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TESARO, Inc. (NASDAQ:TSRO)

Immuno-Oncology License Agreement & Collaboration Conference Call

March 13, 2014 8:30 AM ET

Executives

Jennifer Davis – Senior Director, Corporate Development & Investor Relations

Lonnie Moulder – Chief Executive Officer and Co-Founder

Mary Lynne Hedley – President and Co-Founder

Analysts

Robin Karnauskas – Deutsche Bank

Howard Liang – Leerink Swann

Peter Lawson – Mizuho Securities USA

Operator

Good morning and welcome to the TESARO Conference Call. At this time, all participants are in a listen-only mode. As a reminder, this call is being recorded and webcast.

I’d now like to turn the conference over to Jennifer Davis, Senior Director of Corporate Development and IR at TESARO. Please go ahead.

Jennifer Davis

Thank you, operator. Good morning and thank you for joining us today to discuss our strategic immuno-oncology imitative and collaboration with AnaptysBio. I’m joined today by our CEO, Lonnie Moulder and our President, Dr. Mary Lynne Hedley. Earlier this morning, we issued a press release describing our worldwide collaboration and exclusive license agreement with AnaptysBio. Please note that the slide presentation that we referred to during this call is available on the investor section of our website www.tesarobio.com.

Before we begin, I would like to remind you that discussions during this conference call will include forward-looking statements. These statements are subject to a number of risks and uncertainties that could cause our actual results to differ materially from those described in these forward-looking statements. The factors that could cause actual results to differ are discussed in the press release issued today and in our SEC filings, including our Annual Report on Form 10-K for the year ended December 31, 2012.

We may refer to certain non-GAAP financial measures that involve adjustments to GAAP figures. These non-GAAP financial measures are not a substitute for GAAP financial measures and are unlikely to be comparable to non-GAAP information provided by other companies. We believe non-GAAP measures may be useful to investors as a supplement to, but not as a substitute for, the applicable GAAP number.

I’ll now turn the call over to Lonnie Moulder, CEO of TESARO. Lonnie?

Lonnie Moulder

Thank you, Jen and thank you everyone for joining us today to discuss TESARO’s strategic immuno-oncology imitative and our AnaptysBio collaboration. We are very pleased to announce today the creation of a comprehensive immuno-oncology platform. TESARO has entered to collaboration an exclusive worldwide license agreement with AnaptysBio, a privately held biotech company based in San Diego. To develop and commercialize antibody based products that targets three of the most promising immuno-oncology targets TIM-3, LAG-3 and PD-1.

We believe that ownership of a broad-based immuno-oncology platform uniquely positions TESARO, an emerging oncology focused company as the substantial player in the cancer treatment revolution that is currently taking place. Our strategy will leverage the business development model that’s TESARO was founded upon as we pursue mono-therapy approaches with our immuno-oncology product candidate, as well as combination regiments with our current and future pipeline product candidates. Importantly, we also plan to make our novel antibody available be collaborations to others in academia and companies who may be pursuing new therapies that could benefit from combinations. In addition, this platform will reduce our reliance upon others for access to important immune modulators for oncology or IMOs.

In a moment Mary Lynne will discuss more about this and provide additional details around AnaptysBio’s technology, immuno-oncology and our programs. But first I will briefly comment on our pipeline and provide a high-level overview of the license agreement. This agreement extends our pipeline of product candidates to include monospecific antibody drug candidates targeting, TIM-3, LAG-3 and PD-1 and dual reactive antibody drug candidates targeting PD-1 and TIM-3 and PD-1 and LAG-3.

The first clinical trial from this collaboration will for an anti-PD-1 antibody which we now refer to as TSR-042 and is projected to begin in mid-2015. We expect to advance an additional candidate into clinical trials every one to two quarters thereafter. We believe this collaboration may also augment the value of our PARP inhibitor, niraparib and our ALK/TRK inhibitor TSR-011, and therefore we intend to initiate pre-clinical studies of these agents in combination with TSR-042 this year.

We also continue to advance our three clinical candidates rolapitant, niraparib and TSR-011. We’ve enrolled additional ALK positive and TRK-positive patients into our ongoing Phase 1/2 study of TSR-011 and work is ongoing in support of a controlled release formulation. Our focus with niraparib, is on the strong execution of a NOVA Phase 3 ovarian cancer program and a BRAVO Phase 3 BRCA breast cancer program, while planning for expansion into other indications.

