Jasper Therapeutics, Inc. (JSPR) Earnings Call Transcript & Summary

Good day, and welcome to the Jasper Therapeutics Clinical Update Call. [Operator Instructions] Please note this event is being recorded. I would now like to turn the conference over to Alex Gray, Jasper's Head of Investor Relations. Please go ahead.

Thank you, operator, and thank you to those listening in today. Joining us for the prepared remarks are Ron Martell, CEO; and Dr. Ed Tucker, CMO. Also on the line is Herb Cross, CFO. We will be presenting slides on today's call, which are available via the webinar link and posted to our Investor Relations website. Moving to Slide 2. During today's event, we will be making forward-looking statements based on our estimates and assumptions and our current expectations and projections about future events. All statements other than statements of historical facts made during today's event are forward-looking statements. These statements are subject to a number of risks, assumptions and uncertainties, any of which may be significant, and our actual results may differ materially and adversely from those stated or implied in any forward-looking statements. For a description of risks and factors that could affect our future financial results and business, please refer to the disclosure in the accompanying slides, our most recent Forms 10-K and 10-Q and the reports that we may file on Form 8-K with the Securities and Exchange Commission. All of our statements are made as of today, October 14, 2024, based on information currently available to us. We can give no assurance that these statements will prove to be correct, and you should not rely on any forward-looking statements as predictions of future events. We undertake no duty to update any forward-looking statements, except as required by law. We'll now turn to Slide 3, and I'll hand the call over to Ron Martell. Ron?

Thank you, Alex. Good morning. I'm Ronald Martell, CEO of Jasper Therapeutics. On behalf of my colleagues at Jasper, I'd like to welcome you to our conference call to present the preliminary data from our Phase Ib/IIa SPOTLIGHT trial evaluating briquilimab in Chronic Inducible Urticaria or CIndU, following the press release we issued earlier this morning. Before handing it over to Ed to walk through the data, I'd like to express our excitement to be presenting our first clinical data, demonstrating the ability of briquilimab to deliver rapid and meaningful clinical benefit in chronic urticaria with 10 of 12 participants enrolled in the 120-milligram dose cohort experiencing a complete response. And with 14 of 15 participants enrolled in both dose cohorts of the study, achieving a clinical response within the 6-week preliminary analysis period following the treatment despite high disease burden at baseline. We're also very encouraged by the promising safety and tolerability profile observed in this study with no serious adverse events and no grade 3 or higher adverse events reported. We believe that these data provide strong positive read-through to our other programs in mast cell diseases. And following Ed's remarks, I will review our next steps in CIndU as well as the upcoming milestones in our CSU and asthma programs. Turning to Slide 4. I'd now like to turn the call over to Ed.

