Welcome to the Mesoblast Second Quarter and First Half 2016 Financial Results Conference Call. [Operator Instructions]. Before we begin I would like to read the following forward looking statements, during statements in today's conference call and responses to various questions may constitute forward-looking statements. We wish to caution you that such statements reflect only the company's current expectations and actual events are results may differ material. For more information about factors that could impact these forward-looking statements. Please refer to that risk factors contained in the company's more recent filing for the Securities and Exchange Commission and Australian Securities Exchange. The company undertakes no obligation to update these statements as a result of new information or future events. I'll now turn the call over to Silviu Itescu, Chief Executive Officer.

Good morning, and thank you for joining us on the financial results of the first half and the second quarter ended December 31, 2015. Joining me is Paul Hodgkinson, our CFO. The agenda today will be to talk about our financial results, overview, the review of operations and our forward looking and ongoing focus and commitment. Paul, I would like to hand it to you regarding financial results overview please.

Thanks, Silviu. Turning to slide 5, the first point I wish to make is all the numbers I will talk about in this presentation are in the United States dollars. In terms of the highlights cash on hand is now a 120.8 million and in terms of our cash performance and use of cash we have reduced by more than 25% as we indicated in the guidance in the first quarter against the prior quarter illustrated on the page. In terms of our loss before income tax due to our investment again we have reduced the P&L by 18% or 7.9 million primarily as a result of lower expenses in R&D and lower expenses in our management and admin and we are managing our cash as we’ve stated before to manage through to inflection points. So let's look at a bit more detail. On slide 6, and look at the profit and loss account. In terms of revenue that's been relatively flat so a modest growth of 2% and this is really the difference between this and the comparative period is a recognition of the milestone revenue. On our partners products themselves [ph]. In terms of the loss performance as I said there is an improvement of 18% and when we look inside the main drivers of the R&D expenses so as we are focusing on our Tier 1 platform we have reduced expenditure on the Tier 2 programs. And we've also reduced our labor costs alongside this. In terms of the management and admin we have savings again on labor cost and we’re also benefiting from currency impacts as the majority of our staff are located in Australia inside the management category and we have also reduced IT expenditure. Manufacturing commercialization has offset a little bit, it's 25% higher but this is needed as we launch and bring clinical supply up for our Phase 3 clinical programs. Turning to the cash management in a bit more detail on slide 7, as we have said we have strengthened the cash position to 120 million and obviously that was done through the IPO which was completed in November 2015. Our operating cash burn as we said in the target has been reduced by 25% and we do not see any change to the guidance for the rest of the year so that we indicated in the previous forecast. And we are managing actively to achieve key inflection points on our programs as listed so in terms of our back pain program, rheumatoid arthritis and to file with the FDA for approval of pediatric graft versus host product candidate. Now I'd like to hand back to Silviu for a review of operations.

Thanks, Paul. The highlights operationally for the last six months are on slide 9. Recruitment of all three Tier 1 Phase 3 programs progressing very well in the United States notably MPC-150-IM for Chronic Heart Failure we will talk more about that, our MPC-6 ID program for Chronic Low Back Pain we're recruiting very well across multiple sites in the U.S. and our program for pediatric acute graft as a host disease. With respect to the heart failure program, highlights out of the Phase 3 trials we were very pleased to have seen that the FDA agreed to significantly reduce the program to 600 patients trial following discussions between our commercial partner Teva Pharmaceuticals industries and the FDA. The trial is targeting patients with advanced heart failure and high rates of hospitalizations or death which is the main unmet medical need in the field and recognizes as being said by both regulatory authorities and key opinion leaders. Updated timelines for this shortened trial will be provided in conjunction with our partner Teva. TEMCELL, the product that is being developed in conjunction with JCR in Japan received unconditional approval and reimbursement in Japan for both adult and pediatric graft versus host disease. JCR expects to launch this product in a very short order in Japan certainly during the first quarter of 2016, average reimbursement over a four week multi-dose treatment course in Japan is expected to be in the order of between $115,000 to a maximum of $172,000 if additional dosing is required and Mesoblast is to receive royalties and other payments at predefined thresholds of net sales. We’re very excited to see this product launched in the short term. With respect to MPC-300 IV, our immunomodulatory products for intravenous delivery we've just announced top line results in the Phase 2…

[Operator Instructions]. And our first question comes from Anupam Rama from JPMorgan. Your line is now open.

