Matt Hogan - CFO Jim Brown - President and CEO WeiQi Lin - SVP, R&D, R&D Business Development and Principal Scientist.

Annabel Samimy - Stifel Nicolaus Yi Chen - Rodman & Renshaw Len Yaffe - Kessef Capital Management, LLC.

Greetings, and welcome to the DURECT Third Quarter Earnings Conference Call. At this time, all participants are in a listen-only mode. A brief question-and-answer session will follow the formal presentation. [Operator Instructions] As a reminder, this conference is being recorded. It is now my pleasure to introduce your host, Matt Hogan for DURECT.

Thank you. Mr. Hogan, you may begin..

[Audio starts abruptly] forward-looking statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Further information regarding these and other risks are included in our SEC filings, including our 10-Q under the heading Risk Factors.

Let me now turn briefly to our financials. Total revenue was $3.7 million in the third quarter of 2016 compared to $4.7 million in the third quarter of 2015. Revenue from our R&D collaborations was 352,000 in the third quarter of 2016, as compared to $2.1 million in Q3 2015.

Revenue from this source always fluctuates from quarter-to-quarter depending on the stage of development under the various programs and our role in those programs. Product revenue largely from the sale of ALZET pumps and LACTEL Polymers was $3.4 million in Q3 2016 as compared to $2.7 million in Q3 2015.

Our gross margin on these two product lines was 61% in the third quarter, and these product lines continued to be strongly cash flow positive for us. There was one unusual item in the quarter that’s worth by pointing out.

As you will see from our income statement and will be explained in our 10-Q that we plan to file tomorrow, our overall profit, gross profit and gross margin was affected by a charge of $926,000 that we took during the quarter.

Given the REMOXY Complete Response Letter, we took a hard look at the expected expiration dates of our various lots of [indiscernible] () and prepaid inventory for these raw materials and decided we should take a charge at this time. It’s a noncash charge and that we had already spent money in prior periods.

These [indiscernible] () solely used for REMOXY, but we did expect that will be a major use of them. If in the future we are able to sell some of this material that we’ve written down in Q3 2016, at that time we will report an unusually high gross profit margin as there will be no associated cost of goods sold for that inventory.

R&D expense was $6.8 million in the third quarter of 2016, as compared to $6.7 million in the third quarter of last year. SG&A expenses were $3 million in the third quarter this year as compared to $3.2 million in the third quarter of last year and our net loss for the third quarter was $8.8 million as compared to $6.5 million in Q3 2015.

At September 30 2016, we had cash and investments of $29 million, which compares to $33.9 million at June 30, 2016 and $29.3 million at December 31, 2015. So we had an underlying cash burn rate of $5.7 million in the quarter.

If you exclude around $1.9 million that we raise by selling about 1 million shares through our ATM facility at an average price of $1.87 and excluding the one-time costs associated with our debt refinancing. With that, let me turn the call over to Jim Brown, to discuss non-financial matters in greater detail..

Thank you, Matt, and hello, everyone. I will give an update on our most advanced development programs and then we will open-up the call for questions and answers. We are excited today to be able to share the patient data news on DUR-928.

We feel this may turn out to be a historic time for DURECT shareholders and the patients that may eventually be helped by DUR-928. However, we will begin with our other development programs, leaving DUR-928 for the end. Let's begin with POSIMIR. The primary focus of the POSIMIR team is to persist Phase 3 trial.

We’ve switched over the majority of our active clinical trial sites and their PERSIST trial from part 1 to part 2. Part 2 of the PERSIST trial is the portion in which POSIMIR is compared head-to-head against bupivacaine hydrochloride. We continue to add new sites to the PERSIST part 2 trial.

We currently expect to complete enrollment in the trial in the third quarter of 2017. While this trial was enrolling, the team is reviewing and updating various sections of the NDA with the plan for to be available for resubmission as soon as the PERSIST trial data can be incorporated into the NDA.

With regard to our partnering POSIMER, we’re running a process in which we’re engaging with multiple potential partners. While this process is ongoing, we will let it play out without discussing particular updates. Moving to REMOXY ER. As most of you know, REMOXY ER received a third Complete Response Letter in September.

This new CRL did not reference the chemistry manufacturing and control questions that direct aided Pfizer and Pain Therapeutics in addressing. Rather, this new CRL focused on abuse-deterrent studies and labeling.

