Greetings and welcome to the Cellectis Third Quarter 2017 Financial Results. At this time all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. [Operator Instructions] I would now like to turn the conference over to your host Simon Harnest, Vice President of Corporate Strategy and Finance. Thank you. You may begin.

Thank you very much and welcome everyone to the Cellectis third quarter 2017 financial results conference call. Joining me on the call today with prepared remarks are André Choulika, our Chairman and Chief Executive Officer; Dr. Mathieu Simon our Chief Medical Officer; and Eric Dutang our Chief Financial Officer. Yesterday evening, Cellectis issued a press release reporting our financial results for the third quarter ended September 30, 2017. This press release is available on our website at www.cellectis.com. As a remainder, we will make forward-looking statements regarding financial outlook in addition to regulatory and product development plans. These statements are subject to risks and uncertainties that may cause actual results to differ from those forecasted. A description of these risks can be found in our more recent Form 20-F on file with the SEC. I would now like to turn the call over to André. André Choulika: Thank you, Simon, and good morning everyone. So the third quarter of 2017 has been one of the most remarkable one in our company's history. In June, we initiated Phase 1 clinical trial for UCART123, our first wholly-owned allogeneic CAR T-cell program in AML and BPDCN patients. In July, we successfully fund out and conducted an IPO for our plant science subsidiary Calyxt, creating a tremendous potential of new value creation for shareholders, and most recently our partner Servier has released a first set of interim clinical Phase 1 data for UCART19, the first ever genetic-edited allogeneic CAR T program in pediatric and adult ALL patients. Dr. Simon will go into more details about our clinical program UCART123 and will discuss the ASH abstract by Servier on UCART19 before handing the call over to our CFO, Eric Dutang, who will give an update on our cash position and other financial. With that, I'll pass the call over to Dr. Mathieu Simon, Mathieu?

Thank you, Andre. I would like to start with discussing UCART123 our first wholly-owned CAR T development to reach patient in clinical trials. This is already the certain TALEN gene-edited CAR T program after UCART19 that is not applied in the clinical setting. UCART123 is a gene-edited healthy donar derived CAR T cells that targets CD123 an antigen expressed at the surface of leukemic stem cells in AML as well as on leukemic and other tumor cells such as the BPDCN for your information blastic plasmacytoid dendritic cell neoplasm. AML is a devastating clonal hematopoietic stem cell neoplasm that is characterized by uncontrolled proliferation and accumulation of leukemic blast in bone marrow, peripheral blood and occasionally in other tissues. These cells disrupt normal hematopoiesis and rapidly caused bone marrow failure and death. In the U.S. alone there is an estimated 20,000 UML cases per year with other 10,000 estimated deaths per year. In July, we initiated two separate Phase 1 clinical trials, one in AML patient at Weill Cornell Medical Center in New York led by Professor Gail Roboz and one BPDCN patient at MD Anderson Cancer Center led by Dr. Naveen Pemmaraju. Following the death of a patient in the BPDCN trial in September, the FDA placed both UCART123 trials on clinical hold. We conducted a thorough investigation into this patient death and communicated all findings to the FDA. In response to our analysis, the FDA has recently lift the clinical hold on both studies. Cellectis agreed with the FDA to the following main revision to be implemented in the Phase 1 UCART123 protocol. First, a decrease of the current dose level to 6.25x104 UCART123 cells per kilo, a decrease of the cyclophosphamide dose of the lympho-depleting regimen to 750 milligram per square meter per day of three days…

