Good afternoon, and welcome to the Sangamo BioSciences teleconference to discuss First Quarter 2016 Financial Results. This call is being recorded. I will now pass you over to the coordinator of this event, Dr. Elizabeth Wolffe, Vice President of Corporate Communications.

Thank you, Andrea. Good afternoon and thank you for joining Sangamo's management team on our conference call to discuss the company's first quarter 2016 financial results. Also present during this call are several members of Sangamo's 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; and Dale Ando, Vice President of Therapeutic 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 first quarter financial results, as well as our financial guidance for 2016. Geoff will provide an update on our ZFP Therapeutic programs. And finally, Edward will update you on our goals for the rest of 2016 and beyond. Following that, we will open up the call for questions. As we begin, I'd like to remind everyone the projections and forward-looking statements what we discuss during this conference call are based upon the information that we currently have available. This information will likely change overtime. By discussing our current perception of the market and the future performance of Sangamo with you today, we are not undertaking an 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 date that our comments from today are still valid. We alert you to be aware of risks that are detailed in documents with 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'd 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 first quarter results for 2016, as well as our progress and plans for the development of our ZFP Therapeutic's pipeline. 2016 promises to be a pivotal year for Sangamo as we initiate the first two clinical trials based upon our highly leverageable in Vivo Protein Replacement Platform or IVPRP in the next few months and filed six additional INDs as the year enfolds. As you might imagine, with all of these activities in play, it's been a very busy and exciting quarter for the company and we are making steady progress in all of our ZFP Therapeutic programs. Let me provide some specific details. We have completed all of the major tasks necessary to initiate the Phase 1, 2 clinical trial of our IVPRP-based hemophilia B program. We have made great progress with our lead clinical site at the City of Hope and are on track to dose the first patient on this trial in June. Speaking of this study, we received an unexpected but notable endorsement of our IVPRP approach for hemophilia in a recent review in the New England Journal of Medicine. This was all the more gratifying as the article was co-authored by Dr. Amit Nathwani, Professor in Department of Hematology, University College of London, a key opinion leader in the space and a well respected pioneer of conventional AAV based team therapy for the treatment of hemophilia. In fact, it was Dr. Nathwani's Factor VIII program for hemophilia A that BioMarin in-licensed and on which they recently reported data. Dr. Nathwani provided an excellent overview of our IVPRP based approach to produce therapeutic Factor IX for hemophilia B and noted that "these findings are exciting and suggest an improved…

Thank you, Edward, and good afternoon everyone. As you know after the close of the market today, we released our financial results for the first quarter ended March 31, 2016 and I am pleased to review the highlights of those results with you now. Revenues in the first quarter of 2016 were $3.9 million compared to $13.5 million for the same period in 2015. First quarter 2016 revenues comprise revenue from Sangamo's collaboration agreements with Biogen and Shire enabling technology agreements and approximately 200,000 of revenue from research grants. The decrease in collaboration agreement revenues was primarily due to the amendment of our collaboration and licensing agreement with Shire in September 2015, which return their rights to the hemophilia program to Sangamo, as well as the decrease in revenue under the company's collaboration agreement with Sigma. In the first quarter of 2016, Sangamo recognized $2.0 million of revenues related to research services performed under the collaboration agreement with Biogen and 400,000 of revenues related to research services performed under the collaboration agreement with Shire. In addition pursuant to the agreements entered into with Shire in January 2012 and Biogen in January 2014, Sangamo received upfront payment of $13 million and $20 million respectively. The payment for Shire's been recognized on a straight-line amortization basis over the initial 6 year research term. Beginning in January 2016, the payment for Biogen is been recognized on a straight-line amortization basis over approximately 42-months which reflects the revised service period related to our deliverables under the agreement with Biogen. Sangamo recognized $0.5 million of the Shire upfront payment and 600,000 of the Biogen upfront payment as revenue for the first quarter of 2016. Total operating expenses for the first quarter of 2016 were $20.6 million, compared to $19.7 million for the same period in…

Thanks Ward. As you have heard, we maintain a strong cash position which will enable us to accomplish all of our near and mid-term goals and the value creating data catalysts we have outlined for our therapeutic pipeline. We are on track to achieve these goals and end 2016 with over $150 million in cash. I'd ask Geoff to give you more information about the status of our pipeline and our recent progress in our IVPRP programs. Geoff?

