Charles Theuer - President and CEO Patricia Bitar - Chief Financial Officer.

Tom Shrader - Stifel Nicolaus Chad Messer - Needham & Company Bert Hazlett - BTIG.

Good day, ladies and gentlemen, and welcome to the TRACON Pharmaceuticals Third Quarter 2017 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 Securities and Exchange Commission, including our annual report on Form 10-K for the year ended December 31, 2016, and subsequent quarterly reports on Form 10-Q.

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 thank you for joining us today for TRACON’s third quarter 2017 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, who will review our financial results for the three and nine months ended September 30, 2017. Finally, we will conclude by taking your questions. Let’s begin with our lead product, TRC105, which has the non-proprietary name, carotuximab.

We continue to enroll angiosarcoma patients in a randomized Phase 3 TAPPAS trial. We have opened more than 20 sites in the United States and expect to initiate several European sites by year-end. As a reminder, the initial TAPPAS sample size of 124 patients is designed to detect an improvement of PFS from four to seven months.

In addition, the trial uses an adaptive design that allows for expansion of patient numbers while preserving type 1 error. The design includes an interim analysis we expect to conduct in the second-half of 2018 that should provide substantial insight into the progress of the trial.

In the meantime, we will present updated Phase 1/2 data from angiosarcoma patients treated with TRC105 and Votrient at the Connective Tissue Oncology Society Annual Meeting later this week on November 9.

We believe that TRC105 has broad potential, and TRACON continues to execute on its tier development strategy that includes orphan drug indications, mid-size market indications, and large market indications. In addition to the pivotal TAPPAS trial in angiosarcoma, TRC105 continues to advance in Phase 2 studies in two mid-market indications.

First, we completed accrual of 150 patients into the Phase 2 randomized TRAXAR trial that compares treatment with TRC105 and Inlyta to treatment with single agent Inlyta in patients with clear cell renal cell cancer.

Based on the current rate of events of progression or death that defined the primary endpoint of PFS, we expect to report top line data early next year.

We expect the study to have at least 80 events confirmed by the independent central review committee at the time of the data readout, which should provide at least 70% power to detect an improvement in PFS from 4.8 months with Inlyta to 7.2 months with the combination of TRC105 and Inlyta.

PFS will also be assessed based on predefined levels of two soluble biomarkers, osteopontin and TGF-β receptor III, which correlated with response in the Phase 1b portion of the trial.

Second, we continue to enroll the multi-center Phase 2 trial of TRC105 and Nexavar in liver cancer, where we expect to report safety and initial response data in early 2018.

The goal of this trial is to reproduce the response rate of a completed Phase 1/2 trial of TRC105 and Nexavar in patients with liver cancer that was conducted by the NCI and published in the journal Clinical Cancer Research in August, and in fact, concluded that combination of TRC105 and Nexavar was well tolerated at the recommended single agent doses of both drugs.

Further, the combination demonstrated median overall survival of 15.5 months in all patients, as well as partial response by RECIST in 5% of 15% or 33% of patients treated at the two highest dose levels of TRC105 with Nexavar.

Both of these data points compare favorably with historical single agent Nexavar pivotal trial data that showed a response rate of 2% to 3% by RECIST and overall survival of 10.7 months or less. We also opened the initial site for the Phase 1 trial of TRC105 in combination with Opdivo in patients with non-small cell lung cancer.

The design of this trial was presented at the World Conference on Lung Cancer in Yokohama in October. Opdivo is approved for the treatment of second-line lung cancer with a response rate of approximately 20% in this pivotal trial.

Endoglin is expressed on activated myeloid derived suppressor cells, a cell type implicated in tumor resistance to immunotherapy. And we have observed encouraging activity of endoglin antibodies in combination with PD1 inhibitors in preclinical, syngeneic mouse tumor models.

We expect to present these preclinical, as well as clinical trial data at scientific conferences next year. Data from a Phase 1 trial of TRC105 with a VEGF inhibitor in chemotherapy were also presented at the World Conference on Lung Cancer.

The combination of TRC105, Avastin, Taxol, and Carboplatin was well tolerated, and three of eight evaluable patients or 37% demonstrated a partial response by RECIST. The trial is expected to enroll a total of 18 patients.

In addition, based on activity observed in preclinical models, we have begun discussions with pediatric oncologists to design a trial with TRC105 in combination with approved therapeutics in children with neuroblastoma, which could be funded through a cooperative group.