Thank you, Andre. As previously marked, we have changed the restocking currency of the Group through the related financial statement from euro to U.S. dollar to include the comparison with PF which currently present their financial statement in U.S. dollar. The financial highlight for the third quarter financial results was a successful initial public offering of plant science subsidiary Calyxt, Inc. Calyxt received net proceeds of $58 million after the issuance of 8 million shares at $8 per share. As part of this IPO, Cellectis SA per share 2.5 million shares of common stock of Calyxt for a value of $20 million which is including in the net proceed of $58 million. Cellectis remains the magnet shorter of Calyxt with 79.8%. As of December 2017, Cellectis add $304 million in cash, cash equivalent and financial asset compared to $291 million as of December 31, 2016. The $13 million increase over the nine months period was currently driven by the following element, $38 million proceeds receipt as part of the Calyxt IPO, $7 million proceeds from the sales leaseback transaction at Calyxt, $13 million ForEx impact which were partially offset by $43 million net cash flows used by operating activities. The team continues to execute the strategy with financial discipline. We expect that the cash, cash equivalent and current financial assets position of $304 million as of September 30, 2017, will be sufficient to fund of current operation into 2020. Total revenues were $27 million for the nine months period ended September 30, 2017, compared to $43 million in 2016. Collaboration revenues decreased by $60 million which was notably explained by $8 million one-time actual revenue recorded in the second quarter of 2016 in connection with UCART19 and also explained by $5 million decrease in revenue recognition of upfront payment. Total…

Thank you. At this time, we will be conducting a question-and-answer session. [Operator Instructions] Our first question is from Christopher Marai with Nomura. Please state your question.

I was wondering if you could just touch upon UCART123 for a second, specifically you broke out capillary leak syndrome there in your data sets. Speaking of some ALLs at 50, we heard that in your CD19 treated patients with some of the autologous approaches, they see capillary leak syndrome along with grade 4 CRS. Those seem to come together. So I was wondering if you had any sense on you mean your follow up with FDA and any of your analysis circuits of a patient death whether or not this was a target mediated capillary leak syndrome or this might have been more to due to the CRS? And I have a follow-up. Thank you. André Choulika: Mathieu, you want to get this question.

Yes, I think if FDA has decided to lift to hold that trial because of this at this point of time we're excluding the target mediated syndrome, and we're more thinking of that you know some premedical condition of the patient. That’s why now we're much strict on the selection criteria. I know we're going to treat younger patients at least for the next three patients, 65 years old, we’re going to be very careful about the entry criteria, the patients has to be totally without infections. For example, all those kind of precondition that can trigger this kind of side effect, but at this point you know I will exclude the targeted mediated syndrome for CLL at least that’s the assumption that the PIs ourselves and the [indiscernible], but we’re doing of course [indiscernible] very few patients.

I guess just thinking about the data you've provided for us in the cost of goods and manufacturing. I understand that the GvHD in the trials for both UCART19 and 123 was quite mild. But can you remind us of percentage of cells that have the TCR knockout in both those products? Are they the same? Was it higher in 123 versus 19? Just to kind of call the number 99 point something percent but what was that? André Choulika: Well, yes, actually I can take this one. The criteria for like the release of the batches higher than this were the filtration of our ourselves currently lead to a 99.5 which is a below detection level, so we do not detect any TCR in the batches we released and we believe that our CAR Ts have like -- actually there's -- as you see currently, there's no GvHD and the criteria for the release is largely below like the 99, the 99.5 and below detection level.

Okay, great. Is there any ability to improve that? I mean just maybe one last quick one on your CS1 targeted UCART. Maybe curious if you could elaborate a little bit more on why CS1 rather than the BCMA target that seems relatively validated the autologous side of things? André Choulika: Just to answer very quickly on the question of, can you improve this? Of course, we can improve this and we do have developed technologies to increase this to a higher level even if we think that we're in a very safe place here. Since the first CAR we injected two years and a half ago, the worst thing that has been seen is like a grade 2 CRF on one of the first patients that could not be attributed potentially to our CAR T because the analysis of the cells showed maybe that potentially the skin graft that was there might have been attributed potentially to the bone marrow transplant that was performed prior to the CAR T injection that we had before, but it was essentially suspected mild grade 1 GvHD that disappeared very quickly and is suspected. And in adult, there is no GvHD that has been analyzed up to now. So, we think that to-date at the current level, Cellectis has a very high safety level for the T-cell positive cells and for CS1, yes, that it's a reverse process for production. It means that we have to have to knockout first the CS1 gene in order to suppress from CD8 positive cells. The CS1 gene and to keep perfect balance between CD4 and CD8 and the vials we're producing which is a guarantee as to better product at the end and to suppress crop T-cell reaction. Therefore, the gene editing is a very important step in the preparation of CS1 CAR T and CS1 we believe is a great target for multiple myeloma. So, we're moving ahead with this CART and we hope to file an IND by next year.

