MacroGenics Inc (MGNX) 2014 Q3 法說會逐字稿

Good afternoon. We will begin the MacroGenics second-quarter conference call in just a moment. All participants are in 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, Chief Financial Officer of MacroGenics.

Thank you, operator. Good afternoon, and welcome to MacroGenics' conference call to discuss our third-quarter 2014 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 at our website at www.MacroGenics.com. You can also listen to this conference call via webcast on our website, and it will be archived there for 30 days beginning approximately two hours after the call is completed.

I will point out that in observance of Veterans Day, the SEC is closed today. Therefore, our 10-Q filing will show up at the Edgar site tomorrow before the market opens.

I'd like to remind listeners that we will make forward-looking statements on today's call. 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 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'd 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. We are happy to have the chance to discuss the progress we made during the third quarter as we continue to accomplish the key objectives we set for MacroGenics in 2014.

We advanced our second DART molecule into the clinic this quarter and continue to advance our position in the immuno-oncology field. We also announced a second strategic alliance with Takeda to develop multiple additional DART targets beyond the agreement we announced in May of this year. This second agreement covers four additional candidates beyond MGD010.

In a few minutes, I will review our third-quarter accomplishments in more detail and then provide some key highlights of our pipeline, including an important update to the margetuximab late-stage development program. After our prepared remarks, we will open up the call for the question-and-answer session. But first, I'd like to have the call over to Jim, who will give a brief recap of our financial results.

Thanks, Scott. This afternoon we reported financial results in line with our expectations. Briefly, as we described in our release, MacroGenics had research and development expenses of $18.6 million for the quarter ended September 30, 2014 compared to $11.1 million for the quarter ended September 30, 2013. This increase was in line with our expectations as we continue to move into later-stage clinical trials and add product candidates to our pipeline. We had general and administrative expenses of $3.7 million for the quarter ended September 30, 2014 compared to $2 million for the quarter ended September 30, 2013.

We recorded total revenues consisting primarily of revenue from collaborative research of $18.4 million for the quarter ended September 30, 2014 compared to $20.2 million for the quarter ended September 30, 2013. Collaborative research revenue includes the recognition of deferred revenue from payments received in previous periods as well as payments received during the year.

For the quarter ended September 30, 2014, we had a net operating loss of $3.9 million compared to net income of $6.6 million for the quarter ended September 30, 2013. Our cash and cash equivalents as of September 30, 2014 were $179.2 million compared to $116.5 million as of December 31, 2013.

We also intend to file a shelf registration statement with the SEC covering the potential sale of up to $150 million of securities. Although this facility provides us some fundraising flexibility to more quickly access the capital markets with either equity or debt securities offerings, we don't have any immediate plans to issue any such securities.

Based on the Company's cash balance and current operating plan, MacroGenics continues to expect that its current cash and cash equivalents, combined with anticipated non-equity funding under its various strategic collaborations, should fund the Company's operations into 2017.

With that, I will hand the call back to Scott.

Thanks, Jim. In the third quarter, we extended our track record of advancing our portfolio product candidates, both those fully owned by MacroGenics and those being developed in partnership with our various collaboration partners. As we've stated previously, every product candidate in our portfolio was purpose designed for specific therapeutic application using our proprietary protein engineering technologies. These technologies include our Fc Optimization Platform, which enhances the body's immune system to mediate the killing of cancer cells to antibody-dependent cellular cytotoxicity, or ADCC. And our dual affinity retargeting, or DART, platform which enables the targeting of multiple antigens ourselves by using a single molecule with multiple antibody-like specificities.

We are also able to utilize our proprietary cancer stem-like cell platform, which provides a unique discovery tool to identify cancer targets shared both by tumor-initiating cells and the differentiated cancer cells derived from them. Through the successful integration of these platforms into our product development efforts, we remain on track to have 6 oncology programs in our portfolio in the clinic by the end of 2015 primarily focused on various types of immunotherapy.

I'd like to begin our portfolio review with an announcement we made in our earnings release this evening regarding the development of margetuximab, a monoclonal antibody engineered using our Fc Optimization technology and directed to HER2, which as you know is expressed in many forms of breast, gastroesophageal and other types of solid tumors.

