Thank you, Jeannie, and good afternoon, everyone. Today, Janux issued a press release announcing interim clinical data for the company's JANX007 clinical program. This press release, today's webcast, and corresponding slides are available on our website. Before we begin our prepared remarks, we would like to remind everyone that certain comments made by Janux management on this call will include forward-looking statements. These forward-looking statements are based on current information, assumptions, and expectations that are subject to change and involve a number of risks and uncertainties that may cause actual results to differ materially from those contained in such statements. These and other risks and uncertainties are described in our periodic filings made with the SEC. You are cautioned not to place undue reliance on our forward-looking statements, and the company disclaims any obligation to update those statements. With that, I would like to turn the call over to David Campbell, President and CEO of Janux. Thank you, Chad, and thank you, everybody, for joining today as we present our clinical update, phase I data sets for JANX007 for the treatment of prostate cancer. I'd like to start on this slide to speak to the areas that we've been guiding to our focus for development of 007 going forward. We're primarily focusing in the area of early line taxane-naive patients. This is one of the most rapidly growing segments in the MCRPC space given treatment changes. Historically, as recent as 2018, when the first ARPI was approved in hormone-sensitive, it used to be ARPIs were the standard androgen receptor inhibitors, abiraterone, were the standard MCRPC treatments. At this point in the United States, more than 50% of patients already receive an ARPI in hormone-sensitive. Now when they show up in MCRPC, the mainstay therapies have already been used. The choices for these parents of these patients are typically a taxane, Pluvicto, or an ARPI switch that doesn't work very well. Our view is that this is a ripe opportunity for a compound like JANX007 with a differentiated safety profile and a compelling efficacy profile. With that, I'm now going to walk through a little bit of background. JANX007, first-in-class, first-in-human tumor-activated T-cell engager targeting PSMA. Today, what I'm going to share with you is we've achieved durable responses and radiographic progression-free survival with a manageable safety profile that compares favorably to both approved as well as investigational therapeutics in this space. I will also share with you early results supporting a patient-friendly every-other-week dosing schedule. We've been guiding to early data sets, PSA reduction, CRS profiles, and a handful of patients in our ongoing taxane-naive phase 1b expansion study. At the end, I'm going to share with you some disease burden analysis that we've been performing that suggests JANX007 has demonstrated improved efficacy in lower tumor burden patients, guiding us to our belief of improved efficacy option moving forward into this early taxane-naive patient population. PSMA itself is a clinically validated prostate cancer cell surface antigen. It's highly expressed in bone, lymph node, as well as visceral metastases. There have been a number of T-cell engagers, the bispecifics targeting PSMA, that have demonstrated antitumor activity in multiple clinical trials. However, all of them listed below, there are six that we show here, there have been a couple others, have all been terminated, typically due to safety limitations, lack of efficacy, or combinations thereof. We designed JANX007 to overcome some of these safety limitations in order to meet the needs of prostate cancer patients. On this slide, I just wanted to share with you, get us on the same page, how we're approaching this. On the upper left-hand side, you can see a TRACTr. These incorporate the bispecific. One side binds to the tumor, one side binds to the T-cell. We identify peptide masks shown in red and purple, bind to those domains, block their ability to interact with target. We connect those peptide masks to the bispecific with a peptide linker that incorporates a cleavable linker that's cleaved in the tumor environment. Importantly, in order to support longer intervals of dosing, you can see we also have in blue a half-life extender. This binds to albumin, takes advantage of this clinically validated approach to extend the lifetime of this drug when we dose it. Now, upon entry into healthy tissue, the masks remain in place. There's no proteases to cleave those cleavable linkers. With the masks in place, they don't bind to healthy tissue or T-cell. By blocking that interaction, you're not triggering any pharmacology or any biology in healthy tissue to spare the healthy tissue any adverse events. Upon entry into the tumor tissue, tumor proteases cleave those linkers, release both the red and the purple masks. Importantly, you can see with the purple mask also releases the half-life extender, and that's going to be important in a minute. In the tumor environment now, we have the highly potent bispecific. It's able to form a complex between the T-cell and the tumor cell. That triggers activation of the T-cell, triggers elimination of the tumor cells. Importantly, we do not want to have accumulation of this highly active species in healthy tissue. When this highly active species T-cell engager escapes from the tumor, because it no longer has the half-life extending domain, which is cleaved during activation, it's rapidly cleared. This is allowing us to maintain very low levels of T-cell engager in healthy tissue, even when we drive significant concentrations of the TRACTr. We believe this is what's contributing to our safety profile that has allowed us to develop this drug moving forward. On the next slide, what I want to break down are the five different areas that I'm going to focus on today. We've been guiding for a while, but today we're going to give an overall update on the phase Ia patients. We've now dosed a bit over 100 patients there, provided safety and efficacy data in that expanded set. We've been asking a number