Paul Cox - Director, Investor Relations Jeff Jonas - Chief Executive Officer Kimi Iguchi - Chief Financial Officer Steve Kanes - Chief Medical Officer

Morgan Haller - JPMorgan Ritu Baral - Cowen and Company John Newman - Canaccord Paul Matteis - Leerink Swann & Company Raj Prasad - William Blair

Good morning. Today, we reported our fourth quarter and full-year 2015 financial results, recent corporate highlights and upcoming milestones.

The press release and the presentation slides used on this call can be found on the Investors & Media section of our website at sagerx.com. On Slide 2 of the presentation is the agenda for today’s call.

We will begin the call with prepared remarks by Dr. Jeff Jonas, our Chief Executive Officer and Kimi Iguchi, our Chief Financial Officer.

Following prepared remarks, we will open the call for a Q&A session and we will be joined by Dr. Steve Kanes, our Chief Medical Officer.

On Slide 3 is our safe harbor statement. During today’s call, we may make forward-looking statements, including statements about our expectations as to future clinical development milestones and timelines, the potential results of our activities and evolution of our business and our financial projections.

Actual results may differ materially. The risks and other factors that could cause actual results to differ are discussed in today’s press release and in the risk factors section of our quarterly report on Form 10-Q filed with the Securities and Exchange Commission on November 06, 2015 and other reports filed with the SEC.

Any forward-looking statements represent our views as of today only. We may update these statements in the future, though we disclaim any obligation to do so.

I would now like to turn the call over to Jeff.

Thanks, Paul. I'd like to welcome everyone to our call.

I’ll begin my comments with Slide 4. In 2015 we took big steps towards becoming a fully integrated biopharmaceutical company as we focused on becoming one of the true leaders of innovation in CNS drug development.

And 2016 we think have the opportunity to be a truly transformative year for SAGE. I'm very excited to walk through our extremely active pipeline and all of the milestones we anticipate achieving this year.

Starting with our ongoing Phase 3 STATUS trial of super-refractory status epilepticus and moving on to our additional GABA based clinical indications and our emerging NMDA platform. All of this is possible through our novel scientific platform which recently have offered us the opportunity to develop innovative new treatments for patients with life altering central nervous system disorders and to do so through a rational sequential clinical development approach that we believe gives us the best possible chance of success.

Turning to Slide 5, we'll begin with our lead program SAGE-547 the super-refractory status epilepticus or SRSE which currently has no approved therapy despite the extreme unmet medical need. Following our strong results on our Phase 1-2 study of this devastating disorder, we initiated our Phase 3 STATUS trial this past August.

We anticipate this trial will enroll up to 140 patients to achieve 126 evaluable patients and we intend to initiate up to 150 sites in the U.S., Canada and Europe. So this is a global trial.

This is a randomized, double-blind, placebo-controlled study which is being conducted under a special protocol assessment agreement with the FDA. Enrollment and site openings have gone well, so we were pleased to announce in December that we now expect to read out top-line results from this study in the second half of 2016.

That timing remains on track today. And as a reminder, SAGE-547 SRSE is being developed under the orphan drug law and Fast Track designations.

I'd like to turn now to Slide 6. We have several important milestones that we expect in the first and second half of 2016 with other indications within our GABA-based pipeline as you can see here on Slide 6.

I want to remind folks about our clinical development strategy. In addition to SRSE we believe that we have identified a number of CNS disorders that can potentially be targeted through the mechanism of GABA synaptic and extrasynaptic modulation and building off of our data and proof of principle in SRSE, we have worked to test SAGE-547 and its mechanism in several additional indications in order to validate our hypothesis that these indications may respond to modulations of extrasynaptic GABA.

If we see positive activity in these so called probe studies we believe this gives us confidence in advancing our next generation GABA candidate into those indications. These GABA candidates are not only more potent with similar pharmacology but have optimized PK profiles or pharmacokinetic profiles designed for their target indications.

You can see this concept laid out on Slide 7. Executing on this approach during 2015 we were excited to share data from our Proof-of-Concept study of SAGE-547 in both essential tremor and severe postpartum depression or PPD.

