Charles Theuer - President and CEO Patricia Bitar - CFO.

Chad Messer - Needham & Company Tom Shrader - Stifel Nicolaus Jim Birchenough - Wells Fargo.

Good day, ladies and gentlemen, and welcome to the TRACON Pharmaceuticals Second Quarter 2016 Earnings Conference Call. At this time, all callers are in a listen-only mode. After the speakers' prepared remarks, we will conduct a question-and-answer session and instructions will be given at that time.

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 with the Securities and Exchange Commission, including our Annual Report on Form 10-K for the year ended December 31, 2015, subsequent quarterly reports 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 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 thank you for joining us today for TRACON's second quarter 2016 financial results and business update conference call. I will begin with an update on our pipeline and recent activities. Following that, our Chief Financial Officer, Patricia Bitar, will review our financial results for the three and six months ended June 30, 2016.

Finally, we will conclude by taking questions from call participants. Let's begin with a detailed update on our latest product candidate, TRC105, which now has been designated carotuximab as an international non-proprietary name by the World Health Organization.

We will review recent ASCO presentation and progress towards the initiation of our initial pivotal Phase 3 trial in angiosarcoma. At ASCO, we presented data from our Phase 1/2 study of patients with angiosarcoma, treated with TSC105 and Votrient. In addition, these data were highlighted during the poster discussion section by Dr.

Mrinal Gounder of Memorial Sloan-Kettering Cancer center. All five angiosarcoma patients discussed have radiographic tumor reduction and medium progression free survival or PFS for this subgroup was at least 12.9 months.

Two patients with cutaneous angiosarcoma in the group demonstrated durable complete responses by RESIST, that remain ongoing at 17 and 24 months respectively. Activity was also seen in four additional patients enrolled in the 13 patient angiosarcoma specific cohorts treated with TRC105 and Votrient.

A patient with visceral angiosarcoma in this cohort demonstrated marked reduction of subcutaneous occipital map and complete regression of the single non-target lesion.

This observation of activity in visceral angiosarcoma is important, as our Phase 3 pivotal study comparing Votrient with TRC105 to single agent Votrient, to enroll patients with both cutaneous and visceral disease. As a reminder, cutaneous and visceral angiosarcoma occur in about equal proportions.

Importantly we expect to provide a further update on durable complete responders and additional phase enrolled angiosarcoma specific cohort at the Connective Tissue Oncology Society or CTOS meeting in November. We expect to initiate our Phase 3 randomized trial in the fourth quarter of 2016 following discussions with the FDA and the EMA.

We intend to enroll at least 124 patients in utilizing adaptive design that allows for enrollment of up to 200 patients. The initial sample size of 124 patients is anticipated to provide 80% power to detect a 67% improvement in PFS, assuming an alpha of 0.05. We expect the trial to run over two years and yield interim data in 2018.

At ASCO, we also reported stratified PFS data in patients with soft tissue sarcoma subtypes, other than angiosarcoma enrolled in the Phase 1/2 trial.

Observed tumor endoglin expressions did not correlate with improved PFS in the general soft tissue sarcoma patients, and a median PFS of approximately four months, with similar to that expected with single agent Votrient. It is important to note, that the tumor endoglin expression analysis used archival tumor tissue.

As a result, the endoglin status reflected the state of the tumor and diagnosis prior to treatment chemotherapy, rather than the status of the metastatic disease at the time of entrance into the TRC105 trial.

Tumor heterogeneity with significant period of times been [ph] sampling the treatment and the effects of tumor evolution resulted from prior treatment, could have limited to the ability of archival tumor tissue, to actively reflect tumor endoglin status at the time of initiation of TRC105 treatment.

In order to address this potential issue, we are investigating endoglin status on circulating tumor cells or CTCs as part of the Phase 3 angiosarcoma trial, to determine whether the tumor endoglin expression on cancer cells at the time of actual TRC105 treatment correlates with efficacy.

If this analysis is positive, we may use CTCs to screen general sarcoma patients to establish who may be most responsive to TRC105 treatments. Also at ASCO, we reported promising overall survival data from a single ARM study of TS105 in combination with Avastin in glioblastoma patients who have regressed on prior Avastin treatments.

These patients have a very limited lifespan and the overall survival of 5.7 months of patients treated with TRC105 and Avastin exceeded the historical overall survival of four months observed with Avastin as a single agent.

We expect to have further data from the NCI sponsored randomized Phase 2 trial of TRC105 and Avastin in Avastin-naïve glioblastoma patients in late 2016.