Thank you, Edward. As most of you are aware, IVRPR approach enables us to treat the monogenic disease such as hemophilia or lysosomal storage disorder using ZFNs to target a single addressing the genome of a patient liver at a circled safe harbor side into which we can add a therapeutically relevant replacement gene. The aim is to allow the patient to continuously produce their own therapeutic protein to replace the defective enzymal protein that gives rise to their symptoms. Thus, with a single treatment we have the flexibility to develop ZFP therapeutics to a range of genetic diseases currently being treated using protein or enzyme replacement therapy or ERT and eliminate the need for repeated protein infusions. We chose the albumin gene as our safe harbor, as it is very highly expressed. Albumin being the most abundant protein found in the serum. Adults produce larger amount of albumin about 80 grams per week. It’s safe to co-op the very small percentage of its expression we need to produce therapeutic quantities of a replacement protein. And its highly tissue specific as LVI is made exclusively in the liver. As you heard from Edward, we are in a process of opening Phase I, II clinical trials for our IVPRP programs in both hemophilia B and our first lysosomal storage disorder indication, mucopolysaccharidosis is one or MPS I. MPS I is caused by mutations in the gene in coding the alpha-L-iduronidase enzyme or IDUA, which results as a deficiency of that enzyme in old tissues. Normally IDUA is present in a cell in a structure known as the lysosome, which is like the recycling center of the cell. The enzyme is required to breakdown complex sugar chains called glycosaminoglycans or GAGS, which are produced in most tissues. The inability to degrade GAGS…

Thanks, Geoff. As you have just heard from Geoff, we are entering into a very exciting period for the company with the initiation of two new clinical trials of our in vivo genome editing platform and we are working hard to continue to advance our pipeline leveraging this highly disruptive approach. We remain on-track with our previous guidance for our other programs and the respective milestones, which include the filing of an IND application for our MPS II program in this quarter and for the Factor VII Gaucher and Fabry in the second half of this year. In addition, our collaboration with Biogen continues to go forward and we intend to file an IND application later this quarter for our collaborative beta-thalassemia program. We expect that the IND application for sickle cell disease will be filed by Biogen in the second half of 2016. We are also in good financial position to accomplish all of this and remain on track to end 2016 with more than a $150 million in cash. To state the obvious, clinical execution is a key value driver for us over the next year to 18 months and I can assure you that our team is focused like a laser beam on all of the tasks that drive clinical success. We look forward to keeping you updated on our progress at the following investor conferences and scientific meetings, including the Deutsche Bank Healthcare Conference later this week at ASGCT, which is also to be held later this week and the Jefferies Healthcare Conference in June. I should also note that our Annual meeting of shareholders will be held here at the company headquarters on June 14th and invite you all to attend. This completes our prepared comments. I would now like to open up the call for your questions.

[Operator Instructions] Our first question comes from the line of Charles Duncan with Piper Jaffray. Your line is open.

Thanks for taking the questions. I had just a couple. Edward, just did a great job outlining the expectations for the hemophilia B clinical program. I'm wondering if you could do similarly with MPS I or is that a little bit harder to project in terms of see first cohorts that you may see the first TB activity data or any sense of efficacy out of MPS I?

Sure. Geoff, you want to maybe just come back to what you've discussed in terms of clinical end points and what we'll be looking for in that trial?

Sure Charles. In terms of the underlying sort of pace of those studies, they have the same design - the same interval between patients so we anticipate the same general approach. The MPS study certainly present the opportunity to look at the augmentation of circulating enzyme primarily by measuring it in the white cells, as well as by looking at some of the many sort of clinical outcomes that we can see in those patients, and including the measure of the glycosaminoglycans in the urine. What I just to sort of paint the bigger picture, what we're going to do is evaluate those measures in the subjects while they continue to take the ERT and if we can see clear additive effect, we will then move those programs onto a withdrawal strategy to see whether the underlying production from the liver of those enzymes is able to continue to control the disease. But we expect that those will be sensitive to the effective generation of new enzyme from a liver.

It sounds pretty interesting. It sounds like each patient could be their own control and therefore give you a fair amount of, I guess, discriminative, hard to see any changes even with a few patients.

That would certainly be ideal. To be fair it's a little clearer with Factor IX, it's a simple measurement that is the only - that's the protein that we're trying to produce. But yes exactly, each patient in both of these studies really acts significantly as their own control.

Yes. And then if I could just ask one question in terms of the recent preclinical results in MPS I and II, we were impressed with those from the mirroring model. But do you anticipate being able to present any results from other preclinical studies such as in a non-human primate prior to seeing some of the trial progress with 318 perhaps later this year or next year?

