MacroGenics Inc (MGNX) 2016 Q1 法說會逐字稿

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 first quarter 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. Where it will be archived for 30 days beginning approximately two hours after the call is completed.

I would like to alert listeners 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.

And now I would like to turn the call over to Dr. Scott Koenig, MacroGenics' President and Chief Executive Officer.

Thank you, Jim. I'd like to welcome everyone participating via conference call and webcast today. Thank you for joining us. After a 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 eight molecules in clinical development with six specifically focused in immune-oncology. And have made meaningful progress in our broader pipeline. Our progress has been driven by our cutting edge antibody technologies consisting of our Fc-optimization platform which enhances an antibody's ability to interact with immunoeffector cells and our Dual-Affinity Re-Targeting or DART platform that enables the targeting of two antibody specificities to a single recumbent molecule. MacroGenics remains committed to researching and developing innovative treatment options for patients suffering from cancer, 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 3 developments. But then move to new and exciting developments in our B7-H3 franchise and our growing DART program.

MacroGenics most recently presented promising and positive preclinical data from our B7-H3-based DART molecule at the Keystone Symposium Antibody Drugs Conference in British Columbia, Canada. And several additional preclinical molecules at the 2016 American Association for Cancer Research or AACR annual meeting in New Orleans.

I will provide more detail on this data and our pipeline shortly. But now we would like to turn the call over to Jim to give an overview of our financial results.

Thank you, Scott. This afternoon we recorded financial results in line with our expectations. Briefly as we described in our release, MacroGenics had research and development expenses of $27.3 million for the quarter ended March 31, 2016, compared to $21.5 million for the quarter ended March 31, 2015. This increase was due primarily to increased activity in MacroGenics' preclinical immune checkpoint programs including MGD013, and the initiation of two Phase 1 clinical trials combining enoblituzumab with other compounds. This increase was partially offset by a decrease in margetuximab expense as a result of start-up costs 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 ended 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 the $62.3 million in revenue recognized under the Janssen agreement in the first quarter of 2015.

For the quarter ended March 31, 2016, we had a net loss of $30.3 million compared to net income of $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 at $304.4 million which compares to $339 million which we had as of 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 collaborations should fund MacroGenics' operations into 2018.

And with that, I will hand the call back to Scott.

Thank you, Jim. As previously mentioned, we ended the quarter with eight molecules in clinical development. Six focused on immuno-oncology and two in the autoimmune and infectious disease areas. Five of these clinical molecules were derived from our cutting edge DART platform which we believe is the industry's most versatile [bio] specific or multi-specific antibody technology.

Before I go into some detail, I'd like to note that while MacroGenics' supplies significant resources toward our molecules currently in clinical development we continue to leverage our highly productive discovery in antibody-based engineering technologies 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 five INDs for new molecular entities from our internal R&D efforts over a 19-month period that ended in mid-2015. And we anticipate 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 into our new preclinical data presented at recent industry conferences for several of our current and potential product candidates.

First off, margetuximab our Fc-optimized monoclonal antibody that targets the human epidermal growth factor receptor two continues to be our most advanced clinical program. And we are enrolling patients for the pivotal Phase 3 SOPHIA study for patients with metastatic HER2-positive breast cancer.

In SOPHIA, we are evaluating the efficacy of margetuximab plus chemotherapy. As compared to trastuzumab plus chemotherapy following progression after at least two lines of pervious 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 and treat patients in our Phase 1b/2 trial of margetuximab in combination with pembrolizumab, an anti-PD-1 therapy, in patients with advanced HER2-positive gastric cancer. This trial is being conducted with our collaboration partner Merck. And the team is actively recruiting patients at trial sites in the United States. We plan to expand this study internationally by opening sites in Asia later this year.

Treatment options for these patients are limited, and our proposed combination regimen under investigation would avoid chemotherapy, while exploiting the expected enhanced immune-mediated killing properties of both margetuximab and pembrolizumab.

We continue to see advancements in our other oncology-focused programs within our diverse B7-H3 franchise. As many of you know, our B7-H3 programs focus on a number of the B7 family of molecules that are involved in immune regulation. We continue to advance multiple proprietary programs that target B7-H3 through complementary mechanisms of action and exploit this antigen's broad expression across multiple solid tumor types.