We also continue to discuss clinical investigation of TRC105 in AML, based on data published in the Journal Blood demonstrating endoglin expression on the majority of blasts from AML patients and activity of TRC105 on AML in mouse models.

Neuroblastoma and AML are malignancies with high unmet needs that may represent additional development opportunities for TRC105. Turning now to DE-122, the ophthalmic formulation of TRC105. Considerable progress has been achieved this year in this product candidate’s development for wet AMD by our partner, Santen.

What we had hoped that Santen would report data from the Phase 1/2 PAVE trial at the American Academy of Ophthalmology Annual Meeting in November, the full data set was not available at the time of the abstract submission deadline and the abstract was not selected for presentation.

We now expect that Santen will present the full data set at an ophthalmology conference in the first-half of 2018.

Notably following their evaluation of the safety and bioactivity data from the Phase 1/2 PAVE trial, Santen initiated dosing in the Phase 2 randomized AVANTE study that compares treatment with two different doses of DE-122 combined with Lucentis to treatment with single agent Lucentis in patients with wet AMD.

Trial initiation triggered a $7 million milestone payment to TRACON, which we received during the third quarter. We believe there is a substantial opportunity for agents that target essential angiogenic pathways like endoglin to be developed in combination with VEGF inhibitors for wet AMD.

Recent negative data from companies conducting two separate late-stage studies targeting the PDGF pathway in combination with VEGF inhibitors in wet AMD underscore the high unmet need remaining in this indication. We’ll turn now to our second product candidate, TRC102.

TRC102 is a novel small molecule inhibitor of the DNA base excision repair pathway that is intended to reverse resistance in certain chemo therapeutics.

Based on positive safety, PK and efficacy data of the combination of TRC102 and Temodar, which were presented at ASCO earlier this year, the NCI continues to enroll patients with ovarian, lung and colorectal cancers, which were the tumor types responded to treatment in the Phase 1 trial.

An additional Phase 2 NCI sponsored trial of TRC102 and Temodar in patients with glioblastoma has completed the first stage of accrual.

In addition, a dual arm Phase 1/2 trial consisting of a Phase 2 cohort of TRC102 with Alimta in patients with mesothelioma and the Phase 1 cohort of TRC102 with Alimta and cisplatin in patients with solid tumors is also enrolling.

Finally, our collaboration with Case Western are dosing patients at a Phase 1 trial with TRC102 in combination chemotherapy and radiation therapy in patients with lung cancer. We expect the NCI and Case present data from these trials in 2018.

As part of these studies, we will assess patient tumor samples to determine whether preclinical data showing that Gly pathways expression predicts tumor sensitivity to TRC102 will be validated in the clinic. Late last year, we in-licensed two oncology assets from Janssen.

The first is TRC253, a novel potential best-in-class treatment for prostate cancer. It is a small molecule competitive inhibitor of wild-type androgen receptor and androgen receptor mutations that confer resistance to Xtandi and other drugs approved to treat prostate cancer.

TRC253 is being studied in a Phase 1/2 trial to assess its safety, determine its recommended Phase 2 dose and assess response by PSA levels.

In the Phase 2 portion of the trial, we will incorporate circulating tumor DNA testing in order to allow for biomarker directed therapy of patients who progressed following treatment with an androgen receptor inhibitor.

We are currently dosing the Phase 1 portion of the trial and expect to complete dose escalation and present details of the Phase 2 trial design in early 2018.

If Janssen opts to reacquire the asset prior to or following completion of the Phase 1/2 trial, TRACON will be entitled to receive a $45 million opt-in payment in addition to up to $137.5 million in potential milestones and a low single-digit royalty on any sales.

The Janssen transaction also brought TRC694, a novel small molecule potent inhibitor of NF-kappaB inducing kinase or NIK, that is intended for the treatment of patients with hematological malignancies, including myeloma.

TRACON has an exclusive license to TRC694, and Janssen retains the right of first negotiation should we decide to partner the asset. We continue to perform IND enabling studies with TRC694 and expect to file an IND in 2018.

As you can see, we remain very active on the development front and look forward to a highly productive remainder of 2017 and early 2018 with multiple potential bio enhancing events, including a number of key pipeline-related milestones.

Importantly, we continue to achieve our progress in a cost-effective manner by leveraging the TRACON product development platform that is managing our international Phase 3 TAPPAS trial for TRC105 in angiosarcoma without the significant cost or complexity associated with outsourcing to a global CRO.