It is our hope that Pain Therapeutics will be able to reach an agreement with the FDA regarding what additional data the FDA requires to satisfy them of REMOXY ER's abuse-deterrent capabilities and an appropriate label.

Pain Therapeutics reported in their last SEC filing that subject to discussions with the FDA and their consultants, they expect to be able take approximately -- it will take approximately a year to conduct the actions described in the Complete Response Letter.

Considering the significant opioid problem that exists in the U.S today and our conviction as to the inherent properties of REMOXY ER, we hope this product is eventually approved. But since it's not our NDA, we’re focusing our efforts on the programs that we own and can control. Now onto DUR-928.

DUR-928 is our Epigenomic -- Epigenetic Regulator programs lead product candidate. It's an endogenous small molecule, new chemical entity, which may have broad applicability in several metabolic diseases such as nonalcoholic steatohepatitis or NASH and into acute organ injuries such as acute kidney injury.

Why are we so excited about DUR-928? Well, it breaks down to being the biology, the biochemistry, the animal data and finally the human data. Let's start with the biology. It's an endogenous molecules that we found to be highly conserved.

After the discovery of DUR-928 we developed a test for it and found that healthy subjects from the six species we tested that is mice, rats, hamsters, dogs, monkeys, and humans have the same plasma concentration range. Its endogenous. So its present in the body for a reason.

With the safety profile we’ve seen so far, combined with the effects we have seen in numerous animal models, plus the human patient data that we're announcing today, DUR-928 has demonstrated the potential to help patients with a number of diseases. It's the biochemistry. DUR-928 is a sulfated oxy-sterile. It's epigenetic in function.

That is, after its produced in the mitochondria, it travels into the cytoplasm where its sulfated and then moves into the nucleus were it binds the protein and influences cellular activity via nuclear receptors.

The cell culture work and animal disease model studies we’ve conducted demonstrate that DUR-928 works by affecting nuclear receptors not downstream as one part of a pathway, but rather this molecule acts upstream impacting many genes in many pathways. DUR-928 influences lipid metabolism, inflammation, and cell survival.

As mentioned earlier, the safety profile so far looks very favorable. We’ve dosed animals to the point that we've achieved plasma concentrations that are more than 10,000 times the native levels and we've seen no adverse safety signals of concern.

We've safely reached plasma levels of DUR-928 in humans that have exceeded a 1,000 times the endogenous levels. We are also excited about the animal data. It's a truism that animal data is an imperfect predictor what can happen in man.

That being said, the impressive thing about DUR-928 is a similarity of the responses we observed from the large number of diverse animal models that we’ve conducted at the various CROs we've done work with around the world. Typically, we see positive results the first time we evaluate DUR-928 in a given model.

If it were one or two animal model that would be encouraging, but we've now disclosed data from 10 different animal models, so you can see that we’ve something very different here. When one attempts to translate animal models to the human condition, it can be a difficult translation to make.

That's because human disease is typically more complex and has been generated over a much longer period of time, years versus weeks. The breadth of our animal model work and a specific biochemical biomarker changes that we’ve seen from all of these studies, leads us to believe that we have an opportunity to help patients with these complex diseases.

And finally we're excited because of the human data we’ve seen so far. DUR-928 has demonstrated good safety in more than 80 normal human volunteers that [indiscernible] date and we now have signals of activity in patients.

This activity ties together the biology, the biochemistry, and the animal data that strengthens our conviction that we're developing an important new category of medicine. Simply stated, we all have DUR-928 in our bodies. It helps aid our metabolic inflammatory and survival responses to stressful conditions.

We've safely given large doses of DUR-928 to animals and people. We have DUR-928 positive results in 10 different animal models. And today we announced that we’ve seen clinical chemistry and biomarker responses from cirrhotic and non-cirrhotic NASH patients after receiving just a single dose of DUR-928.

We first introduced 928 to our investors back in March of 2015. At that time, we had just begun our first Phase 1 trial in human volunteers and share data from a limited number of animal pharmacology models.

Over the last 18 months, we've completed four Phase 1 studies, investigating the pharmacokinetics and safety of a single and multiple doses via oral IM and IV routes of administration.

We now have dosed approximately 110 people with DUR-928 and we are now disclosing data from 10 -- we’ve now disclosed data from 10 different animal models, pharmacology studies that suggest a broad range of potential clinical utility for the compound.