Just a quick one for me just on the RA data that was presented earlier yesterday. Just in terms of a clarification here -- are you not seeing any ACR50 or 70 results in the biologic refractory patients or is that data just not been broken out yet? Thanks.

Let me clarify because maybe we weren't clear enough. The entire population of this trial is biologic refractory. So the definition of biologic refractory in this trial was failure of at least one biologic and in fact this is the market opportunity that 30% of patients we felt at least one biologic are all being captured in our trial. In comparison to other classes of drugs including IL6 antagonists, [indiscernible] anti- IL17 therapeutics all of whom are targeting the same biologic refractory population. Those drugs agents have reported in the order of 5% to 15% ACR70 remission rates at best in this target population. We're seeing as high as 20% to 27% of patients achieving ACR 70% or DAS28 remissions at a 12 week end point. So we're very happy with the remission rates that we've seen with a single low dose infusion. I think what we have also started to see a signal of is that in those patients that failed only one or two biologics where the real opportunity exists to put this product in early not at the late end but early as the first biologic in the biologic refracted population, we’re seeing an even greater response and that's where we highlighted the 60% versus 17% matched single biologic failures having achieved an ACR20 and we’re seeing probably half of those patients which achieved ACR20 achieving ACR70. So that's the target population where if we can continue to demonstrate that a single intravenous infusion gives us ACR70 remissions and those remissions are potentially sustained from well beyond 12 weeks and what we're looking at really outcomes at 6 and 12 months then we can start to model out what a remission inducing agent as a single deliverable might start to look like in this unmet need.

And our next question comes from Jason Kolbert from Maxim. Your line is now open.

Can you help me understand when we might see P values and kind of the complete data release? Are you saving for a medical meeting and also can you go into a little bit of detail about exactly what you mean when you talk about mashed placebo treated controls. What does that mean exactly?

Sure. So first of all it's a 24 patient top line data, the full data is 48 patients of course of both cohorts. You are quite correct, there are two major rheumatology meetings, [indiscernible] and American Rheumatology and you would expect that full data will be presented at one of both of those meetings, the upcoming in the next few months. I can tell you that we've got significant values across multiple parameters throughout the 12 week periods and if we were to list them all you would having a very number oriented presentation which I think has a top line interim probably is not appropriate but I think that it is material to the company and I think it's important for our investor base to understand that there is a clear signal of efficacy and more importantly the signal of efficacy is quite different from what has been previously published by other stem cell companies in the space who have not seen a signal of efficacy and the exact same high risk target population which again speaks to I think to the strength of our technology and the potency of the immuno selected MPCs that we’re working with. You asked what does matched controls mean? Patients who are matched for the duration of disease and for number of biologics and I think most importantly and I've highlighted the one to two biologic population when you look at that target population the fact that the placebo of patients did not achieve a high level of ACR20 spontaneously nor ACR50 and 70 spontaneously where 60% of our patients did being matched for the disease severity and biologic use I think speaks for itself.

Silviu, you did mention that you're going to look for data going out. How far should we expect that you're going to be monitoring these patients to see how durable the response is?

I think a true remission is a remission that is durable and doesn’t last 12 weeks and we’re beyond that. Look I can tell you that we're seeing signals that patients who have early remissions maintain remission that through 52 weeks.

That's amazing. Thank you and you know it's also not beyond me to understand that there's no side effects here so you have a completely different profile than you have with traditional biologics. Thank you so much.

And our next question comes from Kevin de Geeter from Ladenburg Thalmann. Your line is now open.

I also wanted to follow up on the RA data, Silviu can you comment with regard to the patients that had ACR70 and I guess numerically they look like all the patients got to ACR50 also at 70s, were those patients tend to have the early onset or was the onset of benefits sort of uncorrelated in this small data set with achieving the ACR70.

No I think -- it's clear from this small data set that if you're going to get a response you're going to get a response within the first -- as early as week one perhaps upto week four but in that very early phase. And if you're going to get a response that is deep in other words ACR50 or 70 you'll see that early as well. So we're clearly getting the sense that a first injection, a first infusion of these cells will have an impact on the immune system early and the degree to which an individual patient responds will also be evident relatively early. And I guess the question as we move forward is how to maximize those responders in the early phases and convert them from an ACR20 to an ACR70.