We believe that Janssen licensing agreement provides validation of our drug development model, and we continue to evaluate additional assets that can leverage our product development platform for the benefit of TRACON and its shareholders.

From a financial perspective, we believe that our existing cash resources will fund currently planned operations to mid 2018.

And we’ll be sufficient to deliver initial response rate data from the multicenter Phase 2 trial of TRC105 in liver cancer, final data from the randomized Phase 2 TRAXAR renal cell cancer trial, safety and bioactivity data from the Phase 1/2 PAVE study in wet AMD, allow transition to the Phase 2 portion of the Phase 1/2 trial of TRC253 and prostate cancer, and support planned manufacturing activities at Lonza for TRC105.

In addition, available financing from our agreement with Aspire Capital provides flexibility to further extend our cash runway. 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 $7.5 million and $8.8 million for the three and nine months ended September 30, 2017, respectively, compared to $0.8 million and $2.8 million for the comparable periods of 2016.

The increase in the 2017 period compared to the 2016 period is primarily attributable to a $7 million milestone earned upon Santen’s initiation of their Phase 2 AVANTE trial in July 2017.

Research and development expenses were $4.3 million and $14.7 million for the three and nine months ended September 30, 2017, respectively, compared to $4.5 million and $16.8 million for the comparable periods of 2016. These decreases were primarily the result of decreased manufacturing expenses related to TRC105 in both of the 2017 periods.

General and administrative expenses were $1.8 million and $5.9 million for the three and nine months ended September 30, 2017, respectively, essentially flat when compared to $1.9 million and $5.9 million for the comparable periods of 2016.

As a result of the $7 million milestone earned from Santen in the three-month period ended September 30, 2017, we had net income of $1.2 million for the 2017 three-month period, compared to a net loss of $5.9 million for the comparable period in 2016.

Our net loss for the nine months ended September 30, 2017 and 2016 was $12.5 million and $20.7 million, respectively. Turning to the balance sheet. At September 30, 2017 our cash, cash equivalents and short-term investments totaled $35.9 million compared to $32 million and $44.4 million at June 30, 2017 and December 31, 2016, respectively.

As we mentioned, we received a milestone payment of $7 million upon the initiation of the AVANTE trial by Santen in the third quarter 2017. In addition, during the third quarter, we received net proceeds of approximately $2.6 million, resulting from sales of approximately 737,000 shares of our common stock through the use of our ATM facility.

We continue to expect our capital resources to be sufficient to fund our currently planned operation to mid-2018. And with that, I will turn the call back over to Charles..

Thank you, Patricia. As we noted, we expect a number of potentially value creating milestones over the next nine months.

For TRC105, we anticipate initial Phase 2 multicenter response rate data in liver cancer and top line Phase 2 TRAXAR trial results in renal cell cancer in early 2018, and we expect the key interim analysis to determine the final study size of the pivotal Phase 3 TAPPAS trial angiosarcoma in the second-half of 2018.

For DE-122, we expect Santen to report Phase 1/2 PAVE safety and bioactivity data in AMD in the first-half of 2018. For TRC253, we expect to advance into the Phase 2 portion of the Phase 1/2 trial in prostate cancer in early 2018.

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

Thank you. [Operator Instructions] And the first question comes from the line of Tom Shrader from Stifel. Your line is now open..

Good afternoon, Charles and Patricia. Good to h ear your voices again..

Hi, Tom..

Hi, Tom..

On the HCC trial, any sense of how many patients we’ll see? And is the 2% or 3% ORR, is that the relevant number anymore, or is it the immunooncology number of more like 17%? Just your thought about what you would want to see you to remain excited about this opportunity?.

Yes. Great question, Tom. Yes. So the 2% to 3% response rate is particular to Nexavar, which is still standard front-line therapy in immunooncology – in liver cancer.

Now, as you all know, there is a comparative trial comparing Nexavar to PD1 checkpoint inhibitor that should readout in the next year or so, and potentially that might change the standard of care. I think our point is that, whether immunooncology agents use first-line and the VEGF inhibitors use second-line or vice versa.

The VEGF inhibitors are still going to be a dominant standard of care in liver cancer. You talk about a disease where frankly, there is a great need for new therapy. So having another agent on top of Nexavar, namely Opdivo, for example, would be great.

But VEGF inhibitors will still be, I think, used in that indication and a single agent will still be very poorly – have very poor efficacy. And so building – being able to build upon that as a dual therapy, I think, we’ll still have a place to play.

