Good afternoon, and welcome to Sangamo BioSciences Teleconference to discuss Fourth Quarter and Full Year 2012 Financial Results. This call is being recorded. I will now pass you over to the coordinator of this event, Dr. Elizabeth Wolffe, Senior Director of Corporate Communications. You may begin.

Thank you, Ashley. Good afternoon, and thank you for joining Sangamo's management team on our conference call to discuss the Company's fourth quarter and full year 2012 financial results. Also present during this call are several members of Sangamo senior management, including Edward Lanphier, President and Chief Executive Officer; Ward Wolff, Executive Vice President and Chief Financial Officer; Geoff Nichol, Executive Vice President of Research and Development; Philip Gregory, Vice President of Research and Chief Scientific Officer; and Dale Ando, Vice President of Development and Chief Medical Officer. Following this introduction, Edward will highlight recent activities and the significant events from the past quarter. Ward will then briefly review fourth quarter and full year financial results of 2012, as well as our financial guidance for 2013. Geoff and Philip will provide an update on our ZFP therapeutic programs, and finally, Edward will update you on our goal for 2013 and beyond. Following that we will open up the call for questions. As we begin, I'd like to remind everyone that the projections and forward-looking statements that we discuss during this conference call are based upon the information that we currently have available. This information will likely to change over time. But by discussing our current perception of the market and the future performance of Sangamo with you today, we are not undertaking any obligation to provide updates in the future. Actual results may differ substantially from what we discuss today and no one should assume at a later time that our comments from today are still valid. We alert you to be aware of risks that are detailed in documents that the company files with the Securities and Exchange Commission, specifically, our Quarterly Reports on Form 10-Q and our Annual Report on Form 10-K. These documents include important factors that could cause the actual results of the company's operations to differ materially from those contained in our projections or forward-looking statements. Now, I would like to turn the call over to Edward.

Thank you, Liz, and thank you all for joining us for our conference call to discuss our fourth quarter and full year results for 2012, as well as our near and midterm plans for the development of our zinc ZFP therapeutics pipeline. We had a very busy fourth quarter and a great start to the New Year setting the pace for an eventful 2013. This end of your call provides us with an opportunity to reflect on the achievements and events of last year, but more importantly, to look ahead and layout our goals for the future. We began to do just that in early December at our analyst and investor briefing and follow that up in the first weeks of January during the annual JPMorgan Healthcare Conference. We used these two venues to accomplish a number of important goals but above all to articulate our vision albeit incredibly ambitious of engineering genetic cures for diseases, not incremental treatments, genetic cures. During those meetings, we provided insight into how we select disease targets for our ZFP therapeutic platform. I have asked Geoff to expand on this later on the call. We also outlined our strategy for the next few years in terms of clinical and preclinical progress as well as our financial outlook. We discussed our preclinical programs and our goal to file seven INDs by the end of the 2015 and explained how we expected to accomplish this within the framework of our current financial expectation. Finally, we articulated how our vision and strategy enables us to create value while mitigating on several levels some of the inherent risk in drug development. If you have not had an opportunity to listen to our analyst briefing, I encourage you to do so. A webcast of the event is still available…

Thank you, Edward and good afternoon everyone. As you know, after the close of the market today, we released our financial results for the fourth quarter and full year ended December 31, 2012 and I’m pleased to review the highlights of those results. Revenues in the fourth quarter of 2012 were $8.9 million compared to $4.7 million for the same period in 2011. Fourth quarter 2012 revenues were comprised of revenue from Sangamo's collaboration agreements with Shire, Dow AgroSciences and Sigma-Aldrich as well as approximately 400,000 of revenue from research grants. As we mentioned in the press release, the increase in collaboration agreement revenues was primarily due to our agreement with Shire as well as an increase in the minimum annual sublicensing revenue from Dow AgroSciences. Total operating expenses for the fourth quarter of 2012 were $12.3 million, compared to $11.1 million for the same period in 2011. Research and development expenses were $9.3 million in the 2012 quarter and $7.9 million for the prior year quarter. The increase is primarily due to increase in external research expenses associated with our preclinical programs, partially offset by lower clinical trials and manufacturing expenses associated with our SB-728-T HIV AIDS program. General and administrative expenses were $3 million for the fourth quarter of 2012 and $3.2 million for the same period in 2011. Non-cash stock based compensation expense was $1.3 million for the quarter with 700,000 in research and development and 600,000 in general and administrative. For the fourth quarter of 2012, we reported a consolidated a net loss of $3.5 million or $0.07 per share compared to a net loss of $6.4 million or $0.12 per share for the fourth quarter of 2011. For the full year 2012, revenues were $21.7 million compared to $10.3 million in 2011 with the increase…