Additionally, we’ve initiated two Phase 1b clinical trials in patients to evaluate the pharmacokinetics in patients with liver and kidney function impairment. At the end of September, we held our first pre-IND meeting with the FDA. At this meeting we discussed the potential of using the DUR-928 to treat acute kidney disease.

Based on this meeting, we will soon be submitting our first IND for DUR-928 and look forward to treating patients in a Phase 2 trial and acute kidney disease next year.

This progress represents a substantial amount of work by the DUR-928 team, because DUR-928 is an endogenous molecules, a lot of investors I meet with understand the market -- the molecules potential. That being said, when meeting with investors one question consistently comes up.

They want to know when we will have evidence in patients reflecting DUR-928's activity from these various animal models. Well, today's the day. Today we're providing a description of data from the first cohort of phase 1b study with DUR-928 in patients with non-alcoholic steatohepatitis.

Data from this cohort show that a single dose provided signals of DUR-928 activity in cirrhotic and non-cirrhotic NASH patients. These DUR-928 data in patients are consistent with the activities that we’ve seen in animal models and in cell culture.

Our first patient trial utilizing DUR-928 is an open-label, single ascending dose safety and pharmacokinetics Phase 1b trial in liver function impaired NASH patients and matched control subjects. The control subjects are matched by age, body mass index and gender, but have normal liver function.

This study is being conducted in successive cohorts, evaluating single dose levels of orally administered DUR-928. The first low-dose cohort consisted of 10 subjects with NASH, four of which was cirrhotic and six were non-cirrhotic and six matched control subjects.

After a pharmacokinetic safety review of this cohort, the study we has proceeded to the higher dose cohort utilizing a dose that is four times larger than the low-dose cohort. Data from the first cohort show the pharmacokinetic parameters between the NASH patients and the match control subjects were comparable.

While the study was not designed to assess the clinical efficacy of DUR-928 as a therapy for NASH, certain clinical chemistry biomarkers for liver function and liver injury were reduced 12 hours after dosing with DUR-928 as compared to before dosing.

Furthermore, high sensitivity C-Reactive Protein, a marker of inflammation, was reduced after dosing with DUR-928.

Interleukin-18, an inflammatory mediator implicated in both liver and kidney diseases, decreased in the NASH patients as soon as a few hours after dosing, and when the -- and the effect was more pronounced in the cirrhotic subjects at 12 hours after dosing. There was little or no change of the interleukin-18 levels in matched control subjects.

In addition, both full length CK18, a generalized cell death marker and cleaved CK18, a cell apoptosis marker, were reduced after DUR-928 treatment in the NASH patients, with the effect being more pronounced in the cirrhotic subjects, and little or no change in the matched control subjects.

Collectively, the reduction of these biomarkers plus results from our animal studies and cell culture studies suggest potential therapeutic activity of DUR-928 for patients with liver disease.

It should be remembered that there is no guarantee that in future studies DUR-928 will demonstrate safety or efficacy in treating NASH or other liver diseases, in larger controlled studies. Dr.

Arun Sanyal, who is a Professor of Medicine, Physiology and Molecular Pathology at Virginia Commonwealth University and the past President of the American Association for the Study of Liver Diseases or AASLD, recently reviewed the data from this trial and was impressed that DUR-928 demonstrated this type of activity signal from a single dose.

We're currently enrolling and dosing subjects in the higher dose cohort for this Phase 1b trial, which we expect to complete in 2016. We expect this trial will enable and inform future studies in patients with liver diseases.

We recently requested a pre-IND meeting with the U.S Food and Drug Administration as a precursor to submitting an IND to enable future liver disease clinical trials in the United States. We’ve a second Phase 1b study with DUR-928 that is also being conducted in Australia.

It's an open-label, single ascending dose safety and pharmacokinetic study in patients with impaired kidney function that is stage 3 and stage 4 chronic kidney disease. This study also includes mass control subjects with normal kidney function.

After PK safety review of the low dose, the study may proceed to a higher dose, assuming both cohorts of dose the study will compromise -- comprise approximately 16 to 18 subjects. We anticipate that we will have results from this trial in 2016 and that this trial will support patient studies in acute kidney injury and/or other kidney diseases.

We recently held a pre-IND meeting with the cardiovascular and renal products division of the FDA to discuss the DUR-928 development program for acute kidney disease.