of dosing regimen questions so that we could begin triggering our pivotal studies. What is the appropriate CRS mitigation that's easy to follow protocol that maintains the grade 1, grade 2 CRS profiles we shared in December? What is the target dose that maximizes efficacy and safety to support Optimus in our phase Ib studies, as well as dosing interval? We know we can dose once weekly. Do we have an opportunity for every other week, which would be a very significant add to this program? Finally, an early update on taxane naive patients looking at early signs of activity and CRS profiles. I'm going to begin with an overview of the phase Ia MCRPC patients' studies that have progressed to this point. On this slide, I'm sharing with you the baseline subject characteristics. In the middle, you can see we provide the December 2024 subjects. We had 16 that we reported on. On the right, you can see now we're going to be talking about 109 patients. We put those both here so that you can see in general, these are very, very closely aligned end-stage MCRPC patients, typically seeing similar prior systemic therapy, similar profiles with respect to bone metastases, as well as lymph node and visceral mets. Very comparable patient populations. However, now we're going to be able to report on a significantly larger patient subset as we go forward. Beginning on this slide, what we've done on this slide as a swim plot, a couple of things. The subjects highlighted in the box, these are all subjects who have received at least the 2 mg target dose, and there's 92 patients out of the 109 that have received greater than or equal to 2 mg target dose. These include a number of different regimens from different target doses, different step doses, different step dose timing, once weekly, every other week, when to start Q2W, and different CRS mitigation procedures. You can appreciate there's a lot of underlying questions going into here, but we can still garner some learnings from this swim plot. First, as you look at the swim plot, the swim lanes are blue if that patient had a soft tissue met that could be evaluated by RECIST, and gray if it was a bone-only disease. What you can see as you look at this, we have a number of patients with significant responses, six, eight, 10, even greater than 12-14 months, both in both subjects with soft tissue mets as well as those with bone-only. What you can also notice is as you look at these, clinical benefit has persisted beyond the RECIST-defined progression in some of these patients. If you start looking at some of these different lanes and you look at the red arrow where there was progressive disease, you can see a number of these patients have continued on drug for a significant number of months. You can see the top patient was out for another half a year. This is being driven by the PI makes the decision that the patient is continuing to derive clinical benefit beyond the RECIST-defined progression in some of these patients. The way to think about this is in the scans, a number of different lesions are evaluated. While the primary lesion, you may have lost control, the other lesions are either under control or actually continuing to be maintained. Quality of life scans is really what goes into the PI making the decision to continue dosing drug even after progression. We're going to circle back to that as we start talking about how to think about our trials coming down the road. What you also notice on the far left is we put the best PSA response or best PSA reduction color-coded in those boxes. What you can see is durability at the top is enriched in subjects that have achieved a PSA 50, 90, or 99, reinforcing to us that the early PSA measure is a clear indicator of what to expect in these patients with really this durability enrichment in this subgroup. As we look at this swim plot, you can see we've got a number of patients still on drug. We've had a number of patients that have had quite durable responses. We also have patients that continue to garner benefit from treatment of 007 even after they've had RECIST-mediated progression. On the next slide, we took a look at radiographic progression-free survival in these studies. In the upper table, we start on the left-hand side with all subjects. You can see in all subjects, the median RPFS comes in at 7.3 months. We also give Kaplan-Meier estimates at three and six months. The May 2025 QW, end of nine patients, that was the press release that we provided back in May where we provided an update on the December patients that reported a median RPFS of 7.9. Going to the right now, we've expanded that group from nine patients up to 29 patients. You can see that the median radiographic progression-free survival has been maintained at 7.9 months. The Kaplan-Meier estimates at three and six months are also still looking positive. On the far right, using the same subjects, now looking at patients who received every other week dosing, we have 19 evaluable patients here. The RPFS was maintained at 8.9 months. You can see our Kaplan-Meier estimates coming in at 76 and 54. On the lower right-hand side, just for comparison purposes, we've got Pluvicto, which is a commercial dose. The other two T-cell engagers, the STEAP1 and the kallikrein 2, at their recommended phase II dose. You can see that our blended groups still compare favorably both in RPFS as well as progression-free survival estimates of six months. What I do want to point out on this is that the subjects, the expansion groups, use the December and May criteria, which is radioligand treatment naive on 6 mg and 9 mg target doses. That allows you to compare those two expansion groups to what we shared with you back in December and May. The overall treatment-related adverse events are summarized on this slide. We made the cardiac greater than or equal to 15%. You can see a fairly well-behaved AE profile here. What we did, you can see we noted a few of these are CRS-associated AEs. This is based upon a publication from Amgen back in 2023. Using that definition, you can see the vast majority of these are secondary to cytokine release, primarily limited to cycle one