Good afternoon. We will begin the MacroGenics' 2016 First Quarter Conference Call in just a moment. All participants are in a listen-only mode at the moment and we will conduct a question-and-answer session at the conclusion of the call. At this point, I will turn the call over to Jim Karrels, Senior Vice President and Chief Financial Officer of MacroGenics.

Thank you, operator. Good afternoon and welcome to MacroGenics' conference call to discuss our 2016 financial and operational results. For anyone who has not had the chance to review our results, we issued a press release this afternoon outlining today's announcement, which is available under the Investors tab on our website at www.macrogenics.com. You can also listen to this conference call via webcast on our website; it will be archived there beginning approximately two hours after the call is completed. I'd like to remind listeners that we will make forward-looking statements on today's call and therefore I would like to also remind you that today's discussion will include statements about the company's future expectations, plans and prospects that constitute forward-looking statements for purposes of the Safe Harbor provision under the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these forward-looking statements as a result of various important factors, including those discussed in the Risk Factors section of our annual, quarterly and current reports filed with the SEC. In addition, any forward-looking statements represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. While we may elect to update these forward-looking statements at some point in the future, we specifically disclaim any obligation to do so even if our views change. Now, I would like to turn the call over to Dr. Scott Koenig, MacroGenics' President and Chief Executive Officer.

Thank you Jim. I would like to welcome everyone participating in the conference call and webcast today. Thank you for joining us. After successful 2015 MacroGenics has been able to use the momentum of the previous year to have a productive first quarter of 2016. We ended the quarter with clinical development with 6 specifically focused in immune-oncology and have made meaningful progress in our broader pipelines. Our confidence has been driven by our cutting edge antibody technologies consisting of our optimization platform which enhances antibodies ability to interact with the immune sector cells and our [ph] retargeting our DART platform that enables the targeting of 2 antibody specificities to single molecule. MacroGenics remains committed to research and developing innovative treatment options for patients suffering from cancer or autoimmune disorders and infectious diseases. So I will begin with the most advanced clinical candidate in our portfolio margetuximab which continues to progress in Phase III development but then moves to new and exciting developments in our B7-H3 franchise and growing DART program. MacroGenics most recently presented promising and positive preclinical data from ur B7-H3 Phase DART molecule at the Keystone Symposia Antibodies as Drugs conference in British Columbia, Canada and several additional preclinical molecule at the 2016 American Association for Cancer Research or AACR annual meeting in New Orleans. I would provide more detail on these data and our pipeline shortly but now would like to turn the call over to Jim to give and overview of our financial results.

Thank you Scott. This afternoon we recorded financial results in line with our expectations. As we described in our release MacroGenics had research and development expenses of $27.3 million for the quarter ended in March 31, 2016 compared to $21.5 million for the quarter ended March 31, 2015? This increase was due primarily to increase activity in MacroGenics preclinical and checkpoint program including MGD013 and administration of 2 Phase I clinical trials combined in over margetuximab with other compounds. This increase is partially offset by decrease margetuximab's expense as a result of start-up cost in 2015 on the SOPHIA study. We had general and administrative expenses of $6.1 million for the quarter ended March 31, 2016 compared to $4.7 million for the quarter March 31, 2015. This increase was primarily due to higher labor related costs including stock based compensation expense. We recorded total revenues consisting primarily of revenue from collaborative research of $2.8 million for the quarter ended March 31, 2016 compared to $71.3 million for the quarter ended March 31, 2015. This decrease is primarily due to $63.2 million in revenue recognized under the Janssen agreement under the first quarter of 2015. For the quarter ended in March 31, 2016 we had net loss of $30.3 million compared to net income $45.1 million for the quarter ended March 31, 2015. Again this large swing was primarily due to the recognition of revenue under the Janssen agreement in early 2015. Our cash and cash equivalents as of March 31, 2016 were $304.4 million which compares to $339 million which we had at December 31, 2015. Based on the company's cash balance and operating plan we are reiterating that our expectation of current cash and cash equivalents combined with anticipated non-equity funding under our very strategic collaboration should fund MacroGenics operation into 2018. With that, I will hand the call back to Scott.