We believe that TRC105 has broad potential, and as a result, TRACON continues to execute on its tiered development strategy, that includes orphan drug indication, mid-sized market indication and large market indication.

In addition to the planned pivotal trial in angiosarcoma, we are also focused on gestational trophoblastic neoplasia or GTN, an indication which includes choriocarcinoma and for which we are pursuing orphan drug designation.

Based on an ongoing durable complete response at month 17 in a patient with choriocarcinoma treated in a compassionate use setting. We plan to initiate a Phase 2 trial in the second half of this year in patients with GTN in the U.S. and the EU.

The primary endpoint of the trial would be response rate, and we believe this trial has the potential to be registration enabled. In addition to the glioblastoma development which I discussed earlier, we are also setting a number of other mid-sized market indications, with short time to event endpoints, including renal cell cancer and liver cancer.

The randomized Phase 2 TRAXAR trial in patients with clear cell, renal cell cancer, compares treatment with TRC105 and Inlyta to treatment with single agent Inlyta in patients who have received one prior VEGF inhibitor. In anticipation of decreased enrollment at U.S.

sites following the approval and launch of Opdivo and Cabometyx in renal cell cancer, we have opened multiple sites and commenced enrollment in the European Union in order to speed approval.

Despite this, we are slightly adjusting our timeline and now anticipate completing enrollment and delivering on the endpoint of PFS in the first half of 2017, rather than the second half of 2016. Although, the exact date will still depend on the number and timing of progression events that occur..

In May, we initiated enrollment in a multicenter Phase 1/2 trial in liver cancer with the primary endpoint of overall response rate. The goal of this study is to validate the robust 40% response rate, who was observed in the 10 patients treated and recommended Phase 2 doses of TRC105 with Nexavar that was reported by the MTI at ASCO in 2015.

For comparison, this is a setting where the response rate of single agent Nexavar has historically been 2%. We expect the NCI to submit data from its trial for publication in a peer reviewed journal this year.

Data from a previously reported trial of TRC105 as a single agent in bladder cancer patients were published in the journal, Clinical Genitourinary Cancer in July. Of note, the main percentage of CD4 positive regulatory T-cells in peripheral blood decreased following TRC105 treatments.

Regulatory T-cells have been implicated [ph] in promoting tumor resistance. We are currently investigating our endoglin antibodies with immune checkpoint inhibitors in preclinical models, to determine whether clinical investigation is warranted.

Finally, further this year, we dosed the initial patients in two larger market indication trials, of Phase 1 trials in TRC105 in combination with Avastin in chemotherapy for first line treatment of patients with lung cancer, and a Phase 1/2 trial of TRC105 in combination with AFINITOR and FEMARA for the new adjuvant treatment of patients with breast cancer.

We believe there is also a significant opportunity for endoglin antibodies to improve treatment options for patients in areas beyond oncology, such as wet AMD. As a reminder, we have partnered global rights to develop our endoglin antibodies in eye disease, including wet AMD with Santen.

Santen continues to recruit patients into their Phase 1/2 trial to assess safety and bioactivity of DE-122 in refractory wet AMD patients. As a reminder, DE-122 is an ophthalmic formulation of TRC105. Fibrosis is the final therapeutic area where endoglin antibodies have demonstrated activity.

In November, we will present preclinical data related to TRACON's endoglin antibodies in models of liver fibrosis and nonalcoholic steatohepatitis or NASH at the annual meeting of the American Association for the Study of Liver Diseases or AASLD.

Turning now to our second project candidate, TRC102; TRC102 is a novel small molecule inhibitor of the DNA-based excision repair pathway. Activation of this pathway triggers resistance to alkylating and anti-metabolic chemotherapeutics, resulting in poor outcomes.

The NCI presented positive safety, pharmacokinetic and efficacy data from its all comer Phase 1 trial with the combination of TRC102 and Temodar at ASCO 2016. The combination of TRC102 and Temodar was both tolerated and partial responses were observed in patients with ovarian, lung and KRAS-positive colorectal cancer.

Enrollment in additional NCI clinical trials with TRC102 is underway. The NCI is enrolling a dual arm Phase 1/2 trial consisting of a Phase 2 cohort of TRC102 with Alimta in patients with mesothelioma; and a Phase 1 cohort of TRC102 with Alimta and Cisplatin in patients with solid tumors.

