Good afternoon and welcome to the Sangamo BioSciences teleconference to discuss Second Quarter 2015 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, Nicole. Good afternoon and thank you for joining Sangamo’s management team on our conference call to discuss the company’s second quarter 2015 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 second quarter 2015 results, as well as our financial guidance for the rest of 2015. And Geoff will provide an update on our ZFP Therapeutic programs. Finally, Edward will update you on our goals for 2015 and beyond. Following that, we will open up the call for questions. As we begin, I would 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 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 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 of 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 2015 second quarter financial results, recent events and accomplishments and our plans for the development of our ZFP Therapeutic pipeline. While not particularly visible to investors, the last couple of months sought a number of important developments in our pipeline that positioned us well to execute on our clinical development plans for both our ex vivo programs in HIV, beta-thalassemia, and sickle cell disease and our in vivo programs in hemophilia, lysosomal storage disorders and Huntington’s disease. On the more visible end of the spectrum, this year we once again had a significant presence at the Annual Meeting of the American Society for Gene and Cell Therapy, or ASGCT, with 18 presentations by Sangamo scientists or collaborators. One presentation describing efficient, targeted integration of genes into the genomes of hematopoeitic stem cells, an alternative to the use of randomly integrating viruses, such as lentiviruses and therefore significant advance for the development of future ex vivo ZFP Therapeutics was selected for the Presidential Symposium, a second ASGCT featured presentation selected as a clinical trial spotlight covered our work on the effect of SB-728-T treatment on reducing the size of the HIV reservoir, a unique feature of our immunological therapy and a critical element in our goal of achieving a functional cure for HIV AIDS. We also presented important proof-of-concept data for our LSD programs and I have asked Geoff Nichol to provide more detail later in the call. Dale Ando, our Chief Medical Officer also provided an update on subjects enrolled in our SB-728 1101 clinical trial. As Dale reported, two out of three subjects enrolled in cohort three of our 1101 study demonstrated control of circulating viral loads at low levels that is…

Thank you, Edward and good afternoon everyone. As you know after the close of the market today, we released our financial results for the second quarter ended June 30, 2015 and I am pleased to review the highlights of those results with you now. Revenues in the second quarter of 2015 were $8.4 million compared to $10.4 million for the same period in 2014. Second quarter 2015 revenues comprised revenue from Sangamo’s collaboration agreements with Shire and Biogen, enabling technology agreements and $600,000 of revenue from research grants. The decrease in revenues compared to the year ago quarter was primarily due to a decrease in revenues from the company’s collaboration with Shire, partially offset by an increase in revenues from our collaboration with Biogen. The decrease in revenues from Shire reflects the timing of manufacturing expenses and natural tapering of research activities as we prepare to file the IND application for the Factor IX program later this year. Sangamo recognized $3.9 million of revenues related to research services performed under the collaboration agreement with Shire and $1.7 million of revenues related to research services provided – performed under the collaboration agreement with Biogen. In addition, pursuant to the agreements entered into with Shire in January 2012 and Biogen in January 2014, Sangamo received upfront payments of $13 million and $20 million respectively. These payments are being recognized as revenue on a straight line, amortization basis over the initial 6-year research term for Shire and approximately 40 months for Biogen. The company recognized $0.5 million of the Shire upfront payment and $1.5 million of the Biogen upfront payment as revenue for the second quarter of 2015. Total operating expenses for the second quarter of 2015 were $20.6 million compared to $17.4 million for the same period in 2014. Research and development…

Thanks Ward. As you have heard, we ended the second quarter with approximately $219 million, a total cash burn of $8 million for the first half of the year. We believe this balance sheet strength enables us to aggressively advance our preclinical pipeline with the goal of filing three new IND there and additional six by the end of 2016 as well as completing our HIV studies in T-cells and making significant progress on our HIV stem cell program. We have a lot going on in the next 18 months and more than sufficient capital to see it through. I have asked Geoff to provide more detail on the recent proof-of-concept data from our in vivo protein replacement LSD programs, how our programs differ from gene therapy approaches that are based on the use of AAV viral vectors and why we believe our strategy has the potential to be more effective as a long-lasting curative therapy? And while this phase of our activities may not be particularly visible, we are aggressively advancing these programs into the clinic and in so doing we will demonstrate the differential technical of our in vivo protein replacement program. Geoff?