And earlier this week, we completed enrollment in the final rolapitant Phase 3 HEC study and we continue to expect that the data will be presented ASCO this year. As you know, we previously reported top line results from the rolapitant pivotal Phase 3 program and we remain on track to submit the rolapitant New Drug Application or NDA, mid-year to the U.S. FDA. We have now completed full database log and analysis of the Rolapitant MEC Phase 3 trial which includes important subgroup and provide for full dataset from all six cycles of therapy very compelling data resulted from these analysis which are targeted for presentation and an upcoming medical meets and these data provide us with even greater enthusiasm for the commercial potential for rolapitant.

In particular a significant portion of the patients enrolled in this trial were from U.S. sites including those that are part of some of the largest Oncology treatment that works based upon our substantial experience in the CINV field and interactions with community Oncology leaders we believe the results from the analysis of the U.S. dataset and our market access strategy could drive significant this year end to CINV guidelines and market updates we look forward to sharing these exciting results with you.

Turning now to the details of the AnaptysBio collaboration and worldwide exclusive license agreements TESARO will pay an AnaptysBio and upfront license fee $17 million as well as provide funding for cost incurred by a AnaptysBio for each development program we expect a report the upfront payment as part of our R&D expense during the first quarter. For each program AnaptysBio is eligible to receive milestone payments totaling $18 million if certain research and development events to achieve including the initiation of two Phase 3 trials plus an additional $19 million associated with certain U.S. and ex-U.S. regulatory submissions and approvals in an initial and subsequent indication and AnaptysBio will earn tiered single digit royalties on worldwide net sales of product that are commercialize plus certain commercial milestone payments in specified levels of annual worldwide net sales are achieved.

And AnaptysBio and TESARO will together complete pre-clinical development of the antibody candidate and TESARO will manage all clinical development, manufacturing regulatory and commercial activities. As a result of this agreement we now expect our average cash utilization excluding the upfront payments through AnaptysBio for the remaining quarters 2014 to be in the range of approximately $13 million for quarter.

With that I’ll turn the call over to Mary Lynne. Mary Lynne?

Mary Lynne Hedley

Thank you Lonnie review the antibody drug candidates identify from this collaboration is the foundation of our platform that will enable to serve to develop novel in Immuno-Oncology product evaluate pharmacy and drug combination attract new potential partners and advance our overall oncology strategy. We believe that immuno-oncology products including antibody directed to TIM-3, LAG-3 and PD-1 will transform cancer treatment and we expect the immunotherapy approaches will become a backbone of cancer therapy regimens across the variety of tumor types.

With this agreement, TESARO had taken the first step and becoming a part of this new paradigm. PD-1, TIM-3 and LAG-3 are the most advanced of the exciting the immuno-oncology targets and many in the field believe that combination of anti-PD-1 with either anti-TIM-3 or anti-LAG-3 antibodies were significantly augment the already in practice clinical activity observed by targeting PD-1 alone.

We are interested in exploring the development of these antibodies and line of therapies in combinations with each other and in combinations with other antitumor agents including niraparib and TSR-011. Having all three of these antibodies in our pipeline, in addition to dual reactive antibodies targeting PD-1, LAG-3 and PD-1, TIM-3 makes TESARO standalone in the immunotherapy space. It provides a competitive advantage for attractive potential and facilitating collaborations with others who have complementary approaches and reduces our reliance on others to access to immuno-oncology agents.

As many of you know, it is a wildly health belief that the immune system is the first line of defense against cancer. A process known as immune surveillance normally keeps cancer in tact as immune cells circulates throughout the body to search out and destroy cancer cell. Tumors ultimately escaping immune system by promoting an immunosuppressive environment in part, by inducing an state of dysfunction in T cell which are important cells that are listed direct and indirect killing of tumors cells.

A dysfunction of T cell population cannot exert key antitumor functions, because they are existed by a persistent exposure to cancer related antigen. Dysfunction of T cells do not pull the trigger or expand their numbers they do not antitumor side effects and nor can major cell tumor cells. We can identify and study these cells because they exhibit the standard expression of markers including PD-1, TIM-3 and LAG-3, on the cell surface. And immune checkpoints such as these proteins served to regulate different phases of T cell activity during the immune response. Although the normal function of these proteins is to maintain immune homeostasis, tumors have evolved to collapse and over express widened for these receptors.