We plan to commence a pivotal Phase III study of margetuximab in HER2-positive metastatic breast cancer in the third quarter of 2015. This decision is based on several factors including clinical data from our ongoing Phase I expansion cohorts, testing a once-every-three-weeks dosing regimen. We are very encouraged by what we've seen in these 10, 15, and 18 migs per kig intermittent dosing cohorts. After follow-up on several of these patients has been completed, we plan to write up this data for publication and presentation at ASCO next year.

Other factors that have influenced our decision include the rapidly changing landscape in the treatment of gastroesophageal cancer, as well as the potential to combined margetuximab with other therapeutics in development to treat gastroesophageal cancer. These developments have created new opportunities to test margetuximab in innovative combination regimens that could be utilized in (inaudible) gastroesophageal cancer therapy. Accordingly, we also plan to initiate Phase I/II combination studies in patients with gastroesophageal cancer and will no longer be initiating the previously announced Phase III magenta study in third-line gastroesophageal cancer patients.

The new Phase III pivotal study will evaluate margetuximab plus chemotherapy against the current standard of care in third-line metastatic breast cancer patients with higher levels of HER2 expression. By which I mean at the 3 plus (inaudible) chemistry or 2 plus by IHC with gene amplification. The standard of care in this patient population varies but tends to be HER2-directed therapy in combination with chemotherapy. We will be discussing these specifics further with the regulators, but we project that the time to BLA filing with this indication should occur in a timeframe similar to that for the previously planned magenta Phase III gastroesophageal cancer study. And we will also plan to conduct an interim analysis to help de-risk the program.

Finally, we continue to enroll our Phase IIa study of margetuximab in patients with metastatic breast cancer whose tumors exhibit lower expression of the HER2 protein and lack evidence of HER2 gene amplification by fish. The dosing for this study is being modified from once weekly to once every three weeks, reflecting the data we have seen to date.

As you might imagine, this plan has taken a significant amount of time and effort and reflects the best thinking about how to develop this program. I'd like to commend the management team for their diligence and creativity in navigating this transition in our plans to something that is even better. This approach reflects considerable feedback from key opinion leaders and payers, targets a broader population of patients, allows us to explore the potential of innovative new combinations for the treatment of gastroesophageal cancer, and overall seeks a higher return on investment for the program.

Moving on to our second Fc-optimized monoclonal antibody in the clinic, I'd like to talk about MGA271, which targets B7-H3, a member of the B7 family of molecules involved in immune regulation. Given the high level of B7-H3 expression on many solid tumor types, we believe that MGA271 has broad potential as currently positioned to be a first-in-class therapeutic agent against this target.

We remain on track to complete enrollment of the three previously defined expansion cohorts of melanoma, prostate and a mixed-tumor type group in our Phase I clinical study of MGA271. We also recently initiated multiple additional monotherapy expansion cohorts across various tumor types including triple-negative breast cancer, head and neck cancer, renal cell cancer, a new melanoma cohort in patients who failed a previous immune therapy, and a cohort consisting of non-small cell lung cancer and bladder cancer patients with the highest level of B7-H3 expression. MacroGenics also plans to initiate further studies of MGA271 in combination with other therapies in 2015.

I'd like to turn now to our dual affinity retargeting, or DART, technology, a platform designed to provide unique advantages over other approaches to create bi-specific or multi-specific molecules, and one that allows us considerable flexibility in developing combination immunotherapy approaches for treating cancer as well as various autoimmune diseases and infectious diseases.

The versatility of this technology has enabled collaborations with several biopharmaceutical companies that has recognized the potential of our DART platform and have partnered with us to utilize this technology. Internally, we have developed over 100 DARTs to date. For the remainder of my remarks, I'd like to focus on the two that are in the clinic and the next on deck.

Our most advanced DART product candidate, MGD006, is a bi-specific molecule that binds to both CD123 and CD3. CD123 is expressed on leukemia and leukemic stem cells but not on normal hematopoietic stem cells, and CD3 is expressed on T cells. MGD006 was our first DART to enter the clinic as specifically designed to engage these two targets by binding to CD3 on T cells and activating them to kill CD123-expressing leukemic cells, which we believe is an ideal illustration of the utility of our DART platform.

We continue to dose patients in our Phase I study of MGD006 in patients with acute myeloid leukemia. Servier partnered with us on this program and exercised its options, taking exclusive license to develop and commercialize MGD006 in certain territories, while MacroGenics retained development and commercialization rights in North America, Japan, Korea and India.