Well, let Geoff or Mike Holmes who's here comment further if need be but there really aren't any other disease models for MPS I and MPS II beyond these mouse models. So what we'll do is use the NHPs as a - for dosing and toxicity, and toxicology but primarily the model systems were done in the rodents Geoff or Mike.

Yes, I mean the only thing I would add Charles is that, as we've gone through these studies, we will continue - we continue to evaluate them, look at histology and various other things then it's possible that as that data accumulates we may present that at a future time. But that's pretty much the basis for our program is the success we're seeing in the model data.

And then final question is regarding the collaboration with Biogen. Edward, I'm wondering if you could update us on that. It seems like positive that they are planning on filing an IND soon per beta thal. And I'm wondering if there have been any changes in the level of engagement or projections on timelines with Biogen in that collaboration?

Well certainly we'll repeat what we just said in the script that our plan is that we will file the beta-thal IND first half of this year and Biogen is previously guided to filing the sickle cell IND in the second half of the year. There's no question that we read the same things you all read in terms of Biogen's continued focus in the CNS space and that's been - we've seen the visibility of that. But in terms of the programs, the data we've generated our enthusiasm for those programs nothing's really changed there.

And the interaction with the team over Biogen, I mean I know it's hard to quantify, but do you feel like, if they were to sell off some of their assets in the similar area that your program would be perhaps bundle with that or how do you -

Charles what's the expression they use in various government things, you know that calls for speculation or - so you know I really don't want to speculate on what Biogen may or may not do as they develop and evolve their strategy. We work on - focus on the things that we can control which is the development of what we think is an incredibly important and differentiated therapeutic program.

Okay, that's helpful. Thank you, guys.

Thank you. Our next question comes from the line of Whitney Ijem with JPMorgan. Your line is open.

Thanks for taking the questions. The first one, I guess I just wanted to kind of circle back with the BioMarin data that you mentioned. I'm just curious if the very early and initial data that we've seen from them has changed how you guys are thinking about target levels of factor expression or kind of what you had hoped for at the highest dose in your studies?

Well, I think the BioMarin data and again Mike and Dale and Geoff are here, and they can certainly add more. But I think the BioMarin data we found to be very impressive, very important data. I will say that it's highly consistent with what we have been aiming towards and what we think is very much a reasonable kind of therapeutic target. And we'll have some preliminary thoughts and data presentations next week or later this week, but Mike we're focused on presenting kind of a comprehensive particularly Factor VIII data in July what's that meeting.

Yes Edward, that's the World Federation of Hemophilia. There's a meeting at the end of July and will be specifically presenting on July 26 and giving a conference of update on hemophilia and specifically our Factor VIII program.

And I think that's probably what I highlighted is the technical platform presentation at ASGCT and then I think a good program update in the context of your question of the BioMarin data in the end of July.

I got it. I'll back in queue. Thanks.

Thank you. Our next question comes from the line of Jim Birchenough with Wells Fargo Securities. Your line is open.

This is actually Yanan Zhu in for Jim. So a couple of questions on the hemophilia B trial design, the low dose of five times 10 to the 12 vector copy per kilogram, could you clarify whether that is a per vector or it's the total of the three vectors used for infusion?

Right, it's the total of the three vectors that we're infusing.

I see. I think I saw the non-human primate data being -- that was presented at the RAC meeting. There I saw the low dose is 1.5 times 10 to the 13. Is there, I guess, the low dose for the clinical trial? Do you expect any efficacy from the current -- this low dose and could you compare related to the non-human primate low dose data?

Well I'll ask Mike or Geoff to comment on the dose element of your question. As you know, we're doing three doses a low dose what we’ve perceive to be a low dose, what we perceive to be a medium dose and then what we perceive to be is the therapeutic or optimal therapeutic dose in the study, it's fairly classic dose escalation. I don't think we'll go into a doze that we don't think has the potential to be therapeutically relevant, but I think the goal here is first time in man is to primarily look at safety and tolerability of the approach. So I'm not from a investor perspective guiding to this for efficacy and perhaps maybe not even the second dose cohort. It's really in the third dose cohort where we are focused on looking at the highest level or the level of efficiency that we're trying to achieve. Mike or Geoff, do you want to comment on the NHP data to dose or where we are on starting dose?

