TRACON Pharmaceuticals Inc (TCON) 2015 Q2 法說會逐字稿

Good day, ladies and gentlemen, and welcome to the TRACON Pharmaceuticals second-quarter 2015 earnings conference call. (Operator Instructions)

During today's call, we will be making certain forward-looking statements, including statements regarding expected timing of clinical trials and results, regulatory activities, future expenses and cash runway, and our development plans and strategy. These statements are subject to various risks that are described in our filings made at the Securities and Exchange Commission, including our annual report on Form 10-K for the year ending December 31, 2014, the second quarterly report on Form 10-Q, and our current reports on Form 8-K. You are cautioned not to place undue reliance on these forward-looking statements and we disclaim any obligation to update such statements.

Now I would like to turn the call over to Dr. Charles Theuer, President and CEO of TRACON Pharmaceuticals. Dr. Theuer?

Good afternoon and welcome to TRACON's second-quarter 2015 financial results and business update conference call. I will start by providing an update on our pipeline and recent activity. After that, our Chief Financial Officer Patricia Bitar will review our second-quarter financials. Finally, we will conclude by taking questions from call participants.

The second quarter 2015 was our first full quarter as a public company and we made significant progress across our pipeline. As a reminder, our lead product, TRC105, is an anti-endoglin antibody that is being studied in the initial indication of sarcoma, renal cell cancer, hepatocellular cancer, glioblastoma, and choriocarcinoma.

Patient enrollment in each of our five Phase 2 trials remains ongoing and we believe positive data from these trials would enable Phase 3 development. In each of the ongoing trials, TRC105 is being dosed in combination with an approved VEGF inhibitor, with the expectation of delivering top-line data in the next 6 to 12 months.

As I referenced earlier, TRACON had a very productive second quarter. We reported positive data for TRC105 in two different oncology indications and we executed a successful end-of-Phase 1 meeting with the FDA. In addition, an IND to study the ophthalmic formulation of TRC105, called DE-122, in wet AMD was filed by our partner Santen.

Importantly, we have achieved this progress in a highly cost-effective manner, which we believe validates our differentiated business strategy of implementing domestic clinical trials using our internal clinical operations team without incurring the cost of outsourcing to a contract research organization.

As I mentioned earlier, we recently announced positive clinical data for two studies with TRC105. Data from an open-label dose escalation and expansion portion of a Phase 1/2 study of TRC105 and Votrient in 18 patients with advanced soft tissue sarcoma were presented at ASCO in June 2015 and highlighted in a poster discussion session.

Eligible patients had received at least one prior line of chemotherapy and most received two or more lines of chemotherapy. Study results indicated that the combination of TRC105 and Votrient was well tolerated and dose-limiting toxicity was not observed. Adverse events characteristic of each individual drug were not increased in frequency nor severity when the two drugs were administered concurrently.

We saw encouraging preliminary signs of activity in this highly pretreated population, including an ongoing complete response by RECIST in a patient with cutaneous angiosarcoma who previously received Votrient and chemotherapy.

As of the ASCO presentation, 46 of 63 patients have been enrolled into the Phase 2 portion of the study, including an additional patient with cutaneous angiosarcoma who also has an ongoing complete response to Votrient and TRC105 treatment by RECIST. Angiosarcoma is a rare sarcoma subtype that highly expresses endoglin in the majority of cases and could be a tumor type that would be particularly responsive to TRC105 treatments.

Given the strong mechanistic rationale and the robust response that angiosarcoma has seen thus far, the ongoing Phase 1/2 trial has been amended to enroll a separate cohort of 13 patients with angiosarcoma. Furthermore, we are currently discussing a separate Phase 3 trial comparing Votrient and TRC105 to Votrient alone in angiosarcoma with investigators.

Many common sarcomas, including leiomyosarcoma and undifferentiated pleomorphic sarcoma also were expressed endoglin on a subset of tumors. We are pursuing a biomarker strategy in the ongoing Phase 2 trial in an effort to correlate endoglin expression with survival. We expect to report data on the primary endpoint of progression free survival stratified by biomarker expression by early 2016. If biomarker expression correlates its efficacy in the general sarcoma population, we may utilize a biomarker as the basis for selecting sarcoma patients for a Phase 2 study in soft tissue sarcoma.