Ultimately we expect a total of 58 patients to enroll in this trial. In addition, a Phase 2 trial of TRC102 with Temodar in 66 patients with glioblastoma was recently initiated.

Finally, enrollment was also initiated in a Phase 1 trial of TRC102 in combination with chemotherapy and radiation therapy in patients with lung cancer sponsored by our collaborators at Case Western.

As you can see, we remain very active on the clinical development front and look forward to highly productive 2016 with multiple potential value enhancing events; including a number of key pipeline related milestones.

Importantly, we continue to advance our progress in a cost-effective manner to the TRACON clinical operations team that manages domestic clinical trials without the significant costs or complexities associated with outsourcing to its CRO.

We are working to extend our highly efficient model to the European Union as well, which should facilitate the planned studies in angiosarcoma and GTN that are expected to begin soon.

From a financial perspective, we continue to anticipate that our current cash resources will fund operations to mid-2017 and be sufficient to deliver the primary endpoint of the ongoing randomized Phase 2 studies of TRC105, support manufacturing activities at Lonza required for regulatory approval, and initiate Phase 3 clinical development in angiosarcoma.

Beyond our internal pipeline we also continue to evaluate product candidates to potentially end license and tend to be opportunistic in this regard. Ideal candidates would leverage the cost effective internal clinical operations capacity at our company.

At this time, I will turn 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 $0.8 million for the three months ended June 30, 2016, and $2 million for the six months ended June 30, 2016, compared to $4.2 million and $5.3 million for the comparable periods of 2015.

The decreases are primarily attributable to a $3 million cash milestone triggered by Santen's filing of an IND in wet AMD in June 2015. Total operating expenses were $8.8 million for the second quarter and $16.3 million for the six months ended June 30, 2016, compared to $6.9 million and $11.7 million for the comparable periods of 2015.

These increases reflect higher expenses in both R&D and G&A. Research and development expenses were $6.8 million for the second quarter and $12.3 million for the six months ended June 30, 2016, compared to $5.4 million and $9.2 million for the comparable periods of 2015.

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 $2 million for the second quarter and $4.1 million for the six months ended June 30, 2016, compared to $1.5 million and $2.5 million for the comparable period of 2015. These increases were primarily attributable to the higher personnel costs resulting from increased headcount.

Our net loss was $8.3 million for the second quarter and $14.8 million for the six months ended June 30, 2016 compared to $2.9 million and $6.9 million for the comparable periods of 2015.

Turning to the balance sheet, at June 30, 2016, our cash, cash equivalents and short term investments totaled $36.2 million compared to $52.2 million at December 31, 2015. As Charles mentioned, we expect our capital resources to be sufficient to fund our currently planned operations to the middle of 2017.

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

Thank you, Patricia. As we noted, we expect a significant number of potential value-creating milestones in the near future. Most important, is the initiation of our pivotal Phase 3 trials, which will be in the orphan drug indication of angiosarcoma, and will commence following concurrence from U.S. and European regulations on trial design.

In addition, in November, we expect to provide an update on data from ongoing and newly enrolled angiosarcoma patients in our current Phase 2 trial at the CTOS meeting, will present preclinical fibrosis data at the AASLD meeting.

Later this year, we expect to initiate dosing of TSC105 in the Phase 2 trial in GTN, a phase that could be registration enabling. By the end of the year, we expect top line Phase 2 data from the NCI randomized glioblastoma trial, and by the first half of 2017, we expect top line data from a randomized Phase 2 TRAXAR renal cell cancer trial.

I look forward to providing further updates regarding our upcoming key milestones throughout 2016. I am confident we have the right strategy in place to deliver on our development and business plans for the benefit of patients and shareholders alike. With that, we will be happy to answer your questions..

[Operator Instructions]. Our first question is from Chad Messer of Needham and Company. Your line is open..

Great. Thanks for taking my questions. So Charles, I know your clinical development model is so far involved not using CROs and you have talked several times about the benefits of that.

Although in the past, I think you said, when you got to Phase 3, that maybe you would, but based on comments you just made in your remarks, it sounds like that's not your intention for the angiosarcoma trial.

Just wondering, if that decision is based on that just being a smaller type of Phase 3, or you alluded to expanding your capabilities to Europe? Is this a longer term play to have more capabilities, so maybe you could handle even larger trials in the future?.

All right Chad, great question. I think it really comes to both the ideas you discussed. So I think first of all, angiosarcoma lends itself to this type of operational model, in a sense that we really know the key investigators in the U.S. and EU, it is a relatively small community.