Now it's very interesting and I just want to maybe quick follow up on this data because I do think it's important. If you sort of look at this data compared to the various data we've seen in biologic refractory patients with the JAK inhibitors that are out there and there are several of them in late development. You know the ACR20 data sort of looks actually pretty similar but you know the chart really seems to for the MPCs really seem to have the strongest benefit out in kind of the ACR70 end of range relative and the question I'm sort of trying to appreciate here is you know with the JAK inhibitors we have seen a pretty significant step down and the portion of patients that ACR50 and 70 relative to ACR20s, you didn't really see that at least beyond to ACR50, is that just an artifact of small numbers or do you think you'll see -- if you get a ACR50 most of those patients you think have a chance of getting something close to a clinical remission?

Look first of all I think we need to be certain, the numbers are small, 24 patients and just as important this is just the low dose, a single infusion of a low dose, right? Having said that it's very clear to us that if they achieve ACR50 they are likely to achieve ACR70, right, we did not see a step down at all and I think really the question here is how to increase the proportion of patients who achieved ACR20 into that ACR50-70 basket. The potential for true remissions and that’s where the unmet need is and that's where the goal of all rheumatologist is. ACR20 is a low bar as you all are aware of, it's the approvable bar but it's a low bar and really this is the question of achieving remission.

One last one if I may then I will back into queue. I mean if you look at the data here for sort of the ACR20s it actually looks [indiscernible] comparing apples and oranges here. But it looks better than any of the data in the label for any of the TNF inhibitors with regard to ACR70. Given the rapid onset of benefit and the potential to have a higher percentage of patients get to have a functional cure are, it doesn't make sense to be looking at this MPCS in front of biologics or in front of TNF inhibitors?

As a small biotech company we have limited resources, so we need to focus on where we deploy those resources. I'm pleased to see is we’re getting these kind of results which is frankly if they continue to be seen this are way better than other classes of drugs in this hard to treat biologic refractory population. And this mirrors very much where we see other products that we’re developing. For example in advanced heart failure or in chronic low back kind. Our cells appear to respond well to signals that they activate them in patients who have active disease. That allows us to really optimize our therapeutic benefit fit in a target population that that if we’re successful will mean a substantial price premium and appropriately reimbursed product. I think you're absolutely right that if a single infusion gives sustained benefit in this hard to treat patient population which allows us to demonstrate an effect in a relatively small Phase 3 kind of program we would of course move this into first line ahead of biologics and look at broadening label and broadening the target population. I would want to mention here that these are fairly large programs and that we wouldn't be doing these programs with that our preferred commercial partner, a particular partner that has major focus in inflammatory arthritis. We’re again -- you would want to in parallel be looking at both the hardest to treat populations as well as the biologic naive populations.

And our next question comes from Alethia Young from Credit Suisse. Your line is now open.

A couple of questions, first one, as it became to. Celgene, kind of I want to understand the relationship of that opt-in and is RA something that's potentially in play there in the discussion?

The answer is no, rheumatoid arthritis as it relates to this product was not part of the opt-in relationship. It was focused primarily on the graft versus host disease and MSC product that’s been used to develop that. So this falls outside of that relationship although again we have a very good relationship with Celgene, our investor and as you would expect that we are talking about this program and others with Celgene and with potentially other partners.

Just continuing on the partnership line, I mean is this something that you think you need to run kind of more patient before you kind have the opportunity that really partner it's real value or would you look at the kind of partner earlier just because of the potential cost.

Again we’re well cashed out to take some of our most mature assets to their natural conclusion and value inflection points. We don't have today sufficient resources to take this program into Phase 3. So your point is correct the right time to partner this is I would think when the full 48 patient data is available to us the second dose cohort but as you know as I've just said we are already in discussions with a number of the large players that have a focus on rheumatoid arthritis and like us they are very keen to see the result of cohort number two.

And can you talk of about how this -- I know again it's small numbers but just compare contrast this kind of tolerability adverse event profile in this population that you’re seeing with your platform versus some heart failure or the back programs kind of help us understand how the platform safety profile is shaping up across different kind of therapeutic classes?