We recently completed an end-of-Phase 1 meeting with the FDA focused on the development of TRC105 in sarcoma. We are now aligned on the nature of the nonclinical studies as well as the manufacturing plan and scale-up activities that will be needed to support the initiation of Phase 3 trials and subsequent submission of a marketing application. As we outsource our production, we will implement our plan in conjunction with our manufacturing partner Lonza.

Also on the regulatory front, during the second quarter, we received fast-track designation from the FDA for the development of TRC105 in renal cell cancer. Going forward, we intend to file applications for orphan drug designation for TRC105 in sarcoma and in gestational trophoblastic neoplasia, or GTN, which is a tumor type which includes choriocarcinoma, by the end of this year.

Like angiosarcoma, GTN highly expresses endoglin and may be particularly responsive to treatment with TRC105. We initiated a Phase 2 trial with the Dana-Farber Cancer Institute in 2015 in a patient with metastatic choriocarcinoma, an aggressive form of GTN. We expect to report data from this patient at the World Congress on Gestational Trophoblastic Disease in September 2015.

We view patients with GTN who have progressed following first-line treatment with chemotherapy as a population with significant unmet need that could be addressed with TRC105. Responses in these tumors are assessed using a simple blood test, which facilitates the assessment of efficacy.

The second indication where positive data were reported at ASCO was hepatocellular cancer. Data from the dose escalation portion of a Phase 2 trial of TRC105 with Nexavar in patients with hepatocellular cancer were presented by the National Cancer Institute, or NCI. 4 of 10 -- or 40% -- of patients treated at the recommended Phase 2 doses of TRC105 of 10 or 15 micrograms per kilogram every 2 weeks demonstrated partial responses by RECIST. For comparison, this is a setting where the expected partial response rate of Nexavar alone has historically been 2%.

The combination of TRC105 and Nexavar was well tolerated the trial. We intend to begin dosing patients in a separate Phase 2 trial of TRC105 and Nexavar in quarter 3 of 2015, with a primary endpoint of overall response rate. We believe that corroboration of the robust response rate reported by NCI would justify the initiation of a Phase 3 trial comparing the combination of TRC105 and Nexavar to Nexavar alone in hepatocellular cancer.

TRC105 is also being studied in two additional randomized controlled Phase 2 trials with data from both trials expected in mid-2016. We are sponsoring the Phase 2 randomized [tracsar] trial in patients with clear cell, renal cell cancer that compares treatment with TRC105 and Inlyta to treatment with Inlyta alone in patients who received one prior VEGF inhibitor.

The NCI is sponsoring a Phase 2 randomized trial comparing treatment with TRC105 and Avastin to treatment with Avastin alone in patients with glioblastoma who have received chemotherapy and radiation therapy, but have not been treated previously with Avastin or another VEGF inhibitor.

We consider our initial indications of sarcoma, renal cell cancer, hepatocellular cancer, glioblastoma, and GTN attractive because the endpoints for regulatory approval may be obtained more quickly than endpoints for other indications. We expect top-line data in each of our ongoing Phase 2 multicenter trials by late 2015 to mid 2016. And if results are positive, we expect to begin dosing patients in Phase 2 trials in one or more indications in the second half of 2016.

Going forward, we plan to initiate four additional clinical trials of TRC105 in combination with existing VEGF inhibitor treatments in large market indications later this year. These include the aforementioned multicenter Phase 2 trial in patients with hepatocellular cancer, a Phase 1/2 trial in patients with breast cancer, a Phase 1 trial in patients with lung cancer, and a Phase 1 trial in patients with colorectal cancer.

Beyond oncology, we are attempting to enhance the treatment landscape in wet AMD. VEGF inhibitor drugs such as Eylea and Lucentis are the current treatments of choice in wet AMD and we believe they represent a backbone therapy upon which to add additional treatments.

The market is large, as annual sales of VEGF inhibitors for ophthalmic indications have reached $7 billion. We have partner global rights to develop our endoglin antibody in eye disease, including wet AMD, with Santen.

Santen filed an IND with the FDA in June 2015 to initiate clinical development of DE-122 in wet AMD. Importantly, the filing of the IND triggered a $3 million milestone payment from Santen to TRACON. As a reminder, DE-122 is the ophthalmic formulation of TRC105.

