Xencor Inc (XNCR) 2015 Q4 法說會逐字稿

Good afternoon and welcome to the Xencor Fourth Quarter and Full-Year 2015 Financial and Operating Results Conference Call.

At this time, all participants are in a listen-only mode. Following the formal marks we will open up the call to your questions. (Operator Instructions)

Please be advised, this call is being recorded at the Company's request. At this time I would like to turn it over to Sarah McCabe, of Stern Investor Relations. Please proceed.

Thank you, Operator. Good afternoon, this is Sarah McCabe with Stern Investor Relations and welcome to Xencor's Fourth Quarter and Full-Year 2015 Financial and Operating Results Conference Call. This afternoon, we issued a press release which outlines the topics we plan to discuss today. The release is available at www.xencor.com.

Today on our call, Bassil Dahiyat, President and CEO, will discuss the Company's business and clinical highlights. Paul Foster, Chief Medical Officer, will discuss the Company's clinical trials. And John Kuch, Vice President of Finance, will review the financial results, and then we will open up the call for your questions.

Before we begin, I would like to remind you that during the course of this conference call, Xencor Management may make forward-looking statements, including statements regarding the Company's research and development, including clinical trial plans for XmAb 5871, XmAb 7195, XmAb 14045 and XmAb 13676.

In its other bispecific product candidates, future financial and operating results, future market conditions, the plans and objectives of the management for future operations, is partnership and licensee status in plans, and the Company's future product offerings. These forward-looking statements are not historical fact, but rather based on Xencor's current expectations and beliefs, and are based on information currently available to us.

The outcome of these events described in these forward-statements is subject to known and unknown risk, uncertainties, and other factors that could cause actual results to differ materially from the results anticipated by these forward-looking statements, including but not limited to, those factors contained in the risk factor section of its most recently filed annual report on form 10-K, or quarterly reports on form 10-Q.

With that, let me pass the call over to Bassil.

Thanks, Sarah, and good afternoon everyone. 2015 was a busy and productive for Xencor. We announced promising data for both of our lead internal monoclonal antibody programs, XmAb5871 and 7195, and positioned two new internal bispecific oncology drug candidates, XmAb14045 and XmAb13676, for initiation of clinical development in 2016. We entered 2015 in a strong financial footing following a successful $115 million equity offering early in 2015 and we grew both our senior management teams and our Board of Directors.

And not only have our partners continued to advance in their seven clinical programs using our XmAb technology, but we also announced a new partnership granting Amgen rights to access our XmAb bispecific technology for use in multiple Amgen candidates. Now, we believe 2016 will be an important execution year for us, as we plan to initiate six clinical trials across four programs. Key to this expansion of our pipeline are our first bispecific oncology programs, which we believe will demonstrate highly potent T-cell activity against tumors combined with the simplicity and robustness of our XmAb antibodies. We also expect our partners to continue to advance the broad licensed XmAb clinical development pipeline.

Now, we'll begin today with an update on XmAb5871; our first-in-class monoclonal antibody that targets CD19 with its variable domain and it uses our proprietary XmAb immune inhibitor Fc domain to target FcgRIIb, a receptor that inhibits B-cell function. So, 5871 has shown potent B-cell inhibition and promising treatment effect in rheumatoid arthritis in a Phase 1-B2A study, and we presented most recently at the American College of Rheumatology meeting in November.

With that, I'll let Paul Foster describe the two new clinical trials that we just started for 5871. Paul?

Thank you, Bassil. We just today announced that we've dosed subjects in two Phase 2 trials evaluating XmAb5871 for the treatment of IgG4 related disease, or IgG4-RD and for systemic lupus erythematosus, or SLE. The first weeks trial is a Phase 2, open-label, pilot study of XmAb5871 when patients with IgG4-RD being conducted at Massachusetts General Hospital by Dr. John Stone. IgG4-RD is a rare, fibril inflammatory auto-immune disorder that affects multiple organs and inflicts 40,000 patients in the US [and] currently has no approved therapies. The disease is characterized by a distinct microscopic appearance in diseased organs, which forms the basis for an objective diagnostic criterion that offers advantages for accurately identifying patients.

As we've described in the past, this study is designed to assess control of disease activity with every other week IV administration of XmAb5871. We plan to enroll approximately 15 subjects for up to 24 weeks of treatment, and the primary endpoint is to evaluate the effect an IgG4-RD responder index to measure treatment activity.