The most advanced B7-H3 target candidate that we have in development is enoblituzumab or MGA271. Which is an Fc-optimized monoclonal

antibody that targets B7-H3. We currently have three ongoing Phase 1 studies of enoblituzumab that are actively recruiting patients. These studies include one monotherapy study and two combination studies with each of ipilimumab and pembrolizumab.

Based on the interim data previously presented at the SITC annual meeting last November, we've expanded the monotherapy study to include an additional prostate cancer cohort. And plan to recruit additional bladder cancer patients in this part of the trial.

We are planning to share updated results from this Phase 1 monotherapy study by the end of the year. MGD009, our B7-H3 by CD3 targeted Fc-bearing DART molecule is being evaluated in a Phase 1 study in patients across multiple solid tumor types.

We recently presented preclinical data of MGD009 at the Keystone Symposia's Antibodies as Drugs conference in March. Our preclinical study demonstrated that MGD009 redirected T-cells to kill B7-H3 expressing human cancer cells from a wide range of tumor types in multiple in vitro and in vivo models.

In human [peripheral blood] mononuclear cell, we constitute in mice, MGD009 demonstrated dose dependent inhibition of growth and regression of B7-H3 expressing tumors. We also demonstrated a linear pharmacokinetics and a prolonged half-life of MGD009 in Cynomolgus monkeys. Supporting the biweekly dosing interval that we are evaluating in the ongoing Phase 1 study.

MacroGenics also presented preclinical research of B7-H3 antibody drug candidates, or ADCs, at the 2016 American Association for Cancer Research, the AACR, annual meeting in April. We presented a poster that evaluated the therapeutic potential of anti-B7-H3 ADCs in multiple in vitro and in vivo models representing human cancer types that overexpress B7-H3.

These data show that the anti-B7-H3 ADCs exhibited specific dose-dependence cytotoxicity toward B7-H3 positive tumor cell lines in vitro and in vivo including breast, lung, ovarian, pancreatic, and prostate cancer cell lines, as well as melanoma. We are pleased with the results of this study and will continue to evaluate the potential application of B7-H3 targeted ADCs within our B7-H3 franchise.

The MGD009 there are currently five other DART molecules in or entering clinical development. Several of our DART molecules are specifically designed to target a known cancer antigen. And are intended to redirect T-cells to kill cancer cells.

MGD006, a CD123 x CD3 targeting DART molecule and MGD007 a gpA33 x CD3 targeting Fc-bearing DART molecule are two programs that are currently being studied in Phase 1 trials with clinical updates for both expected by the end of this year or early 2017.

MGD006 is focusing on patients with AML or MDS. And MGD007 is targeting patients with metastatic colorectal cancer. Also in Phase 1 development is MGD011 also known as JNJ-64052781, a CD19 x CD3 targeting Fc-bearing DART molecule as being developed under our collaboration with Jannsen.

As mentioned earlier, MacroGenics recently presented data relating to several of our preclinical DART molecules at the AACR meeting. In addition to the B7-H3 ADC, we also presented data for MGD013, a PD-1 x LAG-3, dual checkpoint blockade DART molecule.

MacroGenics was able to demonstrate that MGD013 has the potential to promote antitumor activity by simultaneously blocking both PD-1 and LAG-3. MGD013 was shown to block PD-1, PDL-1, PD-1, PDL-2, and LAG-3 and make [C class 2] interactions to levels comparable to those observed with independent constituents.

MGD013 also enhanced T-cell responses upon antigen rechallenge as measured by cytokine secretion to an extent greater than that observed with the independent blockade of each pathway or even when both pathways were inhibited with a combination of anti-PD-1 and anti-LAG-3 mAb. [These] positive data support further development of MGD013 and accordingly we expect to submit an IND application for MGD013 in 2017.

As further demonstration of the productivity of our platform, MacroGenics also introduced three new Fc-bearing CD3 based DART molecules at AACR last month. A [rare one] by CD-3 targeted DART proteins, an IL13R Alpha 2 by CD-3 DART molecule, an FA2 by CD-3 DART molecule. In preclinical studies for each of these molecules, we show potent activity in directing T-cells to kill tumor antigen expressing cells.