Okay and just following up on the TCR knockout. Was there any improvement between the UCART19 knockout levels and the UCART123 product that you could quantify for us? André Choulika: No, actually it's essentially the same technology that has been used during the process and like the first batches that have been made were made at TCR is only big difference between the first injection that we had like three years and a half ago and returning back to -- recurring back to the donor contract manufacturing organization working was called self procured while the first batches have been manufactured in an academic environment, University College London, that’s only difference between the two, but we are still using the same technology even though the technology has evolved a bit.

Okay, so both have the 99.5 below the limited detection TCR knockout. André Choulika: Yes.

Our next question is from [indiscernible] with Ladenburg Thalmann. Please state your question.

So I have a few. I will start with asking about you UCART19. I think you also talked a little bit in the opening remarks. I don’t know if you can provide any additional color regarding the UCART19 trial in U.S. I know it’s been far at the hand, but any color, additional color on the timeline and the trial design for example is going to expend to patients, so eligible for autologous CD19 and CAR T has been to make the transplant option versus requirement? And also thoughts on removing the -- potentially removing the alemtuzumab for lymphodepletion? Any color on that that would be highly appreciated? André Choulika: Simon, do you want to take this one?

Yes, of course the decision is more in the hands of Servier and Pfizer directly. I think the decision has been taking through expand those studies in the U.S. and very soon you really from very large and well renowned institution starting the clinical programs. Basically, the protocol especially on the adult size is going to mimic what has been going I think in the UK at King's College. What we have to take into consideration is probably what, are we going to see in the future, we’re going to see less difficult to treat population because in the first UK stands, we have very hard to treat population. If you take for example the first low dose caused five out of six patients have already undergone transplant and those patients have relapsed between four and six months, that means that we were improving bad shape. So, the goal is to expand those study in the U.S. and probably get to a more if I can say normal population or less hard to treat, but it was the first attempt, it was the way to go at that time when we decided to go. Regarding the question of alemtuzumab, I think there are some discussion to look at product without alemtuzumab, with alemtuzumab, I don’t want to speak on the behalf of my partners, but maybe expansion phases, they will address that discussion through different arms, that’s my feeling. Is alemtuzumab mandatory for CAR T investment as expansion that’s a critical question? We have shown in our first studies I have shown that you can see CAR T circulating between day 7 and day 42 and even longer in the first compensate program. We have shown that UCART123 with that alemtuzumab, we are also a very good persistence. I think that will be the call of our final two partners. It is clear that probably there is recurring pros now the way we’re addressing lymphodepletion in the future I mean because the way we have lymphodepleted those patients was pretty high, I mean we're giving 1 milligram of alemtuzumab per kilo, 1200 milligram total dose per square meter of cyclophosphamide and fludarabine120 microgram per square meters, not total dose. And I know that in the future there will be some changes in the protocol.

And shifting gears, you currently [indiscernible] if you can provide any color on the autopsy finding? And maybe an additional color on what you think of the most specific cause of death for the patient, GvHD patient?

But it's always very difficult to comment because we have kept the decision with FDA, I think that’s the only channel we know that for I think certainly important. I think it's very much too early to say. I mean when we started those studies, we're very much afraid of lack of physicians, lack of investment, lack of CRS. And to our surprise, we have CRS, we have physicians, but we have also some side effects. So I see now what we're doing is starting to -- we're going to start with a much lower dose below that's one a lot below with a better population and the goal is ready to start and to come back to your filings, as we said in 2018 but the study is going to resume in the coming days or weeks. It was the RD of both in condition [indiscernible] TRD FDA recommendation. But I think too early to draw conclusion except the one that we have CRS, we have activity and we have expansion that’s the only thing I can do at this point.

Okay, maybe last question on the finance part. So those $304 million cash, how much of that include the cash out of Cellectis? I think you've integrated it together right?