Thank you Ward, as you have heard we ended 2012 with just over $76 million in line with our guidance of at least $75 million which relative to our historic and projected burn rate is a strong cash position. As we outlined in our analysts briefing we believe that our balance sheet provides a solid basis from which to work and will enable us to complete our ongoing Phase II clinical trials and to bring up to seven products to INDs by the end of 2015. The platform nature of our technology enables us to leverage our work across multiple programs, partnered and proprietary. I've asked Jeff to outline our decision making process and provide more insight into how we prioritize programs and determine how to apply our technology to therapeutic targets that we have chosen. Jeff.

Thanks Edward. As you know, our ZFP platform is unique in that it operates at the DNA level. We've shown this technology to be robust, highly specific and broadly applicable to target any gene that we choose. This gives us a very versatile toolbox, the scope of which cannot be duplicated by small molecules, antibodies or RNA based technology such as Antisense and RNAI. Using ZFPs we can access a range of powerful gene modification outcome, including permanent gene disruption, gene addition or correction as well as the ability to regulate the expression of genes in a cell, turning them up or down to make more or less, of a given protein. This gives us distinct technical advantages and enables us to think very differently about how we address disease particularly so called monogenic diseases caused by a mistake in a single gene such as hemophilia, Huntington's disease or beta thalassemia. This allows us to think not just about treating or alleviating symptoms but about really engineering genetic cures, a whole new paradigm in medicine. So, given the power and breadth of our platform how does one begin to prioritize a therapeutic pipeline, how do we select targets that should, product strategy be to use this technology to its fullest potential. What characteristics do we need in the target disease before we begin to apply our toolbox in a way that can drive a genetic cure? And very importantly, what is the best strategy for delivery in order to achieve the therapeutic effect we're looking for. First, what is a qualified target? There are several essential criteria that we think about. The first is an unambiguous correlation between the gene and the disease. By definition that’s a monogenic disease. For example a mistake in an individual's factor IXG results in…

Thanks Geoff. In addition to broadly covering how we think about our therapeutic product development platform and its applications to different disease targets. We also spoke for the first time about a new strategy that we have been developing our in Vivo Protein Replacement Platform. This is an application that we feel truly represents our ability to reliably make highly specific and precise changes to the genome and one that can be leveraged across multiple monogenic diseases. I have asked Philip to provide you with more details. Philip?

Thanks Edward. Let me begin with some background. As many of you know, in 2012, we published in the journal Nature, the use of our Zinc Finger Nucleases or ZFN technology to permanently correct a mutation in the human factor IX gene effectively providing a genetic cure for hemophilia in a mouse model of the disease. In this instance, we used ZFN specific for the human factor IX gene and a corrective DNA repair sequence encoding a good copy of factor IX. Systemic administration of these ZFNs resulted in the correction of the factor IX gene and production of the corrected protein in the liver of the animal. It restored blood clotting time to normal. We can, of course, design ZFNs to correct a variety of gene targets that are mutated in diseased. (Inaudible) and Alpha 1-antitrypsin deficiency are examples we also published in Nature. For each target, we designed a specific set of ZFNs to precisely bind that individual gene and demonstrated highly efficient gene correction. Thinking along the lines that Edward and Geoff outlined, how do we maximize the value of this incredible technology? We asked ourselves, could we go one step further than doing this one gene at a time? Wouldn’t it be more efficient if we could find a way of leveraging one single site in the genome to treat a host of monogenic diseases requiring enzyme or protein replacement? Could we design one set of ZFNs that would enable us to safely insert a correct copy of any gene at the single site and produce the encoded therapeutic protein from that site. What I am going to describe is what we came up with. Our In Vivo Protein Replacement Platform which is a potentially highly leveragable method of using a single ZFN site to produce…