With the initiation of a Phase I study for the treatment of colorectal cancer, MGD007 is our second DART molecule to enter the clinic, another important milestone for our DART platform technology. MGD007 recognizes both a glycoprotein A33 antigen and CD3. GPA33 is expressed on over 95% of primary and metastatic human colorectal cancers including cancer stem cells, which are thought to be responsible for tumor recurrence and metastasis.

The primary mechanism of action of MGD007 is its ability to redirect T cells via the CD3 component to kill GPA33-expressing colon cancer cells.

During the third quarter, we received a $5 million milestone payment from Servier, triggered by the FDA clearance of the Phase I study. Servier has the option to obtain an exclusive license to develop and commercialize this program in certain territories. But even if it exercises that option, we will still retain development and commercialization rights in North America, Japan, Korea and India.

MGD10 is a DART molecule which simultaneously targets CD32B and CD79B, two B-cell surface proteins, as being developed for the treatment of autoimmune diseases. We expect to initiate a Phase IA study in 2015. In May, we announced that we had entered into an option agreement with Takeda Pharmaceutical Company Limited for the development and commercialization of MGD010. That relationship is going well. And, as you have noticed, in September we announced an expanded partnership with Takeda on the development of up to four more product candidates against jointly selected pairs of molecular targets that incorporate the DART platform.

Finally, I would also like to take this opportunity to talk with you about the newest public member of our portfolio, MGD011, a humanized CD19 by CD3 DART which is one of the two oncology-based DART candidates for which we intend to initiate clinical studies in 2015. MGD011 is designed to redirect T cells to eliminate CD19-expressing cells and has been engineered to address half-life challenges posed by other programs targeting CD19 and CD3. Moreover, MGD011 and our other DART molecules are manufactured using a conventional antibody platform without the complexity of having to genetically modify T cells from individuals as required by other approaches such as chimeric antigen receptor T cells, or CAR T-cells.

MGD011 has a modified Fc domain which allows for extended pharmacokinetic properties and convenient dosing at a once-a-week or longer interval. CD19-targeted therapies have generated a significant amount of excitement, and we believe that MGD011 has the potential to be a best-in-class therapeutic. We will be presenting preclinical MGD011 data at a post a presentation at the ASH annual meeting in December.

I hope that this overview provides everyone with an understanding of the clinical, preclinical and business development opportunities that MacroGenics antibody technology platforms have generated and the significant activity arising from these opportunities.

With that, I'd like to conclude my formal remarks and open up the call for questions. Operator?

(Operator Instructions) Michael Schmidt, Leerink Partners.

Hi. It's actually Jonathan Chang stepping in for Michael Schmidt. Thanks for taking my questions. The first question I have is with regards to your new margetuximab development strategy, can you elaborate on what you have seen so far that led to this decision to begin a pivotal Phase III study in breast cancer? And also, could you elaborate on the decision to evaluate margetuximab in patients with HER2 expression at the 3 plus or 2 plus level by HC with gene amplification versus 1 plus or 2 plus by HC without gene amplification?

Thank you very much, Jonathan. This is Scott. So as you know, on our last conference call I had updated everybody in terms of the expansion of the Phase I study that we were conducting where we were giving the margetuximab to patients on a Q3 weekly basis at three different doses. As I indicated at that time, we were seeing some very encouraging data from those studies. We, in fact, have continued to follow those patients. And the majority of these patients that participated in that part of the study were individuals that had breast cancer, and the majority of those had amplification for 3 plus expression by IHD.

The overall data has shown objective responses at all the three dosing ranges that we tested, and we've seen prolonged treatment of this population both in the individual that had objective responses as well as those patients that experienced stable disease. In composite, this was extremely encouraging, and many of these patients that have participated in this study are still on therapy.

So with the basis of this very encouraging data and follow-up data looking at the pharmacokinetics of this molecule showing that the delivery at two or three weekly intervals paralleled that of those patients that were given six migs on a weekly basis. We felt that, number one, we wanted to go to a Q3 weekly dosing regimen, and with the encouraging study in these amplified populations this was clearly a population that we believed would benefit from margetuximab. I should also point out that virtually all these patients had been on multiple HER2-based therapies. So that was in a large part which triggered our decision moving forward to treat patients in this amplified or over-expressing population.

With regard to your second question, which was what has the experience been with the lower-expressing patients -- the one plus or the 2 plus non-amplified. As I also indicated on our call last time, we are continuing to enroll in that Phase IIa study. We have submitted amendments to the protocol to all the sites participating there -- are getting reviewed by the IRB.