The cash position at Calyxt was $62 million at the end of September 30, 2017. So, you have 238 million for the therapeutic activities.

Okay, maybe a last question. So any guidance internally milestone payments from the Servier for the UCART19 program as you know now treated by dozen patients, any [indiscernible] clinical milestone payments?

We don’t expect to receive milestone payments in 2017. When we give a forecast like through 2020 is truly expecting with your milestones that’s our position.

Our next question is from Peter Lawson with SunTrust Robinson Humphrey. Please state your question.

Andre, just on the 123 trial, how long would you have to exclude the older patients? And do you think that’s going to have an impact on the eventual label? André Choulika: Well, you have to understand that we're still in the dose findings movement. And we started with like 6.25x105, we had approximately no idea this dose was -- actually every cart, the cart, we targeted different target, every like each time it's a new story. So we try to make an educated guess with 6.25x105 currently we're going through a lower dose. The first ID was we had no allentuzemab reconditioning because there were only cycle fluid injection, so we both know this. Now we're in a dose finding, for this dose finding, we think it’s reasonable to move forward in a more selective way with patient in order to try to find the right dose per kg where our 6.25x104, now we're going to re-escalate potentially. We'll see -- once we get there and we start to go into the expansion phase, you see that in expansion Phase, the clinical trial for AML for example and BPDCN for AML is two thirds of the patients are first line patients with complex or like poor cytogenetics. And for BPDCN to task up the patient will be first line, so the population will totally change only for the expansion phase here we do from 9 to 12 patients in Phase 1 and then it will be total different world. Cellectis has no intention to limit itself to what we are currently seeking to find and those findings for UCART123, it's the same thing for 19. If you do those findings, it doesn't mean that it's only -- if like the patients are not responding or not eligible for PALL CART, this doesn't mean that. Who can do more -- do the more can do the less? So we will see afterwards and moving forward we'll start to expand in other indications and so on, but for now we have to find exactly what is the right does per kg and this is what we're doing. So don't take what we are doing currently as probably like the final for BLA, one will go for BLA or probably change this, and we'll try to find the right population. And we think that allogeneic CART for distribution, market access, cost and series like easy to access for patients the fact that a patient don't have to wait for produce of raw material will expand this in a very dramatic way. But now we're still in the dose finding phase. So know the age is only to find the right dose. André Choulika: And I don’t see regulator gestation because you know we have committed to treating an extra patient at 65 years old, the average age for the prognostic in AML in the U.S. is 67 years old. So I don’t think it’s a problem at all.

And Andre, you're kind of in an interesting position where you can re-administer the therapy. What kind of persistence do you think you see with the first administration of the therapy versus the second administration? André Choulika: Well, we believe ourselves have a very significant persistence. When you look at persistent we had for like the 19 trials goes up to 80 days. But Mathieu said something that obviously people have hard time to understand, there is ability to rebuild, one of the patients relapsed CD19 positive two months later after being -- like patient was diagnosed MRD negative, relapsed two months later, and CD19 positive was few months later re-dosed and was put back in MRD negativity. So, the argument of the persistent has a very mild importance, and also we are still at start doses here. For example for 19 is by 5x105 per kg and you know that not 100% of these cells are CD52, so alemtuzumab resistant, so probably a bit above 50% between 50% and 60% these cells are CD52 positive, so between 50,000 and 60,000 cells per kg that are injected. And we’re moving to the next cohort now which is one lot above. So, you have to know that we’re still stepwise moving forward into trying to find exactly what is the right dose, but going for like the argument of the persistence over several years, it's come at the price which is the disease linked to the persistence where you not count a full compartment of cells. Here you have the real drug that you can give several times enrollment, if the patient relapse as you can rebuild those drugs if its 19 positive and you can re-dose to CD19. We see the UCART19, for example if CD19 negative you can re-dose with another CAR T for example if we can have like UCART22 to go in clinic, it’s time to re-dose with UCART22 and so on. So you can see that this span of the potential of the therapy is just showing its small array of lights today, but the potential is huge in the future.

And just finally, do you think you need to lookout MHC close I guess one or two?