Thanks Phillip. So what we’ve tried to do today is give your insight into how we approach targets and implement our strategy in the development of ZFP therapeutic pipeline. Over the next year we expect to make significant progress in delivering on the promise of ZFP therapeutics. We will complete our Phase II clinical trials in our SB-728-T HIV AIDS program. With positive data from these studies we expect to partner in this program for further development and commercialization. You can expect data presentations from these studies in the first and second half of 2013, as well as a presentation in CROI on further immunological data from our earlier trials. Over the next year, we will continue to present data from our partnering programs in hemophilia and Huntington disease and our proprietary program in hemoglobinopathies and lysosomal storage diseases. As we outlined in our analyst briefing in December, our goal is to file INDs in 2014 in hemophilia A and B, a hemoglobinopathy program and our HIV application in stem cells which has been funded by a grant from the California Institute for Regenerative Medicine or CIRM. In 2015, our goal is to file INDs for Huntington’s program with Shire and two lysosomal storage diseases applications. I also hope that our presentations over the past few months have provided you with a sense of how our technology platform and business development strategy can create significant value yet mitigate risk via diversification and leverage. We have distinct therapeutic product development strategies that can be implemented to address a variety of well validated targets. We have a business development model that has enabled us to generate both non-therapeutic and therapeutic partnerships, as well as proprietary programs. And as we have a platform, we can and will seek out further therapeutic partnerships to…

(Operator Instructions). Our first question is from Charles Duncan at Piper Jaffray. Your line is open.

So, my first question is on that upcoming data at CROI. It's clear that your line is going to be additional data from Phase I. Can you help us understand how to think about that with regard to the ongoing Phase II? What would you expect to see?

Well I don't know, I'll speak while Geoff and Dale collect their thoughts on this. I mean I would probably say we're not interested in and particularly front running the actual presentation. I like the way I characterized it before Charles and I'll certainly ask Dale or Geoff if they want to come further, is that at ICAC in September for the first time we really laid out the emulogical underpinnings of this approach, in terms of both durability as well as the type of the T cells that are involved. And I think that you should expect to see further analysis along those lines. I'll pause there and see if Dale or Geoff want to add to that or have any more color on that. No, that about covers what I think we would highlight in terms of the expectations.

Okay, that makes sense Edward. And just to be clear you stated your strategy then, if you have positive data out of these twos to seek a partnership for future development?

That's correct.

And then if we could move on to the INDs within the Shire partnership, could you help us understand some of that needed steps required to get to those INDs and whether or not you'll be increasing visibility on that progress.

Well, again I'll start and happy to have Philip or Geoff or Dale provide more color. And we try to lay out at the analysts briefing some of the major buckets here Charles and so refer people to the specific sections and the analyst briefing we went through, some of the next steps in detail. But essentially what we need to do and starting with the hemophilia program is scale up and from small to large animals, establish the delivery modalities and ratios in terms of delivery and then with that in place move forward into standard GNP production, toxicology studies and IND filing, but that's a very high level representation. Anybody want to drill down on any of that in any more detail?

Yes, I think the critical steps are really showing that we can continue to move up in scale, both in terms of delivery efficiencies to large animals and then upping the scale in terms of manufacturing and that's the, those are the, sort of critical path items for us.

And then success will be defined by the actual filing of INDs or do you anticipate being able to provide some additional information on progress and finally is the filing of an IND pretty much Gant Chart driven or does it require some okay or buy in by Shire?

Well I think I’ll take them step at a time. I think as we mentioned you'll continue to see us present and publish at appropriate disease oriented meetings like the ASH meeting, like ASGCT Society for Neuroscience on pre-clinical efficacy data. I think you'll also see major milestones announced as we move through programs, such as initiation of toxicology studies or things like that. And of course in terms of the actual IND filing, this is a collaboration so we will do and make those decisions in discussions with Shire but I think we are equally motivated, both parties are motivated to move this forward in a high quality way but also as efficiently as possible, so I think we're joined at the hip on that.

Thank you. Our next question is from Liana Moussatos of Wedbush Securities, your line is open.

The two Phase II HIV trials, do you envision reporting them together or this enrolment's different, would you report one out and then the other?

Again I'll start and Dale and Geoff can comment but these are independent studies and so I don’t see one, I don't see them having to be linked in terms of when they're presented or anything like that. I'll give a little bit of color that I've given in the past to others. The Delta-32 heterozygotes study is essentially the same process, the same treatment for all subjects on that study. The engraftment enhancement study is a dose escalation study starting at the lowest dose and then moving up and so one might expect that you would see data from the Delta-32 studies in sufficient numbers earlier than one might see the later stages of the higher dose in the dose escalation Cytoxan studies but that’s a general statement about the process of the trials themselves but I don’t see them necessarily been presented together. Geoff or Dale, any?

I can’t really add a whole lot more color to that. Edward is right. There probably is something of temporal staggering of the two studies but I can’t really elaborate more in terms of exactly how much of each study will present in the preliminary presentation in the first half of the year and obviously we do anticipate being done with both studies by the end of the year.