and a little bit in cycle two. We have a few other observations looking at dry mouth, dysgeusia, hypoacusis. One would be interested as you think about PSMA. The dry mouth, we'll get back to the grade 3. That was at a dose we're not going forward with. All the others are reversible and do not require dose reductions or terminations at this point in time. Overall, a manageable treatment-related adverse event profile continues to support moving this drug forward into earlier lines of therapy. On this slide, we wanted to share with you the overall best PSA reductions on the left and RECIST responses on the right. Keep in mind that this includes all patients. The numbers are provided there. It includes patients less than two treatment cycles and those dosed under less optimal dosing regimens and/or CRS mitigation strategies. In a couple of slides, you'll see exactly what we mean when we get into some of the CRS mitigation strategies that we use and the impact it had on PSA reductions. Overall, in this large expanded group, anybody who's received a target dose greater than or equal to 2 mg, you can see very nice reductions. On the right-hand side, reductions were only observed when we had a target dose of 2 mg or greater. That is why they're all dark blue. You can see RECIST profiles right now, RECIST responses are running at about 30%. The next section that I wanted to go into is addressing the different questions that we were asking about dosing regimen. The first was CRS mitigation. As you remember, back in December, we were using a procedure that allowed wide flexibility to the PIs. We were trying to learn about this new drug modality, so it was critical to give the PIs maximum flexibility when CRS was observed in their clinical site. Now that we've learned a lot more about this drug, we've evaluated a number of specific new protocols that were easy to follow. Our goal was to maintain the G1, G2 CRS profile and the early safety and efficacy data that we shared previously. With that, I'm going to go to the slide where we summarize some of these efforts. On this slide, what you can see on, we're sharing CRS profiles coupled with early PSA reductions. On the far left is the December 2024 data that has already been shared. You can see it's primarily grade 1, g rade 2 CRS. We did have that one grade 3 in a patient who had rabies out in cycle five. PSA reductions, PSA 50 and 90, we're looking very strong at 163%. An example in the middle panel of a CRS mitigation procedure that was not effective. You can see in this particular subset of patients, we had a number of grade 3 CRS events, cycle one, day one, day 15, as well as even out cycle two, day eight. Clearly, it did not meet our was inferior to the December 2024. In addition, if you look at the PSA 50 and 90, you can see it also had an adverse impact on best PSA reductions, significant reductions both in PSA 50 and 90. As you think about overall waterfall plot, keep in mind we asked a number of questions like this that had adverse impacts. On the far right, CRS P2 is indeed a profile that we're moving forward with. You can see the CRS profile is maintained, if not improved, compared to December of 2024, while it maintained PSA reductions similar to what we reported back in December. You see, primarily limited to cycle one, the vast majority of these are grade 1 CRS. As we look at the PSA 50 and 90, you can see we've got a good PSA 50 profile. Twelve out of 14 patients have achieved that. PSA 90, the denominator changed to 13. I just want to spin the notes here. This was a patient who came in with a low PSA value. When they achieved a PSA 50, they became undetectable. We took the conservative route. You could go either way on this. We took the conservative route and just changed the denominator. Other way to do this would have been to say it was eight out of 14, but either way, we're talking about 55% PSA 90. We have a few patients that are still, as you can see, undergoing dosing in cycle two and a little bit into early cycle three. These overall PSA reductions may improve as we go forward, especially some of the PSA 50s and 90s. At this point, we think we've got a profile CRS P2 that we're going to go forward with. CRS P1 is an example just to share with you a little bit of detail on that one. That was actually a toci prophylaxis, and it just didn't work well in our hand. The other evaluations that we looked at was how much DEX, the timing of DEX, DEX plus toci or DEX by itself, etc. We're very pleased with the CRS P2 profile. Clearly, CRS P1 explains some of the grade 3 CRS issues that we had with this program. For comparison purposes, in the light blue box, we provide PSA 50 and 90s for Pluvicto, the STEAP1 program, and the J&J. You can see our PSA reductions with CRS P2 are similar to December 2024 and compare favorably to our competition. I do want to point out, and this is important as we think about continued development of this drug, CRS onset and duration continues to be resolved within one day. Onset is typically between eight and 12 hours. You treat with CRS P2, it's resolved by 24 hours. As we think about down the road, outpatient opportunities, certainly having a well-defined 24-hour window is going to be a benefit with this drug. If you look at most of the other drugs in the area, T-cell engagers typically have variable day of onset from day one to day three or four, typical duration from one day to multiple days of CRS. We think this is another differentiator for our molecule moving forward. On the next slide, I want to spend a little bit of time talking about target dose and dosing interval. As you could imagine, these are tightly integrated. I'm first going to start talking about QW, and then I'm going to talk about Q2W in the next couple of slides. What we've done as we evaluate QW on this slide and Q2W on the next slide is we want to focus on durability as measured by PFS as well as Kaplan-Meier estimates and treatment-related adverse events that are due to the target dose. In order to make sure that we're looking at TRAs that are due to the target dose, we're requiring patients to have been dosed in cycle