For essential tremor last fall we announced positive top-line data in a placebo-controlled Proof-of-Concept trial in 25 patients where we demonstrated clear separation from placebo on efficacy endpoint at the target dose. For severe PPD in a Proof-of-Concept study last year we evaluated four women with severe Hamilton depression scores and demonstrated significant improvement in less than 24 hours on those scores with sustained improvement across 60 hours of treatment.

These data are in line with our hypothesis generated from known animal data that suggests extrasynaptic GABA modulation may play an important role in postpartum depression and perinatal behavior. We recognize that these data were obtained in the open label [matter] [ph].

So to validate that initial signal in postpartum depression we are currently conducting an additional placebo-controlled Phase 2 Proof-of-Concept study in up to 32 patients across multiple centers, who have been diagnosed with severe PPD. We expect this to read out in the first half of this year.

As we establish proof of mechanism with SAGE-547 the second part of our plan comes in the form of SAGE-217, our oral modulator new chemical entity or NCE that has a very similar modulatory mechanism of SAGE-547 but with an optimized PK profile intended for once daily dosing and also designed to be much more potent at both the synaptic and extrasynaptic receptors. SAGE-217 is currently in Phase 1 development and is performing well in healthy volunteers.

If we see the PK/PD and safety data that we hope to do in Phase 1, in the second half of this year we plan to move SAGE-217 into Phase 2 studies in essential tremor, postpartum depression, if the data from SAGE-547 Phase 2 reads out positively, as well as a program encompassing a series of orphan epilepsies where we believe from all of our preclinical work that 217 should have clinically meaningful activity. All of this gets back to our unique approach to CNS drug development using clear binary signals and read throughs across mechanism and preclinical work to efficiently explore initial activity while optimizing a final candidate for a particular indication.

We're very excited to read out both the PPD data in 547 and the Phase 1 data in 217 in the first half of this year and then update you on these three indicators moving forward in the second half of the year. In the meantime, we also continued to invest in the development of next generation GABA candidates further down the pipeline.

This includes SAGE-689 a next generation positive allosteric modulator of GABA A receptors has been optimized to have wide therapeutic window, rapid clearing and [potent] [ph] anti-seizure effect. We believe SAGE-689 can have potential indications where a high degree of anti-seizure activity and sedation is desirable before the introduction of general anesthesia such as in status epilepticus in the emergency room but also in other additional disorders.

We announced back in November that this program had been delayed due to a non-clinical, non-toxicologic request from the FDA and we still expect to initiate our Phase 1 trial in the second half of 2016 assuming the FDA is satisfied with our response. Turning briefly to our NMDA program on Slide 8, I won't spend much time here, but as I had laid out for you in November, this is a piece of our pipeline that we are incredibly excited about.

The NMDA receptor system is one of the key excitatory systems in the central nervous system, and underlies cognition and memory among other functions. We feel that SAGE is right at the forefront of the emerging biology here and we continue to advance our present development candidate SAGE-217 which has been designed to be a first-in-class highly potent and selective modulator of NMDA with an optimized pharmacokinetic profile intended to support oral dosing.

The initial indications are targeted at two orphan indications where NMDA hypofunction or dysfunction has been established. Smith-Lemli-Opitz Syndrome or SLOS syndrome and Anti-NMDA Receptor Encephalitis for which there are no approved therapies.

We believe these are homogeneous populations with peripheral biomarkers that may also be implicated in other larger CNS indications resulting from NMDA receptor hypofunction or dysfunction. And again, going back to our broader CNS development strategy, our approach in our NMDA program echoes what we have done with GABA and that is a broader CNS development strategy pursuing a rationalized approach to further development by first establishing mechanism and proof of activity in smaller indication and then hopefully proceeding to larger markets where we can approach these markets with a biomarker driven strategy.

I'd like to turn now to Slide 9. As I hope you can see we've built on our initial success and development of SAGE-547 and how have what we believe to be an industry leading CNS pipeline with significant potential across a wide range of CNS disorders and we think that we can achieve this goal by targeting fundamental CNS systems such as GABA and NMDA.

