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Sangamo BioSciences, Inc. (NASDAQ:SGMO)

Deutsche Bank 39th Annual Health Care Conference Call

May 8, 2014 4:00 PM ET

Executives

Edward Lanphier – President and Chief Executive Officer

Analysts

Robyn Karnauskas - Deutsche Bank

Robyn Karnauskas - Deutsche Bank

Thank you for joining us today. The next session will be in French. I decided to mix it up a little bit. So for those who don’t understand, don’t worry about it, just send me your questions and I’ll read them English and hopefully he’ll understand. So, next we have Sangamo Biosciences, Edward Lanphier presenting, President and CEO. For those of you who are not familiar with [URN] [ph] there is an app that we are using where we can see questions that you asking anonymously or just raise your hand and we will bring around a mike.

And with that, I think we’re doing a fireside chat, correct? We’ll start with some slides and then we’ll do some questions.

Edward Lanphier

I wonder if I can do forward-looking statements in French as well. All right, 10-K, 10-Q. This presentation will contain forward-looking statements and I refer you to our filings. I think we just filed our 10-K, our 10-Q yesterday. So I’ll refer you to our filings with the SEC.

So in English, Sangamo is focused in the area of genome-editing. Our goal isn’t to treat diseases; our goal is to cure diseases. So it’s an extraordinarily ambitious, incredibly interesting opportunity. It’s driven by a core competency in our ability to engineer a specific type of protein called zinc finger proteins.

This is the most common, the most abundant type of DNA-binding protein in us, in man. It’s also the most abundant class of transcription factor DNA-binding protein on our planet, all the way down to plants and yeast and so on. Because these are modular proteins they can be engineered to target precisely the sequence of DNA we want. And then we can use that ability to physically control the expression of a specific gene or to permanently change, permanently change the nucleic acid sequence of a gene.

What we propose to do is human genetic engineering, physically change and permanently change DNA sequences in a way that we can control the biology of that cell that way we modify that gene. So that’s the goal. We’ve been quite successful in applying the technology broadly, DNA is DNA and we have a large collaboration in the plant area in research. But the principal focus for us is in the area of human therapeutics, and I’ll talk more about that in a moment.

The platform itself, just one slide, we have the ability as I mentioned to engineer zinc finger proteins to target exactly the sequence we want. And then we can attach what we would call functional domain a protein whose normal role it is to either turn on the expression of a gene, turn off the expression of a gene or on the right hand side of the slide, what I’ll talk most about is the ability to target a gene and permanently modify the nucleic acid sequence, either by disrupting the expression of that gene or by doing a targeted insertion at the side of that gene. And I’ll give you examples of both of these outcomes as we go through our programs.

As I’ve mentioned, we’ve been quite successful in monetizing this platform. The earliest collaborations at the bottom of this slide in non-therapeutic areas to-date the collaborations with Dow and Sigma have brought in over $100 million to the company and we retain very significant future milestones and royalties from these collaborations.

About 2.5 years ago, we announced our first therapeutic partnership with Shire in the area of hemophilia and also Huntington’s disease, I’ll talk about those programs. And then in the beginning of this year, we announced our first ex-vivo collaboration in the area of sickle cell disease and beta-thalassemia with Biogen, I’ll talk about those.

But the real focus of Sangamo as I mentioned is the development of novel human therapeutics that are intended to provoke or generate genetic cures. And so how do we think about applying this platform. Well, the technology itself as I mentioned is completely agnostic to the gene. We can target any nucleic acid sequence we want. So the filter through which we think about applying this therapeutically is really delivery.

So we can deliver these engineered zinc finger proteins in vivo and that’s the top. And there we employ a delivery method call AAV, adeno-associated viral vector. We are doing a lot of this in the liver and I’m going to talk about our in vivo protein replacement platform, but we can also use this directly into target issues, such as the brain, such as the eye, such as the lung. We could also do this ex-vivo. We can take cells out of a patient’s body, physically change the DNA with our zinc fingers and then put those cells back in.

We are doing this in differentiated cells, those cells that are in the circulation such as CD4 T-cells, which is the target of HIV. We can also do this in stem cells that once they are modified you can re-engraft back into that same patient and again depending upon the disease and the outcome, change the biology of that disease. So this is the way we think about it.

In blue these are our partnered programs and our strategy in each one of these areas is to partner the lead program and then leverage that investment and that work by a given partner for our own programs, and we’re moving forward in all of these areas.