Dr. Stone, who led the development of this responder index, was currently conducting an international validation study of this disease response index. We expect to report preliminary data from our pilot study in IgG4-RD disease in the first half of 2017. Because IgG4-RD is a newly defined disease, we have the opportunity to be at the fore-front providing and treatment for patients.

We are also evaluating XmAb5871 and in Phase 2, randomized double-blinded placebo-controlled study in SLE. SLE is an inflammatory disease that can affect numerous organs, in which the body's immune system attacks its own healthy tissue. This disease affects an estimated 240,000 patients in the United States each year, and the unmet need remains high, with standard of caring including immunosuppressant medications with numerous side effects and limited efficacy.

SLE is new indication for XmAb5871 which we decided to pursue based on XmAb5871's potency reversible B-cell inhibition and promising treatment effect demonstrated in our Phase 1b/2a study in rheumatoid arthritis, as well as XVIVO results, [we probably] showing inhibition in SLE patient B-cell activation and humeral immunity.

In addition to the signs of activity of the molecule in the rheumatoid arthritis population, a trial designed with a relatively short time to endpoint provided a rationale for pursuing the SLE indication. The Phase 2 SLE trial is a novel design to evaluate the ability of XmAb5871 to maintain the improvement in disease activity after a short course of intra-muscular steroid therapy and in the absence of immunosuppressant medication. This trial design was previously tested in an observational study by Dr. Joan T. Merrill of the Oklahoma Medical Research Foundation, who is the coordinating investigator for the XmAb5871 SLE trial. When background treatments are reduced, six month response rates to a brief course of steroids are known to be low without the addition of an effective therapy. We believe that this trial design allows us to assess the effect of XmAb5871 on SLE disease activity with a shorter time to endpoint, six months, and with fewer patients compared to standard SLE trials, which generally add new medications to the many already being taken by the patient.

The trial is a randomized, double-blind, placebo-controlled multi-dosed trial study being conducted in the US at approximately 20 sites. Approximately 90 SLE patients with be enrolled with a 1:1 randomization of XmAb5871 to placebo. Patients will enter screening with active, non-organ threatening SLE, and importantly, they will discontinue background immunosuppressant medication. Following a short course of IM steroids to quite SLE disease activity, we will randomize patients to XmAb5871,or placebo, and monitor maintenance of the disease activity improvement.

Finally, we also plan to initiate a bioequivalence trial with a subcutaneous formulation of 5871 this year.

Now I'll turn it back over to Bassil.

Thanks, Paul. I'll sum up the 5871 discussion by saying that while our excitement for the potential of 5871 in autoimmune disease is bolstered by the promising results from our Phase 1b/2a study in RA, we decided as we stated before to focus on the development for treatments for diseases with the highest unmet need and are no longer pursuing RA.

Now, development in IgG4-RD and SLE provide complimentary opportunities to start to build the value of 5871 in a portfolio of autoimmune diseases. IgG4-RD is a small new indication with no-proof therapies that Xencor can pursue rapidly, and SLE is a larger indication with a high unmet need and the chance to engage in an innovative trial designed to potentially overcome historical development bottlenecks.

Now, we'll turn to our second lead internal clinical program, XmAb7195. 7195 is our antibody that targets IgE with its variable domain and it uses an identicalXmAb immune inhibitor Fc as 5871, resulting resulting in this case in three distinct mechanisms of action for reducing IgE levels. In particular, rapid clearance of IgE via FcgRIIb binding on liver sign of sinusoidal and epithelial cells. We believe that 7195 has the potential to provide a first-in-class mechanism for reducing IgE that will address the full spectrum of severe asthmatics, including the hardest to treat population with high IgE levels. During 2015, we reported top-line interim data and continued our ongoing Phase 1a trial with 7195 and we look forward to announcing full data from this completed study in the first half of 2016.

As a reminder, this study evaluated a single dose of 7195 in both healthy volunteers and patients with high baseline IgE levels. And in June of 2015, the trial was expanded to include cohorts of healthy volunteers to treat with a split dose of 7195, consisting of a small-priming dose and a second descending dose after one week. The expansion portion of the trial designed to extend in IgE reduction and drug safety following a second infusion.

Top-line interim data from the Part 1 of this phase 1A study was reported in January of 2015. I'll recap that; healthy volunteers received a single dose of 7195. Data showed that our drug is very potent, with a rapid reduction of free IgE levels to below the limit of detection in 90% of treated subjects, including those treated at the lowest dose of 0.3 mg/kg. As well, we saw parallel reductions observed in total IgE. A dose limiting toxicity of transient, asymptomatic thrombocytopenia was also observed as a 3.0 mg/kg dose level.

