TRACON Pharmaceuticals Inc (TCON) 2016 Q2 法說會逐字稿

Good day, ladies and gentlemen, and welcome to the TRACON Pharmaceuticals second quarter 2016 earnings conference call. (Operator Instructions)

During today's call, we will be making 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, subsequently, 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 update such statements.

Now I'd 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 lead product candidate, TRC105, which now has been designated carotuximab as its International Nonproprietary Name by the World Health Organization. We will review recent ASCO presentations and progress toward 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 TRC105 and Votrient. In addition, these data were highlighted during the poster discussion session by Dr. Mrinal Gounder of Memorial Sloan Kettering Cancer Center.

All five angiosarcoma patients discussed had radiographic tumor reductions, and median 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 RECIST that remain ongoing at 17 and 24 months, respectively.

Activity was also seen in four additional patients enrolled in the 13-patient angiosarcoma-specific cohort treated with TRC105 and Votrient. A patient with visceral angiosarcoma in this cohort demonstrated marked reduction of subcutaneous occipital mass 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 will enroll patient 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 patients enrolled in the 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 and utilize an 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 enroll 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 expression did not correlate with improved PFS in the general soft tissue sarcoma patients and the median PFS of approximately four months was 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 at diagnosis prior to treatment with chemotherapy rather than the status of the metastatic disease at the time of entrance into the TRC105 trial.

Tumor heterogeneity, the significant period of time between sampling and treatment and the effects of tumor evolution resulting from prior treatment could have limited the ability of archival tumor tissue to accurately 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 TRC105 in combination with Avastin in glioblastoma patients who have progressed 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 with TRC105 and Avastin in Avastin-naive 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 indications, midsized market indications and large market indications.

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're 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 US and the EU. The primary endpoint of the trial will be response rate, and we believe this trial has the potential to be registration-enabling.

In addition to the glioblastoma development which I discussed earlier, we are also studying a number of other midsized market indications with short time to 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 US 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 accrual. Despite this, we are slightly adjusting our time line and now anticipate completing enrollment and delivering data 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 patients with the primary endpoint of overall response rate. The goal of this study is to validate the robust 40% response rate that was observed in the 10 patients treated at recommended Phase 2 dosing of TRC105 with Nexavar that was reported by the NCI 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 our 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 mean percentage of CD4 positive regulatory T cells in peripheral blood decreased following TRC105 treatment. Regulatory T cells have been implicated 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, earlier this year, we dosed the initial patients in two large market indication trials: a Phase 1 trial of TRC105 in combination with Avastin in chemotherapy for the first-line treatment of patients with lung cancer; and a Phase 1/2 trial of TRC105 in combination with Afinitor and Femara for the neoadjuvant 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 the 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 product candidate, TRC102. TRC102 is a novel small molecule inhibitor of the DNA repair -- base excision repair pathway. Activation of this pathway improves resistance to alkylating and antimetabolite chemotherapeutics resulting in poor outcomes.

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

Enrollment in additional NCI clinical trials of 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 a 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 through the TRACON clinical operations team that manages domestic clinical trials without the significant cost or complexities associated with outsourcing to a CRO. We are working to expand 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 in-license and intend 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 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 $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 periods of 2015. These increases were primarily attributable to 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'll 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 initial pivotal Phase 3 trial, which will be in the orphan drug indication of angiosarcoma and will commence upon concurrence from US and European regulators 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, and we'll present preclinical fibrosis data at the AASLD meeting.

Later this year, we expect to initiate dosing of TRC105 in a Phase 2 trial in GTN, a study 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 our 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 & Company. Your line is open.

Great. Thanks for taking my question. Charles, I know your clinical development model so far involved not using CROs, and you've 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?

Great question. Yes, I think it really comes to both the ideas you discussed. I think first of all angiosarcoma lends itself to this type of operational model in the sense that we really know the key investigators in the US 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 the 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. But at least the early stage orphan drug indication trials beautifully lend themselves toward implementing our model across the pond in the EU as we are doing currently in the US.

All right. Thank you. That makes sense. I guess, even that said, 124 or maybe 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 we've got guidance of cash to mid 2017, but how big is that angiosarcoma relative to all the other things you are spending on?

Yes. I mean, one way to put it in perspective Chad is, the renal cell cancer trial that we're enrolling currently, for instance, is 150 patients. So we have already experience implementing a trial of a size similar to what the Phase 3 angiosarcoma study is, and we may be 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 good 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.

All right. Yes, I think it really comes down to sampling the patients 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've had chemotherapy. Tumor is inherently heterogeneous and so it just may not represent the patient's disease at the time you're assessing them on trial.

The CTCs have the advantage in that you're assessing that at the time they come onto your trial. And so in angiosarcoma, we think there will be some differences in endoglin expression on certain angiosarcomas versus the others. And if 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 it into a more general sarcoma population, with the key advantage being that we're assessing the patient at the time they come on trial as opposed to 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.

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

Good afternoon. Congratulations on carotuximab. That's remarkably pronounceable for the recent (inaudible). A lot of them are just horrendous.

A little bit to where Chad was just questioning. In angiosarcoma, you've treated how many patients? And if I'm getting into embargoed areas, I apologize. But there's an expansion of nine, is that right, and you're quoting four?

Are you not quoting others? Or just run us through what you've done in angio that you can talk about so far.

Sure. Absolutely, Tom. So yes, 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 accruing very nicely. Of that cohort, four patients were treated initially with TRC105 and Votrient and those patients were reported at ASCO.

