do you guys think are the most important to test ultimately how this all will work?.

Well, I think the -- what I am excited about is the overall profile for ITI-007 and being able to address the breadth of symptoms, so I don’t think it’s just one.

I think the important thing is that ITI-007 from the Phase 2 data that we thought improvements in the negative symptoms the depressive symptoms, the improved social -- pro-social effects, with an improved safety profile. So I really do think it’s this whole package I don’t think, I don’t pick out one to say that that’s the important.

It’s really -- it's exciting to be working on this program where we’re seeing the breadth of effect..

And Sharon I ask this every quarter but any additional detail you can give us at this point and what your plans for the Alzheimer’s behavioral studies might be? Has any new data set come out that might inform your strategy?.

And before our next call, you will have those answers. But at this point we’re still not prepared to give you the entire strategy on the next clinical study that will be performing, but you’ll have it soon..

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

Just a couple of follow ups on the bipolar depression opportunity maybe you just thinking about what you said about the learning's from a Phase 2 trial in schizophrenia and the patients there with co-morbid depression, can you help us think about the magnitude of clinical benefit that you would expect to or might expect to see with 007 than the bipolar depression patients and what there you view is clinically meaningful for that patient population?.

Right. Sharon do you want to take that or so I'll just go ahead. So just first you will hear more and detail about the bipolar studies when we put them up on clinical trials but we will be using the [indiscernible] scale for the measuring both the base line as well as the progress.

And I think that it will be yes -- I think it will be a six week study that we will be doing so from both disease for both studies.

So I think that at this point that's probably as much as we're going to be saying about those studies, unless you want you want to add something about bipolar depression in general?.

No I would just say again that the mechanism that we have, the mechanism that ITI-007 has tried-and-true pharmacology and some very unique novel elements as well and the tried-and-true really we feel that there is -- as bipolar disorder is along the spectrum with schizophrenia some would argue that it's an extension of the illness.

So it’s certainly a very strong reason to believe that our pharmacology with tried-and-true around dopamine blockade will work for bipolar disorder.

But then when you coupled out with the nice elements, as I said before about the serotonin re-uptake inhibitor as well as the 5HD2A [ph] coupled with the dopamine, it makes the story excited but the real sequential for this drug came in bipolar depression..

Okay, great. And then just a quick question on the regulatory side.

You obviously had FDA buy in on the trials, but did you actually use or utilize the scientific advice process in Europe for this indication?.

No. We haven’t said anything about any of our European strategy yet we have not been for the moment we have been focusing on America..

Thank you. And our next question comes from the line of Bill Tanner for Guggenheim Securities. Your line is open..

Sharon a couple of topics, just one back on the dementia, wondering if you could comment on when you see the 301 data if there is any kind of the read across those data obviously it's a different indication but it's a same molecule, so anything that might make you more enthusiastic, less enthusiastic.

And then any particular challenges that you see with dementia, you got obviously in older population and curious about any interaction with concomitant meds and then I had a follow up. Please..

Hi. Bill, thanks. We’re all sitting here thinking.

So it's an interesting question on what we learn from the 301 data, what I really look at in terms of positioning ITI-007 for the treatment of behavioral disturbances in dementia is going back to our low dose strategy because we're really looking at the low doses of IIT-007 for the treatment of behavioral disturbances in dementia.

And we had conducted a Phase 2 study earlier in the program in the low dose of 1 to 10 milligram dose range with IIT-007 in patients with primary insomnia and we saw the improvement in sleep -- reductions and wake after sleep onset and the increases in total sleep time in patients with primary insomnia and without any of the cognitive disruption or next day hang over effect.

And then we followed that on more recently with the safety study in patients with dementia and first in healthy subjects and then in patients with dementia to look at the safety profile and in fact in the patients with dementia they came in with whatever medications that they were coming on, in order to look to make sure that we had an appropriate safety signaling and good the PK profile which we did and that and that really got us excited into launching this to forward in the dementia program..

And the one thing I really like is, well that, just thinking about as an extent from our schizophrenia studies to dementia you can see already from our schizophrenia data just now safe and well tolerated a drug it is.

So when you consider our low dose strategy in geriatric patients -- patients with dementia, I get very enthused by the real lower level of adverse effect, better safety that this does potentially will have in that group..

And just what’s known of the chemistry of 007 in denipilizine [ph] there would be no contemplation with drug-drug interaction?.

Yes, Rick..

Okay. Then curious, just had a question on the long acting -- just if you could comment on what kind of perceived technical challenges there maybe or do you think this is relatively straight forward. And then the second part of that would be the timing of the development of that and potential commercial launch relative to the oral..

So I think that as with any LAI development the technical challenges are making sure that you can have drug released over whatever period of time it is that you’re developing LAI for. We think that we are able to do that.

We are still in the preclinical development of long-acting injectable and we expect that we would be in a position to enter the clinic around the end of 2016. So I think until we enter the clinic we’re not going to give you any guidance on when we’ll be on the market, I think.

I would -- speaking of on the market, I just want to remind, Jason asked the question about the EU and scientific advisory board, I would like to say that again we do all of our studies in accordance with everybody’s guidelines including ICH guideline. So we don’t anticipate any unusual regulatory hurdles from other countries..

Thank you. [Operator Instructions] Our next question comes from the line of Seamus Fernandez from Leerink. Your line is open..

Great. Thanks for the follow-up. Sharon just a quick question, as we think about the prospect of the first studies read-out and it’s exceeding similarity to the successful Phase 2 study of the 60 milligram dose.

If the 60 milligram dose were to succeed in this first trial, is there any chance that the Phase 2 could be used as a supportive second positive study basically significantly reducing the regulatory needs of success in the 301 study.

Just wondering how we should think about, is that even a remote possibility?.

We almost got through the whole call without that question. This is Sharon and I think that at this point we’re really not prepared to comment on that. I think -- let us -- just give us a little bit of time, let’s wait and get the results from this first Phase 3 study.

We do however say that the Phase 2 study was a well-designed, fully powered study that of course was submitted to the FDA prior to the enrollment as all of our studies are, so I think that we will update you further once we have the results from the first Phase 3 study. .

Thank you. At this time I’m showing no further questions in the queue. I would like to turn the call back over to Sharon Mates for closing remarks..

Thank you. In closing, we’re pleased with our progress since our last call. We believe ITI-007 represents a meaningful advancement in the treatment of schizophrenia and other neuropsychiatric and neurological disorders.

We are making significant progress towards our goal of helping patients to lead better life more connected with their families and society. We look forward to the exciting months ahead and to the announcement of results from our first Phase 3 schizophrenia trial and our PET study.

Thank you for your participation on our call and operator, you may now disconnect..

Thank you. Thank you, ladies and gentlemen for your participation in today’s conference. This concludes the program. You may all disconnect. Everyone have a great day..