So let me now drill down and be specific. Starting at the bottom of the slide in our stem cell ex vivo approach the most significant disease opportunity in the stem cell replacement area is hemoglobinopathies and specifically sickle cell disease and beta-thalassemia.

We announced in January a collaboration with Biogen, focused on the ability to use zinc finger nucleases to disrupt or knock out the expression of a key regulator of fetal hemoglobin. So in utero and in newborns expressed fetal hemoglobin and that fetal hemoglobin is very efficient in carrying oxygen. But over time BCL11A is expressed, that shuts off the expression of fetal hemoglobin, and at that point our beta-globin takes over. Well, if you have a defective beta-globin gene such as in sickle or in beta-thal, you end up having these oxygen carrying diseases.

If you can turn back on permanently the expression of fetal hemoglobin just as we have in utero or when we were infants, you can get back that normal oxygen-carrying capacity. And so, recent work is a quote from William suggest - in fetal hemoglobin suggest that reactivation of fetal hemoglobin can lead to a single treatment that can cure both beta-thal and sickle.

And so, we’re moving forward with this and our goal is to file an IND on the beta-thal application by the end of this calendar year and in sickle cell with Biogen by the end of next year. That’s our lead program in stem cells. On the ex vivo side, our lead program on the in vivo side directly into the liver is targeting hemophilia, but that same strategy can be applied actually to any of these protein replacement therapy, so how can that work?

Well, what we are able to do is build zinc finger nucleases that target the most potent, the most powerful protein secretor in our body, which is the albumin gene in the liver. We make pounds and pounds of albumin every year, the liver does a great job of secreting that out, people who have one of their albumin gene dysfunctional are completely normal.

What we want to do is capture, [collect] [ph] less than 1% of the albumin promoters in the liver, put downstream from that albumin promoter any gene we want, and we can do this targeting, [exquisite] [ph] targeting by engineering zinc finger nucleases that make a break right at that site, and into that site with the appropriate DNA sequences so-called homology arms that are targeted right to that double-stranded break, we can insert any gene we want. Well it turns out, there is a lot of diseases where protein replacement has been curative, has been a successful therapy.

And so, if we can permanently insert any one of these genes downstream from the albumin promoter, we can get the liver of that person to make therapeutic levels of whatever protein we want. So the pointy edge of the sword for us is the fully funded program with Shire in the area of hemophilia, and we are on track to file INDs for both Factor VIII and Factor IX around the strategy by the end of this calendar year. With this collaboration we retain the rights to other enzyme replacement therapies and our goal is to file two INDs next year for our own account around two lysosomal storage disease targets.

And I don’t think I have to remind you all that there are companies that have been very successful with just one of these products. This strategy is agnostic to any of these and if successful a single treatment could be permanently curative and very disruptive to this very significant market.

Back on the in vivo side now direct target tissue, directly into a target tissue in the brain. This is where we are using a zinc finger transcription factor to turn off, specifically the expression of the disease related gene in Huntington’s disease. Patients with Huntington’s having a normal gene with its normal CAG repeats in the range of 20 CAG repeats, but there are other gene having a very long CAG repeats in the area of 40 or so CAG repeats.

What we’ve been successful in doing both in Huntington’s cells as well as mouse models of Huntington is put a zinc finger into the brain of these mice, where we can selectively shut off completely the expression of the disease related allele and completely ignore the expression of the correct gene expression of the allele. This is a program as I said, we are doing with Shire and we are on track to bring this into the clinic in 2015 as well.

Lastly, also on the ex vivo side is our most mature program. This is where we are going into T-cells, which are the target of HIV, and genetically modifying those cells, so that (a) they cannot be infected by the virus, but (b) they still are capable of [bounding] [ph] an immune response.

So the target we are going after is called CCR5, it’s a co-receptor along with the CD4 receptor that HIV must use to infect cells of the immune system. Absent CCR5, the immune system cells don’t get infected. And that’s been the best proof-of-concept. This is a picture of Timothy Brown from the journal Science. The other side of this picture was Matt Sharp who was one of the patients on our trials.

So the goal here is really two fold, one on the right-hand side of the slide, classic viral replication suppression. Employing the immune system or enabling the immune system to block or stop the acute replication of the virus just as antiretroviral therapies do. The other more chronic and I think more differentiated aspect of this is on the bottom left-hand side, that as these modified T-cells circulate, as they go outside of the blood stream, where actually the majority of CD4 cells are they also have the ability to significantly reduce the reservoir.