Furthermore, they all show antitumor activity in vivo in multiple tumor xenograft models in mice reconstituted with human effectors. We are very encouraged by the results of all three of these studies, and believe these positive data warrant further research into the potential of all three new DART molecules disclosed.

MacroGenics continues to develop new DART-based programs in therapeutic areas outside of cancer including autoimmune disorders and infectious diseases. MGD010 is a CD32B x CD79B DART molecule being developed for B-cell mediated autoimmune disorders. This molecule is being evaluated in a Phase 1A study in normal healthy volunteers. And we expect to report clinical data later this year.

In the infectious disease area, MacroGenics is developing MGD014, a DART molecule that targets latently infected HIV cells, and is our first infectious disease DART molecule planned for clinical testing. We expect to submit an IND application for MGD014 in 2017. MGD014 is being developed under contract awarded to MacroGenics by the National Institute of Allergy and Infectious Diseases for up to $24.5 million.

We continue to identify and evaluate other candidates that target a range of immune regulatory and other molecules using our proprietary platform. In addition to the two IND submissions planned for 2017 that I detailed earlier, namely MGD013 and MGD014, we plan to submit an IND for another antibody product candidate later this year.

All in all, I am very pleased with the progress of our pipeline. In other news from a corporate perspective we just relocated our headquarters to a larger facility in Rockville, Maryland earlier this week. We plan to build out a commercial manufacturing suite within the same facility and are completing the design phase of this strategically important undertaking.

I am proud of the steady progress of the Company during the first quarter, and know we will continue to make strides forward in our pipeline. We look forward to providing data on multiple programs this year while also providing ongoing updates on our continued corporate progress.

This concludes my prepared comments, and we'd now be glad to discuss questions that callers may have. Operator?

(Operator Instructions) Our first question is from Michael Schmidt with Leerink Partners, you may begin.

Hi, it's Jonathan Chang stepping in for Michael. Thanks for taking my question. First, can you talk about the opportunities for enoblituzumab in prostate cancer? Also, could you remind us what are the key questions that you hope the Neoadjuvant prostate cancer study at Johns Hopkins will address?

Thank you, Jonathan. So as you know we are exploring the opportunity of enoblituzumab in 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 in patients who had metastatic prostate cancer showing regression of tumors.

What we intend to do with our current monotherapy study is to expand our exposure by including additional patients this coming year. And hope to update everyone in terms of the progress for the treatment of metastatic prostate cancer.

With regard to the Neoadjuvant study, as was noted at our research day back in October of last year, Dr. Chuck Drake had presented some very exciting data showing that from a historical database of patients that had been treated at Johns Hopkins for primary prostate cancer. For those patients who had undergone a resection of their prostate and those patients who were followed subsequently for a progressive disease.

He identified an up-regulation in B7-H3 gene expression that correlates in those patients that ultimately develop metastatic disease. So we are doing a pilot study which we intend to start later this year in which a patient who have been identified as newly diagnosed patients with prostate cancer with a Gleason score of seven or greater will be enrolled in this study. Initially intended to be 16 patients. Patients will be treated as planned right now on a weekly basis for six doses with enoblituzumab.

They will then undergo a radical prostatectomy, and ultimately we will analyze the tissues for many immune markers, for the appearance of enoblituzumab at the site. And obviously we'll follow those patients over time with regard to progression. This is obviously an initial pilot study, and based on the results will determine how we further pursue this as a Neoadjuvant therapy.

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

Thanks, Jonathan. So as I've indicated on previous calls, we are conducting these combination studies where patients are being treated with three doses of enoblituzumab [at 310 or 15 migs per kg] and then a fixed dose of either ipilimumab or pembrolizumab.

Those escalation studies are ongoing right now. They're proceeding quite nicely. And when we obtain 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 the monotherapy later this year, and as I'd previously indicated if we have sufficient data on the combination studies we'll present it at the same time. If not, it will then move into 2017.