The utility of our endoglin antibodies could also have potential beyond oncology and ophthalmology. Recent preclinical data indicate that endoglin is a key driver of fibrosis and that antibodies to endoglin have the potential to inhibit cardiac and liver fibrosis. We have designated a separate anti-endoglin antibody specifically for fibrosis that is undergoing additional preclinical at testing this time.

Turning now to our second product candidate. TRC102 is a novel clinical stage small molecule inhibitor for the DNA-based excision repair pathway. Activation of this pathway causes resistance to alkylating and antimetabolic chemotherapeutics and its inhibition may result in improved outcomes. TRC102 is currently being studied in combination with the approved chemotherapy drug Temodar in two Phase 1 trials.

Case Western University recently presented clinical data from a Phase 1 trial of intravenous TRC102 and Temodar at ASCO in June, indicating the combination is well tolerated, there were no pharmacologic interactions between the two drugs, TRC102 target concentrations were achieved, and antitumor activity was observed.

These data reinforce data presented by the NCI in April indicating oral TRC102 was well tolerated with Temodar and also demonstrated signs of activity. We are pleased to say that TRC102 was accepted into the [CTIP] program of the NCI and as a result, we expect the NCI to sponsor four additional trials.

These include a Phase 1/2 trial of TRC102 with Temodar in patients with glioblastoma; a Phase 1 trial of TRC102 with Alimta and Cisplatin; a Phase 2 trial of TRC102 with Alimta in patients with mesothelioma; and a Phase 1 trial of TRC102 with Alimta, Cisplatin, and radiation therapy in patients with lung cancer.

As you can see, we have been and remain quite active on the clinical development front. We have made significant progress executing on our clinical development plans in a cost-effective manner through the TRACON operations team that manage domestic trials without the significant cost associated with outsourcing to a contract research organization. In addition, our collaboration with the NCI allows us to broaden the development path for both of our clinical stage assets beyond one or two lead indications.

Our financial position remains strong and we have the resources to complete the five ongoing Phase 2 studies of TRC105, support manufacturing activities at Lonza required for regulatory approval, initiate Phase 2 clinical development, initiate additional trials with TRC105 in large market oncology indications, provide TRC102 for study in clinical trials sponsored by the NCI and Case Western, and pursue additional programs addressing important unmet medical needs, including the development with antibodies to endoglin for fibrosis.

We also continue to evaluate product candidates to potentially in-license and intend to be opportunistic. Ideal candidates would leverage the cost-effective internal operations capacity at our Company and provide value to patients, the Company, and our shareholders.

At this time, I will turn the call over to Patricia Bitar, our Chief Financial Officer, who will provide an update on our financials.

Thank you, Charles, and good afternoon, everyone. TRACON reported collaboration revenue of $4.2 million for the quarter ended June 30, 2015, and $5.3 million for the 6 months ended June 30, 2015, compared to $1.1 million and $1.4 million for the comparable periods of 2014. The increases were due to the Santen agreement being signed in March 2014 and a $3 million milestone that was triggered by Santen's filing of an IND in wet AMD June 2015.

Total operating expenses were $6.9 million for the quarter ended June 30, 2015, and $11.7 million for the 6 months ended June 30, 2015, compared to $2 million and $3.6 million for the comparable periods of 2014. These increases reflect higher expenses in both R&D and G&A.

Research and development expenses were $5.4 million for the quarter ended June 30, 2015, and $9.2 million for the 6 months ended June 30, 2015, compared to $1.6 million and $2.8 million for the comparable periods of 2014. These increases were primarily the result of increased manufacturing and clinical study-related expenses for TRC105 and higher personnel costs resulting from increased headcount.

General and administrative expenses were $1.5 million for the quarter ended June 30, 2015, and $2.5 million for the 6 months ended June 30, 2015, compared to $400,000 and $800,000 for the comparable periods of 2014. These increases were mainly attributable to increase costs associated with becoming a publicly traded company and higher personnel costs resulting from increased headcount.

Our net loss was $2.9 million for the quarter ended June 30, 2015, and $6.9 million for the 6 months ended June 30, 2015, compared to $1 million and $2.3 million for the comparable periods of 2014.