For this year, we plan to initiate a multi-dose trial with a subcutaneous formulation of 7195, and expect to announce initial results from this trial in the first half of 2017. So next, I'd like to discuss our bispecific oncology pipeline. The core of our bispecific programs is a novel XmAb Fc domain, which lets us create a single molecule that combine two targets simultaneously. Now, we believe that this is a flexible approach that allows us to rapidly create drug candidates by combining any two binding domains while maintaining the full-length antibody properties conferred by the XmAb Fc domain, such as favorable in-vevo half-life and simple manufacturing.

Our initial bispecific programs are two targeted antibodies that contain both a tumor antigen binding domain and a cytotoxic T-cell binding domain, in this case CD3. 14 of 45 targets CD123 on acute myeloid leukemia, or AML cells, and CD3 on the other side of the molecule to engage T-cells. It showed sustained and potent completion of targeT-cell s in primate studies from well-tolerated single IV doses. We expect to initiate a clinical trial this year.

13676 targets CD20 on malignant B-cells and, of course, CD3 on the other side for the T-cell engagement. We expect to begin a clinical trial for B-cell malignancies also this year in late 2016. We plan to initiate clinical trials for additional bispecific candidates in 2017, but we'll nominate targets for these trials later this year. The parallel advance of multiple candidates, as well as our partnership with Amgen, are enabled by the simple plug and play portability and robustness of the XmAb Fc domain.

We now see Amgen research and license screening this past September, and it granted Amgen the right to use our XmAb bispecific domains to develop and commercialize five bispecific molecules based on their antibodies. We also licensed [stands] in our pre-clinical T-cell engager against CD38 and CD3; in this case, targeted for multiple myeloma. The Amgen programs consist of pre-determined targets, that is, we know what they are; they were part of the negotiation of the licensed agreement and they complete both T-cell engages for oncology and bispecific antibodies for inflammatory.

Xencor is going to performing initial molecular engineering work, and Amgen will do all development and commercialization of the programs. We received $45 million upfront and are eligible for up to $1.7 billion in milestones, as well as royalty month sales. Amgen is an excellent partner for our bispecific Fc platform; they have a lot of experience with bispecific oncology antibodies, having won the first bispecific [communo-one] antibody in the United States. I'll note that we also announced pre-clinical data for the CD38xCD3 pre-program at the America Society of Hematology in December, which demonstrated the activity tuning possible for our flexible XmAb bispecifics.

Now I'll touch briefly on some of our other partnerships. In the fourth quarter, Alexion Pharmaceuticals exercised an option for a commercial license to Xencor's Xtend antibody technology for use in a therapeutic candidate, which triggered an optional fee payment. And as well they paid a development milestone for an undisclosed molecule against an undisclosed target. In September of 2015, our partners, CSL Limited, through its licensee Janssen Biotech Inc., initiated a Phase 2 clinical trial of CSL362, which is now called JNJ-56022473. It uses our Cytotoxic Fc Domain for the potential treatment of patients with AML. This trial initiation triggered a milestone payment to us.

Finally, I'll turn to the leadership team here at Xencor. In May of 2015 we announced the appointment of Mark Lotz as Vice President of Regulatory Affairs and Wayne Saville, Vice President of Oncology Clinical Development. Together, Mark and Wayne bring more than a combined 60 years of experience at Xencor, in biotech and pharma regulatory affairs and in medical researcher, respectively. And they will contribute greatly to our expanded clinical development efforts. We also appointed A. Bruce Montgomery and Yujiro Hata to our Board of Directors during 2015.

I'm confident these new employments will be invaluable as we continue to develop Xencor into a product-focused company. And with that, I'll turn it over to John Kuch to refer to our financial results.

Thank you, Bassil. In this afternoon's press release, we report a cash equivalence and marketable securities, totaling $193.3 million as of December 31, 2015, compared to $54.7 million as of December 31, 2014. The increase reflects the net proceeds of the $115 million received from completion of our follow-on financing in the first quarter, in addition to milestone and collaboration revenue from partners and collaborators during the full-year 2015.

Revenues for the fourth quarter of 2015 were $21.8 million compared for $5.7 million in the same period of 2014. Revenues for the full-year ended December 31, 2015 were $27.8 million, compared to $9.5 million for the same period in 2014. Revenues in a 3 and 12 month period ended December 31, 2015 were higher than revenues from the same period in 2014, to the milestone and option payments received from our Alexion collaboration and revenue earned from our Amgen collaboration.