Yes, I think, there’s still a good chance it will still be standard first-line therapy, it could be standard second-line therapy. But either way, I think, being able to build upon VEGF inhibition in liver cancer is still a huge opportunity because of such strong unmet need in that particular indication.

That said, to further think about the immunooncology angle in liver cancer, as you know, we are now doing a trial with Opdivo with lung cancer being the initial indication just to have proof-of-concept and show safety. But clearly, that’s a combination we could push into liver cancer, we feel that’s a more productive way forward than say lung cancer.

So the ability to combine with Opdivo will present us with potentially many options in terms of different indications to pursue..

And just to follow-up on that thought and it’s a little bit of a – but the mechanistic angle there is MDSCs?.

It is, Tom. Checkpoint inhibition is really relieving the break, if you will, on T lymphocyte activity within the tumor. Really it doesn’t affect the other half of that immunosuppressive environment, which is the MDSCs.

And exactly endoglin is a marker that is highly expressed in proliferating endothelial cells in tumors like angiosarcoma, which is how it was discovered. But it’s also a myeloid stem cell marker. So it’s highly expressed in myeloid stem cells, including MDSCs and expressions further increase as those cells become activated.

And so, it’s a very good putative target for inhibiting MDSC function in conjunction with PD1 inhibition. And as I mentioned briefly, there’s the preclinical data now that validates that, that has yet to be publicly presented, but do expect to see those data points next year.

So it is a very productive path for us that we are excited to see happen, and do expect to see that trial dose very, very soon. If the site is open that’s conducting that study, which is UAB expect to see additional sites come online in that trial, but do expect to see the first patient treated at UAB in the short-term..

And just one question. So G – MDSCs are also, I think, highly indicated in GBM where things didn’t work well.

Any thought there in closing the loop?.

Yes, I think it’s still critical that to inhibit the MDSC and to see that bear fruit in the clinic, you’ve also got to inhibit the PD1 pathway. So I think, the key is not just saying, we inhibit MDSCs and that alone be sufficient for activity in an immunooncology context.

It’s going to be significant, we hope, in the context of inhibiting the other arm of that immunosuppression, which is the T lymphocyte arm. In other words, if your T lymphocytes are shutdown, whether you liberate the MDSCs, in our view, it’s not going to be sufficient.

The T cell has to be activated through releasing the brake on them through PD1 inhibition and then releasing the brake on the MDSCs could be important in terms of augmenting the effect of immune checkpoint inhibition..

Okay, sounds good. Complicated, but good. Thanks for that questions..

I appreciate it, Tom, as always..

Thank you. And our next question comes from the line of Maury Raycroft from Jefferies..

Hi, this is Michelle [ph] on for Maury. I was just wondering…..

Hi, Michelle..

Hi, how are you?.

Good. Thank you..

So I just had a question on 105 in renal.

Can you walk us through kind of what you are thinking would constitute a positive outcome that would give you confidence to move forward? And then sort of adding on to that, what do you want to see in terms of data sets in your biomarker population? And what kind of delta between the two populations would give you confidence that’s a valid biomarker here?.

Right. Great points, Michelle. So, the overall study is designed to detect an improvement in PFS from an assumed baseline of 4.8 months to 7.2 months with the combination of Inlyta and TRC105. So hitting that endpoint, I think, would be very important to us, and we have expected, at least, 70% power to hit that endpoint.

If you start looking for a greater treatment effect, for instance, if you want to plan or expect to see roughly a three-month improvement from 4.8 months to roughly 7.7 months, you will actually have 80% power to detect that difference.

And I think, if we see anything in that ballpark, 2.5 to three-month improvement overall, will be very excited to have hit endpoint in that trial. I think, even more exciting would be the prospect that a biomarker would predict activity.

And so, if we saw, for instance, the same degree of improvement, say, a 2.4 to a three-month improvement in a biomarker selected population, say, for example, patients with high TGF-β receptor III levels, that would be an absolutely huge advance for the program.

In renal cell, no one has yet to show that a biomarker clearly predicts activity of their drug. If we’re able to show that, I think, we can very nicely carve out a population of patients that should frankly be on our drug in combination with Inlyta and be very forceful in that conviction.

So the biomarker interrogation is an important part of that trial..

Okay.

And then what would be the next step if you do see good data there?.