We’ve treated several 100 patients now with our cells in a variety of disease states. Systemically in these patients with severe rheumatoid arthritis, with diabetic nephropathy, with type 1 diabetes, in the heart we’ve treated now. There was 60 patient Phase 2 trial, there is an ongoing 600 patients trial, so you can imagine we've had several hundred patients worth of exposures. And in the back pain there was a 100 patients Phase 2 trial. At a very wide dose range now we can pretty clearly say that we have not seen any cell related adverse events. Really important, I think it's pretty clear that this therapy is very safe. Patients being followed for at least five years without any kind of outcomes, no short term, no long term adverse events and that's a very different profile to all of the immuno-suppressive agents that are used particularly in inflammatory and autoimmune conditions. In this particular disease state in the biologic refactoring group, in RA one of the major problems of course with TNF antagonist and IL6 antagonist is that they need to be used chronically and they shut down important pathways and have a substantial risk of both neoplasms and opportunistic infections. We have not seen any of those with our treatment and that's probably because we don't shut down chronically any particular immune pathways, what the cells are able to do apparently is act in the short term to switch off multiple pathways sufficiently to reeducate the host in the setting of the immune system probably to reeducate the immune system to reduce inflammatory responses to whatever drives in rheumatoid arthritis. In heart disease to reeducate local endogenous tissue to result in repaired mechanisms in the heart and the disc [ph] but what we don’t see is chronic cells don’t survive long term and they don’t chronically shut down these multiple pathways.

Maybe just one last one that you’ve talked a little bit about -- this approach differed or the safety is different from some of the other stem cell kind of product that we’ve seen, can you just talk a little bit more about that in detail?

I think [indiscernible] is the one that is standing out as being particularly safe given that many hundreds of patients worth of experiences. Look I think IPS and embryonic type of stem cells have a very different mechanism of action, those cells engraft and those cells differentiate down the various parts of tissue. Our cells do not engraft and particularly the fact they are allogeneic, the cell delivery vehicles for biotherapeutics, they are released these biomolecules and have their [indiscernible] tissues. The embryonic stem cells in the IPS line of cells because the engraft need to be monitored for long term to make sure that there's no risk of any kind of cancer expression because of course IPS and embryonic stem cells have the potential to differentiate down the [indiscernible] and potentially can cause cancer. So there is a theoretical risk of cancer with IPS and embryonic stem cells that are long lived and we have not seen any risk of that sort of thing with our cells that basically have a short term survival and basically have their effect based on the fact that they are released.

And our next question comes from Dennis Hulme from Edison. Your line is now open.

First I just wanted to change [indiscernible] on the heart failure program, firstly can you clarify has there been any change to statistical power the reduction in size from 1165 down to 600 and the change of endpoint?

No not at all. That’s a great question. The whole point of this is that we've identified the 20% of heart failure patients, big unmet need, right that continue to be at risk of recurrent hospitalizations and deaths. The fact that these patients have multiple events in a relatively short timeframe means that you can structure a much smaller pivotal trial that uses the exact same powering and assumes a greater event rate in the placebos than we’ve previously assumed and therefore maintain the same treatment benefit, use the same assumed treatment benefit and powering but simply have a much small number of patients. That means that the overall cost of the trial is substantially reduced. The time to completion and recruitment is substantially reduced. And the read out of the results comes in earlier.

Okay. And secondly in relation to the reduction in size, my previous understanding had been that you thought the FDA would require exposure of now something like 1500 to the stem cells to get adequate safety data. It looks like there will fewer patients from that treated. Is the FDA now comfortable with the amount of safety data they will get from the smaller trials?

Yes clearly they are, even more important again comes back to the fact that we're targeting the sicker segment of heart failure patients who really have a risk of death that approaches cancer patients, right and that's the kind of population that the FDA is encouraging sponsors to focus on, patients who have potential breakthrough designation kind of outcomes where mortality is a high risk and of course the pharmacoeconomic benefit comes from preventing multiple hospitalizations in a relatively short timeframe. So given the unmet need and given the severity of the disease and given the fact that the substantial number of patients that have already been recruited have clearly not had any celluloid [ph] adverse events. I think the FDA is comfortable with the number of patients that are going to be exposed. Absolutely.

And our next question comes from David Langsam from Biotech Daily. Your line is now open.

A question about funding and the HARP program and then a couple of questions on the RA. With the current cash burn of just shy of $20 million a quarter and a 120 million in the bank that gives you a runway of 18 months to July 2017. I take it that the 600 patient second confirmatory study would be post regulation or post regulatory approval, am I right on that point? And the funding that you have to take you to the end of that trial?