Thank you, Ron, and good morning, everyone. Before we review the preliminary efficacy and safety results from the SPOTLIGHT study, I want to highlight the high unmet medical need in patients with CIndU. Moving to Slide 5, chronic inducible urticaria is a debilitating condition of the skin and in severe subtypes involves other organs, including the airway, which is going to be catastrophic for certain patients. There are many triggers for the hives, itch and wheels, including heat, cold, sunlight, water and abrasion. The 2 most prevalent subtypes are symptomatic dermographism, or SD caused by skin abrasion and cold urticaria, CU or CCU, caused by moving from warm to cold environments such as air-conditioned rooms or immersion in cooler swimming pools. Mast cells are central to the pathophysiology with degranulation leading to release of inflammatory mediators creating the symptoms of each disease. The most severe outcomes of cold urticaria as an example, can result in laryngeal edema and life-threatening asphyxia. For most patients with CIndU, physical, social and psychological impacts are significant impairments to quality of life, similar to other dermatological diseases, such as psoriasis and atopic dermatitis. Beyond antihistamines, there are no approved treatments available globally for patients with CIndU. The development of briquilimab to deplete mast cells may offer a new paradigm for patients reducing disease burden and improving the quality of life. Let's move to Slide 6, where we show the high-level study design. The trial is enrolling adults with 2 types of CIndU, symptomatic dermographism and cold urticaria, both refractory to antihistamines, we are assessing the ascending single doses of briquilimab from 40 milligrams to 180 milligrams and our centers are located in the EU. We have completed the enrollment of the first 2 cohorts, and we'll begin enrolling our 180-milligram single-dose cohort very shortly. Our key efficacy assessments are the TempTest, the FricTest test and the UCT score during a 12-week observation period and then an extended follow-up period. In addition, we will assess the skin biopsies, the serum tryptase through the course of the study and observe safety and tolerability of the drug. The lower panels show the validated provocation test for each CIndU subtype in the trial. The FricTest is a 4-point assessment and 0 indicates a complete response with a partial response being a 2 or more pin improvement. For the TempTest, which measures temperature thresholds at which hives occur, a complete response is achieved when they tested negative or no hives induced at or below a temperature of 4 degrees Celsius. A partial response is a 4-degree Celsius improvement from baseline. We are presenting 6-week preliminary analysis of all patients currently enrolled into the SPOTLIGHT study, who have now passed the 6 weeks post dose observation period. Now let's go to Slide 7, which summarizes the baseline characteristics of the 2 cohorts. Overall, age, weight and gender of the participants reflects a typical disease demographic for CIndU. Focusing on the larger cohort of 120 milligrams briquilimab, baseline FricTest and cold TempTest scores include a severe disease population of patients enrolled into the cohort. And this is as expected as these patients were refractory to their antihistamines prior to enrolling into the study. Baseline UTC scores for both cohorts were very low. On a 16-point scale, 12 indicates well-controlled disease, and a score of 16 indicates complete control. Therefore, these UCT scores at baseline reiterate the severity of the patient's disease upon enrolling into the study. Now let's move to Slide 8. Briquilimab 120-milligram single dose achieved an 83% or 10 out of 12 complete response rate with an additional patient achieving a partial response during the 6-week period. In the 40-milligram cohort, 1 of the 3 participants enrolled achieved a complete response, and this was in the patients with symptomatic dermographism. We also observed partial responses in 1 other patient with symptomatic dermographism and 1 in a patient with CCU. In the 40 milligrams, cohorts, all 3 participants achieved a clinical response. Now moving to the 120-milligram cohort. 11 out of 12, 92% of the participants achieved either a complete or a partial response. 7 of the 8 participants in the 120-milligram cohort with SD achieved a complete response and the remaining patient achieved a partial response. For the participants with cold urticaria, 3 out of 4 achieved a complete response in the 120-milligram cohort. When combining both the 40-milligram and the 120-milligram cohorts, we saw 14 out of 15 participants or 93% of participants achieved a clinical response in the 6 weeks observation period. Now moving to Slide 9. Slide 9 shows the timing of the clinical responses in relation to serum tryptase measurements. Looking at the means of the 12 participants, we see a rapid fall in tryptase at the first post-dose visit at day 7, remaining well below the baseline value throughout the 6 weeks of observation. The rapid decline in tryptase, consistent with mast cell biology and CK blockade and seen in other studies, correlates with the rapid onset of clinical response. As we observed, 11 out of 12 participants achieved a CR or a PR by week 2. At week 6, 6 out of our 12 patients continue to maintain a complete response and 1 patient continued to maintain a partial response. We will continue to assess the durability of these clinical responses as we complete the trial. In addition, on day 29, 10 of the 12 participants achieved a UCT score of 12 or more, remembering that this is a 16-point scale, indicating that these patients had complete or well-controlled disease. Now moving on to Slide 10, where we show the safety of briquilimab. This shows the cumulative safety results from both cohorts for all patients with a minimum of 6 weeks of follow-up. Briquilimab of 40 milligrams and 120 milligrams was well tolerated with no discontinuations due to safety, no SEs and no grade 3 or higher AEs. There were no AEs of hypersensitivity, no hair or color or skin change colors -- sorry, no hair or skin color changes. The AEs reported in 2 or greater participants are listed in the footnote to the table below, and all were grade 1 or grade 2. The CPK elevations noted in 2 participants were mild and alternative causes were noted. As noted here, we did observe 2 patients who experienced 1 grade 1 neutrophil reduction and -- sorry, we did observe 2 patients who experienced Grade 1 neutrophil reductions, 1 reported at day 94 and 1 reported at day 29. The ANC count fell below the lower limit of normal in the study of 2,000 for those patients, but resolved without clinical sequelae. Moving to Slide 11. This figure shows the mean changes for ANC from baseline for 6 weeks for the 40-milligram and 120-milligram cohorts. Of note, no patients had neutrophil counts below 1,500 during this period of observation, and there was no association with infection. Taken together, these results presented from the SPOTLIGHT trial, including a well-controlled, well-tolerated safety profile with minimal impact on neutrophil counts with high levels of rapid clinical response demonstrate the potential of briquilimab. I will now hand back to our CEO, Rob Martell, for upcoming milestones and closing remarks. Thank you.