Just to refresh your memory on this, we had indicated that we were going to allow patients in on the study who had been on estrogen blockade therapy. We would allow patients who had not progressed from their previous therapies to participate. We also had indicated that we wanted to go to a Q3 weekly dosing regimen. So we anticipate many more patients will get enrolled in this study and expect to complete that study next year.

With regard to the Phase I study, we had very few patients that fit into the category of the 1 plus or non-amplified population. So we had insufficient data to make a decision, and that was a large reason for conducting a separate Phase IIa study.

Okay. Great. That's very helpful. And maybe another question on 006. So bone marrow toxicity has been the general concern, at least with respect to a CAR T approach when targeting CD123 and AML. In that context, we heard from KOLs that it may actually be advantageous to the bi-specific antibody that has a shorter half life. Can you comment on your current dosing regimen for MGD006 and the Phase I trial? And also, when can we expect to see first data from that trial?

Thanks, Jonathan, about the questions on 006. Again, as you recall from my previous comments about 006, we had conducted a very careful study preclinically in cynomolgus monkeys in which our DART molecule, of course, reacts with CD123 specificity in cynomolgus monkeys. And when giving doses that far exceeded those that we anticipate in our clinical study, we did not observe bone marrow toxicity in those studies. And that was in conditions where we had given the animals both continuous infusion over 28 days as well as the current regimen, which is an intermittent dosing regimen in which we dose patients for four days on, three days off and then repeat that for four weeks. So based on those preclinical data, we are very encouraged by that data.

We also indicated previously that the pharmacodynamics effects of this drug showed activity at the nanogram per kig dosing level -- extremely low dosing level. And as a result, when we met with the various regulatory agencies, the FDA in particular, they were encouraged. They were encouraging us to continue and start this dosing at the initial dose where we saw a pharmacodynamic effect. And so again, that started at single-digit nanogram per kig.

Obviously, we are slowly working our way up in the dosing schedule. As you know, for all these immuno-oncology molecules, particularly those that have activating properties, we have to be very judicious on how we do this. We have to be concerned about the safety. So there is slow escalation of the dosing in this patient population. And so therefore I can't give you any particular guidance at this time when we will have the data available. But, as I said, patients are enrolling in the study, and we are moving forward with it.

Great. That's very helpful. And maybe just a final question on your newly disclosed DART molecule, MGD011. So CD19 is a fairly crowded space. I'm curious to know what drove the decision to develop a CD19 target in DART, what your development plans are for this product. And whether MGD011 is part of any existing partnership. Thanks.

Great question. Thank you for that. And as you recall in previous discussions, as a proof of principle way back when we were first developing our DART program, one of the first molecules we developed was a CD3 by CD19 where we compared the properties of the DART containing these specificities with that as a bi-molecule. And as we have previously published in 2011, we showed salutary properties of our DART molecule compared to the bi-molecule.

We did not actually anticipate initially going into the clinic with this molecule. As you know, we moved forward with MGD006 and MGD007 as our first two molecules. But despite the fact or encouraged by the fact that other technologies have proven very beneficial to patients with ALL and in some patients with non-Hodgkin's lymphoma. And in particular, the data that we have now generated in preclinical studies, we were extremely encouraged about the prospects for this molecule.

First of all, as we have indicated, this DART molecule is engineered as monovalent specificities for the CD3 and CD19 targets, and it includes an ST domain that dramatically increases the half life of this molecule. I am particularly encouraged, as I have indicated -- we indicated earlier this week, the preclinical data for this molecule will be presented at ASH in December. So I encourage everybody to take a look at the data at the poster session there.

But in my 40 years of working in various animal model systems, this is some of the best data I have seen in various tumor model systems. So with the properties of, A, being able to create an off-the-shelf molecule that can be used universally in patients and with NHL and potentially ALL and other indications as well, and the ability of being able to give this less frequently than current therapies, I think we have a potential to be a first-in-class, best-in-class molecule.

And is MGD011 part of any existing partnership?

It is not.

Okay. Thank you very much.

Steve Byrne, Bank of America.

So Scott, what do you expect the comparator arm to be in your Phase III study in HER2-positive metastatic breast?