three. So these are the treatment-related adverse events in cycle three and beyond. That gets around reducing the signal because remember, the majority of our AEs occur in cycle one and cycle two, which would reduce the discrimination that we have here, as well as really giving us that information in this particular is really allows us to compare these target doses without other confounding events. Looking at efficacy and durability on the top, you can see 3 mg, 6 mg, 9 mg, 12 mg. Essentially, they're all within line of sight of each other. We've got different RPFS, and some of these groups you can see are pretty darn small as we look at the radiographic PFS. Looking at Kaplan-Meier estimates at three to six months, you could say you could go forward with any one of these four doses. As we looked into safety on the bottom, you can see looking at grade 3, we're running about 30%-40% out here, very manageable profile with the 3 mg, 6 mg, and 9 mg QW. Once we get out to the 12 mg, you can see that's up to five out of the five patients had a grade 3 adverse event out in cycle three or beyond. Based upon that, we prioritize three, six, and nine target doses as our preferred doses going forward. Early study, we're looking at 6 mg QW in our taxane naive. The next cohort we'll talk about on the next page. Based on this, we've prioritized 3 mg, 6 mg, and mg. Our preference right now is probably at 6 mg, but we're leaving a little bit of flexibility there as we go forward in taxane-naive patients. We will talk about why in a few slides. On this slide is an evaluation looking at QW versus Q2W. Once again, we're evaluating radiographic PFS and Kaplan-Meier curves to compare QW versus Q2W. We're focusing on cycle three and beyond treatment-related adverse events. That is when Q2W starts. It also minimizes CRS confounders, like we said on the previous. The subjects continue to be, as they have been from our early radioligand-naive patients, the same as the expansion group that I shared with you earlier, that have received at least one target dose in cycle three. Based on this, looking at the Kaplan-Meier evaluations, you can see what we had to do here is we had to combine 6 mg and 9 mg just so we had enough subjects to be able to evaluate via Kaplan-Meier. From that evaluation, you can see our RPFS is maintained when we went from 7.9 at QW to 8.9 at Q2W. Our Kaplan-Meier estimates at three months compare favorably. At six months, you can see a little bit of a loss. What we've noted is once we get these patients out to their Q2W, they have very nice durable responses. That is why you could see a little bit of a loss at six months and still maintain a very favorable median RPFS. As we look at safety, once again, looking at cycle three and beyond, comparable overall adverse event profiles, but you can see that there's a reduction in the grade 3 AE profiles, 35% down to 21%. Based on this, these initial results support a patient-friendly Q2W dosing schedule. As I pointed out, the first cohort in our taxane naive is a target dose of 6 mg and it's 2 mg qweekly. We started that before we had this data set. The next cohort will be Q2W, presumably at 6 mg target dose. Finally, I wanted to share with you some of the early data that we've generated in our taxane naive patients. We've been guiding that this is going to be a handful of patients, small number, early data looking at PSA reductions in CRS. On this slide is shared with you the best PSA reduction to date as well as CRS profiles in these patients. The asterisks on the PSA reduction, just to note that dosing is ongoing, subjects are still in early dosing cycles. Those PSA reductions may improve as we go forward. To provide you with a snapshot of where we're at on these four patients at this point, you can see very nice, you've got a patient at PSA 90, a couple have already achieved a PSA 70, and they've all done this with three out of the four have a grade 1 CRS profile. On the right-hand side, looking at CRS, you can see once again, primarily limited to dose one, beyond dose one at this point, still early data. We're looking at fevers in some of the patients, a couple of the patients in cycle one and cycle two. Early and deep PSA reductions coupled with a manageable CRS profile, we think is encouraging as we start thinking about our opportunities in taxane naive patients moving forward. This also is early data to reinforce CRS P2 is behaving as we would hope it would in these patients. On this slide, I want to shift gears slightly. We now have enough patients, and we started breaking down the patients into different subsets, looking at their radiographic PFS and primarily looking at disease burden. What we've done on the left-hand side, you can see we've got 63 patients, and these patients are radioligand naive, same as the expansion groups, contain 3mg, 6mg, and 9mg target doses, as well as QW and Q2W. We've now got 63 patients. You can see the Kaplan-Meier and Gray, very nice RPFS at 7.9 months. We then evaluated, we're evaluating a number of different models. They're all directionally pointing the same way where we can use different criteria for a high tumor burden versus a low tumor burden. As we break these out, the high disease burden patients in red have a reduced RPFS down to about 7.3 months, a meaningful number of patients here at 39. Interestingly, I think what one would expect based on the T-cell engager space, as we look at the low tumor burden patients, you can see we've improved that out to 10 and a half months. Very encouraging profiles as we think about moving to earlier lines of therapy. What we've done on the right-hand side is using these clinical marker surrogates, we've provided the breakdown of low versus high in the different subsets we've evaluated, the all-patient population today, the December taxane-exposed versus the phase Ib taxane-naive. When we look at the sum total of this data, it suggests a potential for an improved RPFS as we move into earlier lines of patients with a lower tumor burden, especially looking at these phase Ib taxane-naive patients. As you think about the likelihood of Janux having a desired RPFS