Well, for now you see that for example UCART123, there was no alemtuzumab preconditioning. In the patients it was only [indiscernible] and the cells expanded well for 19 like the cells stayed for over 80 days with MHC there. If there is a need in the future to piece, we have to go and knockout MHC we will do it, but if you pile up knockout that are composer for the performance of the product, it’s better to avoid this. Because you can do other knockout that can be good for the performance such as for example you can knockout PD1 or as of the future for example CARTs like CS1, UCARTCS1, you cannot knockout CS1, For 30 age, you can knockout 38. So the number of knockout don’t have to be piled up just for the beauty of it, it has to have a necessity. If the cell for example 123 was only a plain PCR outside knockout, no MHC, no CD52 can in grasp and expand in the patient then well I can ask you to question. Why would you have MHC knockout for persistence? Well, here it comes like the second argument that I said before while if the CARs rejected and can re-dose the patients afterwards. We have the longer experience in the field of allogeneic CARs now and we have been what series of patient and we're starting to have like a very good insight of how the cells expand, behave like the durability of these cells in the patient where they go, what they do. So, I think that now we can have a like deep information about that.

Our next question is from Nick Abbott with Wells Fargo. Please state your question.

Good morning. It’s Nick. Jim's traveling this morning. But first of all I congratulations on getting clinical hold lift. I’m sure that's a great relief. And so maybe just starting there on 123, did you discuss a split dosing regimen as another potential ways to try and address the safety challenge? And part of my reasons for asking that is, we just saw its root analysis on JCAR015 by Juno and it was fairly clear that you could identify which patients are most likely to get into trouble early on. So I was wondering whether you discussed split dosing I know some of the protocols had day 123 but obviously doesn’t have to be that?

No, we do not discuss split dosing because according to PIs and ourselves, as split dosing is very useful when you address infusion toxicities and we're not seeing infusion toxicities. We’ve seen more, some CRS. So in that case, we don’t believe that it is the avenue to pursue that’s why I mean very clearly we got the consensus with the FDA that diminishing the dose was more the way to go rather than to split dose between day one and day two. At the end, the total dose would have been the same given. So we went more through a better and more careful selection of the patients. Keep in mind that our first patient that unfortunately died. It was a difficult patient to treat. So I think he was not a classical patient that usually we include in those. There are early doses carrying Phase 1, so it's more careful selection in patients. And where you've seen the dose because again it came as a surprise, a lot of people had expected that an allogeneic CAR T were best persisted that allogeneic CAR T would not have expanded and what we've seen in the first two CD123 patients is completely the contrary. So, we believe that as we're starting with a lower dose where the toxicity, the side effect would be more manageable, it could be easier, not to ability to find much the optimum dose and the optimum and the safety profile of this drug more quickly in a more organized way.

And if you -- as you go forward, do you intend the dose level would be a log higher or you wouldn’t make such a leap?

No…

I guess depend on dose level one really don’t they?

The plan is go back and if we see that, the more careful selection of the patients give us the appropriate result then we will come back to the original first dose, that’s within we have with the FDA. I mean that’s if we don’t show activities, if we show activities and if we have a good side effect five that maybe the dose that in that case when we do [indiscernible] patient to confirm the does. But our plan is really to go back, 65 years old population to eliminate some comorbidities like the infection, status at the time of the injection which is pretty important one because that’s the triggering agent of the CRS. Also probably we're not going to give GSF [indiscernible] during the first three weeks because that’s also something that can enhance the cytokine expression. So we have decided to postpone the new results integration as to the 28th. Those can [indiscernible] will come back, if we have the lower activity, we will come back to the original guidance.

Okay. And as part of your discussions with FDA, did you review the protocol for using rituximab as a kill switch.

Not at all, there has never been challenged, never been in question. I mean in fact FDA went -- the discussion we had with the FDA was very much the same than the conclusion we get from our PI and our addition safety boards on the two institutions MD Anderson and Cornell Weill.