Thanks, Edward and good afternoon to everyone. Our in vivo protein replacement platform, or IVPRP, is an efficient, leveragable and potentially curative approach to diseases that are currently treated using enzyme replacement therapies, or ERT. Our platform was designed to add a corrective therapeutic replacement gene into a so-called Safe Harbor site in the genome. This strategy has several advantages over conventional gene therapy approaches, particularly in terms of the potential durability of the effect. We have developed the IVPRP with significant funding from Shire for the hemophilia A and B programs and have leveraged the same strategy for our own programs in LSDs. We have named the first two LSD targets, Hunter and Hurler syndromes, but also have active research programs in several other LSDs. The IVPRP enables us to treat a monogenic disease, such as hemophilia or a lysosomal storage disease by targeting a single address in the genome of a patient’s liver as a so-called Safe Harbor site into which we can add a replacement therapeutic gene. This allows the patient to produce their own source of therapeutic protein to replace the defective enzyme that gives rise to their symptoms. The approach gives us the flexibility to develop ZFP Therapeutics to essentially any disease currently being treated using protein replacement therapies using a single set of ZFNs. We chose the albumin gene as our Safe Harbor as it has all the properties that we desire. Firs, it’s very highly expressed, being the most abundant protein found in the serum. Adults produce about 80 grams of albumin for a week, which is about 9 pounds of albumin per year. Second, it’s safe to co-opt the very small percentage of its expression needed to produce therapeutic quantities of a replacement protein. And third, it’s highly tissue-specific as albumin is…

Thanks Jeff. So as you have heard there is an awful lot going on at Sangamo. We are focused on filing INDs for hemophilia B, Hunter and Hurler syndrome in the next several months and an additional six INDs in hemophilia A, beta-thalassemia or sickle cell disease, Huntington’s disease and an additional two LSD indications, a very busy and important year and a half ahead. I also want to update you on some internal organizational developments that have occurred this quarter. On the R&D front we have promoted Dr. Michael Holmes from Vice President of genome editing research to Vice President of research. Mike has been with the company for 14 years plus. And among his many accomplishments has most recently been leading our in vivo approach. In addition, Curt Herberts, who has been with Sangamo for nearly 5 years and has played an important role in the business development group, senior director of corporate development and strategy has been promoted to Vice President of Corporate Development. Congratulations Mike and Curt, very well deserved. As this is probably clear we have a very busy second half of the year ahead of us and we look forward to keeping you informed of our progress. In the immediate future we will be making corporate presentations at the Wedbush Securities Life Sciences Management Access Conference on August 11 and the Morgan Stanley Global Healthcare Conference on September 18, both of which will be webcast and available on the Sangamo website. As far as scientific updates are concerned, as I mentioned earlier, additional updates from our 1101 trial will also be provided at this year’s ICAAC meeting. This concludes our prepared comments. I would now like to open up the call for your questions.

Thank you. [Operator Instructions] Our first question comes from the line of Cory Kasimov of JPMorgan. Your line is now open.

Great. This is Whitney on for Cory. Thanks for taking the questions. First one and I am not sure how much you can say here, but just wondering if the Shire, Baxalta hubbub have changed how you are thinking about your partnership or timelines or if there is anything notable there?

Well, it’s only been a couple days, right. And unclear of what’s going on. But no I think the answer is it hasn’t changed anything.

Got it. And then just given the mechanism of action if your approach in beta cell and sickle cell, just wondering if there are patients who may be better candidates for gene editing versus gene therapy, it’s like they have higher baseline levels of fetal hemoglobin or anything like?

Good question. Geoff and Dale do you want to discuss them?

Yes. I will actually pass it over to Dale.

Yes. I think we are using the BCLG to operate hemoglobin F, so we are very keen about looking at patients that may have a good response to hydroxyurea or slightly better hemoglobin F levels. But other than that there is no clear genetic element that would favor patients for the gene editing.

Yes. What we do know – it’s Geoff here. What we do know is that if for whatever reason you have a genetic background that favors the production of the hemoglobin S, then you tend to have reduced symptoms certainly a beta-thal and potentially also for sickle cell. Now whether that helps in terms of adding to the effect of switching off the Enhancer to BCL11A I think remains to be same. And certainly we would anticipate that switching off that Enhancer is at the very, very top end of the naturally occurring genetic changes that promote hemoglobin F that occur in very, very, very, very rare individuals who basically have a BCL11A knockout already in their genetic makeup. So anything that we can do will be significantly out of range compared with the genetic background of the patient. But an interaction is always possible, but that will depend on clinical trials.

Got it. Thanks.

Thanks, Whitney.

Thank you. Our next question comes from the line of Charles Duncan of Piper Jaffray. Your line is now open.

Hi, it’s Roy in for Charles. Thanks for taking my questions. I think previously you guys were going to do the beta-thal Phase 1 and Biogen was going to do sickle cell, is that still the organization that planned or is one company going to take hold?

Yes, I think that’s largely the guidance. Sangamo is going to take the lead on the Phase 1/2 trial on beta-thal. And I don’t think we have given formal guidance on sickle, but I think it’s likely that Biogen will have a much greater role in that if not fully taking the lead on that.

Okay, great. And then a little bit surprising, but the data for the Enhancer knockout looks little better than the BCL11 gene knockout based on global ratios. I think there is noise across experiment or just something about the general health assaults?

Can you repeat the front end of that question again?

Yes, the data on the Enhancer knockout, the gene now kind of look little better with Enhancer knockout based on the global ratio?

