Good afternoon and welcome to the CytomX 2017 Midyear Update Call. At this time, all participants are in a listen-only mode. Later we will conduct a question-and-answer session and instructions will follow at that time. Please be aware that today's conference call is being recorded. I'd now like to introduce the first speaker Debanjan Ray, CytomX Chief Financial Officer and Head of Corporate Development. You may begin.

Thank you, operator. Good afternoon and thank you for joining us for our midyear update on the CytomX Therapeutics business. Here with me today is CytomX's President and Chief Executive Officer, Dr. Sean McCarthy. Before we begin, I would like to remind you that we will be making forward-looking statements during this call including guidance on cash utilization, the evolution of our pipeline and expectations for our collaborations. Because forward-looking statements relate to the future, they are subject to inherent uncertainties and risks that are difficult to predict and many of which are outside of our control. Important risks and uncertainties are set forth in our most recent public filings with the SEC at sec.gov, including our form 10-Q filed today on August 7, 2017. We undertake no obligation to update any forward-looking statements whether as a result of new information, future developments or otherwise. A webcast of this call will be available on the Investor Relations page at CytomX's website at cytomx.com. I would now like to turn the call over to Sean.

Thanks, Debanjan and good afternoon, everybody. Very pleased to be here today to provide a midyear update on our progress here at CytomX. During the first half of the year, we continue to advance the deep and differentiated oncology pipeline of potentially transformative property therapeutics that are focused on some of the most compelling targets for the treatment of cancer. Throughout the year the team has executed flawlessly on our operating plan, setting the stage for several important clinical milestones in 2018. Before I cover program updates, just a brief reminder that Probody Therapeutics are designed to exploit certain unique conditions present in the tumor microenvironment with the goal of more effectively localizing antibody binding and activity, while limiting activity and healthy tissues. Our pipeline built of this unique platform technology includes proprietary cancer immunotherapies against clinically-validated targets such as PD-L1 and CTLA-4 and first in class, Probody pro conjugates against highly attractive targets such as CD166 and CD71. These latter targets having been considered in inaccessible to conventional antibody drug conjugates due to their presence on normal tissue, we believe presents some very unique opportunities. CytomX also has strategic collaborations with several leading Biopharma companies such as AbbVie, Bristol-Myers Squibb, Pfizer, ImmunoGen and I'll provide a few collaboration updates a bit later on today's call. So now let's turn to our recent accomplishments, I'm delighted to say that we now have two wholly-owned product candidates in clinical studies. Most recently, we initiated the first clinical trial of a Probody drug conjugate or PDC that we refer to as CX-2009. PDC's are unique first-in-class molecules that target highly and broadly expressed tumor actions, previously considered inaccessible given their presence on normal tissue. We're extremely excited about the potential of PDCs because they allow us to potentially unlock an entirely new…

Thank you, Sean. Prior to turning the call over for questions, I'd like to review selected financial highlights from the second quarter. We ended the second quarter with cash, cash equivalents and investments of $335.9 million. As Sean mentioned, the strong balance sheet allows us to fund operations into 2020 and gives us ample opportunity to advance CX-072 and CX-2009 to clinical proof of concept. Revenue was $8.8 million for three months ended June 30, 2017 compared to $3.1 million for three months ended June 30, 2016. This increase was primarily attributable to recognize revenue from the upfront payment received from the BMS in connection with the expansion of the existing collaboration. The $200 million upfront received from the expanded collaboration will be recognized over the next eight years. In addition, we will receive a $15 million milestone from AbbVie, which will be recognized -- received and recognized in the third quarter of this year. Research and development expenses were $28.1 million for the three months ended June 30, 2017, compared to $12.7 million for the three months ended June 30, 2016. This increase was primarily attributable to a $10 million sub license payment made to UCSB, which was triggered by the receipt of the $200 million upfront payment from BMS in connection with the expanded collaboration. The $10 million sublicense fee to UCSB also caused our loss per share to increase to $0.69 this quarter versus $0.39 in the comparable period last year. With that operator, we would now like to turn the call over for questions.

Thank you. [Operator instructions] First question is from Ying Huang of Bank of America. Your line is open.

Hi. Thanks for taking the questions and congrats on the progress. Couple of quick ones. First on the enrollment of lead program CX-072, can you talk a little bit more about the enrollment and also whether you're seeing more competition for enrolment because I noticed that now we're expecting data to first be reported next year instead of late 2017? And then I have a question on the two clinical programs next year. I assume that's the AbbVie and also the Bristol CTLA program. Can you talk about where [that is] for the AbbVie program? Is that also expected to enter clinic next year? Thank you.

So, with regard to enrollment, as I said, we're very pleased with how enrollment has been going. We’ve taken a fairly aggressive approach with regard to site initiations. We have more than 20 sites open now in the U.S. and ex U.S. and enrollment frankly is tracking ahead of schedule. I think we’ve been guiding for some time that the study readout for 072 and also for 2009 will be 2018 events. I think that we do of course have a broad-based translational program in place and still possible something could emerge from that over the course of this year, but I think it's really best to think about data emerging for the study in 2018. But again, we're very pleased with how our enrollment has progressed with the monotherapy to allow us to open up those two combination cohorts. With regards to the partner programs, yes, you're right, the two partner programs that I alluded to are indeed the CTLA-4 Probody with Bristol, which is making terrific progress and the AbbVie partnered CX-2029 CD71 targeting PDC. That AbbVie program we are planning a 2018 I&D. We’re not in a position to guide more specifically just yet. But we’re very pleased with the progress and obviously as announced have entered into GLP toxicology studies. So, the program is moving forward very nicely.