Research and development expenditures for the fourth quarter of 2015 were $10.9 million, compared to $5.1 million for the same period in 2014. Our [main] expenses for the full-year ended December 31, 2015, were $34.1 million compared to $18.5 million for the same period in 2014. Research and development expenditures for 2015 were greater than expenditures in 2014 due to additional spending on XmAb5871 clinical programs and on our bispecific programs.

General and administrative expenses in the fourth quarter in 2015 were $3.4 million, compared to $2 million for the same period in 2014. G&A expenses for the full-year ended December 31, 2015 with $12 million, compared to $7.5 million for the same period of 2014. Additional spending on SG&A in 2015 reflects additional compensation costs and legal fees. Non-cash, share-based compensation for the full-year 2015 was $4.9 million, compared to $1.9 million for the full-year 2014. Net income for the fourth quarter of 2015 was $7.8 million, compared to a net loss of $1.3 million for the same period in 2014. The net income earned in the quarter reflects revenue earned from our Alexion and Amgen collaborations. Net loss for the full-year of 2015 was $17.6 million, or $0.45 per share on a fully diluted basis, compared to a net loss of $16.4 million, or $0.52 on a fully diluted per share basis for the full-year 2015.

This increased loss for 2015 over 2014 is primarily due to additional R&D spending. The total shares outstanding as of December 31, 2015 was $40,551,039, which reflect the additional 8.625 million shares issued in our follow-on financing in the first quarter 2015. Based on current operating plans, we continue to expect that we have sufficient cash to fund research and development programs and operations through 2019, and expect to end 2016 with approximately $150 million in cash, cash equivalents, and marketable securities.

With that, we would now like to open up the call to your questions. Operator?

(Operator Instructions) Michael Schmidt with Leerink Partners.

I had one on the lupus study for 5871, [about also]. I guess B-cell targeting has been a fairly difficult mechanism I guess historically in Lupus, if you think back to the failed Retoxomap studies, Corlizomap, Orenizo; all those have not have been as successful, I guess. How comfortable are you with the mechanism in Lupus of 5871?

Well, I think the mechanism is supported by the Exstevio data where we demonstrated, and this was in a paper we published about - in 2011 in Journal of Hematology demonstrating that with, I think, around 28 lupus patient B-cell samples where we able to inhibit to the same extent we could inhibit healthy donor B-cell samples using 5871. So in habited activation, inhibit [humoral] responses in reconstituted skid mice models. And this was quite similar to the data we saw for our RA Exdevio studies.

And so, I think that helps bolster our confidence that our agent can do something with lupus B-cells. I think the B-Cell hypothesis in SLE generally, yes is mixed, I think you do have to remember the first newly approved agent in lupus in 30 or 40 years was Venlista, an antibody that acts by inhibiting B-cells. So, I think that B-Cells play a role in lupus is pretty clear, and I think that as a therapeutic intervention there's very good support, at least as good as any other axis or modality.

I'll maybe ask Paul to comment on part of the point of this trial design is to try to tease apart what your drug might do from many of the conflicting factors that typically have gone into lupus drug clinical trials.

This trial is designed to give us some proof of activity in lupus. And based on the results of this trial will determine whether or not we go on for full development.

Let me try to understand the phase two design. So, it sounds like you're getting patients in through admission, so to speak, with steroid and then trying to maintain them in that state with your drug while the patient is expected to decline. Is that the way to understand it? What is the end-point that you are actually looking at after six months?

That's correct. We're taking patients and they're being - their (inaudible) activity is being cooled down with IM steroids. So each patient gets the same steroid course. And then we look to see if we can maintain that disease improvement over the course of six months of therapy with the expectation that placebo patients are going to all return to their baseline disease activity, or worse, during that six month period. And what's import is that as part of this we remove their background immunosuppressants.

And what are you actually measuring as end-point?

We're measuring disease activity by [Saleno Seld A and bilag], and so they need to reach a certain degree of disease improvement on steroids before they get randomized. And then we look for a worsening of the disease activity by [Saleno Seld or Bi Lag]. In addition, the investigator has to think that that increased disease activity warrants treatment, warrants additional medication to their therapeutic regime.

And are you considering a biomarker strategy down the road for this indication?

We are going to be collecting a number of bio markers during the study and we'll have to evaluate the data at the end of the study.