Right. Yes, I think – I think we would argue that they are essentially equivalent in terms of fetal activation, but Geoff do you want to – I think we would argue that they are essentially equivalent.

Yes. I mean I think given what you typically see in these experiments with some allowance of variation and so on we would come down with an equivalent statement. Small differences probably are not telling us a large amount given all of those factors. Okay, that makes sense. And then on your first LSD programs, do you think you are going to go into patients that are diagnosed by genotype, is that a feasible approach and going forward is there going to be someone that’s manifested a clinical phenotype? Thanks.

Dale or Geoff, do you want to discuss the initial sort of the cool criteria for those studies?

Yes. We will basically use genotyping to select out the patients. And basically, the phenotype of these patients is very difficult to differentiate between 100s of Hurlers except for the most severe forms of Hurlers. So we will need to sequence the genes.

Okay, I hope that answers your question. If you are asking are we going to treat people who have only just been diagnosed early in life by genotyping rather than treating people who already are suffering from the disease, basically I believe we are biasing towards people already suffering from the actual phenotypic manifestations of the disease. But obviously, they will be confirmed, the actual nature of the disease will be confirmed by genotyping.

Okay, that’s helpful. Thank you.

[Operator Instructions] Our next question comes from the line of Chris Howerton of Jefferies. Your line is now open.

Hi, thanks for taking the questions. Just Geoff, I didn’t quite catch you, did you say that based upon the presentations at ASGCT, you still had dosing to work out for IVPRP, I just wasn’t quite sure exactly what you said regarding dosing?

On which program?

For the IVPRP as it relates to the LSD programs?

Yes. Well, Geoff, go ahead. I mean, I think we have presented data on both the dose escalation as well as in disease models. So, I don’t know Geoff maybe you have a better sene of what the question is aiming at?

Yes, I mean, look just to be clear, we have great data from the models that we have already published on. We are feeling good about the dose range and the dose-related effects that we are seeing. We continue with given that the IND is going to happen targeting the year end, we continue to complete IND-related studies, but we are feeling good about the data that we have already put out there in terms of being indicative of what we are likely to see in the final studies that are ongoing now.

Okay, alright. That’s helpful. And I guess previously for the beta-thalassemia trial design, you talked about getting around 10 patients that would be transfusion-dependent, are your expectations in line with that or is there any reason you think that, that might change in future?

In terms of total patients on the Phase 1 and Phase 2 study?

Yes.

Yes, I think that, that’s the general number that we are guiding to. Geoff or Dale, is there any update on that?

No, I think that’s absolutely clear. It’s the Phase 1 design that we talked about earlier. You could understand that it’s probably not going to be a whole lot different just because we are affecting the Enhancer of the underlying pharmacodynamics. We expect to be essentially the same and have demonstrated that in animal models.

Sure, okay. And then just one last quick question, in regards to targeting the Enhancer of BCL11A, you kind of highlighted the advantage of it being erythroid specific, are there any other advantages that you would like to – you can speak to or anything else that might be pertinent in terms of efficacy or safety?

I think the principal – the material advantage that the Enhancer brings is really the erythroid specificity and I think that’s the critical piece. As more work is done and as we prepare to present and publish that work, we will have an opportunity to give a more thorough picture, but I think having the knockout and fetal activation, but the knockout of BCL11A expression just in red blood cells and the erythroid lineage is really the material change in the rationale for the approach. Is there anything else to add, Geoff?

Yes. Look, I mean, what we know is that it’s erythroid-specific. That’s the most important thing and that’s certainly what we have clearly demonstrated in our studies. We have also demonstrated that it appears to be just as active and just as effective in promoting fetal expression as the total knockout. And so it’s with an abundance of caution that clearly if there is an erythroid nonspecific effect, there are a lot of other cell types that are around, but certainly we know that there is an effect of BCL11A knockout on B-cells that’s well-known and that was an issue that we understood with the knockout given the fact that we were expecting some mixed chimerism that was not in itself a problem, neither to us nor to Biogen nor to the agency, but there are a lot of other cell types. And so it just seems to make a lot of sense to avoid any possible future effects becoming manifest due to that, even though we are not really seeing any in the initial studies. So, that’s the sort of underlying approach as well as the opportunity at this stage given that we had really moved so fast on the Enhancer to essentially consolidate the programs at an earlier point than perhaps we had initially anticipated just for good drug development housekeeping.

Sure, okay. Alright, well thanks for taking the question.

Thank you. And our next question comes from the line of Charles Duncan of Piper Jaffray. Your line is now open.

Hi, guys. Thanks for taking the follow-up. Just a quick question on actually the pan-ISD [ph] I realized upon your study, but you also have plenty to present anything in ICAAC and do you have any ideas when we might see some data from that study?

I don’t know on either question.

Okay, thanks.

Thank you. I am showing no further questions at this time. I would hand the call back over to management for any closing remarks.

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

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