Thank you, Ed. Moving to Slide 13. One of the key takeaways from these data is that they reinforce the potential for an optimal biologic dose strategy with briquilimab in mast cell diseases. As Ed discussed, we have now shown that briquilimab is able to rapidly drive clinical responses as well as deep reductions in tryptase with durability of clinical benefit at the 120-milligram dose level, all while demonstrating a favorable tolerability profile with the mild and transient impact on neutrophil counts observed. These attributes, along with briquilimab's 9-day half-life should allow patients to achieve clinical response shortly after treatment, then have the drug washout allowing the return of c-Kit signaling followed by redosing prior to the return of symptoms. Taken together, we view these data as supportive of an optimal biologic dose approach as well as a positive readthrough to our other mast cell programs. On Slide 14, is a summary of our operational updates for SPOTLIGHT and BEACON studies. As Ed noted, we have added a 180-milligram cohort to the SPOTLIGHT study, which has already been cleared by regulatory authorities and will soon begin enrolling patients. We expect to present the full data from the study in the first half of next year. In our press release this morning, we also announced that we are planning to report initial data from all cohorts in the BEACON study, including the 180-milligram Q8-week cohort during the week of January 6, 2025. Moving to Slide 15. Our upcoming mast cell franchise milestones. In addition to the milestones I just mentioned in CSU and CIndU, we're looking forward to enrolling our first patient in the Phase Ib/IIa challenge study evaluating briquilimab in patients with asthma later this quarter. And we're also excited to announce that we anticipate selecting a fourth mast cell indication in the first half of next year and launching a clinical study in the back half of the year. To conclude on Slide 16. As I've said before, 2024 is a transformational year for Jasper, now highlighted by clinical data demonstrating that briquilimab can drive substantial clinical benefit in chronic urticaria. We are particularly encouraged by the combination of robust efficacy, rapid onset of effect, durability of clinical response and safety that was observed. On the efficacy side, 93% of all patients achieved a clinical benefit. And in the 120-milligram cohort, an 83% complete response rate was observed. The effects of briquilimab on tryptase reduction and clinical response, we're also seeing soon after dosing with 93% of patients enrolled in the 120-milligram cohort, achieving a CR or PR at day 15. And on the promising safety profile, briquilimab has been well tolerated in the study with no SAEs and no AEs of grade 3 or higher, and no AEs related to anemia and skin or hair color changes reported. We look forward to presenting full SPOTLIGHT study results in the first half of next year. The safety profile thus far gives us confidence to continue to explore briquilimab at higher doses and optimal dose frequencies in mast cell diseases. On behalf of the entire Jasper team, thank you to the investigators and the patients who participated in the SPOTLIGHT study. With that, I'd like to open the meeting to questions, only related to the SPOTLIGHT study, and please note that we will not be discussing the BEACON study as it remains a blinded study at this time. Operator?

[Operator Instructions] The first question today comes from Yaron Werber with TD Cowen.

Congrats on the nice data. I got a question maybe and a quick follow-up. So when we look at the CR/PR 92%, the CR 83%, it looks really good. I mean, obviously, this is the 120 dose and presumably, you're still trying to figure out which dose you're going to take forward into CIndU, and you might want to take a higher dose forward. Am I thinking about this correctly? And also, what's your latest thoughts on -- I'm just trying to get a sense of durability as relating to serum tryptase levels. You're seeing a nice reduction, but you're obviously not totally maximizing it. So is this just a question of dose? And then how are you thinking about dosing frequencies. Are you considering potentially Q4 weeks, given the data from a competitor? Or are you sticking to Q8 and 12?

Thank you for the question. Yes. I think that these data really reinforce, first of all, that we have an active drug and that gives us great confidence that we can drive meaningful responses. I think as we think about doses and it's one reason why we added the 180 and is thinking about the data forthcoming from the BEACON study. The real question is how do we sequence these doses. So maybe with that, I'll turn it over to Ed. Ed?

Yes. Thanks, Ron. Thanks, Yaron. We are incredibly pleased with the results today from the 120-milligram cohort in the SPOTLIGHT study. We demonstrate the clinical responses, both at the 40-milligram and the 120-milligram, which demonstrates both biological activity, which is what Ron was mentioning, but also as well that the responses were durable out to 6 weeks, which was the cutoff for this data. What does that mean for the sort of looking ahead, I think certainly, the results are comparable with prior data. And also as well, we have the opportunity to test further and analyze further the higher doses being tested in BEACON and now in the SPOTLIGHT study as well with the 180-milligram cohort being started. What does that mean? It possibly means that the depth of our responses could be deeper and the durability could be longer, but I think on its own, the 120 in itself is very encouraging from a drug perspective and also a dosing frequency perspective. So we anticipate that both this data here and the additional data will provide us a lot of insights in deciding what those doses and frequencies will be in our registrational programs for CIndU and CSU.