Thank you Jim. As previously mentioned we ended the quarter with 8 molecules in clinical development. 6 focused on the immuno-oncology and 2 on the autoimmune and infectious disease area. 5 of these clinical molecules was derived from our cutting edge DART platform which we believe is the industry's most personal bio-specific or multi-specific antibody technology. Before I go into some detail I would like to note that when MacroGenics applied significant resources to DART molecules currently in clinical development we continued to leverage our highly productive discovery in antibody based engineering technology to identify new drug candidates to add to our growing pipeline. This has been a consistent theme over time that has resulted in our robust pipeline. We submitted a total of 5 INDs with new molecular entities from our new molecular inter R&D efforts over 19 months period that ended in mid-2015 and we anticipated continuing to submit at least one new IND per year for the next several years. Let me now update you on our current pipeline and also provide further details about our new preclinical data presented at recent industry conferences where several of our current and potential future product candidates. First of all margetuximab, our Fc-optimized volatile antibody that targets the human epidermal growth factor receptor 2 continues to be our most advanced clinical program and we are enrolling patients for the clinical Phase III Sophia study for patients with HER-2 positive metastatic breast cancer. In Sophia we are evaluating the efficacy of margetuximab plus chemotherapy as compared to trastuzumab plus chemotherapy following progression of at least two lines of previous therapy in approximately 530 patients in the United States and Europe. We expect to complete the Sophia trial in 2018. We are also continuing to enroll new patients in our Phase 1b/2…

[Operator Instructions] our first question is from Michael Schmidt from Leerink Partners, you may begin.

Hi this is Jonathan Chang stepping in for Michael, thanks for taking my question. First, can you talk about the opportunity for enoblituzumab and prostate cancer? Also could you remind us, what are the key questions you hope to answer in the prostate cancer studies?

Thank you Jonathan, as you know we are exploring the opportunity of enoblituzumab and a number of different cancer types including prostate cancer as we presented at the SITC meeting, we were encouraged by some of the observations we saw of patients with metastatic prostate cancer showing regression of tumors. What we intend to do with our current mono therapy study is to expand our exposure by including additional patients this coming year and hope to update everyone in terms of the progress in the streaming of metastatic prostate cancer. With regards to the co-agilent as noted at our research say back in October last year, Dr. Chuck represented very exciting data showing that from historical data base of patients that had been treated at John Hopkins for primary prostate cancer. For those patients who had undergone resection of their prostate and those patients who were followed subsequently for progressive disease he identifies an up-regulation in B7-H3 gene expression that correlates in those patients that ultimately developed metastatic disease. So we are doing a pilot study which we intend to start later this year in which patients who have identified as newly diagnosed patients with prostate cancer with a score of 7 or greater and will be enrolled in the study. Initially extended to be 16 patients, patients will be treated as plan right now on a weekly basis for a fixed doses with of enoblituzumab. They will then undergo a radical and openly we will analyze the tissues for many of new markers for the appearance of enoblituzumab and obviously we will follow the patients overtime with regards to progression. This is obviously a initial title study and based on the results we will determine how we further proceed in the therapy.

Great, thank you. And also on enoblituzumab when might we see the data from the combination studies with ipilimumab and pembrolizumab?

Thanks Jonathan so as I indicated on previous calls we are conducting these combination studies where patients are being treated with 3 doses of enoblituzumab and then a fixed dose of either ipilimumba or pembrolizumab. Those escalation studies are ongoing right now. They are proceeding quite nicely and when we attain the dose that we want to move forward for more intense evaluation we plan to expand that initially into four different tumor types. And we expect to present as I said earlier data on a monetary related this year and as I previously indicated we have sufficient data on the combination studies we will present it at the same time. If not we will load them and move into 2017.

Great thank you and a last one, you provided a variety of encouraging updates like early stage programs of AACR, can you talk about how you are thinking of these assets in terms of development for business development strategy?

Yes thank you very much for the question. As you know we have been very successful over many years in entering into very successful partnerships, this is both for developing assets for the benefit of patients as well as providing us with non-diluted capital in these cases and also the expertise of the partner in help from moving many of these programs forward. Where we are given that we have so many assets, some that we have newly disclosed at the meetings I descried earlier today, plus many others that are still in our research portfolio we intend to engage companies both those who have interest in working with us in a co-operative fashion, particularly in cases where we can make commercialization rights for many of these molecules. We also are looking for opportunities where assets which we fund are very promising but a partner may have unusual expertise in an area looking for both types of partnerships as well so you should look forward to further discussions about our business development strategy during the course of the year.