And importantly, in the EU, care is very nicely centralized with respect to treating rare sarcoma subtypes. So given that, involving the European sites and incorporating that into our model makes a lot of sense, and it's really facilitated by studying an orphan drug indication like angiosarcoma.

As you talk about a larger study, I think it’s a study-by-study question. GTN is another small indication where we also expect to be able and have identified key sites in Europe that we can implement the study using our model.

As you look at a large global say Phase 3 lung cancer trial, that's a separate decision and we have to kind of cross that bridge when we come to it. So at least the early stage orphan drug indication trials, dutifully lend themselves towards implementing our model across the pond that we are currently doing in the U.S..

All right. Thank you. That makes sense. I guess, even that said, 124 may be as many as 200 patients is still a pretty good sized trial.

Just wondering if it's possible to get more of a sense of what that impact is going to be on your spending going forward? I know you have got guidance of cash in mid 2017, but how big is that angiosarcoma relative to all the other things you are spending on?.

Yeah. I mean, one way to put in perspective Chad is, you know, at the renal cell cancer trial they were enrolling currently, which was 150 patients.

So we have already experienced implementing a trial of a size similar to what the base for angiosarcoma study is, and we have been able to do that comfortably within our current budgets, and that's going to be true with the angiosarcoma Phase 3 as well..

All right. And then -- and I just apologize, I can't write and take in information quite as fast as you can say it, I believe you talked about measuring endoglin levels on circulating tumor cells in the angiosarcoma Phase 3 study, and if you thought you had some correlations there, maybe going back to sarcoma at large.

And I was just wondering if you could, maybe one more time explain why you thought that would be successful versus the endoglin correlations that you already tried to do in general sarcoma?.

I think it really comes down to sampling the patient at the appropriate time in their clinical history. Archival tumor tissue unfortunately in sarcoma, usually means sampling the patient at the primary diagnosis years ahead of when they actually come on to our trial, they had chemotherapy, tumor is inherently heterogeneous.

And so it just may not represent the patient's disease at the time you are assessing them on trial. The CTCs have the advantage and that you are assessing that at the time they come on to your trial.

And so -- in angiosarcoma, we think there will be some differences in the end of expression of certain angiosarcomas versus the others, for instance, patients with CTCs that express endoglin are most responsive in our angiosarcoma Phase 3.

That will give us the idea, that maybe we can take that observation and translate into more general sarcoma population, with the key advantage being that we are assessing the patient at the time they come on trial, as opposed -- based on some tissue, that was procured in a retrospective fashion, in many cases years before they were actually treated with TRC105..

All right, thanks. That makes a lot of sense..

Appreciate your questions, Chad. Thank you..

Thank you. Our next question is from Tom Shrader of Stifel. Your line is open..

Good afternoon..

Hi Tom..

Congratulations on carotuximab, that's remarkably pronounceable for the recent --.

Appreciate it..

A lot of them are just horrendous. A little bit to where Chad was just questioning; in angiosarcoma, you have treated how many patients? And if I am getting into embargoed areas, I apologize, but there is an expansion of nine, is that right, and you are quoting four.

Are you not quoting others, or just run us through what you have done in angio and talk about it so far?.

Absolutely Tom. So yeah, we treated five patients initially as part of the original Phase 2 study, and then we opened up the 13 patient angiosarcoma cohort, which is now growing very nicely. Of that cohort, four patients were treated initially with TRC105 and Votrient, and those patients were recorded at ASCO.

Some other patients on that expanded cohort initially treated with TRC105 as a single agent, and then at the time that they progressed, they are then allowed to receive the combination, and those are patients that will update data at CTOS.

And in addition, we are going to enroll more patients beyond just the initial 13 patient cohort, until we open the Phase 3, they won't receive a combination of both TRC105 and Votrient, just to give those patients a place to go, that's an incredible unmet depopulation.

So in summary, so far, we have released data on nine patients, five from the original cohort, or from the angiosarcoma specific cohort that have received the combination from day one. Additional patients have received TRC105 as a single agent and then will convert to the combination.

The reason we are doing that, is just to see if there is significant single agent activity to justify expiration there. We don't think there will be. We think it's absolutely essentially that you concurrently inhibit both the VEGF and the endoglin pathways concurrently in order to see optimal activity.

But I think we need to show that for sure, as we have seen complete response with the combination, and we want to make sure that they are not something we would see with single agent TRC 105 as well..