in these patients, we think this data suggests the opportunity that as we move into these earlier lines of patients, we are going to continue to see improved PFS profiles. I would argue that this is consistent with what we've seen with a number of T-cell engagers. The way to think about that is patients have a better functioning immune system, they have a lower tumor burden, lower tumor growth rate, all of those conspire to improve the responses in low tumor burden patients. In summary, just want to highlight we've identified our doses and regimens moving forward based upon our overall MCRPC patients Ia study. We have identified an easy-to-follow protocol that has maintained the grade 1 to CRS safety profile, also maintained our PSA reductions. We have identified and prioritized the 6 mg and 9 mg target doses as the best combination of safety and efficacy. We've also evaluated and selected could go forward with QW, but importantly also with Q2W, looking at 6 mg and 9 mg, which demonstrate the best combination of safety and efficacy in a Q2W setting. In taxane naive, our early phase Ib has demonstrated rapid and deep PSA reductions with primarily grade 1 CRS. Based upon this, the data we've generated continues to compare favorably to historical data in this heavily treated, pretreated MCRPC patient setting. In the next section, I'd like to walk you through a couple of slides how we're thinking about clinical developments of JANX007 going forward. I shared with you in my first slide why we're focusing because of the landscape changing, we're really focusing on that taxane naive earlier line patient subset. Our clinical plans continue to be what we shared with you since last year. We're evaluating JANX007 in monotherapy as well as in combination with darolutamide in taxane naive pre-Pluvicto MCRPC patients. We and others are learning as we went through this with KOLs and our clinicians. This is the largest and growing MCRPC setting. If we think about, I believe enzalutamide is going to go generic next year, we expect that's going to drive even additional uptake of these androgen receptor inhibitors and hormone sensitive, really creating an opportunity if we can differentiate from right now the drugs that they have available to them are pretty much not differentiated, and we'll talk about that in a little bit, taxane or Pluvicto. If we could come in with a differentiated safety and efficacy profile, we see that as an outstanding opportunity, and we continue to focus our efforts in that area. We've also noticed that we're going to evaluate the JANX007 in PARP inhibitor refractory patients. Right now, there are no approved therapies for these patients. Once they no longer respond to the PARP inhibitors, that may provide an opportunity for an expedited approval on this site. Considerations: we need and will continue to evaluate Pluvicto uptake, new clinical data with that in both the taxane-naive setting as well as the hormone-sensitive setting, and we'll adjust our plans accordingly. We're fully aware of the recent approval of taxane and PSMAfore. That's with an ARPI switch. A couple of data sets that came out at recent ESMO, there was a Canadian study that evaluated or compared taxane-naive patients that we're targeting also, taxane as a control compared to Pluvicto. They demonstrated that Pluvicto had no demonstrated RPFS time to deterioration differences and essentially had the same overall survival as taxane, actually with taxane maybe having a slightly better overall survival. So we're aware of that study. There was also the PSMA addition study in hormone-sensitive demonstrating while there was an improved RPFS, there was not an improved overall survival, there was a lower quality of life coupled with a slight increase in secondary malignancies and kidney events with two-year follow-up. Based on these recent studies that have been reported, we think these support and actually strengthen our rationale for why we are focused on this taxane-naive pre-Pluvicto patients. On the next slide, I wanted to highlight something that others have noted and we think is important as you think about the opportunities for T-cell engagers going forward. What we are doing here is we are comparing radiographic PFS with overall survival. In the upper panel, we have got Kimmtrak, tarlatamab, tarlatamab in two different lines of setting for small cell lung. What others have noted and we're noting here is if you look at the RPFS compared to the control, the T-cell engagers had a minimal improvement in improved RPFS, 0.4 to one month compared to the control. However, there was a significant improvement, an outsized improvement as you went from PFS to overall survival. You can see it went from 0.4 to 5.7, 5.3 in 13 months. It looks like early data set, two different T-cell engagers, but while they may not have a significant impact on RPFS, and we've seen this with other immuno-oncology drugs, you can see an outsized improvement in overall survival. Now let's compare that with Pluvicto. We've got a couple of different studies. We've got the third line, we've got the taxane naive, where the RPFS compared to control is significant. It's 3.7, 5.3 months, but you get much less of an overall survival improvement. What we've done on the bottom is looking at taxane, that Canadian study, we just reversed the order, prostate cancer. You can see taxane even, while it has an RPFS of 2.1 improvement compared to control, you can see once again an outsized, slightly outsized, not as good as what you see with the T-cell engagers improvement in overall survival. Assuming this sort of relationship holds as you think about our early RPFS around 7.9 months in end-stage patients, this provides a rationale which allows us to think about why that might improve as we go into earlier lines of patients. Remembering in prostate cancer, approval is typically based on your overall survival. We think it's a positive that the T-cell engagers, early data sets, clinical data sets are showing this outsized overall survival improvement. On this slide is my final slide. Just want to wrap up a few things here. Conclusions: we've achieved