As a way to evade immune surveillance and suppress immune responses. All of which result in disease progression. Interaction of T cells expressing PD-1, TIM-3 or LAG-3 which tumor cells or stroma expressing ligands for these checkpoint receptors send negative signals into the T cells which result in [indiscernible] or apoptosis. Blocking the interaction of checkpoint receptors in their ligands reversed the state of T cell exhaustion and restores the antitumor activity and affect the temporal lobe produced long-term clinical benefit in patient.

Indeed, some patients with treated with blocking antibodies to the experience remissions to well over five years. Some of the most durable responses have been observed following anti PD-1 antibody treatment of patients with metastatic melanoma, renal cell carcinoma, and non-small cell lung cancer. As promising as PD-1 antibody present to-date, PD-1 blockade along does not restore full T cell responsiveness and only a subset of patients respond.

Combination approaches leading to blockade of other checkpoint proteins such as TIM-3 and LAG-3 together with PD-1 may substantially enhance the potential of this approach, and benefit the largest number of patient across the widest range of tumor types. We have chosen to partner with AnaptysBio because in our belief their approach to antibody generation is designed for the identification of high potency antibodies with characteristics that predict desired pharmacologic property. The AnaptysBio mammalian cell display system allows for the simultaneous selection of high antibody expression, antibody stability and robust biophysical features that result in optimal pharmacokinetic properties necessary for successful clinical development.

Coupled with their in vitro affinity maturation SHM-XEL platform even difficult to drug target such as TIM-3 can be readily attract. Today AnaptysBio has used this platform to improve upon desired characteristics for over 20 antibody molecules for multiple third party relationships. We’re enthusiastic about working with our collaborator that Anaptys and have a great deal of respect of what they have been able to accomplish with its platform.

PD-1 is in an immune checkpoint receptor that negatively regulate T cell function. The ligands of PD-1, PDL-1 is expressed on many tumor cells and expression has been linked to core clinical outcomes in a variety of cancers. Interaction of PD-1 on a T cell with PDL-1 and tumor cells something negative signal to T cells which results in a suppression of the T cell response. Anti-PD-l antibodies blocks this interaction and restore T cell activity within tumor sites as measured by increased T cell proliferation, increased secretion of protected cytokines and enhance killing.

Anti-PD-1 treatment produces significant in vivo efficacy in murine tumor model and has shown remarkable clinical result in several studies to-date. Most notably in patients with non-small cell lung cancer and melanoma were reported one year survival rate range from 60% to 80%. TSR-042 to is an anti-PD-1 antibody 10 times more potent than a competitor antibody and enhances human T cell activation in a model that is predictive of clinical activity. We expect to begin clinical trials of TSR-042 our anti-PD-1 antibody candidate in mid 2015. TIM-3 represents one of the most interesting new candidates for checkpoint blockade, TIM-3 like PD-1 is a marker of T cell exhaustion or dysfunction, TIM-3 engagement [indiscernible] inactivates T cell, TIM-3 and PD-1 are co-expressed on a large percentage of T cells isolated directly from human tumors treatment of these cells with anti-TIM-3 antibodies restores functionality.

Data from pre-clinical models provide evident that tumor regression and cures following combination treatment with anti-TIM-3 and PD-1 antibodies.

Today it has been difficult to generate highly potent anti-TIM-3 antibodies by conventional methods. And to our knowledge, there are no TIM-3 antibodies currently being tested in clinical studies. The AnaptysBio platform has enabled generation of anti-TIM-3 antibodies with the activity that [indiscernible] as that of other molecules are restoring T cell activity. We anticipate selecting our final TIM-3 antibodies for clinical development during the second quarter of 2014.

The third LAG of our immuno-oncology platform consistent antibodies directed to LAG-3. LAG-3 is co-expressed with PD-1 on exhausted and dysfunctional T cells. Association with the ligand MHC class II results a negative signaling and inactivation of T cells. LAG-3 and PD-1 at synergistically to mediate tumor induced non-responsiveness.

Pre-clinical studies have demonstrated tumor regression and cares in most tumor-bearing animals following treatment with anti-LAG-3 and anti-PD-1 antibody. To our knowledge, only a single LAG-3 antibody has been introduced into the clinics. TESARO’s lead antibody is a potent MHC class II blocker and restores T cell functionality. We expect to select a LAG-3 antibody for clinical development in the third quarter of 2014. Pre-clinical data shows enhanced activity of dual checkpoint blockade. Treatment of tumor-bearing animals with anti-TIM-3 together with anti-PD-1 is more effective of reducing tumor growth, than treatment with either antibody alone.