And as I told you, at CROI we reported nine out of nine patients who’re now three years of all had a material reduction in their reservoir, their HIV reservoir, and a concomitant increase in their CD4 counts. So the greatest amount of visibility around this program was just about two months ago, early March, where the early work was published in the New England Journal of Medicine that was work that was done with the University of Pennsylvania and Carl June. And then we updated on the program the next day actually here in Boston at the Conference on Retroviruses and Opportunistic Infections.

I won’t go through each one of these points, but the basic concept is this. What we’ve shown is a highly statistically significant correlation between the number of these modified cells that we reinfused back into an HIV patient, where both of the CCR5 genes have been knocked out and that correlates directly to a reduction in viral load. And so, those are the studies that are really the focus for us right now. We’ve completed two studies, one, where we took patients who already had one of their CCR5 genes naturally disrupted, the so-called delta-32 heterozygotes. And in that case of the seven evaluable patients, two of those became undetectable during the treatment interruption. And one of those as of two months ago at last report was out 31 weeks in – with functional control of his virus while not on antiretroviral therapy.

The other approach we’ve taken is borrowing a page from the play book of cancer immunotherapy using a Cytoxan preconditioning, where we get significant engraftment enhancement of these modified cells.

It’s that study that we’re now moving forward into a Phase II trial and here the second major bullet point suggest, we’ve achieved an optimal dose of Cytoxan preconditioning and we are moving into a 12-patient Phase II trial, we expect to complete the accrual and treatment of that study this calendar year and have data from that study in the first half of next year. And we will update on the program in a couple of weeks at the American Society of Gene & Cell Therapy in Washington.

So that’s a very quick overview of the programs that we’ve talked about in our strategy in picking them; this is a timeline for IND filing. So data on the top left out of the HIV program we just presented at CROI and we should have data out of this Phase II trial in the first half of 2015. Four INDs this year, a stem cell IND mid-year in HIV, and then three INDs, two of the hemophilia INDs and the beta-thal IND by the end of the year, and then four more by the end of 2015.

We also acquired a company Ceregene last summer. They had an ongoing fully enrolled, fully treated study in Alzheimers, it employees AAV expressing nerve growth factor in the brain and we expect data from that study also in 2015.

In terms of near-term, I point you to the American Society of Gene & Cell Therapy. This is a conference that we have typically had significant presentations, I think, we are well over a dozen this year, and we will be putting out information around those, and so a significant update on those.

In terms of financial guidance, I think many of you know that we did a successful financing earlier in March, where we’ve raised $100 million; yesterday, sorry Tuesday, first quarter call we announced that we ended the quarter with $245 million in cash. We’re guiding to ending this year with at least $225 million and then with the milestone payment from the Shire and Biogen collaborations on the research funding, you can see directionally our burn rate while we move those eight INDs forward is virtually non-existent.

So the funded partnerships while attaining significant ownership of proprietary programs has – is a balanced business model and that really brings you to the summary. So the straw that stirs the drink here is really just core competency of being able to engineer zinc finger proteins to target exactly the DNA sequence we want, and because we can do that, because we can permanently change nucleic acid sequences, our goal is not to develop a better longer lasting therapy. Our goal is to physically and permanently change DNA in a way that it can cure diseases. So, again, I said it upfront, I’m going to say it again. This is not unambitious, it’s very ambitious, but if we’re successful, it could truly change the course of medicine for many of these patients with monogenic diseases.

We’re well on track in terms of proof-of-concept around this. We’ve been in the clinic with the zinc finger nuclease for five years, so we understand the regulatory path, the manufacturing path and the development that we are applying that in areas where we think the targets, there is an unambiguous correlation between the target and the disease and where the delivery strategies are well worked out and not a variable with the equation.

As I mentioned, we are on track to file up to eight INDs by the end of 2015, and we have more than sufficient capital to get us there even while forward integrating in our own programs, both in terms of clinical development as well as internal manufacturing.

And lastly, because we are a platform company, we’ve had the luxury of developing a strategy that I think can drive near-term proof-of-concept, but retain long-term value. So a business model where we’ve balanced what we’ve partnered and what we’ve been able to retain, and where we think we can get leverage to forward integrate, we’ve also looked at the diversity of therapeutic strategies in vivo, ex vivo, stem cells, differentiated cells, and we are working on targets again that are very well validated.