durable responses, good RPFS, manageable safety profile, compares favorably to the other T-cell engagers and approved therapeutics. We have durable responses in patients with both bone-only disease as well as subjects with soft tissue mets. Some of our competitors are focusing on bone-only disease due to lack of activity in soft tissue mets. We think having the ability to do both will be an important differentiator for our compound. Initial results clearly support moving forward with the Q2W dosing schedule, which we're very excited about. That also may open up additional opportunities as we think about continued development to 007. Favorable activity in taxane-naive phase Ib expansion study has also been shared with you today. I want to wrap up. This is as we think about why JANX007, why we think it may be successful as we move forward into these earlier lines of therapy, right now focusing on taxane-naive, maybe focusing in other areas down the road. We have shared with you lower disease burden. We have an improved RPFS with 007. That is exactly what you have as you move into earlier lines of therapy. The PFS and overall survival trends from Kimmtrak and tarlatamab suggest T-cell engagers may deliver greater overall survival benefits relative to their PFS. Coming back to the swim plots, evidence of clinical benefit in some of our patients treated PI choice to treat beyond RECIST-defined progression because they were still garnering benefit reinforces these observations. Based on all of this, we're full speed ahead developing JANX007 both in our monotherapy and our combination studies going forward. With that, I wanted to leave plenty of time for questions, and I will hand off and open up the line to questions from the different people. At this time, I would like to remind everyone in order to ask a question, press star, then the number one on your telephone keypad. Again, we do ask you limit yourself to one question and one follow-up, and then rejoin the queue. Your first question comes from the line of Josh Schimmer with Cantor. Please go ahead. Thanks for taking that question. Actually, I have a couple, but hopefully they're quite quick. First, were there any differences in the rates of CRS or ADAs in the Q2 week versus the Q1 week regimen? Was the grade 5 adverse event a first cycle event or subsequent? Can you frame the market size for the PARP inhibitor prostate cancer indication, refractory prostate cancer indication? Thanks. All right. Rates of CRS are going to be identical. Keep in mind that when we the first two cycles, whether it's QW or Q2W or once weekly, what we've learned from evaluating when to start Q2W dosing, we started after cycle one, we started after cycle two, we've learned that it's important with 007 to drive maximum PSA reduction in those first two cycles. The best way to do that is with once weekly dosing. As CRS is primarily a cycle one, cycle two, you'll understand why there's no different rates of CRS between Q2W versus QW. Josh, you asked a slew of questions. I would say pick another one, and I'll go with that one also. All right. The market size for PARP inhibitor refractory prostate cancer? Yeah. Right now, we've got that penciled at a bit over $500 million and growing as the PARP inhibitor evaluations, genetic evaluations are being used more and more in hormone-sensitive prostate cancer. That's only increasing this patient subset over time or better identifying patients who actually will be receiving the PARP inhibitors. Great. Thank you. Your next question comes from the line of Brad Canino with Guggenheim. Please go ahead. Hey, afternoon, and thanks for the comprehensive update, David. One of the questions I continue to hear with these data is that since 007 has clearly the best in class PSA, why is its RPFS equivalent to other TCEs and Pluvicto and shouldn't it be better than that? A two-parter for me. First, it would just be good to hear how you'd respond to this question now with so much data out there for this program. Second, what do you think are the implications of these equivalent late-line durability data as you strategize to bring 007 forward into the early lines of therapy in prostate cancer? Thank you. A couple of good points. You asked me to compare it to Pluvicto. I think this slide is how we think about that. Pluvicto has shown outsized RPFS and a reduced overall survival improvement and contrasted that with the T-cell engagers, which are the exact opposite. We are looking right now, if we hold a similar relationship, one could expect an outsized overall survival. The other way to think about that is our RPFS in 7.9 months right now is in a blended evaluation where we're evaluating, mixing Q2W, suboptimal doses, suboptimal CRS regimens. They're all in there. That's a blended number. We're comparing it right now to Pluvicto on a commercial dose. I think that there's an opportunity just simply by once we start looking at and defining our phase II dose, I would expect the numbers to get slightly better. More importantly, I think as we move into earlier lines of therapy, because as we're looking on this particular slide, you can see the RPFS is 8.6-9.3 months, so say nine months. That's in a first line to third line patient population. We're in a fourth line, fifth line. Simply moving into earlier, we would expect our 7.9 PFS to get better. I think all of those conspire to why we believe that our overall reductions right now, it's just a function. We have a blended. We're in end stage. As we move into earlier, we expect our numbers to get better, coupled with the expectation T-cell engagers are showing this interesting outsized overall survival response relative to their PFS. Your next question comes from the line of Marc Frahm with TD Cowen. Please go ahead. Thanks for taking my questions. Maybe one just on the RECIST responses to start. Can you confirm who was able to actually confirm and how many of those are maybe still unconfirmed, but they're maybe ongoing or unfortunately are not ongoing on treatment still? Yeah. We haven't broken that down other than to say this was a mix of confirmed and unconfirmed. I don't know the