I'd like to just walk quickly through the anticipated milestones I covered here on Slide 9. In 2016 we expect data from the Phase 2 study of SAGE-547 in severe PPD and a Phase 1 read out from SAGE-217 during the first half of this year.

We anticipate data from the Phase 3 STATUS trial in the second half of 2016. Continuations upon first half readout we anticipate potential initiations of several Phase 2 studies with SAGE-217 including the study in essential tremor, postpartum depression and orphan epilepsies in the second half of 2016.

And we expect to initiate our Phase 1 program with SAGE-689 in the second half of this year. So as you can see, we have a number of important inflexion points we hope to achieve over the next 12 months that we hope will lead us closer to becoming a commercial stage biopharmaceutical company and will also that we hope will help define our late stage pipeline in GABA related and NMDA related indications.

I'd like to thank you all for your attention and now I'd like to turn the call over to Kimi to discuss our financials before we get to Q&A.

Thank you, Jeff. On Slide 10 we have a summary of our financial results for the fourth quarter and full-year 2015.

Cash and cash equivalents at the end of the year totaled $186.8 million. This does not include funds from our recent public offering which raised approximately $140.4 million in net proceeds.

Research and development expenses for the fourth quarter were $20.4 million including $1.6 million of non-cash stock based compensation expense and $69.4 million for the full year 2015 which included $5.9 million of non-cash stock based compensation expense. Moving to general and administrative expenses for the fourth quarter they were $8.2 million including $2.5 million of non-cash stock based compensation expense and $25.3 million for the full year 2015 including $9.3 million of non-cash stock based compensation expense.

We reported a net loss in the fourth quarter of $28.6 million and $94.5 million for the full year 2015. As of February 16, we had 32 million shares outstanding.

In the coming quarters we expect to see increases in operating expenses as we complete our Phase 3 STATUS trial with SAGE-547 in SRSE and continue to advance our clinical development and discovery efforts and also engage in activities directed at a potential NDA filing and commercial launch and further grow our infrastructure and organization. Based on our current operating plan, we expect our cash and cash equivalents and the net proceeds of $140 million from the offering will be sufficient to fund our current operations and through the beginning of 2018.

Before we open up the call over to Q&A, I'd like to remind you that we plan to attend a number of upcoming conferences in the first quarter which are listed on Slide 11. These include the Epilepsy Foundation Pipeline Conference, which is taking place in San Francisco on February 25 and 26; the Cowen Healthcare Conference where we will be presenting at 04:00 PM Eastern Time on March 07; the American Chemical Society National Meeting & Exposition taking place in San Diego from March 13 to March 17; and the American Academy of Neurology Annual Meeting or AAN taking place in Vancouver from April 15 to April 21.

We will now like to open the call for Q&A. Operator?

Hey, good morning guys, this is Morgan on for Cory. I just had a quick question and this may be getting a little bit of ahead, but can you kind of talk about what preliminary commercial preparation that you may have ongoing right now for 547, what kind of steps are you taking now to ensure that everything moves on efficiently given you have positive data at the end of the year?

Hey, good morning and thanks for the question. We've taken a number of steps as you know to maybe I'll answer the question because you don’t know, to prepare pre-commercially.

So we've begin as you know we're doing payer research both here and overseas based on what we project could be a target product profile and that will also give us an idea looking at potential reimbursement channel. So we're doing, that's already occurring and as you know with the acceleration of our time line and the compression of the time that DEA could have to review which is but shortened by statute last year we've also begun hiring in particular areas in terms of brand management.

We've also brought in the former Head of Supply Chain from Cubist, Heinrich Schlieker, who is now running our supply chain organization to help make sure we have our manufacturing supply chain locked down. In addition, we are building up our medical science liaison group and as well as our medical affairs group.

And as Kimi noted earlier, we are now beginning to publish and present more broadly this year as the data come through and as we anticipate many of our patents we'll be filing, so it'll be free to speak about structures and things of that nature. So we have a fair number of initiatives underway in preparation - prelaunch preparation.