Turning to the balance sheet, at June 30, 2015, our cash and cash equivalents totaled $61.2 million compared to $65.3 million at March 31, 2015. As Charles mentioned, the IND filing by Santen triggered a $3 million cash milestone payment, which we received subsequent June 30, 2015. And as result is not included in the reported $61.2 million cash and cash equivalent balance. We continue to expect our current resources to be sufficient to fund our currently planned operations for at least the next 18 months.

And with that, I will turn the call back over to Charles.

Thank you, Patricia. As we noted, we expect to have a significant number of potential value-creating milestones in the new future. These include: results from a Phase 2 trial of TRC105 in choriocarcinoma; orphan drug designation by the FDA for TRC105 in one or more indications before the end of the year; initiation of multiple TRC105 clinical trials in large market indications by the end of the year; as well as the initiation of multiple TRC102 trials by the NCI.

We also expect initial Phase 2 top-line data from our ongoing trial of TRC105 and Votrient in sarcoma by early 2016, including data from the key endpoint of progression free survival in sarcoma subtypes that highly express endoglin, including angiosarcoma.

In summary, I appreciate the support of our investors during an exciting first half of 2015 and look forward to reporting further updates regarding our upcoming key milestones. I'm confident that we have the resources in place to deliver on our development and business plans for the benefit of shareholders and patients alike.

With that, we will be happy to answer questions.

(Operator Instructions) Tom Shrader, Stifel.

Congratulations on first quarter. I have a question about the angiosarcoma trial. I think you said 13 patients. Is that something that you would be waiting for to start a Phase 3 trial or that would be open label and used to help generate a Phase 3 trial? And would a Phase 3 trial have to be controlled?

Hi, Tom. Great question. So with respect to angiosarcoma, we have been very impressed with the responses we've seen thus far in the Phase 2 trial. And given that and given a response -- and given investigator input, our thought is that making a trial available for angiosarcoma patients now is a way to address an unmet need and gain further experience in angiosarcoma, which includes, for example, both cutaneous and visceral forms. That said, we are planning it that the current time of moving into Phase 3 next year in 2016 in angiosarcoma.

In terms of design of that trial, there are multiple options. I think an option that has resonated with investigators currently is Votrient with or without TRC105 is a putitive Phase 3 pivotal study. That I think is attractive for several reasons.

We are building upon up backbone VEGF inhibitor therapy, which mechanistically makes sense when you target the endoglin pathway. The overall PFS in angiosarcoma with VEGF inhibitors alone is not very impressive and so you can clearly build upon what's a fairly unimpressive PFS by adding on to the established standard-of-care.

So currently, that's our plan moving forward. But we will continue to discuss plans with investigators in order to develop the optimal plan moving forward with respect to Phase 3.

Okay. And two quick questions on the new trials. The breast cancer trial -- there's no VEGF inhibitor in there. And given the history of Avastin, what's the thinking there?

Yes, the breast cancer trial is a neoadjuvant study combining -- with an mTOR inhibitor and then an aromatase inhibitor. There is -- it's an investigator-sponsored trial. It's done by an investigator who actually did study Avastin in the neoadjuvant setting and was very impressed with its ability to potentiate both mTOR and aromatase inhibitors in the neoadjuvant setting.

Given that angiogenesis inhibition seemed to be active in the neoadjuvant setting, his thought was to study TRC105 as another inhibitor of angiogenesis with that same pairing of agents, with the expectation of seeing a significant pathologic complete response rate.

We have not studied our drug with an mTOR inhibitor, but mTOR inhibitors do have anti-angiogenic effects. We do think that's a combination that will be interesting to study. And we do like the fact that at a neoadjuvant trial, you will have rapid assessment in terms of response to the tumor access at the time of the mastectomy just after neoadjuvant therapy is initiated.

Okay. And in colorectal cancer, why with Stivarga? Some of your best data ever is with Avastin in colorectal cancer. What's the thought there?

It's a great question, Tom. With respect to colorectal cancer, we are committed to moving forward in that indication. And our current discussions have centered on Stivarga. And I would mention that -- I would note that with respect to the final trial design, there is still consideration of adding onto Avastin. To your point, we had impressive activity with Avastin in colorectal cancer in a Phase 1/2 study. Also another possibility will be adding on CYRAMZA, the Lilly VEGF inhibitor.