So you could have a press release on one and then press release on the other, or would you have one press release with top-line data for both in the first half?

The possibilities are mindboggling. Yes, I don’t think that we are planning this to be, not to be glib about it, around press releases we are really driven by the data and by sufficient amount of data to make a sincere legitimate credible scientific presentation.

What do you mean by sufficient amount of data, certain number of patients?

Yes, certain number of patients who have a sufficient amount of time that we can make a reasonable clinical observation.

Then what number would that be?

That would be a sufficient number.

Okay. In 2014, you mentioned the INDs and then another group of INDs was at 2013 or 2015, for Huntington and lysosomal storage diseases?

I must have slurred my words, 2015 for Huntington and to lysosomal storage disease targets.

And in 2014, what were the ones that you mentioned again?

Two hemophilia targets, factor VIII and factor IX, the stem cell based HIV program that we are doing in collaboration with City of Hope and (CIRM) and the hemoglobinopathies program for CD34 cells.

(Operator Instructions). Our next question is from Elemer Piros of Burrill Securities. Your line is open.

What I would like to ask Edward is, and this is related to what Charles was asking about the IND enabling studies, if you could give us an idea, if there are any peculiarities, differences between when you are getting ready for an in Vivo as opposed to an ex Vivo trial, and as you go from small animals to larger animals and to humans, the delivery system, would it remain the same?

Let me repeat the questions, just so I have it. You are asking about sort of preclinical development path to IND filing and the differences, potential process or hurdles that might be different for an in Vivo therapy versus and ex Vivo therapy, is that right?

That is exactly correct. And if there are any changes; for example as you work up from mice to non-human primates to humans in terms of the way you deliver the therapy?

Yes, again I will again I’ll go first here. I’m not sure that I’m the right person that I am also looking around the room to see who wants to raise their hand to jump on it. Yes, I think the path under Ciber and you know this is both under Ciber both in the division of cell and gene therapy, is well-well established. And for instance for our in Vivo approaches, both factor VIII and factor IX, lysosomal storage diseases, Huntington’s were using an NAAV vector. There have been, I don’t know what the right numbers. I will take thousands of patients who have been treated with AAD under dozens and dozens of INDs and so there is a well-established path in terms of toxicology studies, CNC, release criteria for the vector and so on so forth and Dale has been through this dozens of times with the programs. On the cell therapy side, again, same sorts of issues, well established path for characterization of the initial material characterization of release criteria and so on and so forth. And in terms of toxicology studies again, well established processes. With that said I mean, Dale are there any things that you would point out that differ between, I’ll just take toxicology studies for cell based therapies versus vector therapies.

In general, human cell based therapy, there is really no good animal model per se to show us exactly what’s being done and in general you put those cells into compromised mice to look at safety and whatever parameters if any that can be evaluated whereas the direct viral vector therapies often can be mimicked in animals and where appropriate we will do those for both preclinical and for safety. So that’s the major difference.

And in terms of factor use as you; for example if you think about the Factor IX program, these are all scaling up. The same sort of delivery system used as it goes from?

This is Philip. For our in Vivo programs for example we will be using the identical vector systems for the both small animal studies, the large animal studies, and obviously those will be the ones that we are multiplying ultimately take to clinic. So there is no change in the vector used between a small animal safety testing and/or efficacy testing and the ones that we used for large animals are ultimately declined.

Okay and certainly Elemer, in our in Vivo vectors are at no associated virus and we have access to at least two strings of AAV which are effective for delivery to deliver. So that’s the approach there. The ex Vivo approaches don’t use an AAV. There are various approaches that we can take to getting the encoded ZFNs and ZFPs into the cell and clearly the toxicological issues with in Vivo tend to deal with systemic delivery and so on we still face the fact that we are targeting the human genome without therapeutic and it’s not usually possible to fund exactly for same site in animals for the specific agent in the Vivo setting. In the ex Vivo setting we can modify human cells and put those into animals again as they will a set highly artificial situation but there the issues are engraftment and the systems and continued help of the cells and the animals during the time that you can maintain those human cells ex Vivo in those immuno deficient animals.

Thank you. I'm not showing any further questions in the queue. I’d like to turn the call back to management for any further remarks.

Great. We’d like to thank you for joining us and we look forward to speaking with you again when we release our first quarter financial information. We will be available later today if there are any follow-up questions. Thank you.

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