Obviously that will depend on the outcome of the Phase 3 program which is still performing well and on track to report out in the second half of this year.

Okay great, thanks a lot.

You bet.

Hi guys, good morning. Thanks for taking the question.

I wanted to just dig in a little further on the status of your Phase 2 PPD study, is that open and how is enrollment going, can you give us any more details on the design and powering of that study other than the 32 patients?

The base of study is enrolling. We've almost completed opening up all the sites.

There will be 10 to 15 sites. We've had a lot of interest in this study and it is on track.

As you know it is, as I have described it is a reasonably straightforward design and the design was informed by the original open label data in terms of that treatment protocol, the dosing protocol, the primary and secondary endpoints as well as the followup up to 30 days. So it is doing quite well and it is on target to report out in the first half of this year.

Are the entry criteria for the patients pretty identical to the pilot study?

Yes, they are, I think one of the caveat, one of the process we've taken at the company is to use each study to inform the next study and so since we had, although is open label I want to make sure I point that out, we had very dramatic results in the first four patients. We determined at that point that we should keep the same inclusion, exclusion criteria.

The only modification that we've been allowed to now is that women who are breastfeeding we have now been granted a waiver by the FDA to include women who wish to breastfeed they have to pump the milk and not use it but they are now allowed to be enrolled. So that's the only difference which obviously we're very encouraged by and so that's it, otherwise same endpoint, very straightforward design.

No bells and whistles. It is a very, very straightforward clinical design.

And my followup is on 547 in SRSE, the tightening of the timeline around the data that you have given us, can you tell if that's driven by your visibility on event rate or your visibility on just enrollment?

It is actually driven by all those factors. Steve's team who is here and he can give more granularity.

We had a working model that assumes certain population prevalence, it assumes certain enrollment rate and assumes a certain time period for opening up sites. Remember many of these sites are not classical clinical trial sites, they are actually working IC used and as we had a pretty broad range when we started and as a result the tightening of the timeline really comes to all those factors on the model that our confidence in the actual prevalence, the enrollment rate as well as our ability to open up sites quite expeditiously we've had a lot of interest in sites both here and in Europe as well, so all of those things moved forward well.

The other point I'd make is when we started the estimation for launch period we had assumed because this is a GABA mechanism although we don’t know that there was a possibility that DEA would at least want to pass judgment on scheduling and as you know historically that can take 12 months or more and we had that baked into our launch plan. And this gets back to the first question as well.

In December the Congress passed a law that now mandates DEA has only 90 days to decide on scheduling and remember that can't start until the NDA is approved. So that was always another unknown that has now been removed and that was the other reason we accelerated the timeline in addition to the fact that the trial is performing well.

Got it and my last question is on your NMDA program, can you give us anymore detail on the mechanism there, I know there is a variety of pipeline programs that affect either the NMDA the channel or an allosteric site and what the mechanism, what your mechanism might mean for future indications?

The SAGE team a number of years ago, about three years ago, published data with collaborators that identified 24-Hydroxycholesterol as the probably possibly the native positive allosteric modulator of NMDA in the brain. And so - and we knowing that this was an oxysterol which some of you know is now a very interesting mechanism to lot of basic scientists in terms of neuroscience.

So we decided and understood at that point that we had a potential breakthough in terms of a molecular scaffold that could impact NMDA activity. So 718 was born from this original discovery and it is we believe our first in class positive allosteric modulator of NMDA.

And so 718 has been designed much like 217 and I apologized for the numbers our chemistry guys aren’t good chemistry namers, but 718 is we believe will also be like 217 orally available as well as highly potent possibly once daily therapy. So our belief is that as a first in class we decided to focus on positive allosteric modulator because no one has really having done this successfully.

And we already have non-GLP tox on this compound. It is an IND enabling toxicology now, but the non-GLP tox suggests it is behaving as we anticipated as a reasonably – as a very on target positive allosteric modulator without any of the associated cytotoxicities that have often been hypothesized to encumber this particular mechanism.