Similarly, treatment of tumor-bearing animals with anti-LAG-3 together with anti-PD-1 is more effective at reducing tumor growth than treatment with either antibody alone. Dual blockade can produce tumor regression in the majority of tumor-bearing animals and provide the rationale for combination clinical studies with monospecific antibody. We also plan to develop dual reactive antibodies to TIM-3, PD-1 and LAG-3, PD-1 which may provide certain benefits in comparison to treating patients with two monospecific antibodies, including improved activity and safety, coupled with reduced costs to the healthcare system.

There is melting evident that the combination of PD-1 blockade with other anti-tumor agents could provide synergistic anti-tumor activity. [Indiscernible] in T cell lymphomas induce expression of PD-1 ligand and make these tumors more immunosuppressive and possibly more responsive to combination treatment with anti-PD-1 antibody and in ALK inhibitor. Tumors with high mutational burden such as triple-negative breast cancer and BRCA positive tumors are considered to be the most immune responsive. We plan to initiate pre-clinical studies to evaluate the effect of PD-1 antibodies in combination with TSR-011 and niraparib during this year. In summary, we are very excited about this collaboration and our platform is immuno-oncology program. This platform provides the portfolio of candidates focused on high value targets augments the value of our other pipeline candidates. And enhances our prospects for future collaboration.

We have a number of upcoming milestones related to advancing these drug candidates. We anticipate selecting candidate for our anti-TIM-3 antibody in Q2, 2014 which could be a first-in-class candidate. Selecting an anti-LAG-3 antibody candidate by Q3, 2014 and selecting dual reactive antibody clinical candidate targeting PD-1, TIM-3 and PD-1, LAG-3 by first quarter 2015.

We plan to begin preclinical investigation at TSR-042, with each of TSR-011 and niraparib in 2014 and we expect to begin our first clinical trial at TSR-042 in mid 2015. We look forward to updating you over the next several quarters on the progress we’ve made across the multiple programs within our immuno-oncology platform.

Lonnie Moulder

Operator, at this point could we please poll for questions?

Question-and-Answer Session

Operator

(Operator Instructions) Our first question comes Robin Karnauskas of Deutsche Bank.

Robyn Karnauskas – Deutsche Bank

Hi guys, congratulations and we’re really excited about this agreement. I guess a couple of questions, so how do you derisk potential for cost, a combination of CTLA and PD-1 was a little bit toxic, and when you think about combining these new targets how do you derisk that preclinically, and then what is the advantage and what is the challenge of entering this phase fleet and along with that you mentioned the cost, that how are you thinking about developing these drugs and making sure that your combo cost down? Thanks

Mary Lynne Hedley

Well, I can take the first part of that. So that obviously CTLA-4 combinations for example PD-1 have resulted in about 16% of patients having immune-related neuro fatal or fatal AEs such as enterocolitis, hepatotox, pneumonitis. There is a difference though the thing CTLA-4 and TIM-3 and LAG-3 and PD-1. The CTLA-4 is much more – it’s much more than on-off switch whereas PD-1 and TIM-3 and LAG-3 are more likely a stat so I guess you can describe it that way. So, one of the thought – thinking is that the combination of PD-1 with these other more mild immune modulators may be less toxic overall.

In addition and we know that TIM-3 and LAG-3 are up-regulated after CTLA-4 in the T cell activation cascade, so it could be that when you block TIM-3 and LAG-3 in combination with PD-1 and may be monospecific T cells that are in the tumor environment which obviously is going to lead to a greater safety profile.

Lonnie Moulder

And clearly Robin, and all of you on the phone I think there is an understanding with this new paradigm that there is a substantial market opportunity I was looking at a report from a equity research analyst the other day that targeted an overall $35 billion opportunity for immuno-oncology I don’t know if that’s the right number, but it’s quite substantial. And if you look at what we’ve brought in here, we intend to be a player in that very large opportunity.

Our anti-PD-1 antibody will be developed of course in select indications and in novel combinations at various lines of therapies is going to be quite a bit of room for a number of agents out there. And our TIM-3 antibody could be first-in-class, and we’ll entering into clinic next year. The LAG-3 antibody there is only one in the clinic ahead of us that we’re aware of, so we’re really not that far behind. And as you know there is a platform approach here that we can take advantage of, and that we can use these antibodies to enhance our current pipeline drugs and anything else we might bring into our pipeline over time.