Certainly, its Geoff here, certainly what we're striving to do is look at the NHP data and come up with the dose, a starting dose in the clinical study that to Edward's point offers on the one hand a low enough dose to able to start a study with reasonable safety, but on the other hand offer some opportunity for efficacy and looking at the NHP data overall and Mike may want to comment on this you know, it’s clearly a threshold, it is close to the threshold active dose that we saw in the non-human primate study. So that's the rationale, obviously it remains to be seen what the effect in humans is going to be compared with the effect in non-human primates ,and I think coming back to Edward's point about speculation let's see what we see in the clinical trials, but even if it is - even if there is a close relationship between NHP dose and human dose, we may see that a lowest dose obviously, but let's be a little more circumspect and expect to see it at the second or the third dose as being much more likely.

Great. Another question is in the conventional AAV, gene therapy for hemophilia, in those approaches anti-capsid T-cell response has been observed, which led to the liver enzyme elevation. In your gene therapy approach could you comment on the likelihood of that happening? One thing is you do have three vectors, so the number of vectors is greater per infusion. But could you just in general comment on the possibility of inducing T-cells responses?

Yes, certainly. It's the total vector - we think what's important is the total vector dose which remains in the same zone as we have seen for example with recent BioMarin data. If you actually look at their dose range, it's pretty much the same dose ranges, we are putting forward. And as best we understand it, these LFT changes are driven by just the total amount of capsid, and the capsid is the same on every virion, no matter what's it got sort of inside in its DNA. So we think that it should be driven by the total vector dose whether there's an affected serotype on this is also another area of speculation simply it remains to be seen and as we've described before, we're going to be taking as with all of the trials in this area, a fairly close watch on the patients to make sure that their LFTs are well monitored and will treat steroids currently we're saying we'll follow the approach of actually treating these events when they occur. But as you have certainly heard from BioMarin, there is always the option of going earlier in order to essentially prophylaxis against that possibility and obviously that will depend on the way the study actually unfolds.

Got it. That's very helpful. I have a last question on, one comment that's made by Dr. Nathwani in his New England Journal review article. He mentioned that polymorphism of albumin gene may prevent this approach to be used universally. Do you have some sense of how they extend that polymorphism and how it impacts the use of the product candidate?

Well I think in any Genome Editing approach, you select the target sequence and given the specificity of the Zinc Finger approach, we think we have great precision around that target. To the extent that there is a polymorphism or in a very, very well element of population, then you're absolutely right, given the specificity of our approach, then it will not be affected, but we think that's an extraordinarily rare and true in the hypothetical, extraordinarily in the practical.

Got it. Thank you very much.

[Operator Instructions] Our next question comes from the line of Gena Wang with Jefferies. Your line is open.

This is [indiscernible] for Gena. Just first one clarification question, so for the hemophilia B Phase1/2 trial, so I was just going to apply prophylactic steroid use or you thought you mentioned that you’re going to use that but will that prophylactic in the protocol?

Without being dismissed Geoff, do you want to repeat what you just said.

Yes, so just to clarify, the protocol as written at present is to not use prophylactic steroids to monitor patients closely, and use steroids as necessary we think, that's still the rational approach given that this has got Zinc Fingers and various other reagents in it that are not typically present in more standard gene therapy approaches. But I think as I signaled, we will have a relatively lower to moving towards the use of prophylactic steroid approach which I think we've always said the field is likely to move to and I think we are seeing that is indeed coming to pass.

Okay. Got it. And then my second question is about the new IND. So I just wonder especially for the two - in the first half of the year, have you guys passed through the RAC Meeting, if not so when would that be scheduled?

It’s a timely question, [indiscernible] thank you. As you may have noted, the NIH recently put out new guidelines relative to the Recombinant Advisory Committee. And so instead of in the past filing with the RAC, RAC determining whether they wanted to have a public review of the protocol or not, one files an IND, one then goes to the IRB of the given institution, and that IRB makes a determination about whether they need RAC or want RAC review. So, it’s a new approach, it's a new protocol and I guess at this point, you'll just have to stay tuned and we'll see what the - our collaborative institutions want our need for their IRBs.

Okay. All right. Thank you so much.

Thank you. This concludes today's Q&A session. I would now like to turn the call back over to Mr. Lanphier for any closing remarks.

Great. Thank you. We'd like to thank you for joining us. And we look forward to speaking with you again when we release our second quarter 2016 financial information. We'll 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 the program. And you may all disconnect. Everyone, have a great day.