And presumably as you think about the clinical trials for CS1 and 22, the experience you've had with 123 will influence your starting dose there or I mean I know Andre every CAR, every target is different, but do you feel like going forward you're going to be starting in the 104 range? André Choulika: I feel each target is different. I think Andre 2 minutes much more CD19 story, so at this point we have not filed the IND but the plan is probably not to do very much different that we do to do with CD19. CS1 it’s a completely different story because it’s a different target, different kind of population also. We have not self assessed the dosing, but again we believe that each CAR is different. Each CAR is different, it's also very much patient dependent, comorbidities in burdens of -- it's a difficult science but the goal is really for reach strong realm to individualize the dosing scheme.

The question was asked earlier about BCMA versus CS1. Have you looked? I mean I know your partner is developing a BCMA comp, but have you looked pre-clinically at the relative merit of a CS1 CAR versus a BCMA CAR, I mean obviously again we heard [indiscernible] about soluble BCMA and that's been discussed quite widely as potentially reducing the efficacy in the BCMA CAR, but what are your thoughts about BCMA versus CS1. André Choulika: As you know we are collaborating with the MD Anderson with one of the best multi-myeloma doctors you know Professor [Lussky]. We recognized that BCMA is a very good target but according to Professor Dr. [Lussky] you know our CB38 or CS1 could also be two very good targets. CS1 has the advantage that first of all we are the only company that can gene-edit you know the CAR T in order to remove CS1 on the surface of our own T cells in order to avoid self destruction, so that's already a point where we have two advantages of competition. And also we like the damage CS1 expression which is pure expression with all this very few of target toxicities, very few of target expression. We also love CDS38 because we looked at this product cell, it's the antibody, daratumumab has been extremely successful in clinic. It's a more complex development because you know CD38 is expression all the tissues other than the myeloma cells that's why we've decided to give full priority I mean to CS1, and we're going to start as soon as possible with Professor [Augustine] with all these tablets and you know the Pfizer our partner is progressing on this year and the residue way that is BCMA is a very good target. We had that is month before we signed the deal with Pfizer that's two very good targets.

We have a follow-up question from [Lanxin Lee]. Please state your question.

So I just have a clear follow-up of the any -- any thoughts on for UCART19 in DLBCL because it's a larger indication than ALL? And also I think autologous CD19 CAR T data kind of indicated that the system requirements maybe lastly in DLBCL versus ALL because the NCR start issue led there, but autologous CAR T about one minus $.50 but the second though [indiscernible] doable remission without a transplant. So, I don’t know what’s your plan or thoughts on expanding UCART19 into DLBCL, any color there? André Choulika: Well, I think it will be a very logical strategy to go after this disease, but that’s going to be the decision of our two partners Servier and Pfizer. And keep in mind that we are still at the very early stage. We are there looking at the product ALL with very difficult to treat the population with very, very low dose. We are -- as André was saying, we’re 1 to 2x106 cells per kilo. Keep in mind that the results that we are presenting today have been optical lease dose, if you look at the [indiscernible] patient information prospectus, they are recommending to you as the same product at 1.2 to 2.5x108 kilos. So, we have very preliminary stage of the [indiscernible] I’m very happy already to report those, what we call a very impressed, very outstanding results for such a low. Regarding the strategy of our partners, I think it would make sense you know once we have developed the product in ALL to look at all the lymphodepletion patient and probably also to change a CLL. I mean that’s the decision that would be taken by our two partners. And I’m sure, if you looking at the size of the market, looking at the similar transactional signs that we apply to others disease like the lymphoma disease, and now we know that we have a good owning that we have persistence that we can go in each node because probably we have the execution persistence. It makes a lot of sense to grow after the indication, but that’s the UCART19 is their part.

Ladies and gentlemen, we have reached at end of our question-and-answer session. I would like to turn the call back over to Simon Harnest for closing remarks.

Yes, thank you very much again to everyone for the great questions. And thank you for the team for this great Q&A session. Feel free to shoot me an email directly or call me directly at anytime, if you have any follow up questions. And we’re looking forward to seeing you soon at the coming conferences. Thank you so much.

Thank you. This concludes today’s conference. You may disconnect your line at this. And thank you for your participation.