Thank you the next question comes from Dan Chattier [ph] with Jeannie. You may begin.

Hey good afternoon, thank you for taking my questions here. Just starting up on LAG-3, given the raw interest on LAG-3 especially from the pharma, could you talk to the single agent LAG-3 being run in a single molecule, target specificity two agents independently being pursued by molecule?

As you know and as stated, several companies that are developing different antibodies directly against LAG-3, what was very striking from our study which we are very excited was the development of a DART molecule that incorporates specificity for PD1 & LAG-3 and during the development of this molecule was the fact that as the DART molecule in terms of biologically functional both in the context of activating primary responses into spine as well as recollagen specificity responses we found that the DART molecule composed of targeting LAG-3 and PD1 resulted in superior performance compared to two separate antibodies to the same target. So we are very encouraged by the enhanced activity as seen with the single molecule. Obviously for patients, if it turns out that this is clinically successful, this is obviously easier to administer, hopefully we will see even better efficacy in that combination as compared to individual molecules and openly pharma-economic standpoint a single molecule is certainly going to be cheaper than two individual antibodies.

Great and then on the CD123, do you have plans to initiate enrollment in Europe, could you update on enrollment and any data timing and how do you think the CD123 DART is positioned versus the CD123 programs?

Thank you. Regards to Europe as I indicated before we intend to open six sites in Europe, we have filed with the regulatory agencies in various countries. We have done site initiations in at least I know one or more sites and we expect enrollment of first patients in Europe imminently. The expectation as I indicated before between the sites in the U.S. and the Europe we hope to complete the dose escalation studies, later this year. We have also indicated we are looking at other alternatives dosing regiments, again to look for the optimal delivery of this drug to get the best efficacy and obviously the best entry profile. And this will be added on to our current study. We plan to update the community later this year on the status of the program and where we plan to go in 2017.

And one last question, the CD19 DART given the very broad program pursue by Janssen any thoughts on it? Thank you so much for taking the questions.

And I didn't answer your CD123 question, so let me finish that question which was CD123 cortisol versus the DART molecule and as you have noted before in our preclinical studies the potency of desired molecules fair quite nicely compared to the data that has been generated with the cortisol's maybe with the same target that we are pursuing and the same is true of those directed to CD123. So optimally we will see how the program stares fares in the critic but the ease in which the patient can be best monitored from a safety perspective, all these things we see as satisfactory parameters that would consult well for the DART platform. With regards to the MGD011 (CD19 X CD3) a program that has been pursued in the clinic by Janssen, they have the opportunity to present the data, we have no control over the timing of that but they have indicated to us that they will be about this but I can't give you any more specifics about when this will occur but hopefully we will see some data within the course of the next year.

Thank you. The next question is from Christopher Morai with Oppenheimer. You may begin.

Good afternoon and thanks for taking the questions. Congratulations on the progress. First question on the Phase 1, I was wondering if you could provide us any updates on the recruitment on how those goes to first Phase and sort of looking at your projections of enrolled at least in U.S.?

It's going really well, we have I believe 5 or 6 sites open in the U.S., and we plan to have up to 10 sites in the U.S. the studies going exceptionally well. As you can recall two doses of margetuximab and then fixed doses of ipilimumab but I am very encourage by the speed at which this is enrolling. Also, as I noted before we will branch out in sites in Asia. We expect those regulatory filings to occur imminently and hopefully start enrolling patients either later this year or next year.

Our expectation is to be able to report this time in 2017.

Great, sounds good progress and then secondly, I think you touched upon this but with respect to GD users in the Phase 1 trial. I think you touched upon the potential to perhaps to adjust dose or are you looking at dose titration or how do you look at adjustments here and I was wondering it was really a reflection of the potency of the DARTs in particular side effects we are seeing or is there some opportunity between patients which happen to be correlated with some of the central side-effects?