We will use feedback from this meeting, as well as our feedback from our clinical advisors in order to file the IND to enable kidney disease clinical trials to begin in the United States. We have previously communicated the biological activity of DUR-928 have been demonstrated in eight different animal disease models, involving three animal species.

These models represented acute organ injury and chronic disorders involving kidney, liver, brain, and multi-organ injuries. Today we’re reporting on two additional animal disease models. First of these is a second study in a mouse model of advanced NASH, the STAM model.

In this model, which is conducted by a Contract Research Organization in Japan, NASH is induced in diabetic mice that are fed a high fat diet. In a previously reported study in this model, the treatment with DUR-928 was initiated when the fatty liver -- when fatty liver had formed and stopped after fibrosis have been developed.

Daily oral administration of DUR-928 for four weeks resulted in inhibition of the progression of liver inflammation, hepatocyte ballooning and fibrosis. In our latest study in this model, the treatment was initiated after fibrosis had formed and stopped after nodules had developed.

Daily oral administration of DUR-928 for four weeks resulted in a statistically significant reduction of the fibrosis and hepatocyte ballooning as compared to the placebo control. The fibrosis seen at the end of the study in the DUR-928 treated animals was less than that seen at the beginning of the treatment.

The hepatocyte ballooning seen at the end of the study in the DUR-928 treatment group was significantly lower than at the beginning of the treatment. The second animal study we’re announcing today is a bile duct ligation model in rat. This is a model for cholestatic liver diseases such as Primary Sclerosing Cholangitis or PSC.

In two studies, conducted by a CRO in Canada, the bile duct was surgically ligated, resulting in cholestatic inflammatory liver injury.

Daily oral administration for nine days of DUR-928 demonstrated a significant improvement in body temperature and body weight, as well as a statistically significant reduction in total bilirubin, including both direct and indirect bilirubin.

We look forward to completing the ongoing clinical studies in Australia to submitting the INDs and initiating Phase 2 studies with DUR-928 in the U.S next year. I want to thank you for your time. And with that, we will now take any questions you might have..

Thank you. We will now be conducting a question-and-answer session. [Operator Instructions] Thank you. Our first question comes from the line of Annabel Samimy. Please proceed with your question..

Hi, guys. Thanks for taking the question. Glad to finally see little bit of data that we can talk about.

So, maybe you can first tell, at a similar stage of development in some of the other programs that have been worked on, what are the kind of -- are these typical of a kind of [indiscernible] and some of the active compounds? And to follow-up from that when you think of that, how are you going to move this in Phase 2? What kind of endpoints you’re going to be looking at for this population? Thanks..

First of all, I’m not aware of other compounds that have shown this kind of activity from a single dose.

But I think the reason we're so excited about is that we have seen similar results in our animal models and then we dose them for some weeks, we see the end results of the histopathological improvements and the disease circumstance improvements, we're certainly really pleased to see the IL-18 and the CK 18 data that was certainly -- that was an endpoint that I think Gilead pointed too, which in one of the recent studies as [indiscernible].

Lin, do you want to maybe look at -- some of these will be used as endpoints, right?.

I think at these biomarkers we’re always looking with a interest and then -- because it's kind of indicates the drugs activity. However, in the Phase 2 clinical trial, we will certainly use FDA -- will discuss with FDA and then use the endpoints, which is clinically relevant ….

Right..

… and then, yes, the FDA call out -- collaborating with the FDA to select, for example, those serum creatinine levels in the AKI trial that would certainly be a relevant -- clinically relevant markers..

Right.

I mean, some of these biomarkers will be also measured, but it's really what they’re looking for in the acute kidney will be the creatinine levels and moving onto dialysis and death, those are the things [multiple speakers]?.

Yes, it had to the clinically relevant endpoints..

Each study will be different..

Yes..

Yes, I guess, I was wondering [indiscernible] are you moving on to NASH, are you looking for activity in kidney and then moving on to kidney?.

We are looking at both..

Yes..

Okay. All right. Thank you..

Sure..

Our next question comes from the line of Yi Chen. Please proceed with your question..

Hi. Thank you for taking my questions. My first question is, you mentioned that in the first cohorts after DUR-928 trial in NASH, there were four cirrhotic and six non-cirrhotic patients.