percentages off the top of my head. Okay. Maybe just on the idea of this PARP refractory population kind of as a potentially rapid path to approval, obviously this is prostate cancer in general is a very IRA-exposed population. Just maybe can you talk through the strategic rationale there versus potentially waiting for a broader approval before you kind of start the IRA clock? Keep in mind by generating the data, the IRA clock does not start until you actually file for registration. That would be a decision that we would make later. The way to think about this is if we have an opportunity for an expedited path to approval that financially makes sense, we will evaluate how far away we are on our combo or monotherapy with 007. That is a decision that we will make later. It'll be based upon market opportunity size, where we're at on that taxane naive study, how far away are we from registrational data there. Marc, we don't have to make that decision today. All we're doing today is triggering the study, generate the data, then we'll talk with the FDA, see if there's even an expedited path. The way that I think about it is we're putting together a data set. We don't have to trigger that IRA clock until or unless we decide that's the right thing to do. That's a few years down the road. Okay. That's helpful. Maybe if I can squeeze in just on the CRS mitigation strategies you presented, the kind of December versus strategy one, strategy two. Can you just mostly the two versus December, just kind of give us a sense of the magnitude of the difference of the kind of days on therapy or dose of steroids that those patients are getting? We have not provided the details on P2. The amount of time that they remain on CRS mitigation is comparable between all of these. It is really just what was done, the timing and size of the dose is really all that varies here. At this point in time, other than sharing CRS P1 was toci prophylaxis, we are not sharing what P2 was. We have got a number of people in the space close to us. We are just going to keep that as competitive information for a little bit longer. Thank you. Your next question comes from the line of Matt Fitz with William Blair. Please go ahead. Thanks for taking my questions and providing a lot more data than I was expecting. Josh tried to ask about some details on that grade 5 cardiac arrest, so maybe I'll just follow up with that. I guess just how many dosing regimens and cohorts do you think you'll ultimately need to evaluate in the phase Ib? I know you can do myriad of six and nine target dose in Q week and Q2 week, but just curious if you'll evaluate all of those, I guess. No. We've mapped out our expectation is two, three max. It has to be two because we're deciding what to take into Project Optimus, and we want to make wise choices. Our expectation is it will be two different to the QW versus the Q2W. If we find something surprising, then it would only require one more. We expect to get in and out on two, and that will give us the data set. We need to talk with the FDA about Project Optimus. Just any additional details on that cardiac arrest patient, was that during the initial step-up with CRS or anything like that? No, it was not related to CRS. It was a cardiac arrest in a patient with a pre-existing history of DIC, which we note here. I think the site even went back and forth whether or not to attribute it to drug. To be conservative and careful in the end, it's been attributed to drug, even though we could find no direct reason why that should be the case. Okay. If I can ask one more. How did you define tumor burden as being low or high in slide 20? I guess just confidence that a pre-taxane patient population would really, in general, have that low tumor burden, or you might doctors see this data and want to put patients with, I guess, more aggressive higher tumor burden disease on trial? Sorry about that. For some reason, it looks like I lost. Can you hear me? Yeah, I can hear you. Okay. Here we are. On this particular slide, thank you. I had some technical difficulties. We have a number of different models. You can look at different clinical markers of bone disease, of soft tissue mets. You could add on top CT DNA mutations. There are a number of these models that different groups have used. We've used variations of all of them. They all directionally point in the same direction. As we look at our own data, granted, it's very, very small for our patients at this point in time. Keep in mind over time what these patients are going to be looking like, more and more matches. They're going to be coming off of hormone-sensitive prostate cancer treatment. This will be their first foray into MCRPC. If you look at the low versus high, already just looking at historical data, you can say first-line patients have a lower tumor burden than second and third. That is certainly going to hold. We also think the landscape treatment trends where what we're talking about is what is going to be the first treatment in MCRPC following hormone-sensitive. Those patients are typically going to be in the low stage. Got it. Thank you for my questions. Your next question comes from the line of Karina Rabayeva with Truist. Please go ahead. Hello. Hi, guys. Thanks for taking the question. You show that CRS profile included in early line patients with predominantly grade 1 CRS compared to later line patients. Could this potentially support using the outpatient setting? Yes. Yes, when we look at the CRS P2 profile right now, where the vast majority of patients are grade 1, which is a fever, outpatient right now, if you look at what's going on in CAR-T and hematology with the T-cell engagers, it's typically stay close to the unit. With a drug like ours and that particular profile, we think that would be very supportive of an outpatient treatment paradigm going forward. Okay. Thank you. I have one more question. In patients where the PI decided to treat beyond progression, what do you know about the target lesions that were enlarging? Could this be potentially an influx of T-cells? Yes. I think what you're asking is it's pseudoinflammation based upon the inflammatory