Let me answer that, I’ve to go to be circumspect how I answer this because our partner Teva is running the program and we haven't publicly yet updated the revised timelines and we will be together shortly. Having said that I think it's Teva intends to run trial number two in parallel to trial number one, not in sequence, number one. Number two obviously reducing the trial size number one trial Phase 3 to 600 patients means that it now comes within the timeframe of our budgetary allocations. Again I just want to state that Teva is responsible for funding that program, not Mesoblast but there are some important value inflection points including that futility interim analysis and completion of recruitment that I think it's fair to say will fall in within our counter budgetary timelines.

So is the second confirmatory study as you understand that post regulatory approval of the first study on the basis of first study or is required for regulatory approval?.

Look I think those are the kind of discussions that Teva and we will be having with the FDA and we will be updating the market but I think I just want to emphasize that the target patient population is very similar to a breakthrough designation type of population that is previously been looked at by the valley FDA in but heart failure and oncology trials. We will be updating the market in the next quarter about the strategy but clearly targeting a very sick patient population with no alternatives makes this a much more streamlined program.

I guess what I'm getting at a very simple why is the trial of 1200 patients is not actually smaller than the trial of 1165?

I just said that the trial is 600 patients, that’s the Phase 3 trial that is currently active.

But then there is a second one and I'm assuming that that is a mandatory trial?

The second you’re asking me is whether, the you’re asking me is whether the second trial is mandatory before approval or after approval? The answer I'm saying to you is that’s a discussion that Teva and Mesoblast will continue to have with the FDA and we will update the market as soon as we have that information.

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

Just a quick follow up on some of the RA questions certainly lot of positive progress there. If you look at the ACR20 and 50 and 70 those are indexes of combined specific criteria. As you parse the data can you tell us are you seen improvements in specific criteria within RA such as pain, movement or joint tenderness especially -- well obviously in the patients that aren't seeing complete remission.

So obviously the ACR criteria is a composite of multiple components and what's really striking to us and in fact we’re saying significant or trends towards significant across multiple components. We will of course update the market more fully on which components but yes I think the physicians in the current [ph] global assessment, pain scores, swollen joints, functional disability scores we’re seeing all of those substantially impacted by a single low dose infusion of our cells. So we're very pleased by that.

Okay. And that kind of comprehensive response lend itself to a more sustained response usually so that’s good to hear. You mentioned that ACR20 is the approvable bar with regard to the FDA, I know it's early days but in your conversations with doctors and I know you have low side effects but what are they really want to see before they will you know consider prescribing something?

Look if any new drug was able to achieve an ACR50 end point that was significant powered against placebo, it would clearly take the market. ACR20 is a very low bar it just means 20% improvements in symptoms and signs [ph], 50% improvement in symptoms and signs becomes a clinically meaningful end point and we’re targeting 50% improvements in other diseases with ourselves including chronic low back pain. We ought to be achieving 50% improvement in symptoms and signs in this disease as well. You know with no side effects, right, now that's really important. The last thing you want is a drug that gives you these kind of improvements and cures you through all sorts of other side effects which is obviously easy to do with immuno-suppersives. But a safe product that gives you at least a 50% improvement in ACR50 would immediately be a frontline agent and if on top of that you're able to do achieve true remissions, durable remissions meaning 6, 12 month remissions with a single course of therapy I think that's exactly what every rheumatologist treating this patient population is looking for.

And then just getting back to the heart failure program really quickly. You're going to Phase 3 which is now 600 patients and then that confirmatory study that’s also up 600 patients and you get to cut down on your timeline significantly going from 1100 some to some 600 patients. With the second study running at the same time how is enrollment? You’ve plenty of patients that you’re feeling like running the two together is challenging with regard to identifying the patients or if you just got pretty good runway there.

So obviously our [indiscernible] has not started trial number two yet. Logistics are now underway, part of the approach is to broaden the program across Europe and have equal number of sites in Europe recruiting as they are in the U.S. At the moment trial number one, is substantially recruited out of the 600 patients using only U.S. sites. The intention is to broaden this quite rapidly over the next couple of months into Europe and then be in a position to start trial number two the that overlaps Europe and the U.S. I think we have the ability to do that in parallel, I think it's really more of a funding issue and our partner Teva is responsible for funding the program so I think I would have to sort of to further those discussions to Teva.

Our next question comes from Tanushree Jain of Bell Potter Securities. Your line is now open.