So currently, our plan is Stivarga. But I would make clear that that is still a topic up for discussion in terms of the optimal backbone therapy to pair with TRC105 in colorectal cancer.

Okay, great. Thanks for the detail.

Chad Messer, Needham.

Great. Thanks for taking my question, Charles, and getting an update from you guys. As always, a bit of a whirlwind. I just have a couple of questions and one is on the biomarker strategy in sarcoma.

The rationale makes complete and total sense to me. Just wondering why so far it's been -- your discussions about biomarker strategy have been limited to sarcoma? And does it make sense to look at that in some of the other indications as well?

Hi, Chad; appreciate the question. So there are certain tumors that highly express endoglin on the tumor cells, whereas every solid tumor will highly express endoglin on the tumor vessels. And that's why every solid tumor is potentially a target for TRC105 as a therapeutic.

But those tumors that highly express the target on tumor cells may be particularly responsive to the therapy and that's why mechanistically it made sense to see activity in angiosarcoma. We further hope that mechanistically, choriocarcinoma will be similarly responsive, for example.

There are other tumors beyond choriocarcinoma, beyond angiosarcoma, that do express endoglin on tumor cells. One in particular we're interested in is melanoma. And then beyond that is the general soft tissue sarcoma population, where you see expression on certain subtypes and not on others.

So with respect to sarcoma in general, angiosarcoma, high expressive endoglin on tumor and vessels, that is its own, if you will, biomarker subtype. But in the general sarcoma population, we will interrogate the other subtypes to see if direct expression on tumor will stratify those more responsive sarcoma subtypes from those that are less responsive. We could employ a similar approach in melanoma and we are envisioning that is a future indication.

There are other tumor types -- for instance, colorectal cancer -- where you don't expect tumor expression, that the expression is really on the vessels. And hence, building onto VEGF inhibitor therapies in colorectal cancer makes sense without, if you will, a biomarker stratification.

All right; thank you. That makes sense. My other question is on the end-of-Phase 1 meeting you had, I guess, which was specific for sarcoma. In terms of what you worked out and kind of got on the same page with the FDA there, is there other issues for other indications that you have to go back and work things out?

And when you talk about things like nonclinical studies in manufacturing, I would imagine a lot of that should apply to any indication you would go into. Just wondering if there are additional details that would need to be fleshed out in similar meetings in the future?

An excellent point. When we submitted a request for an end-of-Phase 1 meeting, we had to pick an indication, if you will. And given the robust activity we've seen in sarcoma, specifically angiosarcoma, that was the indication we picked.

But the key I think with end-of-Phase 1 meeting is, as you pointed out, that it's really gaining concurrence on general program attributes that enable study in multiple indications. And that is the nonclinical and the manufacturing activities that will be needed to support Phase 3 development, regardless of indication. And then also commercialization.

And we were really pleased coming out of the meeting in terms of the alignment we gained with respect to those two categories: namely, nonclinical testing and also manufacturing scale-up in order to support Phase 2 trials in angiosarcoma, sarcoma in general, but also will be applicable across multiple indications.

All right. I thought that might be the case, but thought it was worth asking. Thanks.

Yes, we definitely were thinking what indication we should name. Because we definitely had multiple choices there.

All right. Makes sense. Thanks.

(Operator Instructions) Matthew Andrews, Wells Fargo Security.

Thanks for the chance to ask some questions. Charles, can you just go back through the numbers again on the end for angiosarcoma and the ongoing study and the responses you've seen? Two: when you report data later this year in the sarcoma study, are you going to provide Choi and RECIST response results?

And then lastly, for the pivotal study in angiosarcoma and if you move into general sarcoma population with the biomarker strategy, do you expect to use Choi or RECIST? Or is the primary endpoint going to be PFS or to be determined based on future discussions with FDA? Thanks.

Sure, no, appreciate that. Matt, thank you for your questions. So with respect to angiosarcoma, with respect to the initial Phase 1 trial, we had enrolled a cutaneous angiosarcoma patient in whom we saw that complete response that's now ongoing at 45 weeks. And the patient had progressed on Votrient previously, which we thought was fairly impressive.