Great, thank you. And maybe just one last one. You provided a variety of encouraging updates at early-stage programs at AACR. Can you talk about how you're thinking about these assets in terms of a development or a 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 a very successful partnership. This is both for developing the asset for the benefit of patients as well as providing us with non-diluted capital in many of these cases. And also the expertise of the partner in help moving many of these programs forward. Where we are given that we have so many assets some that we've newly disclosed at the meetings I described 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 cooperative fashion. Particularly in cases where we can maintain 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 to develop those type 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 Debjit Chattopadhyay with Janney, you may begin.

Hi, good afternoon. Can you hear me?

Yes, hi Debjit.

Hi guys, thank you for taking my questions here. Just starting up on the LAG-3. Given the broad interest in LAG-3 especially from big pharma, could you talk to the single agent LAG-3 PD-1 combo in a single molecule? Target specificity, (inaudible) versus two agents independently being pursued by (inaudible).

Yes, so as you know and as stated there are several companies that are developing an independent antibody directed against LAG-3. What was very striking from our study, which we're very excited, was the development of a DART molecule that incorporates specificities both for PD-1 and LAG.

And unanticipated during the development of this molecule was the fact that as a DART molecule in terms of biologically functional assays both in the context of activating primary responses induced by [staphylococcal enterotoxin] B as well as a recall antigen specific responses to tetanus toxoid. We found that the DART molecule composed of [targeting] LAG-3 and PD-1 resulted in superior performance compared to two separate antibodies to the same target.

So we're very encouraged by the enhanced activity seen with a single molecule. Obviously for patients if it turns out that this is clinically successful this is obviously easier to administer. Hopefully, we'll see even better efficacy in that combination compared to individual molecules. And ultimately from a pharmacoeconomics standpoint a single molecule is certainly going to be cheaper than two individual antibodies.

Great. And then on the CD123, you had plans to initiate enrollment in Europe. Could you update on some of the enrollment and any data timing? And how do you think the CD123 DART is positioned versus the CD123 (inaudible) programs?

Well, thank you, Debjit. So with regard to Europe as I've indicated before we intend to open six sites in Europe. We have filed with the regulatory agencies in the various countries. We've done site initiation visits in at least I know one or more sites. And we expect enrollment of first patients in Europe imminently.

The expectation as I've indicated before between the sites in the US and in Europe we hope to complete the intra-patient dose escalation studies later this year. We've also indicated that we're looking at some other alternative dosing regimens. Again to look for optimal delivery of this drug to get the best efficacy and obviously the best safety profile. And this will be added onto 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 if I may. The CD19 DART given the very broad program pursued by Janssen, any thoughts on when we could see some data on it? Thank you so much for taking my questions.

Yes. No, thanks, Debjit, and I didn't answer your CAR T-cell. Let me just finish that question, which was the CD-123 CAR T-cells versus the DART molecule. And as we've noted before in our preclinical studies the potency of the DART molecules fair quite nicely compared to data that has been generated with CAR T-cells to many of the same targets that we're pursuing. And I think the same is true of those directed to CD123.

So ultimately, we'll see how the program fairs in the clinic, but the ease in which you can give the drug. The way the patient can be best monitored from a safety perspective, the cost of goods, all of these things we see as salutatory parameters that would bode well for the DART platform.

With regard to the MGD011 CD19 x CD3 program that is being pursued in the clinic by Jannsen. 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 (inaudible) about this. But I can't give you any more specifics about when this will occur. But hopefully we'll see some data within the course of the next year.

Thank you. The next question is from Christopher Marai with Oppenheimer, you may begin.

Hi, good afternoon. Thanks for taking the questions. Congrats on all the progress. First question really on the Phase 1, 2 aspect. I was wondering if you could provide us any updates on recruitment? I know during the quarter you dosed your first patient. How's that looking? Sort of your projection for having [that full interval] at least in the US and then I'll add a follow up, thanks.

Yes, thanks, Chris. The study is going very well. We have I believe five or six sites open in the US. We plan to have up to ten sites in the US. The study is going exceptionally well. As you recall we were looking at two doses of margetuximab, ten and fifteen [mg per kg] and then the fixed dose of pembrolizumab. But I'm very encouraged by the speed in which this is enrolling.