So we decided that therefore we, that we brought the drug forward and we also understand from the animal data that this is a mechanism that ought to be useful in cognition, attention and other areas of CNS function. And our approach to development was to therefore we said rather than going to the large markets first, because people have talked about these programs in Alzheimer's or autism, our translational group identified two disorders that I’ve mentioned on the call both of which have known NMDA hypofunction which therefore ought to be modulated and attenuated by treatment with 718 that we get through Phase 1.

They both also have peripheral biomarkers associated with their, with a particular comp at the symptomatology that extend into large markets such as Alzheimer's and other encephalitis as well as autism. So our hope is that even though we can get indications in these rare diseases that we can take the data if they are positive and then use it prospectively to find biomarker which has a known symptom complex associated with it and move then into larger markets with this molecule.

The other part of the NMDA program is the NMDA that the NAM or the negative allosteric modulator program that’s a little bit further behind and we are exploring a potential, a number of potential approaches here on that and will have more news about that probably later this year or early next year.

Great, thanks for taking all the questions guys.

You bet.

Hi, guys thanks a lot for taking my questions. The first question I have is Jeff, can you comment on what you guys are seeing in terms of the screened failure rate 4.5, 4.7 in terms of that initial weaning attempt and is that relatively in line with your expectations when you designed the study?

We are not doing it – thanks for the question, firstly, this is - as a Phase 3 program the primary goal for the company is to maintain the integrity of the program. It is completely blinded and so we are not doing interim looks or any of that nature.

All we can tell you is that it is well on track to report out in the second half of this year. One of the reasons we put out the evaluable versus the screens rate is that was based on the, and we've been too careful to do that in anticipation of this kind of question.

That’s why we tell people we anticipate needing to enroll about 140 patients or randomized to get about 126 evaluable, but other than that we are really not, we’re not doing any interim looks. I would point out though that one of the major advantages of this study is that we are doing this qualifying wean and that of course helps to regularize and homogenize the population and make sure that the patients we are treating actually had true diagnosis of SRSE.

Okay and can you give us just a sense qualitatively if, I mean initial data read out if you will be talking at all about some of the secondary end points and I know if you have made that decision yet?

Our basic, this kind of, let me kind of say this, this will be an obviously it is positive, this will be an NDA filing. So our intent will be right now our plan is to give out the primary endpoints along with what typically is associated with this type of reporting out top-line results as well as safety and safety data, ADOs dropouts due to death, discontinuation and things like that.

And we may give some granularity around the weaning in terms of the efficacy, but we will have several secondary endpoints many of which are designed to look at pharmacoeconomic advantages of this approach and those we will probably wait for publication and publication or scientific presentation.

Okay and then in terms of 217 you talked about several different indications where you are planning on looking at the agent. So given your comments regarding large indications versus small indications, if you had the choice between all three of PPD, orphan epilepsies and essential tremor would you have a bias at this point towards going for smaller indications versus larger indications or is it simply just let's look at what the data tell us and then let's decide about what size indications to focus on.

Well, firstly I love all my children, so let me just begin by saying that. And right now I think that these are all areas where we think, I think that you answered it, it going to be driven largely by clinical feasibility and our ability to impact patients' health and care and improve patients' lives.

Yes obviously, the great unknown is postpartum depression. If that were to report out positively from 547 that has very broad implications for what this mechanism could do not only in postpartum depression, but in other forms of depression or either sex linked depression or generalized depression.

So that could change our thinking candidly about how we approach Phase 2. We already have very good data in tremor we believe and so that I think looks to be something we would also think to have to really consider hard because that clinical feasibility we think is quite good and for orphan epilepsies, we have such a profound database historically about this mechanism.

So all of these we think are highly feasible and have already been arguably somewhat de-risked. I think as you say to conclude, it’s really going to depend on how postpartum depression reads out and what how the drug will continue to perform in Phase 1.

We are getting that's in the middle, we are already in multiple ascending doses. The drug is performing very well.