So I wonder whether that is by the result of random enrollment or that was designed by choice? And also based on the reported initial biomarker results, the press release said that the effect both for IL-18, and CK 18, the effect was more pronounced in cirrhotic subjects at 12 hours of the dosing.

So does that indicate that in the higher dose cohort you will preferentially enroll cirrhotic patients or not?.

Lin?.

Well, the number of cirrhotic patients versus non-cirrhotic patients was determined by design. So at the beginning of the study, we'd like to have about roughly half of the cirrhotic and half of the non-cirrhotic.

So, for that matter and for the next cohort, we will still have half of -- about half of the patient cirrhotic and another half will be non-cirrhotic..

Okay. So ….

And then the effect about biomarkers, the effect we saw more pronounced in the cirrhotic patients and then which is actually exciting to us, totally. And then that makes perfect sense in terms of the drug effect.

And if you look -- as a matter of fact, if you look at absolute numbers, both these markers in the cirrhotic patients, they’re lot higher than the non-cirrhotic patients. Of course, that the -- all the NASH patients are lot higher than the matched control subjects..

I see.

So, have you reviewed the actual dose of the low dose so far?.

No, this is the lowest dose we have indeed [ph]..

We haven't disclosed what that is..

No? Okay.

So, pending future results of the complete Phase 1b trial, would you target the both cirrhotic and non-cirrhotic patient groups or you could essentially -- based on that you could choose one of those?.

That’s a good question. And then, in fact we’re going through a rollout of detailed plan for the liver disease trial probably later..

Yes, not too log from now..

Yes..

But it's important also to make note of the -- some of the [indiscernible] done recently as well. That went [indiscernible]..

Yes. And certainly that result is very encouraging to us..

Right..

We saw particularly whether we saw more pronounced effect in cirrhotic patient, which they’re certainly -- or these markers are lot higher than the matched control subjects or non-cirrhotic patients that makes very good sense for us..

That’s right..

So the higher dose will enroll approximately the same number of subjects?.

Yes. Yes..

Yes. Yes..

Okay, got it.

So we should expect to see the results from a higher dose in early 2017?.

We hope sooner..

Yes. That’s our goal..

Yes..

Okay. Thank you..

Sure..

Thanks..

Our next question comes from the line of Frank. Please proceed with your question..

Hi. This is Frank [indiscernible] actually on for Jim Molloy. Thanks for taking the questions. First, a couple on timeline.

So is it fair to think that for POSIMIR we should be expecting that data 4Q '17 at this point? And then, the IND filings for both DUR-928 programs, should those -- is the goal here to have those INDs filed by the end of '16?.

Yes, first with regard to the data on POSIMIR, yes fourth quarter is our objective. And for the 928 piece we're working towards at least one this year, right. We will see how the year unfolds and make it to, but if not, it will be early on next year for the second..

Okay, great. And then, so if everything goes well here hopefully to get that data by end of the year here to finish the Phase 1bs.

Should we expect Phase 2 to start right away as soon as possible in the first quarter?.

Well, yes we’re going to start the Phase 2 as quickly as we can. And what we will do is in the not-too-distant future and I don't know exactly when, but in the -- over the next near-term, we will be outlining our strategy for 928 going forward. And that will be which acute trials, which chronic trials we’re going to be doing and in kind of what order.

So you will -- you understand the first three or four trials that we're looking at doing and then from there it will unfold. But our objective will be to get data out of patients from the Phase 2 work as quickly as we can..

Understood. And then, just lastly on the human data.

Was this in line with expectations when you look at it and you guys were thinking or when you speak with KOL's is this for just a single dose at the lowest dose we’re not sure what that is yet, but is this kind of a lot better than expected?.

I have to say that it is better than I expected. And then, we did not expect, as Jim said earlier, the study was not designed to look at the effect -- the biological effect of 928 rather than look at the safety and PK. Of course, we collected all the biomarkers as much as we could.

So, we were able to see that the effect after a single low dose exposure, it was certainly better than we expected. The drug appear to be more potent than we expected. And then -- so that’s why we’re very encouraged..

We are also encouraged, because if you look at the animal data, you can see in some of these models, the product models is those had some influence on the biomarkers and that later translated weeks later into histology and better outcomes.

So our expectations is this should translate as well, given this endogenous, given the safety profile and now everyone has been asking, when are you going to see something this people will, the first time through it the lowest dose we have. So we’re actually really pleased, very happy to have this, and I think it's wonderful..