With respect to the Phase 2 portion we reported at ASCO, the second patient cutaneous sarcoma that was treated also had a complete response. And really that was the basis for now enrolling a separate cohort of 13 patients with angiosarcoma and we do expect to see that enroll starting relatively soon and then moving forward into 2016.

But the overall Phase 2 study of 63 patients in general soft tissue sarcoma is enrolling very well. We disclosed 45 patients, 63 in at ASCO, and we expect full enrollment well before end of the year.

Now on that study, the endpoint is progression free survival and that is by RECIST criteria. In terms of Choi criteria, that is an analysis we could do separate after the study is over, if you will, using a central radiographic review. But to be clear, the main criteria applied to that study in terms of defining progression free survival and response is RECIST. And that will be the criteria that will be used to assess PFS both in patients that express the endoglin on the tumor tissue directly and those that do not.

In terms of thinking forward into Phase 3, with respect to sarcoma, whether it be soft tissue sarcoma or angiosarcoma, our thought is that PFS is an approvable endpoint. That was the endpoint that was the basis for approval of Votrient in sarcoma in the PALETTE study. And so that would be a bang, if you will, to standard paradigm in that disease. It would be progression free survival by RECIST.

In the Phase 2 study, we could incorporate -- and logically you would incorporate a separate analysis of Choi criteria because I think Choi criteria is an interesting criteria. But to be clear, the endpoint for approval as we think about sarcoma is PFS and it would be defined by a RECIST criteria.

Okay. So just two CRs with angiosarcoma -- not three, correct?

We have two CRs. And the two phases would be cutaneous angiosarcoma and treated to date in that trial, correct.

Got it. Okay. And then just lastly, just curious if you could give us a sense of the level of interest, some of the comments by clinicians at the sarcoma poster for 105 at ASCO. Was there a common theme or question to you and/or the lead investigator presenting the data? Just curious sort of what the feedback has been from ASCO for that.

No, I appreciate that, Matthew. It was a busy poster. You know, angiosarcoma, like soft tissue sarcoma in general, it is a very difficult disease. It's treated with first-line chemotherapy; it's treated with pazopanib. The PFS, even in patients who respond, is about four months; the overall survival is about a year. It's a tough disease.

So it's the incomplete responses in that type of disease was -- generated a fair amount of enthusiasm, both among people at our Company and also among investigators. That's really been the impetus to move this forward, open up a separate cohort of patients in the existing trial to give additional patients the opportunity to see the drug, but also to move forward aggressively in finding a Phase 3 trial. So that was driven by investigator enthusiasm as a result of that poster.

I think it was remarkable in the poster discussion session at ASCO when you - the last slide presented in that session was the picture of the complete responders from our study. And that just gives you an idea of the enthusiasm, even within that session, by the presenting physician around the activity we've seen thus far in that indication.

Okay, great. Thank you.

Debjit Chattopadhyay, ROTH Capital Partners.

Thanks for the questions here. Just a hypothetical question here on angiosarcoma. Given the data from Inlyta versus a Nexavar, what would be logical combination? I understand the current 13 patient expansion is with Votrient. Going forward, would Nexavar make sense to look -- just to look at it, given the data from Nexavar in angiosarcoma per say?

It's a good question. So Nexavar is not approved in sarcoma, but they have reported use in a separate trial that was not submitted for label expansion. That said -- there's some activity of Nexavar in angiosarcoma. The partial response rate was about 15%.

That said, Votrient was approved in soft tissue sarcoma, which includes angiosarcoma. So from a regulatory perspective, we think it's more productive to use Votrient as an approved agent as a backbone therapy, for instance, if you were to do a randomized Phase 3 trial.

You know, I do think that Votrient, even though it doesn't have as much independent data in angiosarcoma as does Nexavar, will probably have a very similar type of response rate -- say 15% is what we're projecting. And the PFS will also be very similar, which again is not impressive about four months.

And so we are actually using Nexavar as a surrogate for the statistical analysis and planning for the Phase 3 trial. But we do plan to move forward with Votrient just because approved. And so from a regulatory standpoint, it makes development much more [vassle]

Great. And then when you start thinking about choriocarcinoma, at what point do you go back to the FDA to discuss what the logical trial design is for chorio?