We are comfortable in saying it’s going to be a very potent drug and it’s likely to be a once-daily – a drug used once daily. So right now it’s moving very well on track and so I think that is the other piece of the puzzle that is how 217 finally performs in the Phase 1 program as to where how we sequence the introduction of Phase 2.

I think the other implicit comment or inferential thing that one can infer from your question is that, this is a mechanism that is likely to be quite potent and have a broad potential use across multiple indications. We believe we probably had the industry leading platform in this particular mechanism.

So we will be looking opportunistically not only for 217, but some of our follow on compounds of where we might use them as we get the readouts from Phase 1.

Great, thank you.

Thanks John.

Hey guys, thanks for taking the question.

Hi Paul, how are you?

Doing well, thanks Jeff. We have a couple, the first one is on the 140 patients enrolled versus to get 126.

Can you expound upon what could exclude a patient from being in the 126 sample from the initial 140 sample that first enrolls?

Yes, basically remember we had – we described this when we did the Phase 2 and so a few patients either died before they could have a drug administered or their complications preclude completion of treatment and an obvious complication of the underlying disorder, so somebody with a stroke bleeds out or and things like that. Occasionally there will be, a family may decide to withdraw consent for treatment given the extent and circumstances from which these patients suffer.

So those are the kinds of things that occur and so as a result in order to give some, I know we had the same ratio in the Phase 2 which was 25 enrolled, 22 evaluable and so that is how we did that. We just wanted to give some clarity in terms of the number of patients we projected, we would need to screen.

The other point of course is that we - these are - we also remember I pointed this out to the earlier question, we are doing a lean attempt on trial prior to randomization. So, some of that variability will be removed.

So that is the reasoning behind that.

Okay. And Jeff is the evaluable population the one that is evaluated in the FDA approval by TT analysis?

It’s a randomized double-blind study and it’s likely that we will use, it is a discussion we will have and frankly that will depend on the nature of the exclusion. And so for example, it’s an old statistical conundrum.

We used to call this a school bus problem where if your patients are coming in to be their first treatment [ph] and the school bus crashes they are - they have been randomized, do you include them in and are they are evaluable. This is a unique population and so that is a discussion that is in the stats, but we haven’t made it public because it was a discussion and something we were very happy with the outcome of the agency.

Okay, great. And then I have one more pipeline question, so we have done some more reading on alepregmadilone and the mechanism and I found that beyond its effects on GABA it’s mechanism is more multifaceted.

The drug also can work on some various progesterone receptors. So when you think about using this as a probe molecule and subsequently moving forward with SAGE-217 to what extent does SAGE-217 fully replicate alepregmadilone's pharmacology and in these various indications how confident are you that it is all its effect on GABA that could be driving a benefit in PPD, tremor, et cetera?

If you look at the Annual Day and then we can get some more details if you want, but basically the concentration required for the off target effects are much higher than those – than aloe's effect on GABA and in fact if you look at some of the animal data progesterone by example, has often not been useful in the same indications in the animal data where alepregmadilone has been active. The second point I would make is that if you look at the data we have already published and made published or made public, we’ve already shown for aloe [ph] it has GABA-ergic like effects in animal models that are replicated say for example in beta power for EEG in humans across indications.

Those same effects that we see that we believe are GABA-eargic are also seen by 217. We think that – so we don’t think there is anything magical about the off target effects of aloe [ph] and if you look at the data set for PPD it is pretty clear that is an extrasynaptic effect not a more promiscuous effect based on off target.

The 217 data in animals really does look very similar though more pleasant than 547, which suggests in and of itself that the mechanism is GABA-ergically driven, not by these off target effects. I would also make the final point is that we believe that for a chronic oral therapy that the ideal pharmacology is one that's clean with minimal off target and of course that has been our thesis in moving forward both 217 or chronic oral use as well as 689 for more complicated use in the emergency room.

Okay. And just one quick follow up, have you done, I know animal models in depression are highly flawed, but have you done any animal work on SAGE-217 in depression and things like the four swim test or other various animal models?

I’m going to turn it to Steve.