environment of the T-cell engager. I would not say that. I would say, especially as we're looking at those patients in the swim plot, we've got out around seven, eight months where they've progressed. I would not consider that, nor would the radiographer consider that to be an inflammatory. That looks to us like it is actually progression of the primary lesion. However, as we pointed out, in order for the PI to keep that patient on drug, and you can see we've got at least one or two for another half a year or so, that's because the other lesions that aren't part of the RECIST evaluation either went away, were reduced, or certainly weren't growing, or their quality of life improved. It's really a PI call. I would not try to say that that's due to pseudoinflammation at this point. Okay. Thank you. Your next question comes from the line of Jeff LaRosa with Leerink Partners. Please go ahead. Hi, David. Thanks for taking the question here. I want a little bit on the Q2W dosing schedule. I guess high level, would you say the totality of the data supports Q2W over once weekly? Could you maybe dig a little bit more into why the six months RPFS dropped relative to what you're seeing with once weekly? Were patients sufficiently have enough sufficient follow-up beyond six months to sort of evaluate that? On that safety, I know you looked at CRS and totality, but anything else with liver enzymes increases, salivary tox, or anything else that looks different in that schedule? When we've evaluated the Kaplan-Meier curves, what we've noted is once these patients make it out to around six months, they have a nice durable response. You could start thinking about different we've lost the high tumor burden patients, and these are the low tumor burden patients. As the study went on, we've noted an increase in high burden patients as the drug appeared to work. PIs are using it more. In the end, what we would say is if they make it out that far, they have a nice durable response, and that's what's driving the RPFS, even though we're at 60%. That basically means that line stayed flat for quite a while before for another close to three months before it breached the 50% line. That just gives you an idea of how prolonged the response is out there. Now, with respect to safety, you noted CRS. I want to come back and the safety that we're summarizing on this slide is cycle three and beyond. There is no difference in CRS. On Josh's question, the first two weeks dosing QW versus Q2W is the same. So for all intents and purposes, those first two, three weeks look the same. What this is pointing is when we start the Q2W, which is cycle three, what does the safety profile look like from there on out? These are small numbers, but at least it's pointing in the right direction as we look at the grade three adverse event profile, which would not be CRS at this point. You can see an improvement as we went to Q2W, which is which one probably could expect given the exposure levels are reduced over time as you do Q2W versus QW. Would you say you prefer the Q2W over QW at this point? Yes. We are very excited about the Q2W and are looking forward to starting that cohort as rapidly as we can. While I'm talking, given the different growth rates as you move into earlier lines of therapy, we're also excited about Q2W. If we're able to do this in a rapidly growing, fairly high tumor burden compared to a first-line patient with a Q2W, we think we have an even better chance of having at least as good a profile as we move into those early li ne taxane naive patients. Your next question comes from the line of Jonathan Miller with Evercore ISI. Please go ahead. Hi, guys. Thanks for taking the question, and thanks for all the great granular data. I would love to get a little bit deeper into some of the drivers of, I guess, the differences in RPFS maybe. Obviously, you're going forward with the 6 mg doses, Q2W, but I'm curious, when you say, "David, really you could have developed any of those middle doses, 3 mg, 3 mg, 6 mg, 9 mg," can you talk a little bit about what you were seeing at nine meg or at three meg that are those differences in RPFS real differences in RPFS given the patient numbers that you have and what was driving six months? I guess the same question really about the tumor burden result. I guess it probably doesn't surprise any of us that low tumor burden patients do better. Do you really see materially better than expected RPFS on the T-cell engager versus just seeing better RPFS because they have less tumor? Two parts. I've got the QW slide up here. Jon, happy to take your question. I want to point out my view of the efficacy is the four of these were comparable. To your point, the RPFS, not enough numbers here. Look more at the Kaplan-Meier estimates, and they're all within a line of sight of each other. On efficacy, durability, there wasn't a clear differentiator here, which is you could have gone forward with 3 mg, 6 mg, 9 mg, or 12 mg. It was more as we got into the safety, looking at the adverse events in cycle three and beyond, where you see you went from about 30%-40% up to about 100% of grade threes. It was really that number, Jon, that drove us away to deprioritize the 12 mg dose. The next question was around the RPFS. I agree. There's nothing here that is overly surprising. It's just good to see the data. It's very interesting to see an RPFS now in a low tumor burden patient of about 24 patients, which is about 10.5 months, which if you then extrapolate over taxane naive, say, "Okay, we have an opportunity to look like that," and then you go back to Pluvicto, and that particular patient population has an RPFS ranging from 8.6-9.3. If we do indeed come in at 10.5 or thereabouts, would be a positive. On this slide, we have the opportunity that appears to be unique to the immuno-oncology and the T-cell engagers to have an even greater impact on overall survival than RPFS. When we put all of that together, Jon is why we view this as a directionally important and positive data set. Ladies and gentlemen, due to time constraints, that concludes today's call. Thank you all for joining. You may now disconnect.