Yes, great question. I think, if we have a clear biomarker enabled strategy in renal cell cancer, the thought would be to push that forward in a randomized study with the biomarker being the basis for enrollment of those patients.

In a general sense, showing activity with Inlyta will, I think, have great read throughs for other indications, where you have endoglin expression on the tumor vasculature. I think also we need to take into account where the landscape of renal cell is going.

And I think, Tom addressed the fact that immunooncology agents may make an impact on liver cancer, clearly, they’ve already made that impact in renal cell. And we are seeing a lot of trials, for example, combining checkpoint inhibitors with VEGF inhibitors in the first-line setting.

And I think it’s logical to expect those may become the dominant standard of care, namely a VEGF inhibitor like Inlyta may be first-line approved with a PD1 inhibitor. And if that’s the case, our thought would be to build upon that dual agent. So we clearly have evidence that TRC105 combines well with VEGF inhibitors.

We are in the midst of developing data that we combine with checkpoint inhibitors. And if we can show that, then the next logical step would be combining TRC105 with a combination of a VEGF inhibitor plus a checkpoint inhibitor, which could be dominant standard of care in renal cell. So we would definitely want to take that into account.

And pending our combination study with Opdivo, that might be the next logical trial in renal cell as opposed to just combining with VEGF TKI. So long answer to your question, Michelle.

But I think, what we have to do is really look at the landscape, look at the emerging data with TRC105 with checkpoint inhibitors, and see what makes the most sense from a commercial and clinical development perspective..

Okay. And then on your MDSC comments from earlier, I just was wondering if you’d seen any evidence of immune activity.

You’ve had a lot of studies with 105 and just not – yes, have you seen any evidence in immune activity in the clinic?.

Yes, great question, Michelle. So the NCI has done a couple of single arm trials with TRC105 as a single agent in bladder cancer also prostate cancer. And they did see some mild effects, I would say, mild effects on T regulatory cells, but statistically significant effects on Tregs in those studies.

So the preclinical data I talked about already, but there is also some clinical data that’s published – that indicates that we had some effects on T cells in the peripheral circulation.

And that’s, I think, another point in favor of assessing the immunooncology angle for inhibiting the immune pathway with TRC105 on top of the preclinical data I referenced earlier..

Okay. And then just one more..

Yes, please..

On 253, so how common is the 876L mutation?.

Right. Yes, great question. So we are basing our data mainly on the Janssen Phase 1 study of apalutamide. So during the Phase 1/2 study of apalutamide, which as I think most people know has now been filed formally as an NDA application for approval. But during the Phase 1/2 study, the F876L mutation was interrogated.

And based on those data, we expect a prevalence in patients who progress following apalutamide or enzalutamide of approximately 10% to 15%. And so we use those percentages in order to predict a number of patients to be screened to detect the mutation.

I should point out the following though, as precision medicine evolves, there are many centers that treat prostate cancers that are proactively using NGS sequencing to broadly sequence the androgen receptor in their failing patients.

And as part of that sequencing profile, they will identify F867L mutants independent of enrolling patients in our study. So that really will help us. So, for example, there’s a center that uses a technology where they routinely fully sequence the androgen receptor at a time of progression on enzalutamide, for example.

They’ll know that patient has the F876 mutation and they will be recruited to have that patient come into our study right away.

So that we’ll be looking for the mutation proactively in patients that don’t know the base for the resistance, but we’ll also take those patients where we do know the base resistance if that mutation based on NGS sequencing that outside of our trial in getting those patients into our studies.

And the reason we can do that productively is that a lot of the centers, the real key prostate cancer treatment of excellence centers in this country are part of our trial.

So there are two ways really to get patients on trial, patients that take the test and detect the mutation and patients that already have the known mutation through participating in NGS sequencing protocols that are standard at some of these centers for excellence..

Okay.

And then should we expect data in 2018? And then would it be in a meeting or would you like to top line in a press release?.

So in 2018, what we expect to do is be making the transition in the 253 trial from Phase 1 to Phase 2 formally. And that I think, will give people confidence that this drug is safe since we are taking the drug now out of Phase 1 into formal Phase 2.

In terms of full disclosure of data, we’ll discuss those opportunities and options with our partner, Janssen. But what we do expect to be able to, at least, provide is that, we have moved into the Phase 2 portion of the study in early 2018, which should give you confidence on the safety profile of the drug..

Okay. Thank you..

Thank you, Michelle..