Yes, so we've - the animal models that we’ve been looking at have primarily been in the areas of seizure, some level of anxiety and sedation. As we get more data and in this case we are following clinical data as opposed to relying on what I will consider to be somewhat not as predictive animal models in terms of depression though we disclosed information as well.

I think the one point we've made as Steve alluded to, as expected 217 dose and animal dose appear to have [indiscernible] and we do see this and there is some preliminary data humans as well, so I think from this standpoint we will rate the PPD program, I think will be somewhat prohibitive for this and if that program reads out positively we will pursue, more actively pursue some of the work for validation. Let me just say this, you probably know this and I know it is not meant to be a trick question, a lot of rats have drowned in the service of developing antidepressants to no avail.

The forced swim test learnt this has had imperfect translation to clinical activity. So I think for 217 and 547 in particular, I think this is a great example where leading with human data is really the proper approach.

And as I say, if we see such activity we can then reverse engineer some animal data, but I think the human data is really obviously going to be the most compelling.

Sure, it makes sense. Okay, thanks guys.

Hey guys, thanks for taking the question. Can you just clarify the lean prior randomization in the STATUS trial, so you guys who are qualifying lean in the 24 hours post and then you guys – so I just need a little clarification in that?

Yes, actually that’s right. Thanks Raj, I mean I'd let Steve give you some more granularity on that.

Yes, when patients are enrolled what we'll do is ensure that within the first 24 hours we’ll do what's called a qualifying wean. That's to ensure the patients remain in status up that begins before being randomized.

So regardless of what their history had said before they have been enrolled, we want to ensure that closure to read possible they remain in Status prior to being randomized into trial.

Okay and then regarding SAGE-217 what internally which you consider a success in the phase 1 trial is it a better safety profile in the 547, is it a better PK profile and then what doses are you using how does that compare with the 547 doses that you have used in the approved concept trials?

So that the Phase 1 like any standard Phase 1 is healthy volunteers is really trying to help us understand both the exposure as well as the safety. So in terms of exposure and PK what we are looking for are the things that Jeff was referring to which is good oral bioavailability measures which case we mean very robust and we have parameters for those, who needs to have very clear oral bioavailability that would not be dose limiting and the other would be to confirm what we've been seeing in animal models which has to do with a long half supported once day.

So those will be considered, sort of swinging out of the part, home runs in terms of what we would expect. Of course the other part is the safety and safety both in single and multiple dosing, so these are sort of the base line.

The other things we are looking into and I think it speaks to your other question which is, what is the dose ranging that we need to be in and there we have been using EEG as a way of identifying what would be the appropriate dose ranges against variety of indications. So as we've discussed, in the past we’ve used data power as a way of understanding the levels of exposure not necessarily dosing that would have predictable GABA related effects in essential tremor and in postpartum depression and we'll use that as an indication of what sort of doses be get selected to Phase 2.

So basically what Steve said is we’ll have Pharmaco EEG and I think that the point that we want to emphasize is that we have shown data power to be pretty closely correlated with activity in the tremor program. So we really have a very powerful and reasonable biomarker that I think will inform, how good a drug 217 is likely to be moving forward.

So we’ll get a sense of therapeutic index and things of that nature. So when this concludes in Phase 1 we will have single ascending dose, multiple ascending dose, obviously standard PK and some pharmacodynamics, which I think will go a long way to either risk or de-risk our further development of the molecule.

But as Steve said and I said, right now its performing as well as we could have hoped.

Okay and one last question, Kimi with all these [indiscernible] guys have what goes on in the financial model with 2018 is that assuming everything works and we’re going to Phase 2 and everything just and the ramp as well, just a little clarity on that?

Yes, it’s really it’s the pipeline that we showed in the slide deck is all the problems that will move forward. I think at this point PPD is where we don’t have visibility into what the Phase 2 would look like and so that one is we know we’ll need to revaluate.

Great, thank you.

Thank you everybody for your attention this morning and we think 2016 is going to be a transformative year for the company and we appreciate your interest and support and everyone have a great day.