And then it sounds like your working on the SubQ formulation. I guess, when do you think the phase two will wrap up and when do you think - I guess will the SubQ be ready for phase three? And then secondly, are you looking at a partnering strategy down the road or trying to develop this in house?

Our goal is to have the SubQ formulation ready for new trials that would start in 2017 or later. So the SubQ study is going to start this year for contention bioequivalence, and then from there we'll go to hopefully having it ready for any future studies. We think that it is an important feature of the eventual product profile.

From an overall business strategy around the compound, I think what we want to do right now is establish multiple areas, multiple disease indications where 5871 has established activity where we can again clearly get answers from the phase two studies that we're designing. And I think this innovative lupus study design that Dr. Joan Merrill at Oklahoma is collaborating with us on. I think this is an important step for clarifying the kind of answers we can get out of a lupus phase two trial, which is often confounded, as you pointed out in the past.

I think having multiple indications where we can demonstrate 5871 has an impact I think positions us in different ways. For I224RD, that's an area where you could conceive of driving forward all the way to development by yourself, depending on what kind of a registrational path you can negotiate with the regulatory authorities. I think lupus is an area where it certainly opens up a broad array of potential partnering opportunities if you choose to go that way because of the very large size of the market and the high unmet need.

There's, yes, a lot of mid and late stage clinical development going on with lupus, but I think the opportunity still remains very, very high. So we want to have those multiple options so we can find the best path for the molecule. Keep the option open in the more rapid to develop I224RD, which is really going to be the nearer term story as we build the broader value around the outfit as a whole.

David Nierengarten with WedBush.

Hey, maybe it's kind of an additional question on the lupus study. As we all know the most studies took 1,600 patient to tease out their effect. What kind of effect size do you think you might see, or any studies are pointing to what kind of effect size you might see to give us confidence that maybe you can do it with fewer patients in a shorter timeframe?

I'll let Paul comment. I think what I can say at the outset is there are no published studies yet that point this out. However, there is certainly general experience that guides us on patients who are off their immunosuppressants.

Without having done the trial, we can't really say what effect that we will see. We do know that in this type of design if you're on placebo that virtually every patient will have relapsed or gone back to their level disease activity by six months. So we're looking to see a clinically substantially increased proportion of patients at six months who have not returned to their disease activity level.

It's a withdrawal trial is one way to look at it. You're withdrawing the therapies that often maintain a certain percentage of patients so that you can clarify the activity of your drug.

And then I guess on the next question would be just a follow-up on how clinically relevant that is, given a patient's propensity to maintain steroid use or switch to a more aggressive regimen, include [Plomusta] or different agent?

Based on our discussion with the investigators, [including] Dr. Merrill, we think that what we're targeting here is to look for a fairly large benefit from this. How that translates into overall clinical benefit of the patient population. That would be the subject of a further development in the design of those trials. We look at this trial similar to what Dipliomab did in Asthma and what they would do with medication looked at exacerbation rates.

So that will give us clarity on what's going on. Now, one thing I will point out is that there currently is no act of guidance from the FDA on what a registrational development program for lupus would look like. There had been one based on Venlistas approval, they had sort of put out guidance, but they withdrew that a few years ago, because I think of a lack of general acceptance among the medical community. So looking for new strategies in lupus drug development is something that people have been talking about for a long time, and we're sort of jumping into the forefront of that and we're going to run this study and see where it takes us.

Christopher Marai with Oppenheimer.

First maybe if you could just clarify roughly the cost of the phase two trial in lupus while we're on that topic. And secondly, perhaps when we expect to get some updates on the data from the IgG4 program as well?

Sure. So, we don't break out the costs for individual trials, and I will say that it's completely contained within the financial guidance that we've been giving for a while now, that is the cost of this trial. It's 90 patients, six month treatment period. I think that keeps it well within what we as a small company would call a reasonable size phase two. But it is all within our guidance. It doesn't change our financial guidance at all. We would expect to provide first data on the IgG4-RD study in the first half of 2017.

And then just with respect to lupus; any data timeline there? And then with respect to the sub-continuous formulation of 7195, how is that coming, when it that going to be ready for patients?

We would expect top-line data from the 5871 lupus trial in 2018. and the 7195 sub-containous formulation is expected to start a phase one multi-dose trial middle of this year.

And then maybe remind us real quickly on the SubQ trial design for 7195; that's going to be a multiple ascending dose, is that correct?