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

And in addition, we're going to enroll more patients beyond just the initial 13-patient cohort until we open the Phase 3 that will receive the combination of both TRC105 and Votrient. Just to give those patients a place to go. That's an incredible unmet need population.

So in summary, so far, we've released data on nine patients, five in the original cohort, four 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're doing that is just to see if there's significant single-agent activity to justify exploration there. We don't think there will be. We think it's absolutely essential 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 responses with the combination. And we want to make sure that they're not something we would see with single agent TRC105 as well.

And it sounds like back to the endoglin levels must matter hypothesis, I kind of felt like maybe that had -- you'd backed off that after the all comers sarcoma data. But now it's -- I mean, is it just the sense that it has to be relevant or has there been some data that has you back kind of thinking about that?

No, the way I'm thinking about it -- I think there are certain tumors where the endothelial cell is the cancer and it's 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 a malignancy of placental tissue which is pure vascular tissue which also reflects endothelial tissue and that will densely express endoglin as well.

So I think that certain tumors where the endothelial cell biology drives that cancer, I think that's where we'll be especially active and that's where we've seen durable complete responses -- both those indications. So I think there is one category of endoglin biology driving the cancer where I think we're going to continue to see robust activity.

Outside of that tumor type, for instance, general sarcoma, there are certain sarcomas where we, at least, on archival specimens, you'll see endoglin tumor expressions, certain ones you will not. There we still think there's a chance that endoglin tumor expression will still drive the 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 onto trial as opposed to relying on archival specimens to dictate that.

So I'd say there are two categories, the tumors where endoglin biology drives the disease, which is then endothelial-based cancers. And then the broader population, say, of sarcoma patients where certain subtypes will continue to be responsive and identifying those as key.

And I would point out, we had another complete response in that sarcoma trial that was a non-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 the TRC102 bullet point, that's as high as I've ever seen a TRC102 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, it's just looking at the numbers, but are these patients where you would never have seen a response to straight Temodar?

Yes, I think 102 is becoming more and more exciting to us. And I think also the NCI remains very excited about that program. I think the excitement around that poster was palpable at ASCO.

Those are three tumor types where alkylating therapy is not considered to be highly active. So seeing those partial responses -- and I've mentioned that three of those response were durable, lasting more than six months -- was extremely encouraging. And that's why there's continued excitement. That's why now there's a Phase 2 study with Temodar 102 in glioblastoma.

So I do think those are meaningful responses. And I do think we'll see more definitive data coming out of Phase 2.

Right. And were all those 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 that not every patient treated in that trial was at the go-forward dose, as opposed to a significant dose escalation as part of that trial.

Okay. And then just real quick on TRAXAR. You're expanding to stay in sort of uncorrupted second line. Is that -- are you determined to do that rather than to try this, 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 failed one and only one VEGF inhibitor. If you're going to allow multiple VEGF inhibitors and have an incredibly fractured population, you're going to damage your ability to see efficacy.

I think to our credit, we recognized that there was going to be advancement in the standard of care in renal cell cancer. When we say we've dosed now in the European Union, that reflects planning that started last year.

So this is an expected development. We planned for it. We now have 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.

(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 -- you're talking about a hazard ratio of 0.33. Is that right?

The hazard -- sorry, Jim, and 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 median PFS has been three months, which emphasizes how tough a disease that is. So we'd be looking to take median PFS from three to five months which would represent a hazard ratio of 0.67.

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

Yes. So the power at 124 patients is 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 a priori to fixed design 200 patients you'd get that power level, but 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 -- are there -- have there been any tumor types yet where we've validated endoglin levels as determining responsiveness to 105? And is there plans to look at circulating tumor cells outside of sarcoma perhaps in HCC or other indications?

Yes, 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 further studies to your point.

Yes, I do think -- and this plays a little bit to my response to the second of Tom's questions. In a sense angiosarcoma is the ultimate validation for endoglin tumor expression. Angiosarcoma as an endothelial cell malignancy highly expresses endoglin virtually on every single case, 19 out of 20 cases that were assessed by archival tumor tissue analysis.

So I think that in a sense has validated our approach that tumors that highly express endoglin like 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 isn't a tremendously long cash runway. So what non-dilutive means might just have to extend that runway?

And is there any -- when you look at the spend right now and say we think we're going to get the biggest bang for our buck from angiosarcoma and GTN, what proportion of your spending is that, if you needed to kind of narrow the spend to extend the runway? I'm just trying to get a sense of how we can push that beyond mid-2017.

Sure. Yes, I think in terms of non-dilutive ways to track capital at TRACON, I'd 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 the second is the opportunity to partner TRC105 in oncology, which we think also could attract significant non-dilutive capital between now and 2017.

The third would be potential partnership in fibrosis, which also could attract capital and significant capital. I would remind 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 but I would say it's not an overwhelming part of the spend in the sense that 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 fourth quarter this year and in the meantime to attract additional capital to the company whether by non-dilutive financing or potentially through a capital raise.

Yes. I guess where I was coming from, Charles, is the opposite, that angiosarcoma and GTN seem to be where you've had your strongest results, but you're really going -- you're pursuing a very broad development plan. And would you perhaps narrow your development plan to extend your cash runway for angiosarcoma and GTN, I guess is what I'm wondering.

Right, right. Yes, I think if you look at where we -- that spend would be relatively incremental if we -- 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 not just the product for the angiosarcoma Phase 3, but also we're beginning registration-enabling studies so that we'll 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 of 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'll remain -- we'll do that in a very capital efficient manner, and we'll raise capital to support those programs.

In terms of limiting 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.

Got it. Thanks for taking the questions, Charles.

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.

Great. Well thank you everyone especially the call participants for the 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.