Thank you. And our next question comes from the line of Chad Messer from Needham & Company. Your line is now open..

Hi, Chad..

Hi. Hi, thanks for taking my question. There is always so much to track with you, guys.

Maybe just to start off, can you give us a sense of what we should expect later this week at CTOS? I mean, presumably, is it more patients and longer follow-up? And if so, how much?.

Yes, I mean, I think that’s exactly the answer, Chad. So, we initially presented data on nine patients with angiosarcoma as we are enrolled in the initial trial of TRC105 in a broad sarcoma population.

We, after that point started enrolling selectively into sarcoma patients in an expansion cohort based on the fact that we had seen significant activity in the angiosarcoma patients. So you can expect updated data on a broader cohort of patients with angiosarcoma treated with the combination, including the PFS in those populations of patients.

We’ll also present some PK data using a dosing scheme whereby we use weekly dosing for four weeks and then go to a hybrid scheme of every two weeks thereafter, which would present, I think, an easier dose schedule for TRC105 and subsequent trials. So those are the two main things you’ll see at CTOS, which is only two days away.

We’ll present those data on Thursday of this week..

Okay. And then by just going back to an earlier discussion on renal cell, so it seems like you already see a lot of jockeying for frontline combinations of specific KIs with specific checkpoint inhibitors.

Just wondering how much of a challenge do you think that poses for you? It seems you might have to sort of hitch up to one of those wagons specifically and it will be a while before we know who wins?.

Yes, I mean, it’s – and it’s hard to say who is going to win, right? I mean, each company is doing an independent trial of their drug checkpoint inhibitor versus the TKI alone. No one is really going head-to-head to compare really to prove that their TKI with – I mean, checkpoint inhibitor is really better than someone else.

So it’s going to be a bunch of trials that, if you will, compare data that’s in an uncontrolled setting. And so I think that will remain nebulous for quite sometime. I think, it’s an excellent point. I think, for us, we feel confident that we can combine with most any VEGF inhibitor. We’ve done it with Sorafenib. We’ve done it with Nexavar.

We’ve done it with Votrient. We’ve done with Inlyta. We combined well across the board. So I think, combining with the VEGF TKI is not the question, it’s which one to pick.

And to your point, it may be driven by business considerations, because it will be hard, I think, to ferret out based on the multiple trials that deliver data given that they are not really comparing against each other, which is the better drug.

So, there will be a lot of considerations in that decision, some of which will be clinical development considerations and some will be business considerations as well..

I appreciate the insight..

Yes. Yes, thanks, Chad..

Thank you. And our next question comes from the line of Bert Hazlett from BTIG. Your line is now open..

Yes, just very briefly, you covered a lot of ground, just the 253 inflection point, I guess, the….

Yes..

As you progress with initial data with 253, what – are there specific points where the opt-in needs to be triggered by Janssen, or can they do that at any time? Thanks very much..

Thanks. We appreciate the question. Yes, the opt-in can happen at any time up until – at the point we deliver the definitive Phase 1/2 data then the clock starts, which is a 90-day clock that they can opt-in after full Phase 1/2 is presented to them. But they can opt-in at any time until that point.

For us, in terms of important points in that trial, I do think moving from Phase 1 to Phase 2 is an important point in that trial, because it’s telling the world that that drug is safe enough to move into a Phase 2 study, that there is no significant safety signal, which given that’s a potential best-in-class drug, it should make it a very valuable commodity.

The thing with that drug, we emphasized its ability to inhibit mutations formed in resistance as basis for resistance to Xtandi and apalutamide. But also be clear, that it is as active on the wild type androgen receptor as both of those drugs, and that’s what makes it potentially best-in-class.

As the actual wild-type AR, but it also gets these mutations sort of base for resistance to where we think it will be the two dominant players in that space. So even though we’ll develop it initially in the mutant population, this drug could move into the front-line setting.

And so, the fact that we say this drug is moving into Phase 2, which tells the world this is a safe drug. We’re confidence that Janssen will – it will probably be in Janssen’s best interest to opt-in and reacquire the drug at the appropriate time for them. Any other….

Thank you. And I’m not showing any further questions at this time. I would now like to now turn the call back over to Dr. Charles for any closing remarks..

Well, thanks very much for your questions and your interest. Have a great day, and we look forward to hearing from you again soon..

Ladies and gentlemen, thank you for participating in today’s conference. This does conclude the program and you may all disconnect. Everyone, have a nice day..