That's a great question, Steve. As we have indicated, it is likely to be a HER2-targeted containing regimen with chemotherapy. At this point, we would like to discuss the trial with regulators, particularly the FDA, before we give details about the trial and the design of the trial. But as I indicated earlier today, we have met and discussed this with KOLs. We had an advisory committee meeting about the design of this trial. We've also met with payers, and they have been very enthusiastic and very supportive of how we are going forward with the design. But what I will hold off is giving you the details about the comparator arm until we meet with the regulators.

Would you anticipate the patients to be enrolled to have previously progressed on a HER2 therapy?

Absolutely. It is likely they would have had two previous -- in a majority of the cases, two previous HER2-containing therapies.

And with respect to the ongoing study that you have in low HER2 expression in the non-amplified tumors, is it worse waiting to see the results of that before you move ahead into a Phase III program?

No. We -- the data that we have to date has shown extremely encouraging data in the amplified population. And so we feel that those patients with HER2 amplification or overexpression by IHC would certainly benefit by this treatment. Obviously, we will have to see the results of that study. Independently, if we do see also a significant signal in the lower expressing population, we would entertain the prospects of conducting a separate study in that population for looking at its benefits.

And given your HER2 product, margetuximab, differs from the others in that you to engage the immune system. Is there any synergy by combining it with a checkpoint inhibitor?

I think that's an excellent question. Clearly, as you know, the field is looking at various combination therapies. We have done some preclinical work showing that combination of margetuximab with other agents that may be immune modifying could have benefit. And so that's certainly an area that we are considering for designing future studies of how patients could best benefit by various combinations of immune therapies, both those that are on the market as well as those that we are developing ourselves.

Okay. And then I guess similar, in a couple of your DARTs -- are CD3 -- at least one of the binding areas domains is CD3. Do you have data that would suggest that those would also benefit or have synergy by combining with the checkpoint inhibitor?

So I'm not quite -- so combining a CD3-directed DART with a checkpoint inhibitor, is that the question you are asking?

It is. Yes.

Okay. Because those model systems are very difficult to test and invariably require surrogate molecules, we have not modeled that in in vivo systems. We have suggestions from in vitro data that is very encouraging, but at this point we have no in vivo data looking at that combination. But that clearly is an obvious pathway that is right for exploring.

Okay. Thank you.

(Operator Instructions) Chris Marai, Oppenheimer.

First, just on 007, your DART in colorectal, I think you have previously mentioned that this might also have efficacy in hematological malignancies. And you have given often very strong early data that comes out of these Hmong trials. I was wondering, why did you decide to bring it forward in colorectal first? And would we expect to see some additional trials later in a Hmong setting?

I'm sorry if that was your impression. I'm not quite clear how you came to that conclusion. Just to refresh your memory, GPA33 is restricted to gastrointestinal tissues. What we have previously shown is that GPA33 is highly overexpressed on almost all colorectal cancer tissues as well as the colorectal cancer stem cells.

We've also indicated that approximately a half of all gastric -- gastroesophageal cancer patients specimens and those from patients with pancreatic cancer are also positive for GPA33. We have no data to show any expression of GPA33 in hematological malignancies, so maybe it's a crossover from some of the other molecules, but it isn't the 007.

Got it. Maybe I'm confusing my numbers, then. No worries. But with I guess respect, then, to combination therapies in 007, obviously some immune modulatory molecules in [vivo] maybe could eventually be combined as opposed with a molecule like this. But there was some great talks at (inaudible) over the weekend really regarding small molecule kinase inhibitors and their potential role in synergizing with therapies -- T cell therapies specifically that target solid tumors. And I was just wondering have you thought about potential combinations there?

Not only have we thought about potential combinations, we've actually begun to explore combinations pre-clinically of 007, with exactly the things that you are describing both in terms of the small molecule opportunities as well as other immune-based therapies. So, again, we're going to dose escalate the 007 molecule, get to the dose that we think will give the best therapeutic benefit and safety profile in a patient, and then look at the potential of combining this both with the small molecules, as you have alluded to, as well as other immune-based therapies.

Okay. Great. And then I guess finally with respect to 271, you had noted that you had treated some patients who had been previously exposed to prior immunotherapies. I was just wondering if going forward you might attempt to re-treat these patients, not just with 271 as a single agent but also potentially with these immunotherapies, and if you have sort of looked at trial designs around that. Thanks.

So just for clarification, what we announced today is that part of the expanded monotherapy cohort will include melanoma patients that are selected specifically for being on other immune-based therapies -- and as you could imagine, which drugs they most likely will be.