Yes, particularly as you see that in our all Phase 1 trial in the house based subjects, we cannot see much of these effect and no markers up or above. Just like what we saw in order to ….

In order to Animal..

… and more studies, but so we don’t know what it would be the effective dose in human. So we cannot expect to see that anything change and this is lower dose..

Right..

By now we did. We know the drug is more potent than we expected..

Right. And if it's in line with our theory that this is a stress -- classic stress hormone that [indiscernible] damage in the body to be able to have it and do it [indiscernible]. So, it's very -- it's really just -- its wonderful news. It's definitely a treat not a trick on this Halloween..

That’s great. Well, thank you very much. That does it for me..

Sure..

Our next question comes from the line of Len. Please proceed with your question..

Hi. This is Len Yaffe. I had three questions on DUR-928 [indiscernible]. The first is, for assets in the NASH category from preclinical through phase to be completely paid between $150 million to $700 million for [indiscernible] to the product.

And I was just wondering when you will be presenting data at a medical meeting that may attract interest given where your market cap currently is? Second question is, my knowledge is you have the only compound that’s showing efficacy as it relates to fibrosis in both liver disease and kidney disease.

So is the drug act by the same mechanism in each of those and if so, would that tend to lend even more support for the efficacy of this compound. And the last question is, given that this is a sulfated version of a naturally endogenous compound, could you let us know about the patent like of the compound, so that won't be a question in future times..

Okay. Well, so it's actually is an endogenous market. It's not a sulfated version of it.

So to take the last one first, we do have I think six different patent families going forward for the molecule and some of which issued a number haven't and we're constantly -- some of the reasons why we are being a cryptic on dose and things like that is, we’re still looking to file new patents, so we expect to have new -- I think we’re well protected from patent standpoint.

And then with regard to when the data will be presented? WeiQi Lin, I will let you address that one and the fibrosis reduction and the kidney and liver, the mechanism same which I think you can address that as well..

We are probably looking at putting some of the data together and then submit the abstract to the ESO [ph] meeting for next year..

Right. And what about the connection between the fact that we see something that these mechanisms are [indiscernible] very similar between the hepatic and renal, so maybe you can address …..

Yes, actually I think the reason this molecule works in a variety different disease models as we’re doubting from different [indiscernible] or resulting from different organ injury and then essentially, if you look at and ultimately at the end all the puzzle -- genetic pathways were all identical.

It's always involved, if not as left at accumulation that will be always involved in inflammation and a cell death. So for this molecule, earlier Jim mentioned it's an epigenetic regulator.

It regulates lipid metabolism and then decrease the process lipid accumulation and then regulate inflammatory responses, but only at the diseased stage and then also promoting cell survival only at the disease state, it makes perfect sense for a variety different model that’s actually always our thinking to look at which would be the next model to go.

And then, so that we can use that as the method of use patent filing. And then essentially a lot of diseases, if not all of it, a lot of diseases they essentially go the same common pathway, it's the inflammation and the cell death...

I think that's really true when we met with the FDA at the end of September for the pre-IND meeting for the kidney trial, we spend some time discussing these data, because we have these data in hand at that point, with the FDA and they were quite encouraged by what we saw only in the animals, but the fact we’re seeing this in humans.

And they were reflecting that with regard to the kidney potential of the product..

Yes, yes..

Great. Thank you so much..

There are no further questions at this time. I would like to turn the floor back over to Mr. Hogan for closing comments..

Okay. Just a very brief comments, which is Jim Brown will actually be in New York in mid-November at two conferences. We put one of them in the press release, which is the Stifel conference on Tuesday the 15th where we actually make a presentation, but also do one-on-ones with the conference.

The day before that, the Investment Bank Mizuho is also having a conference and Jim will be there doing one-on-one meetings only. There are no corporate presentations.

So if happened to be an institutional investor in the New York area and you like to meet with Jim on either of those dates and conferences, please go through the conference coordinators at Mizuho or Stifel.

And then beyond that, to the extend people have further questions, please always feel comfortable calling the company or emailing us, we will be happy to get on the phone with you and spend more time trying to explain the science and where we're going. With that, thank you for your interest and your attention..

That concludes today’s teleconference. You may disconnect your lines at this time. Thank you for your participation..