It's going to be a multi-dose study in healthy volunteers with a parallel group design that is different dose levels but simultaneously, because we've established a range of doses from our single dose study. And we will look for, of course, the safety and tolerability as well as look at biomarkers such as IGE levels. And we would expect to report that data in the first half of 2017.

Arlinda Lee with Candacorden.

First maybe just to clarify; the top-line data that your expecting in first half of 2017 for 5871 and IgG4 related disease, is that top-line or full data and medical meeting?

That will be top-line.

And then is that the same for a parallel multi-dose 7195 data?

Yes. We would expect that to be a top-line announcement at the outset as per both the full release; that would be later than the first half of 2017 full data.

And then maybe a question for John. Can you provide additional color on the Alexion, Amgen split on the revenue line?

Are you talking about the breakdown of the revenue? Yes, that will be detailed in the SEC filings. The Amgen gets a little bit complicated because you breakup the upfront into the deliverable CD38, CD3 preclinical compound and the five discovery programs that we're going to be doing simonial engineering work of. So, I think it's about $13.75 million was for the Amgen and then the Alexion is $7 million, $8 million. And I think that should all be broken out in our 10K filing, which should be posted shortly.

And then maybe you can talk a little bit about your philosophies going forward on additional bispecifics. We saw in the AACR abstract title that you guys had a presentation for PSMA MCD3, and we were wondering if you were interested in going to immuno-oncology and what your thoughts are there.

Yes. So, our philosophy for the additional bio-specific candidates we have beyond the 13676 and 14045 is to as rapidly as we can use this plug and play bispecific capability to put forward new molecules. We expect around the middle of this year to announce our new leads. And what we plan on doing is have one new lead that's a CD3 by specific. So, a T-cell targeter against specific tumor cells. We'll disclose the target at that time. And the other lead we'll have will actually be a duel checkpoint bispecific. So, that is a molecule that binds two different T-cell checkpoints and inhibits both checkpoints simultaneously. The idea there being to increase the selectivity of checkpoint inhibition to the more highly checkpoint repressed cells that are typically more abundant in tumors. So, those are the two kinds of candidates we'll announce the details of later on. And the idea is to continue to expand our efforts in oncology-based around our bispecific capabilities.

Michael Schmidt with with Leerink Partners.

I just had one more on 7195 in terms of expectations for this update coming in the second quarter. Can you remind us, are those all higher IGE patients in this update, and I guess, how many patients have been treated at this point?

So for the trial it is - so, the data we have not presented yet is for parts two and three of that phase 1A trial. The part two of that trial is in high IGE subjects treated with a single dose of 7195. Part three of that trial, which was the part we announced as a new portion, an additional portion in June of last year is in healthy volunteers using a split dose with one small priming dose followed by a second escalating dose. The data from those two parts as well as the full data from the previous top-lined part one that we released in healthy volunteers, will all be presented later this year at a major medical meeting.

Does that answer your question, or were you also asking about the trial we're about to start?

Yes. So, on this trial, I guess, how many patients have been treated -

-- for the trial. Parts two and three have been completed, and we're right now cleaning up the data and preparing it for presentation.

And remind me the single dose high IGE subjects, are those treated at 1/6 dose or at ascending doses as well?

That was ascending doses.

And you said it will be top-line in the first half and then the conference in the second half, is that correct?

I'm sorry, no. For this phase 1A study, the IV study, it will be full data presented this half at a medical conference. I think for our subcutaneous study we expect to have top-line data in the first half of 2017 from the subcutaneous 7915 study we plan to start mid-year, and we would have full data from that at a later data which we would announce.

And then last question, remind me of the Alexion royalty rate?

It's low single digits for the access to our extend technology.

There are no additional questions, so at this time I would like to turn the call back to Xencor CEO, Bassial Dahiyat, for closing comments.

So to close, we have a very full slate of development activities for the year ahead. We continue to grow and advance our Xmap pipeline, so in addition to the two XMap 5871 phase two trials we started, we plan to start clinical trials to test the subcutaneous delivery of both 5871 and 7195.

In addition, we also plan to initiate the human testing of our first bispecific anti-bodies, XMap's 14045 for AML, and XMap's 13676 for the treatment of B-cell malignacies. Further, we're going to nominate additional internal bio-specific candidates.

And then last, we plan to report full data from the completed phase 1A trial of XMap 7195 in the first half of this year. Thanks again for your time and we look forward to updating you on our progress soon.

Ladies and gentlemen, this does conclude today's program and you may all disconnect. Everybody have a wonderful day.