The next question comes from Gavin Clark-Gartner with Evercore ISI.

This is Yesha on for Gavin. I just have a quick follow-up on that previous question. And albeit maybe there's not enough PK/PD modeling data yet. But based on the existing data, what level of tryptase reductions do you think you can get in those higher 180 to 40 mg doses? And how long do you think those reductions will be able to persist for?

Good morning, Yesha, and thank you for that question. I think as you point out here, the study is still early in its preliminary data and we will be looking at those PK and PD markers moving forward. And again, we're pleased by the tryptase reduction that we observed in the study with this dose level. I think the question will be, as we move up in doses, would we see additional reduction in the tryptase. Ed, anything you care to add to that?

Yes. Thanks, Ron. Thanks, Yesha. I think one of the things that's very encouraging is the speed at which the tryptase was reduced and then that was correlated with the rapid onset of clinical responses in the SPOTLIGHT study. That, again, indicates the strong biologic activity against the mast cells. And so the readthrough from there, as we anticipate when we run those analysis, the PK/PD analysis across a wider population of patients, both in the SPOTLIGHT study and also have the BEACON data available early next year. That will be very informing for us with regards to, again, those dose selections for the registrational program. One would anticipate that, yes, tryptase will be deeper and more prolonged in its reductions as you ascend the doses in the 2 studies.

I think 1 additional comment as it relates to that is, as we all know, tryptase is an interesting biomarker, but it continues to be in precise both -- on both leading edges from the reduction of tryptase, just how much tryptase reduction is necessary to drive a clinical response. And then the return of tryptase is imprecise in correlating to efficacy. As you noted, even though tryptase is continuing to rise in the tail here of the 6 weeks, we still maintained 6 complete responses, even the fact that tryptase is rising. So it's 1 of the things we will continue as Jasper to be a leader in this field is exploring and working with subject matter experts here to better understand tryptase in this disease and how better to use that biomarker because at this point, it still is a bit crude as a biomarker.

The next question comes from Gregory Renza with RBC Capital.

Congrats on the nice data. Maybe just in keeping with the tryptase theme, if I may, I'm just curious how the recovery at day 6 may be aligned with your expectations. Is this earlier than you were expecting? And as you just think of just adding some comments on how this could improve with the higher dosing as you've alluded to? And just certainly related, as you think about that lower dose at 40 mg, just wondering if you could talk a bit about the effect of the 40 mg on tryptase and the kinetic profile. Congrats again.

Greg, thank you for that question. Ed?

Yes. Thanks, Ron. Thanks, Greg. I think the tryptase recovery, certainly, we have discussed that in the past that tryptase recovery can come from a number of different sources. I think what's really key here is looking at the clinical responses at the 120. With regards to dose response, I think it's fair to say we see a clear dose response from the 40 milligrams to the 120, both in terms of responses and also in the tryptase. When we look at the tryptase itself on the 40 milligrams, we do see a similar depression in tryptase, be it a smaller incremental reduction in tryptase and then the durability of that tryptase reduction is shorter than in the 120. What the inference acknowledging small numbers is that, number one, that is a dose response. But the second is that this longer-lasting tryptase reduction is certainly a sign of mast cell depletion as opposed to mast cell inhibition, which is what we think we saw in the 40 milligrams, and that's very consistent with our experience from prior studies. And so we think that the optimal biologic dosing has been demonstrated here in the 120-milligram dose where we're getting mast cell depletion on a single administration of briquilimab that is lasting out to 6 weeks, both clinically and also in the reductions of tryptase.

The next question comes from Ben Burnett with Stifel.

And I'll also add my congrats on the data. I do want to follow just on this line of questioning around tryptase because I think it's super interesting. Just to clarify from that last comment, were you able to look at mast cell recovery? I know in the past, you've kind of mentioned that as another proxy to consider. So just curious, if you looked at the mast cell recovery in this data set and if that corresponded with symptoms or symptom relapse? And then if I could just also ask for a little bit of clarity on the BEACON data that we're about to get next year, kind of how many patients across the various dose cohorts could we get? And would we get material number of patients at the 240 mg dose cohort?

Ben, thank you for the question. So a couple of high-level answers. On the BEACON study, yes, we will provide 12-week follow-up data on all cohorts, including the 240-milligram and the 180-milligram Q8 week as well. So all study -- all patients in all cohorts, including the 240 and the 180 Q8 week with a minimum of 12 weeks on all of the patients in that study. Regarding mast cell recovery, we are taking biopsies from these patients. Those data are not available at this time, but we do look forward to looking at those biopsies to better understand both the timing of the mast cells, the depth of the mast cell depletion and the timing of the recovery.