In the inclusion of the first cohort of melanoma patients, we also had a couple of patients who had been on prior immunotherapy. And so as a result, given now that pembrolizumab is now approved and (inaudible) is approved, clearly most of these patients with melanoma will have experienced this -- one or both of these drugs. We also wanted to expand our experience of looking at this population in combination of MGA271 going forward. And so that was the basis of the design of this new part of the study.

Great. Thanks for taking my questions.

Stephen Willey, Stifel.

Just with respect to 271, I know that the three initial monotherapy cohorts, I think, have completed enrollment I think it was last quarter. I'm just kind of wondering at this point if there is any additional clarity with respect to when that data may be communicated in and in what form.

Thanks, Steve. Just actually to correct that, as you recall on the last call, we anticipate completing enrollment in those three cohorts by the end of this year. Just to update you, we are on track. One of those cohorts is totally completely enrolled. A second one is one patient away, and the third one a few patients away. So we are close to finishing the enrollment by the end of this year. Clearly, patients will get continuous therapy into 2015. And as I have indicated, as that data is accumulated, we will find the right forum to presenting this data at a major meeting.

But clearly, as indicated today, we would like to get a larger body of data looking at other indications starting this year. And as I have also indicated, starting next year we are going to be combining 271 with a number of different other agents to look at the effects of combination therapy. So I expect 2015 will have several opportunities to present an update on 271.

Okay. And you talked about how 007 you are evaluating preclinically both with other immune modulators and with small molecules. Are those kind of combinations in the planning stages for 271 as well, clinically?

Clearly, that I can definitely say -- obviously in the thoughts for combination therapy for 271, we have actually protocols that have been submitted and are being reviewed. And we intend to look at combinations. And clearly, the opportunity to look with other immunotherapies that are available to us will be conducted. So, yes, for 271 that will definitely will happen.

Okay. And just with respect to the plans to evaluate the additional combination regimens in gastroesophageal, I guess are those going to be in earlier lines of therapy? And maybe what are those agents that you are going to be looking to combine margetuximab with?

Thanks for the question, Steve, and being able to address that. Obviously, the whole landscape for the treatment of gastroesophageal cancer has dramatically changed this past year. As all of you know, ramucirumab was approved in April of this year. The recent data from the rainbow study this fall with the approval in the chemotherapy paclitaxel-treated populations and second line has been approved.

At the end of September, Merck presented their data showing about a 31% response rate of pembrolizumab -- overall response rate of pembrolizumab in gastric cancer. We also know that Roche has indicated that the [catsilla] data is likely to come out earlier than first anticipated. So with that change of that landscape and with our own data that we have been generating internally looking at combinations of our molecules of margetuximab with other therapies showing additive or, in some cases, synergistic opportunities, we think that it was very important for us to recognize that change of landscape and now look at the potential of opportunities. Instead of treating patients in third-line gastric cancer to be able to now combine this with one or more agents to get to earlier lines of therapy. So we are very excited about this opportunity, and I think it makes sense for the patients.

Okay. Thanks.

Chris Marai, Oppenheimer.

Just given broadly your partnering on the DART molecules and DART platform, I was wondering if you could help elaborate on what sort of provoked you to retain rights to certain DART molecules for certain targets or indications. Just roughly how you view that landscape in terms of your partnerships. Thanks.

Thanks very much, Chris. So as you know, historically MacroGenics has been very active in finding ways of bringing non-dilutive capital into the Company to both advance the platforms as well as developing potential commercial opportunities. And as you sure have noticed, particularly in the past couple of partnerships, we have spent a lot of effort in trying to retain significant commercial rights for these programs.

There are obviously occasions where a partner will come to us with interest in using our platform to pursue targets that we might not have any particular interest in pursuing ourselves. And so what we have decided to do is to have a balanced opportunity both to bring in additional non-dilutive capital in this manner or to partner with a company where we can both develop the compound and leave us with a large opportunity for commercialization of those molecules. And what I can indicate is that you should expect more of these opportunities to arise both near term and in the future.

Thanks.

Thank you. And that concludes our question-and-answer session for today. I would like to turn the conference back to management for any closing comments.

Well, first, I'd like to thank everyone again for joining us and let you all know that we look forward to updating you on each of the programs that we discussed today as we continue to make progress throughout the rest of 2014. Thanks very much.

Thank you. Ladies and gentlemen, thank you for your participation in today's conference. This does conclude the program, and you may now disconnect. Everyone have a good day.