Sounds like you are back to the endoglin levels must matter hypothesis.

I kind of feel that maybe that had -- you had backed off that after the all comer sarcoma data, but now it -- is it just a sense that it has to be relevant, or has there been some data that has you back kind of thinking about that?.

The way I think about it -- I think there are certain tumors where the endothelial cell is the cancer and is driving the entire tumor. That's angiosarcoma, that's a malignancy of endothelial cells, which are dense endoglin expressing cells.

That's choriocarcinoma, which is also malignancy of placental tissue, which is pure vascular tissue, which also reflects endothelial tissue, and that will dense express endoglin as well. So I think that certain tumors, where the endothelial cell biology drives that cancer.

I think that's where we will be especially active, and that's where we are seeing durable complete responses, both of those indications. So I think, there is one category of endoglin biology driving cancer, where I think we are going to continue to see robust activity.

Outside of that tumor type, for instance, general sarcoma; there are certain sarcomas, where we, at least in our [indiscernible] assessment, you will see endoglin tumor expressions, in certain ones, you will not.

There we still think there is a chance, that endoglin tumor expression will still drive disease and thereby, those tumors will be more susceptible to therapy. I just think we have to classify those tumors more in a relevant context. Meaning, when they come on to trials as opposed to relying on archival specimen, they dictate that.

So I'd say there are two categories; the tumors where endoglin biology drives the disease, which is endothelial cell based cancers, and then the broader population say, of sarcoma patients, where certain subtypes will continue to be responsive and identify those as key [ph]; and I would point out, we had another complete response in that sarcoma trial that was running on a angiosarcoma patient.

That patient clearly is responsive to therapy. We have to be able to identify those patients and the CTC approach makes a lot more sense, because of the acute interrogation versus the retrospective interrogation that archival tumor tissue represents..

Okay. And with the TRC102 bullet point, that's as high as I have ever seen a TRC bullet point in your standard list? It's usually more like 12 or 13.

So do you feel these data are pretty definitive? I mean, just looking at these numbers, but are these numbers where you would never have seen a response to straight Temodar?.

I think 1 or 2 is becoming more and more exciting to us, and I think also, the NCI remains very excited by that program. I think the excitement around that post was palpable at ASCO. Those are three tumor types, we are outlaying therapies not considered to be highly active.

So seeing those partial [ph] responses, and I had mentioned that three of those responses for durable last more than six months, was extremely encouraging. And that's why there is continued excitement and that's why now there is a Phase 2 study with Temodar 1 and 2 in glioblastoma.

So I do think those are meaningful responses, and I do think we will see more definite data coming out of Phase 2..

Right.

And were all these patients at the go forward dose, or is there some dose escalation in here? So maybe the fraction of responders could be better?.

Agree with you on that point. But every patient in that trial was at the go forward. Of course, the significant dose escalation was part of that trial..

Okay. And then just real quick on TRAXAR; you are expanding to stay in sort of uncorrupted second line.

Are you determined to do that, rather than to try to say after some of the new drugs, is that what's going on?.

Absolutely Tom. I think it's absolutely critical that we stay in patients that have HER1 and only one VEGF inhibitor. If you are going to allow multiple VEGF inhibitors and have an incredibly affected [ph] population, you are going to damage your ability to the efficacy.

I think to our credit, we recognize that there was going to be advancement in the standard of care in renal cell cancer. When we say we dose now in the European Union, that reflects planning that started last year. So this is an expected development we planned for, now sites opening across four European countries that will support this trial.

And that allows us to, as you said, maintain a trial that's not corrupted by compromising the eligibility criteria..

All right. Perfect. Thanks for all the color, Charles..

Appreciate the questions Tom..

Thank you. [Operator Instructions]. Our next question is from Jim Birchenough of Wells Fargo. Your line is open..

Hi guys. Thanks for the update, a few follow-ups; just wanted to follow-up on the Phase 3 -- I want to make sure I heard 67% risk reduction.

So is that -- are you talking about a hazard ratio of 0.33, is that right?.

Jim, thanks for your question. The hazard ratio is 0.67. So as an example, based on previous studies of Votrient as a single agent in angiosarcoma, the mean PFS is in three months, which emphasizes how tough a disease that is. So we would be looking to take mean [ph] PFS from three to five months, which represent a hazard ratio of 0.67..

And if you had to take it to 200 patients, what would the study be powered to attack at that patient level in those events?.