Great question. So choriocarcinoma is an area where there actually are no, frankly, approved drugs. There is a standard-of -care in first-line in terms of chemotherapy that is used. And then following that, there's nothing that's, if you will, standard-of-care. So our view with respect to choriocarcinoma is that patients who progress following first-line chemotherapy represents the unmet need in which we should develop our drug.

The other huge advantage in choriocarcinoma is that beta-HCG is a simple serum pregnancy test is the standard, the gold standard for assessment of response, which allows a rapid assessment of response.

With respect to designing the trial, which could include use of TRC105 as a single agent, we do need to discuss that with the FDA in terms of the endpoint for approval, which could be overall response rate. What level of beta-HCG decline would define our overall response? And these also to be vetted with the FDA.

And the level of response in refractory setting that essentially could support approval also would need to be vetted with the FDA. So those are all key questions we would need to discuss with the FDA at an end-of-Phase 2 meeting.

Great. And then one more on the -- just a follow-up on the breast cancer question before. These patients are largely receptor-positive patients. But there's pretty much a vacuum when it comes to triple negative or even lower expressing HER2, [the 1 plus -- especially the 1 plus via IT]. So I'm wondering is there any kind of synergy for TRC105 in these two settings?

It's a great question. We had done a trial earlier that we reported of combining TRC105 with [Zolota], which was in HER2 negative breast cancer, that included patients with triple negative breast cancer in that trial. So we have clearly combined with a chemotherapeutic that is a standard in triple negative breast cancer.

And there is interest to continue to study triple negative breast cancer. I think as you can appreciate, we have a quite broad pipeline and are studying a quite broad number of tumor types as we move forward currently. And so triple negative breast cancer currently is not a top priority with respect to the indications planned, but it is something to consider down the line.

And I might've missed it: what's the logical endpoint for the breast cancer study here? Are you looking at response rates?

It is pathologic complete response rate. So this is a neoadjuvant study whereby women treated with breast cancer who were planned to undergo mastectomy are treated with therapy prior to the planned surgery. And then at the time planned surgery, the tissue is assessed, looking for a pathologic complete response as the key endpoint for the study.

Great. Thank you, Charles.

Ling Wang, Oppenheimer.

Thanks for taking my questions. A follow-up on the soft tissue sarcoma. First of all, I wanted to clarify the time for initial data from the Phase 2 portion. Is it going to be a year end this year or next year? And also for the 13 patient angiosarcoma cohort, are you going to limit to the [13] years type?

Could you repeat that last sentence one more time, Ling?

Sure. So in the angiosarcoma cohort, the 13 patients, are you going to enroll just a few [tenures] angiosarcoma or different types of angiosarcoma as well?

Understood; appreciate the question. So with respect to the Phase 2 study, as I mentioned that's ongoing at this time, the full enrollment being 63 patients, which is on top of the 18 patients' data that we reported at ASCO, that's a total of 81 patients. We do expect full enrollment this year. In terms of full correlation of PFS with biomarker expression -- namely endocrine expression on the tumor -- we do expect that in early 2016.

The angiosarcoma cohort we expect to open very soon. That will be any type of angiosarcoma, both cutaneous and visceral. And I think that will be very useful in terms of seeing -- we have very little experience thus far treating visceral angiosarcoma.

So as part of that 13-patient study, we hope to see further activity in cutaneous angiosarcoma. But also we hope to see activity in visceral angiosarcoma. Ideally, we would like to enroll both types in a Phase 3 trial and that data from that specific cohort will be useful to make that determination.

Got it. And also for the single patient choriocarcinoma, can you comment on -- by the time the data will be presented, how long are the patients will be on the drug? And perhaps any color on the patient characteristic?

Yes, with respect to the choriocarcinoma patient, we do expect presentation at that World Congress Gestational Trophoblastic Disease. In terms of commenting on specific aspects of the patient, I cannot comment at this time, Ling, other than to say it's a patient who has seen prior therapy and was refractory with respect to those prior therapies. But September is not that far away, so we hope to be able to report that data in a relatively short time frame.

Okay, thank you.

Thank you. And at this time, I'm showing no further participants in the queue. I would like to turn the call back to management for any further remarks.

Well, thank you again for the questions and thank you to everyone for participating today. Look forward to catching up again in the near future. And have a great day.

Ladies and gentlemen, thank you for your participation on today's conference. This concludes the program. You may now disconnect. Everyone, have a great day.