Thank you, Sean.

Our next question is from Boris Peaker of Cowen. Your line is open.

Great. Thank you for taking my questions. The first one, I’d like to focus maybe on the 072 program specifically the BRAF combo arm. You mentioned that you believe that the doublet combo, could potentially be better than a mega triplet. I’m just curious what would need to see from this arm of the study to confirm this thesis and also if you may have any plans to actually run a triplet with a MAC inhibitor?

Yeah. Hey, Boris, great question. So, as I said, clearly the field is evolving quickly in this context. Just to rewind a little bit and outline the rationale going into this particular arm, you'll recall that the initial clinical experience with PD-L1 with atezo and vemurafenib has shown considerable potential in terms of activity. But very severe toxicity, such that full dose of that combination is not achievable in patients and so our objective is to -- we are asking the question, and bear in mind that vemurafenib alone, does not display the types of toxicities that we’re seeing in those patients. So there seems to be something about putting them on top of PD-L1 backbone that amplifies its toxicity. So, the experiment, the way doing it, the hypothesis is that in the context of a targeted more systemically [close] PD-L1, in other words the Probody then can be tolerated in patients and the full dose given and therefore the full benefits realized by patients. We believe that the potential benefit of that doublet could be meaningful and potentially superior to the emerging data for the triplet, the atezo vem Cobi triplet, which was read out in terms of initial data, but still we've it still waiting on overall survival data. So, our objective is to do a simple experiment with the doublet rather than over complicating the experiment, by now putting on a MAC inhibitor. There is one additional reason to not put on MAC inhibitor, which is evidenced that the MAC inhibitor itself is somewhat immunosuppressive which could complicate things even further. So, we think this is a clean experiment. We believe the rationale is still very solid, and as I mentioned, the arm is open and enrolling at this point in time/

So, it sounds, just to make sure I understand you. The key here is to focus more on kind of the dose reductions or fraction of patients that may need it or may not need it more so than perhaps making conclusion based on any kind of specific response rates?

Our objective would be to avoid -- again, the hypothesis here is that, we would avoid dose reduction and therefore be able to maximize the benefit for patients.

Great. Thank you very much for taking my questions.

Thanks Boris.

Our next question is from Christopher Marai of Nomura. Your line is open.

Hi, Sean, Thanks for taking the question and congrats on all the progress. Just wondering actually if you could elaborate a little perhaps on plans going forward with Probody technology in the T-cell redirecting the bio-specific space, and we've seen obviously some posters you guys have put up and some interesting data in the solid tumor settings recently from various competitors. So, I was wondering if you could perhaps comment on use of Probodies in a solid tumor versus non-solid tumor, or liquid tumor setting and then progress that you’ve been making there with Probody that redirect T cell? Thank you.

Great. Hi, Chris. Thanks for the question. Yeah, we remain very excited about this application of the technology. We think there is a very clear need for safer, more effective T-cell engaging by specifics in the solid tumor setting. We have made great progress. Some of this work as you’ve seen has been published that you alluded to with an EGFR CD3 format, where we’ve been able to expand therapeutic window very substantially, pre-clinically and we’re concurrent thinking through our next steps for that another molecules in terms of advancing into our pipeline. You mentioned recent progress, I think I would point to the Roche CEA CD3 data at ASCO, which I think was encouraging for sure. A level of proof of concept that T cell redirection can be effective in early data, but it can be effective in solid tumors. We again, a bit like with our Probody drug conjugate strategy, we believe that we can unlock a new universal targets for solid tumors for this importance and emerging modality and we remain very committed to this research at this time.

And then just maybe one quick follow-up, you remind us that the BMS extended collaboration. Does that include any T-cell redirecting Probodies or am I mistaken? Thanks.

So again, the expansion of the relationship, six additional oncology targets, two additional non-oncology targets and they are able to select the T-cell by specific format for certain targets should they wish?

Great. Thank you. Congrats on the progress.

Great. Thank you.

[Operator instructions] Next question is from Biren Amin of Jefferies. Your line is open.

Yeah. Thanks for taking my questions. CX-072, can you just discuss the immunogenicity profile that you’ve seen to date from the ongoing trials?

Too early to tell, Biren and hi, by the way. Thanks for the question. So, we're ready to say at this point is, no DLTs observed to date. We'll be doing comprehensive PK analysis in the coming months.

Okay. And Sean I think you mentioned that you wanted at least with 072 proceed into a monotherapy study with the tumor type that sensitive to PD1. I am pretty sure, you’re probably not going to discuss what that tumor type is today. But is one of the considerations that you could file a regulatory filing on Phase 2 data, when you chose that tumor type. And secondly, are you developing a companion diagnostic, and if so, are you currently using that in the current monotherapy and combo studies?

Great questions, Biren. With regard to the first, of course, indication, selection is internally linked with in this area or clinical development, is intimately linked with potential registration strategy. It's too early to comment any further on that. With regard to companion diagnostic, just to make sure I understand the question. Are you asking about, PD-L1 levels, are you asking about something else.

Yeah. Are you evaluating PD-L1 levels currently in the ongoing monotherapy in the epi combo studies?

We are. We're certainly measuring PD-L1 status, we are not selecting patients in these early arms of the study. That’s something that we are consider doing a bit further down the road.

Got it. Thank you.

Thank you.

Thank you. There are no further questions at this time. I'd like to turn the call over to Debanjan Ray for any closing remarks.

That concludes our call and our Q&A session. Thank you very much.