So, the whole package together I think does position us very well competitively in this quite substantial market. As far as cost in the system I think over time that probably the opportunities to think through just how in fact, one can combine multiple, higher priced products in the U.S. and in the other regions of the world where there are of course pricing controls in place and there we’ll need to be interesting business models to do that, but one approach could be using dual reactive antibodies where we’re hitting two targets at once and bringing forward a product that can actually manage that cost equation. So that’s how we think about it.

Robyn Karnauskas – Deutsche Bank

That’s really helpful, and one follow-up if I could. How is your PD-1 differentiated and what is the pre-clinical support for combo without any PARP you have that yet?

Mary Lynne Hedley

Yes.

Robyn Karnauskas – Deutsche Bank

And there is two follow-ups.

Mary Lynne Hedley

Yes. So, I think in terms of the overall differentiation of the PD-1 antibody. As we demonstrated or showed in the slide there is at least a tenfold increase in potency in comparison to one of the competitor antibody.

But our focus – and I guess I should also point out that just the inactive platform alone, allows for the selection of very high affinity antibodies that are specifically geared towards having all of the characteristics you would want as you move into the clinic.

So, this technology allows for the simultaneous selection of subnanomolar or nanomolar potency for binding in addition to the direct functionality such as T cell activation, specificity to minimize potential safety risk the active – the activity with homologous proteins to enable IND enabling studies, high expression to enable scale-up and manufacturing and all the typical biophysical properties that you want for having low clearance comps and minimizing downstream manufacturing challenges.

So, I think based on what we’ve seen today the antibodies all have a very desirable characteristics around this regards, they’re extremely potent and 10 times more potent ion the case of PD-1 antibody. And our focus really though isn’t necessarily competing in the melanoma non-small lung cancer state, it’s on identifying specific indications where we think we can play a role and in promoting novel combination.

Robyn Karnauskas – Deutsche Bank

All right, thank you.

Operator

Our next question comes from Howard Liang with Leerink.

Howard Liang – Leerink Swann

Hi, thanks very much and congrats.

Lonnie Moulder

Good morning Howard.

Howard Liang – Leerink Swann

Good morning, can you hear me?

Lonnie Moulder

Yes.

Howard Liang – Leerink Swann

Sorry. Congrats. So, on the – I guess a question on the order of these agents entering to the clinic. So after PD-1, so we assume in TIM-3, LAG-3 the noted, bispecific antibodies?

Mary Lynne Hedley

Correct.

Howard Liang – Leerink Swann

Okay. On the TIM-3, I think there is some IP I think what they would view to be blocking IP from your competitors or one of the competitors what’s your view on the IP whether you have freedom to operate in the TIM-3 area?

Mary Lynne Hedley

Yes, our anticipation is based on what we understand from the patents that have issued today and the outstanding patent application that we should not have an issue from a freedom to operate perspective. And again, in particular focused what we intend to have a commercial antibody.

Howard Liang – Leerink Swann

Okay. In terms of the advantage of bispecific antibody in vision cost advantage can you talk about it potential advantage from a clinical perspective I assume this is based on co-expression of TIM-3 or LAG-3, with PD-1, can you talk about how often we see the co-expression and in what tumor types?

Mary Lynne Hedley

Sure, so you are absolutely right, I mean, in addition to obviously reducing cost to the healthcare system, we know that T cell – so if you think about tumor infiltrating T cells, so we call them TILs, so the TILs and the tumor many times co-express either PD-1, TIM-3 or PD-1, LAG-3. And it turns out that that actually may be related to the tumor type. So for example, if you take TILs out of ovarian cancer patients we know that these are high expresses of LAG-3 and PD-1. Whereas if you look at melanoma patients and you remove TILs, we see high over expression of TIM-3 and PD-1. And interesting, when you take those out of the tumors, in those patients and you treat them with these anti-TIM-3 and PD-1 or anti-LAG-3 and PD-1 antibody, you can restore the activity of those T cells.

So I think in terms of the actual dual specificity, when you use each of those different approaches may be dependent on the tumor type that you’re going after. And that may be relative to obviously how patients or how specific regent physiologically relates to PD-1 and TIM-3 or PD-1 and LAG-3. So, I think from a perspective of increased safety not having obviously two antibodies which could potentially lead to anti-antibodies or and also having just any cost activity minimized, gives you an opportunity to provide the efficacy that you need by targeting these cells, but not the potential for safety.

Howard Liang – Leerink Swann

Okay, thanks very much.

Lonnie Moulder

Yes.

Operator

Our next question comes from Peter Lawson of Mizuho.

Peter Lawson – Mizuho Securities USA

Sorry I may have missed this, but from the PD-1 what indications are you going to be given after?