We know that a mistake in Factor VIII leads to clotting deficiencies. We know the replacement of the correct factor VIII leads to clotting normality. We can put Factor VIII in we believe we can get normal expression of Factor VIII in a permanent way. And lastly, we’ve removed the balance sheet risk in the company.

So Robyn with that, I’m happy go back to French.

Question-and-Answer Session

Robyn Karnauskas - Deutsche Bank

So a question in French, could you please describe how your drug differs from the BlueBird technology and how it might compare?

Edward Lanphier

The principal - I think an example of the differentiation is in the beta-thalassemia sickle cell program, I would say that’s a good vehicle to talk about. So where we’re identical is, we’ll both take and isolate CD34 stem cells from a patient with a sickle cell, right.

The Bluebird approach takes a vector, a lentiviral vector that has in it a promoter that will drive the expression of the beta-globin gene. They transfect those autologous CD34 cells with the lentiviral vector, it integrates into the genome of the – of those stem cells, and then those stem cells are re-engrafted back in the patient and the expression of beta-globin should give a normal beta-globin, normal sickle or non-sickle phenotype and normal oxygen capacity.

Our approach focuses on a non-viral delivery. It focuses on delivery of zinc finger nucleases via messenger RNA and electroporation. So we put these zinc finger nucleases into the CD34 stem cells for a very short period of time, 48 hours, 72 hours they are there and then they are gone. There is nothing left behind. Those zinc fingers target the BCL11A gene, which when disrupted or knocked out allows for expression of fetal hemoglobin, which gives you the oxygen-carrying capacity.

So the two fundamental differences, one is the target. They are replacing the beta-globin gene, we’re knocking out BCL11A. And then the other is, I guess, I’d call it specificity. One, we know precisely where we are, BCL11 knocking it out and inserting nothing into the genome. The Lentiviral vectors inserted into the genome, that’s how they get the permanent expression in stem cell, but they do so on a random way. And so, whatever the opposite of specific is, is random, and that’s the principal difference.

Robyn Karnauskas - Deutsche Bank

And if necessary say down the line duration wasn’t there, would you be able to re–challenge and would they be able to re-challenge without immune response?

Edward Lanphier

Well we are not putting a virus in, so…

Robyn Karnauskas - Deutsche Bank

So you should be able to re-challenge…

Edward Lanphier

That’s correct, that’s correct. And the same thing is true of, just to expand that point, in the modification that we are making in our CCR5 T-cell protocol, I didn’t emphasize it. But historically, we’ve used an adenovirus to deliver the CCR5 nucleases, we are now using mRNA, which allows us to repeat and repeat if we want to. So exactly right, no viral components in the sickle cell program for our approach.

Robyn Karnauskas - Deutsche Bank

And then just to follow-up, Bluebird will have data in man for their viral approaches. What is the read to success with your drug in sickle cell or this could start with beta-thalassemia, so what is the read there? How do you think investors should view if their data is positive this year the read and success for you?

Edward Lanphier

I think in the – from an efficacy perspective, I hope they are successful; I hope there is a positive outcome. I think ultimately the difference is going to account - I don’t think there is going to be a difference in terms of the target, in terms of oxygen-carrying capacity of fetal [inaudible]. I think the real issue is going to come down ultimately to specificity, which really is a derivative of safety. And a very, very different product profile of randomly integrated viral vector versus no viral vector, no random integration, single site specific modification.

Robyn Karnauskas - Deutsche Bank

Okay. I’ll push back in there a little bit…

Edward Lanphier

Sure.

Robyn Karnauskas - Deutsche Bank

[Well, you need] [ph] a lot of patients to see potentially or a lot of time to see - unless one gets cancer, in the first year of giving the drug, that may take a lot of time to see what the proof is of your product theoretically. You may not be able to see the differences and advantages of your approach versus their approach and how would you push back on that?

Edward Lanphier

Well, I guess, I hope that never happens…

Robyn Karnauskas - Deutsche Bank

Right.

Edward Lanphier

But I think mathematically, you can do the math on that, but I think there is a clear product distinction between the potential for [that and not] [ph].

Robyn Karnauskas - Deutsche Bank

Okay. A couple of questions from the audience?