Just two quick ones for me. First on the heart failure trial. Silviu if I recall correctly between Teva and FDA there was a test of superiority decided when 50% of events have occurred. Now with the change in the trial design and the size what number of events are we looking at to test that -- test of overwhelming efficacy.

So obviously we will continue to have an interim analysis for futility and overwhelming efficacy based on heart failure match. We are still calculating the precise numbers of events needed for that. I think it will be very close to what you just said but we haven't got that quite written in stone yet. What it means of course is that on the futility analysis on the primary endpoint will be moved substantially forward from where it was previously time to date because if we're talking about roughly 50% of the events in an 1100 patient trial versus 50% of the events in a 600 patient trial you’re talking about much earlier time to this futility analysis if it's roughly around the same kind of numbers. But let us come back to you with a more formal timeline as Teva and ourselves come to agreement on this but I would say that's kind of upshot will be of the futility and overwhelming efficacy analysis.

And just a second question for me. So for the RA trial, so far across all your other programs we've seen. I think apart from disk that the high dose has worked better than the low dose, now in terms of mechanistically can you give us the rationale of what you think might be the case for the RA program?

Well based on our previous large animal studies in rheumatoid arthritis and modeling in sheep for example. We see that the cells intravenously migrates to inflammatory joints and also migrate to a central immune organ such as the spleen and lymph nodes. It's very hard to imagine that a dramatic improvement in many joints can be due to the cells going to each one of these joints. So it's much more likely that the cells home to the site of the immune activation. Again as I said lymph nodes and spleen and look what is the right optimal dose, is it a million cells per kilogram? Is it 2 million cells per kilogram, is it two doses of 1 million cells per kilogram a week apart, those are the kind of kinetics that we're now exploring and we will get a much better feel of that when cohort number two is completed. But it'll be somewhere in this order and I don't think it's going to be -- it will require a lot more than one to two million cells per kilogram at one of two infusions.

And our next question comes from Marc Sinatra from Lodge Partners. Your line is now open.

Just a quick question, since we’re getting a little bit closer to some news flow from the CHF trial, while we have had some but this is expected news flow. How is AMI trial in Europe going the one that you and Teva are jointly funding? That’s been going a while now and we haven't heard much from it, can you just give us an update?

That’s one of our Tier 2 programs. And we expect to have data during the course of this calendar year for sure on this program. It's going well, there have been no adverse events, of course we've recruited reasonably well I think we'll be updating the market on results from this program. Again on positive results we would need to consider with our partner how best to move into a pivotal trial in post-MI patients and who are the right patient population. It may be that the post-MI patients at highest risk of heart failure a group that overlaps with the current half pool maybe the appropriate pivotal target population but again we will update the market as we complete those results.

Okay. Just from a theoretical point of view, I mean would you expect similar results in AMI as you would in CHF or would you expect divergent results or semi-divergent results, I'm just I don't know--

So for the big difference of course is that the AMI patients are relatively healthy when they get AMI and we’re targeting the sickest AMI patients and trying to prevent severe heart failure. Patients who are currently treating in the heart failure Phase 3 program are at the other end of the extreme that the end stage whether it's due to previous heart attacks or not they now have a very large style dilated hearts and what we're trying to do is to reverse the problem. And prevent the slippery slide to hospitalization and death. You’re talking about a prophylactic program on the one hand and then restored program on the other hand. There's no doubt that that the prophylactic program in heart attacks will need to be narrowed down to that segment who have had the largest heart attacks and who have had acute half failure that that we can impact on quickly so that we don't get into a large Phase 3 program where the majority of patients don't need the therapy. So I say it's about narrowing the front very much to the sickest patients who can be helped by this therapy which is going to have a premium pricing.

And your last question comes from Chris Kallos from Morningstar. Your line is now open.

I just got one regarding the Celgene agreement, that must be coming up close to being expiring, can I get an update on what the outcome of that has been?

We continue to have good discussions with Celgene around graft versus host disease and other inflammatory conditions and those discussions are on foot for the next few months as other discussions continue as well in some of our other very important areas including chronic low back pain with other partners.

And I'm showing no further questions. I will now like to turn the call back over to Silviu for any further remarks.

Well again we thank you all for joining us this morning and we're very excited by our recent results, our continued progress in our Phase 3 programs, our near term expectation that the first industry manufactured stem cell product will be launched in Japan and hopefully we will be able to update the market on near term revenues as a result of our royalties from that program and other milestones as they come to hand. Thank you very much.

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