Also as I've noted before we are going to open sites in Asia. We expect those regulatory filings to occur imminently. And hopefully start enrolling patients some time either later this year or early next year.

Our expectation is to be able to report data sometime in 2017.

Yes.

Great, sounds like good progress. And then secondly, and I think you touched upon this, but with respect to MGD006 in the Phase 1 trial I guess you touched upon potential for protocol changes perhaps to allow physicians to adjust dose. Are you looking at dose titration or how do you look at adjustments here?

And I was just wondering is that really a reflection of the potency of the DART and particular side effects you're seeing or is there some heterogeneity between patients and disease burden which happens to be correlated with some of the potential side effects. What's really the thought process behind perhaps updating those protocols?

Yes, no. Thanks for the question. As you point out quite rightly there's extreme heterogeneity in this population of AML patients, and certainly with MDS patients as well. This is really being pursued to get the best combination of efficacy and safety. As you recall in our toxicology studies that we conducted in Cynomolgus monkeys we had dosed those monkeys on a schedule initially of either four days of drugs, then three days off of drugs. And then repeated that for four weeks.

We then had a parallel schedule of animals being treated continuously over a 28-day period. And we saw no real difference in terms of the toxicity profiles in the Cynomolgus monkeys. And so what we initially decided to do is treat the patients with a four day on, three day off schedule.

Initially, it was 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 past the four-week interval. And now we're again looking at is it possible both in terms of interpatient dose escalation to get the maximum dose on the four day on, three day off schedule? And then look at alternative dosing where we may keep patients on continuously. So this is just again to get the best scheme to treat these patients.

Thank you. The next question comes from Yigal Nochomovitz with Citi. You may begin.

Yes, hi. Thanks. Just a question on the AACR presentations. You presented five preclinical molecules there. Can you give us any sense as to which of those is more likely to be advanced into an IND filing? Thanks.

So I'm not going to tip our hat on this one, Yigal, thanks for the question. Obviously, of the five you know specifically MGD013, the PD-1 led by LAG-3 we plan to be in the clinic in the first half of the year next year. So that is definitely going in. With regard to the three additional DART molecules and the one B7-H3 ADC molecule we are continuing with the preclinical development 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 ones specifically we want to move forward as a clinical development.

And just one sort of strategic question on the B7-H3 franchise. I mean you saw the ADC construct at AACR. Obviously, you have the DART and you have the Fc-optimized version of the antibody. So you potentially could have three B7-H3 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 is there one that's going to end up winning out commercially in the end? What are your thoughts there?

So we are fairly agnostic with regard to which programs we move forward in. In fact, all three with a caveat that we pass the ADC through toxicology and we select that to move forward into the clinic. But with your hypothetical there, we look at this mechanistically working quite differently.

As you saw for instance with the enoblituzumab, the Fc-optimized antibody. As you know this allows mechanistically to kill targets through macrophages and K-cells. What we had shown very nicely is that we were also able to induce a expansion of particular T-cell clones in patients treated with this.

So mechanistically we're seeing both the engagement of a innate immunity as well as the generation of T-cell responses. With regard to the MGD009 molecule, here we're redirecting T-cells irrespective of specificity to the site. So in cases for instance where there's a [porosity] of T-cells at the localized site, the ability to engage any T-cells and bring them there to induce killing effects could allow for the elaboration of a T-cell response which normally does not occur.

With regard to the ADCs we see great prospects here particularly in the case of very bulky tumors. You almost see this as an opportunity to function like a chemotherapy to reduce the size of bulky masses of tumors. So we think all three have great prospects, we actually envision there a time that we could combine these therapies either among this class of drugs or with other molecules in the checkpoint space.

Okay, thank you very much, Scott.

Thanks.

Thank you. (Operator Instructions) The next question comes from Stephen Willey with Stifel, you may begin.

Hi, this is Philomena in for Stephen Willey. Thanks so much for taking my questions. We just have two related questions regarding the data that was presented at the AACR for MGD013. We found it interesting that there's this enhanced antigen specific cytokine secretion in response to tetanus toxoid [recall assay], and we wondered whether you'll be assessing any other recall responses to antigens other than tetanus toxoid? And whether you have examined this enhanced cytokine secretion with other DARTS?