Unidentified Analyst

Yes, could you just explain with the HIV viral infection, you go in and effect a gene if I understand it correctly in the patient, which has some sort of efficacy, could you explain how that works, please?

Edward Lanphier

Sure. The strategy or the hypothesis in our HIV program involves the receptor on the surface of T-Cells CCR5. HIV uses two receptors, co-receptors to infect the CD4 T-cells. One is the CD4 receptor, the other is CCR5, absent CCR5 those cells do not get infected. And there are people largely Caucasians of Northern European descent, about 1% of that population have a natural mutation in both of their CCR5 genes. They are perfectly normal, it could be anybody. Their immune systems are perfectly normal, but they cannot and do not get infected by the HIV virus.

And so, again, there is lots of data around that. Our goal and our approach is to potentially recapitulate that genotype/phenotype. So knock out the CCR5 gene, have CCR5 negative T-Cells that don’t get infected by the virus, but are still capable of [daunting] [ph] and augmenting an antiviral response. And the data we have to-date suggest that the greater the amount of dual knock out by a allelic knockout of CCR5, the greater the effect on acute viral replication.

Unidentified Analyst

The lysosomal diseases and inserting the gene attached to the albumin promoter…

Edward Lanphier

Yes.

Unidentified Analyst

…the FDA is used to seeing enzyme replacements milligram or milligrams per kilogram.

Edward Lanphier

Yes.

Unidentified Analyst

Is your technology precise enough that you can give them comfort with the dosing effect and then also how do you adjust as a patient, these are pediatric patients, they grow up, they need more of enzyme replacement as well, so how do you adjust for that?

Edward Lanphier

Yes, great question. So I’ll first take the dose titration. And we’ve presented these data, I think for the last two years at ASH where we’ve shown that the amount of AAV that we use to deliver the nucleases is directly [qualitative] [ph] to the amount of liver modification, albumin modification and subsequent protein expression. That’s a fairly tight window, and we’ve done that on a couple of different enzyme replacements. But I think the work that’s largely been done is in the Factor IX; we presented is largely in the Factor IX space. So we can control dose or we can control levels of protein secretion based upon the dose of AAV.

In terms of pediatric situation, this is where I actually think we have a very distinct advantage [inaudible] but this is a compare and contrast not that sort of conventional gene therapy. So conventional gene therapy you put an AAV vector into the liver of a hemophiliac and express Factor VIII driven by the [promoter] [ph]. AAV does not integrate, such as the opposite of lenti. So over time particularly in the pediatric patient as those liver cells divide, because it’s not in the endogenous gene, you are going to get a washout over time of that expression. So it will go down and we’ve published works where we’ve done partial [hepatectomies] [ph] in mouse models where we’ve cut out half the liver in a – and showing what the cDNA goes down. But our approach where we can get therapeutic levels of the Factor VIII in a young patient, because it integrates as that liver grows, as those cells divide, all of the progeny will have that endogenous gene modification. And so we expect to see normal levels or constant levels as the liver divides. So it’s really the principal differential, technical advantage of targeted insertion versus transient gene expression.

Robyn Karnauskas - Deutsche Bank

So with your hemophilia approaches, can you re-challenge as well with hemophilia approaches?

Edward Lanphier

Re-challenge, retreatment with AAV is problematic.

Robyn Karnauskas - Deutsche Bank

Right.

Edward Lanphier

And so one of the reasons why I sort of long-windedly went through this issue of conventional approaches washing out is the challenge of retreatment. But if we can permanently insert the Factor VIII gene in the albumin locus, all of those future cells will have that modification. So conceptually and quite frankly the preclinical data support that we won’t have to retreat.

Robyn Karnauskas - Deutsche Bank

When I spoke to you in the beginning, you’re still seeing sustained three, four years out expression in these patients, like how long will it take to actually prove your thesis correct, that your technology is [inaudible] different and better for patients?

Edward Lanphier

Yes. Well, I think it’s going to take some time, but if I – if you look at any of the – if you look at the animal models it depends on really turnover of the liver and in this case the liver. And so it’s going to take several years. The opposite is true, however, in tissues that don’t turn over rapidly. So the brain, for instance, put AAV into the brain, you can get long, long-term expression, because brain doesn’t turn over quite so much, right, similarly retreatment in the eye, because it’s immune protected. But liver is a tissue that turns over relatively rapidly depending on the individual – depending on the disease state. But over time, the expression levels of AAV, we expect will wash out.