Yeah no. If answer the question, so as you point out quite rightly there is extreme heterogeneity in this population of male patients and certainly with MDF patients as well. This is really being pursued to get the best of combination of efficacy and safety. As you recalled in our toxicology studies that we conducted in cynomolgus monkeys, we had--those monkeys are the schedule initially of either four days of drugs then three days off of drugs and then repeat of that for four weeks. We then had a parallel schedule of animals being treated continuously over a twenty eight day period and we saw no real difference in terms of the toxicity profiles in the cynomolgus monkey. And so what we initially decided to do is treat the patient with a four-day on three-day off schedule. Initially with limited to a month when we had a very favorable safety profile, we filed with the FDA the ability to continue to treat those patients capacitance of four weeks of interval and now we're again looking at; is it possible both in terms of intra-patient thoughts of stimulation to get the maximum dose on the four day or three day off schedule and then look at alternate dosing where we made key patients on continually. So this is just again to get the best scheme to treat these patients.

Thank you. The next question comes from Lue Garol [ph].

Hi, thanks. Just a question on the AACR presentation, you presented five pre- clinical molecules there, give us any sense as to which of those is more likely to be advanced into an I and D filing? Thanks.

So I'm not going to tip my hand on this one Lue Gaal, thanks for the question. Obviously of the five, you know specifically MGDO13, is we plan to be in the clinic in the first half of the year next year so that is definitely going in. With regards to the three additional dark molecules and the one D7H380C molecule; we are continuing with the pre- clinical developments of all the molecules. We obviously want to look at the bar of toxicology in primates and we will make a decision in terms of prioritization but at this point we're not ready to disclose which one specifically we want to move forward as the clinical development.

And just one sort of strategic question on the B7H3 franchise, I mean, you saw the ADC construct at ADCR, obviously you have the dart and you have the version of the antibody. So you potentially could have three BC7H3 molecules in the clinic, what are your thoughts on how you're going to manage that portfolio? Is it a situation where you'll sort of take them all forward or there's one that is going end up winning out commercially in the end? What are your thoughts there?

So you know we are fairly agnostic with regards to which programs we move forward and in fact all three, you know with the caveat that we pass the ADC through the toxicology and we select as we move forward to clinic. But with your hypothetical there, we look at this as mechanistically working quite differently. As you saw for instance with the ST optimized antibody, as you know this allows mechanistically to kill targets through microphages and K cells, but we had shown very nicely is that we were also able to induce an expansion of the particular T cells clones in patients treated with it. So mechanistically we're seeing faulty engagements of the innate immunity as well as the generation of T cell responses. With regards to the NGDO9 molecule, here where we're redirecting T cells of irrespective of specificity to the site so in cases for instance where there's a parchity of T cells at the localized site, the ability to engage any T cells and bring them there to induce killing effects for the elaboration of a T cell response which normally does not occur. With regards to the ADCs, we see great prospects here particularly in the case of very bulky tumours. You could almost see this as an opportunity to function like a chemotherapy to reduce of the size of bulky masses of tumours. So we don't --you know we think all three have a great prospect, we actually envision there are times that we can combine these therapies either among this plant drug or with other molecules in the check point space.

Okay, thank you very much.

Thank you. [Operator Instructions] The next question comes from Steven Willy with Stifle. You may begin.

Hi this is Sill [ph] in for Steven Willy. Thanks so much for taking my question. I just have two related questions regarding the data that was presented at ADCR for MGDL13. We found it interesting that there's this enhanced antigen specific cytokine secretion and response to tetanus toxoid. We call RC and we wondered whether you'll be assessing any other, we call responses, to antigens other than tetanus toxoid and whether you have examined this enhanced cytokine secretion with other dots.

Thanks for that question. This data that we generated was quite recent on the tetanus response and do you know we had presented the preliminary data with the Toxin B data showing enhanced response. But we are actually expecting to look at other antigens as well but this is the first one where we have looked at the combination of two check points in a dark molecule to look for this enhanced response. But certainly as we developed other combinations together, we will devise that to determine whether this next mechanism is pervasive.

And so do you think that maybe this can be exploited within a vaccine setting perhaps?

Well, in a way as you know mechanistically people are looking at shutting down the inhibitory check point's pathways as a way to enhance responses so real clearly we have had investigators talk to us about the prospects of using these star like molecules in that context. So yes I think that is something that in the future could be exploited.

Thank you very much and congrats on the progress made thus far.

Thank you so much.

Thank you. The next question comes from Matthew Harrison with Morgan Stanley. You may begin.

Hello, this is David Lee [ph] for Matt. First question is, can you just give a rundown of what type of data we should expect to see; either this data in the coming quarters in the various star programs and what's the timing of that as the present?