So to power at 124 patients at 80% as we discussed, if you push it to 200 patients, you will preserve that power level and possibly have a higher power level. So it's not a fixed patient design. So it never gives you the exact power, that if you went straight [indiscernible], the fixed design of 200 patients, you get that power level.

So what it will do is guarantee the power will always be 80% or better, by allowing that adaptation if you will..

Got it.

And then just following up on endoglin levels; can you remind us -- have there been any tumor types yet, where we validated endoglin levels as determining responsiveness to 105 and is there plans to look at circulating tumor cells outside of sarcoma perhaps, in ADCC or other indications?.

It’s a great question on the CTC aspect. I think, once we move forward with respect to implementing the CTC analysis in the Phase 3 angiosarcoma trial, we will consider for other studies to your point. I do think, and this points a little bit to my response to Tom's question, angiosarcoma is the ultimate validation for endoglin tumor expression.

Angiosarcoma is an endothelial cell malignancy, highly expressed endoglin virtually on every single case, 19 out of 20 cases that were assessed by archival tumor tissue analysis. So I think that in essence has validated our approach that, tumors that highly express endoglin angiosarcoma have been the most responsive to therapy.

The key now is to try to take that into other tumor types, general sarcoma included..

And then just a final question, and it relates to your cash runway; mid 2017 is a tremendously long cash runway.

So what non-dilutive gains might you have to extend that runway, and is there any -- when you look at the spend right now and say, we think we had the biggest thing for our block in angiosarcoma and GTN, what proportion of your spending is that, if you needed to kind of narrow the spend to extend the runway? I am just trying to get a sense of how we can push that beyond mid 2017?.

Sure. I think, in terms of non-dilutive ways to try capital at TRACON, I put those in three categories; one is our continued relation with Santen in AMD. We expect additional development stage milestones in that relationship that will help extend the runway.

And then second, is the opportunity to partner TRC105 in oncology, which we think also could attract non-dilutive attract between now and 2017. The third would be potential partnership in fibrosis, which also could attract capital and significant capital.

I would remind to you that, we did do a preclinical deal in AMD with Santen in 2014 which was a double digit upfront payment to TRACON. We think the fibrosis program potentially is as valuable, if not more valuable. So I think those are three areas where non-dilutive capital could help us between now and mid 2017.

In terms of the angiosarcoma experience, that is a significant -- part of the spend I would say is not an overwhelming part of the spend, in a sense that internalized operations model makes that trial doable at a cost that is much-much less than you would associate with a typical Phase 3 trial.

So we could improve the runway by delaying that study, but that's not our intent. Our intent is to continue that study on track, initiate the trial in the fourth quarter of this year, and in the meantime, to attract additional capital to the company, whether by non-dilutive financing, or potentially through a capital raise..

Yeah. I guess where I was coming from Charles, is the opposite of angiosarcoma and GTN seemed to be where you had your strongest results.

But you are really going -- and your are pursuing a very broad development plan and would you perhaps narrow all your development plans to extend your cash runway for angiosarcoma and GTN, I guess, is what I am wondering?.

I think if you look at where we build that, that spend would be relatively incremental, at least for instance -- the trials that are driving capital expense is renal cell, which, again is moving forward quite nicely, given the European sites now enrolling. Liver cancer is a relatively small trial, it has not cost us a lot of capital.

Our Phase 1 trial has cost us incredibly low amount of capital.

I mean, probably the biggest spend that we don't talk about, Jim, is the CMC, which is the production of antibody by Lonza, that will support, such as the product with the angiosarcoma Phase 3, but also, we are beginning registration enabling studies, so that we will be ready to file a BLA from a CMC perspective, that complements where we are from a clinical development perspective.

So those are important elements that are the priorities for the company. The majority spend moving forward will be the CMC to support registration and the angiosarcoma, those will be the two major spends from a clinical development perspective, and also from a CMC perspective.

And we will remain -- we will do that in a very capital efficient manner, and we will raise capital to support those programs. In terms of limited spend in other areas, I don't think it will make a material difference in terms of where our runway goes for the short term..

Thanks for taking the questions Charles..

Great questions. Thanks Jim..

Thank you. At this time, I see no other questions in queue. I'd like to turn it back to Dr. Theuer for any closing comments..

Well thank you everyone, especially call participants for their time and questions. Have a nice day. We look forward to speaking with you again soon..

Ladies and gentlemen, thank you for your participation in today's conference. This concludes your program. You may now disconnect..