Philomena, thanks for that question. This data that we generated was quite recent on the tetanus response. As you know, we had presented the preliminary data with the [staphylococcal enterotoxin] B data showing the 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 checkpoints in a DART molecule to look for this enhanced response. But certainly as we develop other combinations together we will devise assays to determine whether this 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 checkpoint pathways as a way to enhance responses. So clearly, we have had investigators talk to us about the prospects of using these DART-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.

Hi, this is David Lebowitz in for Matt. First question is could you just give a rundown of what type of data we should expect to see? I know there's some data in the coming quarters from the various DART programs, and what the timing of that is at present?

Yes, sure, David. So as we noted today the MGD010 molecule which is our CD32B x CD79B which was a single-dose escalation study in normal volunteers. We have indicated that we will be presenting at a scientific meeting some of the results from the clinical trial. We will have an announcement for the timing, but that is the first one you should expect new data to be presented.

As I indicated earlier today, we will provide updates on the MGD006 molecule CD123 x CD3 later this year. The specific forum in which we presented we have not determine that as of yet. We have indicated that MGD007 which is our gpA33 x CD3 we're likely to present an update either later this year or first quarter in 2017, based again on the timing of certain scientific meetings.

The expectations on MGD011, the CD19 x CD3, is in the hands of Jannsen. But I'm hoping that data would be presented sooner 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 know that the combining PD-1 and LAG-3 is certainly quite interesting, intriguing. I'm just curious as to your thoughts on the potential changes in safety profile when you start compounding by adding more than one checkpoint inhibiter into [a by specific].

David, that's a very good question. And obviously in the case of checkpoints that have seen immunological complications because of the blockade, you have to be very concerned about combining these. To date, we are obviously going to be pursuing these in toxicology studies in monkeys that express these targets.

We'll obviously look for any evidence of toxicity in those settings. Of course these can not necessarily predict what happens in humans. And therefore, as expected, most of these molecules we start at very low doses and move up 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 already, BMS has entered into clinical studies for a combination of PD-1 and LAG-3 as separate molecules. And so I guess we'll learn lessons there with regard to that specific combination. But clearly we are always concerned about safety in the patients.

Thanks for taking my questions.

Thank you. The next question comes from Christopher Marai with 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 the doses for MGD006 x 123 [five specific]. So I think data that we've seen to date from other molecules suggest that that target should be pretty safe to target.

I'm wondering are there potential safety issues you've eluded to really a result of retargeting T-cells here? And is that sort of a cytokine release syndrome or other sort of immune side effect that you're seeing?

And then with respect to the potency if you're talking more broadly, obviously potency can be an issue when it comes to those types of side effects. Have you been working on any internal technologies that might modulate the potencies of these molecules? And then if not, do you anticipate that you would kind of modulate these either through pretreatment (inaudible) patient or maybe steroids to blunt the T-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 premedication or in cases of cytokine responses to those patients that has continued to allow us to dose the 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 dose escalation in this population because of a safety issue. So let me set that straight number one.

With regard to the modulation and the potency, again we have seen no reason at this point as you have implied to actually reduce the potency of these molecules for engagement. Having said that, as you note from our previous scientific presentations most notably at our research day we have constructed alternative molecules which we called our Trident platform. Where we can more selectively engage specific T-cell populations.

An illustration that we had shown at our previous meeting was the engagement more selectively of CD8 cells versus CD4 cells as a way to recruit to tumor targets. And the result was a maximum killing effect with a virtual diminution of the cytokine profile most associated with CD4 activation.

So we have the opportunity to devise molecules with alternative cytokine profiles and still retain maximum therapeutic value. But at this point, there is nothing to say that is required to pursue a CD123 x CD3 target. And right now all we're trying to do is optimize the conditions to best deliver the drug to give the best therapeutic value and the best safety profile.

Great. Thank you for clearing that up. And just one last one. What's the current headcount at MacroGenics now? Thanks.

I think we're about 287.

Yes.

Great, thanks guys. Have a good night.

Thank you.

Thanks, Chris.

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

Thank you, Operator. And thanks 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 gentleman, this concludes today's conference. Thanks for your participation and have a wonderful day.