Mary Lynne Hedley

So I think Peter we will update you related to that, as we’re closer to the clinic I think it would be premature for us to, at this point tell you what that would be. We of course have very specific ideas about where we would go, but I think it would be more wise of us to just with that further and then give an update.

Peter Lawson – Mizuho Securities USA

And then just on the platform, do you have the ability to select the lower toxicity or is it just a really kind of focused around the kind of antibodies?

Mary Lynne Hedley

So lower toxicity or we think of lower toxicity as potentially related to across the activity and certainly there is the ability to eliminate any cross reactivity that one might be a typical IND enabling studies that we do with antibodies just to look any cross reactivity taken in tissues outside of where you would expect to see PD-1, TIM-3 or LAG-3. So you can eliminate cross reactivity with this type of a platform. We also want to select for a very low clearance and the reason for that is to have the antibody around for a longer period of time and of lower doses. So that also in some ways can enhance safety by using lower doses of the antibody. So all of those has been built into the process for selecting the LAG-3, TIM-3 and PD-1 antibodies.

Peter Lawson – Mizuho Securities USA

Then, any kind of IP issues you could have for entrant any of the marketplaces for TIM-3, LAG-3 or PD-1?

Mary Lynne Hedley

None that we have identified.

Peter Lawson – Mizuho Securities USA

Okay. Thanks so much.

Mary Lynne Hedley

You’re welcome.

Operator

(Operator Instructions) Our next question comes from Yaron Werber from Citi.

Unidentified Analyst

Thank you for taking the questions. This is Chris in for Yaron. I had a two part question. First, can you speak a little bit more about the scope of this agreement and the actual number of antibodies, it looks like an Anaptys is also a partner of several other biotech companies. And then second part, besides the novel targets can you speak a little bit more about how you think these antibodies are differentiated versus some of the competition active in the space? Thank you.

Mary Lynne Hedley

So the agreement covers five antibodies, monospecific antibodies to PD-1, LAG-3 and TIM-3 and two dual reactive antibodies of PD-1, TIM-3 and the PD-1, LAG-3 antibody. And I think in terms of the differentiation I was all – I think I pretty already went into the advantage that using the AnaptysBio system to select an affinity in match rate antibodies covers. So it’s this ability to essentially have unprecedented diversity in terms of selection of antibodies I mean, three times 10 to 12 combinations are currently available.

And as a factor that really limit stage in [indiscernible] technologies but in addition to this high level of diversity there is an ability using the in vitro selection system to select out antibodies that have all of the desired characteristics that you are want moving forward, whether that be extremely high affinity which in potency which of course is relevant. But there are all the other characteristics of antibodies that ultimately make them ideal clinical candidates that reduced cost reactivity with any human tissues which minimizes the potential safety risk.

The ability to select for antibodies in a mammalian system increases likely that you’re going to be able to have high levels of expressions, you’re going to be able to scale up and manufacture the antibodies, you’re going to have biophysical properties that results in both clearance.

In terms of selecting the dual reactive antibodies, visibility to select in vitro very high affinity antibody is particularly relevant. Because you can imagine if you want to bispecific antibody meaning as CVR regions in the antibody which are controlling what the antibody binds to. You want to be, if you want high affinity for two separate targets you’re going to have to go through a lot of different candidates and affinity maturation in order to select out those candidates. So using an active file system you’re able to put yourself in a competitive advantage to do that successfully with a high level of diversity that their antibody libraries. But also quickly.

So I think in particular in the dual reactive space this put us in a very significant advantage. And I guess I would also point out TIM-3, TIM-3 has been traditionally just a very difficult molecule to treat antibodies too it’s not a particularly immunogenic molecule so having a stability to select in vitro will allow us to pull out an extremely potent with again all of these desired characteristics associated with it.

Lonnie Moulder

And just one follow-up on the AnaptysBio partnership relationships. We have an exclusive arrangement as it relates to immuno-oncology they have many other partnerships in other therapeutic areas.

Jennifer Davis

Okay, operator I think that concludes our Q&A.

Operator

Okay. I’d now like to turn the conference back over to Lonnie Moulder for closing remarks.

Lonnie Moulder

Well thank you – thank you everyone for joining this morning. We really look forward to working with AnaptysBio team to advance these programs and deliver these new products to patients. Thank you and for your interest in TESORO and have a great day.

Operator

Ladies and gentlemen, this concludes TESARO’s conference call. You may all disconnect at this time.

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