Yes, sure David. So as we noted today the NGDO10 molecule which is our CD32B by CD79B which was a single dose escalation study in normal volunteers, we had indicated that we will be presenting at a scientific meeting from the results of the clinical trial. We will have an announcement at -- for the timing. So that is the first one you should expect new data to be presented. As I indicated earlier today, we will provide updates on the NGDO6 molecules, CD123 by CD3 later this year. The specific forum in which we'll present it, we have not the terms as of yet. You know we have indicated that NGDO7 which is our GPA33 by CD3, we are likely to present an update either later this year or first quarter in 2017 based again on the timing of certain scientific meeting. The expectations on NGDO11; that's CD19 by CD3, is in the hands of the absence but I'm hoping that data will be presented as soon rather than later. And with respect to the other programs; they're just too early to give you any guidance on the timing.

Thank you for that and jumping over to a different topic. I noted the combining TD1 and Lag3 certainly quite interesting, intriguing. I'm just curious just your thoughts on the potential changes and safety profile when you start compounding by adding more than one check point inhibitor and do it by specific.

David that is a very, very good question and obviously in the case of check points that have seen immunological complications because of the blockade, you have to be very concerned about combining these. To date you know we are obviously going to be pursuing these in toxicology studies in monkeys that express these -- of these targets. We will obviously look for any evidence of toxicity in those settings. Of course these cannot necessarily project what happens in humans and therefore as expected, most of these molecules. We started you know very low doses and we worked in a very safe fashion. We will obviously use the experiences others have had at looking at the safety profile of these individual molecules but as you know array of BMS as incident to clinical studies for a combination of PD1 in the last three as separate molecules. And so I guess we'll learn lessons there with regards to that specific combination. But clearly we are always concerned about safety in the patient.

Thanks for taking my questions.

Thank you. The next question comes from Chris Vromeri [ph] Oppenheimer. You may begin.

Hi guys, thanks for taking the follow up. Sorry I think we got cut off on the last one but I wanted to actually elaborate a little bit on your changes in those doses for MGD006 at 1.35 specific. So if data that we've seen to date from other molecules tested at target, should be pretty safe to target, I'm wondering if you know are the potential safety issues you've alluded to -- you know are really result of targeting it; re-targeting T cells here and that sort of like cytokine release syndrome or other sort of immune side effect that you are seeing. And then with respect to the potency of your darts more broadly, obviously potency can be an issue when it comes to those types of side effects; have you been working on an internal technology as it might -- you know modulate the potencies of these molecules and then if not, do you anticipate that kind of modulate these either through pre- treatments that involves the patient or maybe steroids as a quantity of your cell response? Thank you.

So Chris I'm actually going to challenge you on your first premise which is the concern about the safety profile. We have observed as expected cytokine associated responses but quite manageable with pre- medication or in cases of cytokine's responses to those patients that has continued to allow us to dose patients in higher doses. And as I said before, at this point we're looking at intra- patient dose escalation and expect to identify the maximum dose. But we have not stopped the continuous dose escalation in this population because of a safety issue. So let me set that strain number 1, with regards to the modulation of the palsy again we have seen no reason at this point as you have implied to actually reduce the palsy of these molecules for engagement. Having said that as you know from a previous scientific presentations most notable research say, we have constructed an alternative molecule which we call our trident platform where we can more selectively engage specific piece of our population in illustration that we had shown at a previous meeting was the engagement more selectively of CD8 cells verses CD4 cells as a way to recruit to tumor targets and the result was a maximum killing of that with a virtual demolition of the cidatrin-profile most associated with the CD4 observation so we have the opportunity to divide molecules with alternative cidatrin-profiles and still retain maximum therapeutic values but at this point there is nothing to say that is required for to pursue a CD123x CD3 target and right now all we are trying to do is optimize the condition but that is to deliver the drug and give the best therapeutic value and the best safety profile.

Great, thank you for bringing that up and just one last one, what is the current head count at Macrogenics now?

I think we are about 287.

Great, thank guys.

Thanks.

Thank you. This concludes the question-and-answer session. I'll now turn the call back over to Dr. Scott Koenig for closing remarks.

Thank you, operator. And thank you to everyone listening and participating. As always we appreciate your interest and look forward to providing updates throughout the quarter. Have a good afternoon.

Ladies and gentlemen, this concludes today's conference, Thanks for your participation have a wonderful day.