Robyn Karnauskas - Deutsche Bank

Okay.

Unidentified Analyst

[Inaudible] in terms of scaling up the operation when you go to the market, so I mean, in your opinion, I mean, with your technology, how easy or difficult it is to have commercial scale manufacturing in-house?

Edward Lanphier

Sure. Well, it’s going to be different for in vivo products versus ex vivo, but let’s start with in vivo. The scale up of commercial levels of AAV could be done in space twice this size, in terms of a single product, particularly for some of the smaller indications, I mean, we are not talking about millions of patients in these areas. So it’s a very reasonable, significant, but reasonable amount of manufacturing infrastructure and has been done several times, a multiple groups.

The ex vivo size is larger, more complicated, every product is an individual batch. So you don’t have the off-the-shelf products. And the infrastructure required at least in the current manufacturing or current kind of establishments that have to be done and the release that – the testing has to be done is relatively significant. I think I know there are very real efforts going on to automate those processes. If you look at some of the funding that CIRM, the California Institute for Regenerative Medicine is done in terms of request for proposals for automated cell processing. Those kinds of developments although they don’t exist yet, I think will go a long, long way to improving the consistency on a batch to batch basis of autologous – modified autologous cells and will reduce the costs not only from a labor point of view, but because of the consistency and calibration of these future instruments will reduce the amount [release] [ph] testing that has to be done on those, and quite frankly can bring some of these therapies out of just sort of first world infrastructures potentially into developing countries.

So manufacturing for in vivo off-the-shelf products is pretty straightforward. Currently, manufacturing of autologous cell therapies, whether it’s stem cells or CD4 cells is not assembly line. You’re building a [call] [ph] one at a time, but I think there is a lot of effort and a lot of energy that will change that over the next 5 to 10 years.

Robyn Karnauskas - Deutsche Bank

So for the HIV side after looking at Gilead’s model, which has cells out to 2029 eventfully there will be no branded HIV therapies [that I’m sure] [ph] people are looking for the next thing that will bring in revenue for HIV. I’m just thinking about what do you think it takes for a partner, what you think it’s takes for pharma to see, the proof-of-concept here, I mean, you have some data. So what does it take to believe in this kind of therapy for HIV?

Edward Lanphier

I think we need to show acute viral functional control of the virus in the absence of antiretroviral therapy. So in other words, we need to infuse these modified cells, weigh the period of time, take patients off of antiretroviral therapy and then give sufficient amount of time for this therapy, this modified immune system, to control acute viral replication as measured in the blood, which is essentially the standard for antiretroviral therapies.

It’s a longer process if you want to talk about reservoir, depletion, and immune reconstitution, but the most direct endpoint, and I think to your point in terms of because that’s our strategy, that’s our stated business objective is is post Phase 2, pre-pivotal studies is to partner this program. So I actually have an informed answer for once.

What we want to see is in a percentage of these patients functional control of the virus, in a durable way.

Robyn Karnauskas - Deutsche Bank

Is there any - durable way, the only thing that worries me is like what happens if like it stops not being durable.

Edward Lanphier

Go back on ART.

Robyn Karnauskas - Deutsche Bank

But like I – that’s why they’re so focused on seeing everyday making sure you’re compliant, so like, you have to know the day that the drug wasn’t working, where they will be able to - they would have to monitor…?

Edward Lanphier

Well I think people would be monitored certainly in the clinical trials and durability side of things. But ultimately the other element of this while we’re looking for acute viral load control, the element of mechanism that will ultimately drive a curative outcome or long-term functional control is reservoir depletion, and really eroding away these large stores of virus in the body.

And that’s what this strategy can do, which ART cannot do, it doesn’t touch the reservoir.

Robyn Karnauskas - Deutsche Bank

Last question, I know we’re out of time. So RNA, [inaudible] is being used for hepatitis B, how do you think gene therapy [inaudible] in hepatitis B; it seems like there could be a real opportunity?

Edward Lanphier

Yes, I think there is. It’s an area we’ve looked, I don’t think we’ve published, no. We’ve looked at several liver based approaches both from a knockout perspective and on a [expression] [ph] perspective, and I think there are opportunities there.

Robyn Karnauskas - Deutsche Bank

When will we hear about those…?

Edward Lanphier

I don’t know. Not today.

Robyn Karnauskas - Deutsche Bank

Okay. All right. Thank you very much.

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