The next question comes from Pete Stavropoulos with Cantor Fitzgerald.

Congrats on the data. Clearly suggests there's a pharmacological activity leading to a clinical response. I understand that this is a single dose. But curious on how these data sort of in combination with the Phase I PK/PD data, have you thinking about whether you may need to incorporate a loading dose?

Pete, and thank you. Yes, as you know, the healthy volunteer data really helped inform us for our dose selections in -- both in this study as well as in the BEACON study. And the 80 and the 120 dose that we chose here, as a reminder, the 80 is where we thought that, that threshold of saturation might come into play. We now know that even at the 40 level for some patients, we were able to get there. The median in the healthy volunteer at the 158 level, and that's why we chose the 120 and the 180 dose levels here. So I think they're quite informative, now backed up with these data. And Ed, maybe you want to speak a little bit more about the optimal biologic dosing here and why we're looking at these different dose levels and intervals.

Yes. Thanks, Ron, and thanks, Pete, for the question. I think with regards to the loading dose, I think once we have all the data in from the SPOTLIGHT and the BEACON study, we'll be able to conduct a full analysis, including the mast cell depletion, the mast cell recovery measured in the biopsies and then also correlating that with the tryptase measures, both on the downward deflection and also the recovery as well. So we're going to have a lot of data at the end of these 2 studies. As you may recall, we're testing doses, which we anticipate therapeutic from 80 milligrams, although we did see biologic responses here today in the 40 milligrams in the SPOTLIGHT study, but we're testing 80 milligrams all the way through to 240 milligrams in the BEACON study as well. That will inform us in terms of our dose selections moving into a potential registration study where we'll have that data in hand next year and make those decisions. So we haven't made a final decision on whether or not we need a loading dose. I think we need to see the data first. But all of this looks very encouraging, as Ron said, from a 120, we have a lot of head space with regards to those additional doses and also testing the frequencies as well, which is very important for us, the 8 and the 12-week dosing frequencies at the higher doses in BEACON.

Congratulations once again.

The next question comes from Matt Phipps with William Blair.

Congrats on this initial positive look here. First off, just what drove the decision to make an interim analysis of the SPOTLIGHT study at a 6-week time point as opposed to the 12-week primary endpoint?

Ed?

Thanks, Ron. Thanks, Matt. We had this analysis in mind because the patients have all completed the 6 weeks. As you may recall, patients on the 120-milligram dose, we anticipate would have cleared that drug around the 4 weeks period acknowledging the half-life of this product. And so we thought that the 6-week data was highly relevant for the field, but also for ourselves, so we could examine the efficacy and safety once the drug is cleared out. And so having this data and also patients who are further along from a safety perspective, it was important to share this data with the community.

Great. And then looking at, again, some of the tryptase data, I know that's been a focus. The baseline for that 120 mg dose shows a very wide range, including a patient all the way up to '25. Just curious if you saw a benefit across such a wide range of serum tryptases or maybe that high patient was a tougher to treat patient or something? And you said greatest reduction of a mean of 66%. Just curious if you have what the median reduction was given this wide range?

Yes. With regards to the tryptases, in the 120, there were a couple of patients who are a little bit higher than the upper limits of normal. But that's to be expected in this community of patients. You do get outliers of tryptase. And we saw that in some of the other studies for both CIndU and CSU. So not completely unexpected. With regards to additional analyses looking at individual patients, I think that we will do those analysis later down the line once we have more data in. The one other thing I would just mention about the tryptases is that we did see tryptases from baseline to the level below quantification by week 2. So again, this is important information in terms of those individual patients and how they're responding to the drug with regards to tryptase.

Great. And maybe 1 last question. Just as far as when we're thinking about the BEACON trial, the way that neutropenia AEs will be reported, is it a lower limited normal 2,000 as the cutoff for any neutropenia or -- yes, just how should we be thinking about that?

Yes. So for the BEACON study, this is located in Europe, the lower limits of normal for the protocol were 2,000. And we had -- we did not see any patients fall below the 1,500 mark. Now from a clinical perspective, one does not anticipate any clinical sequelae at neutrophil levels of 1,500. So we feel very reassured that the drug is doing its job in reducing the symptoms for these patients without compromising safety with regards to the ANC counts. So again, we look forward to sharing more data later in the year from a broader population as well.

Thank you, Matt. And we have time for about 2 more questions.

The next question comes from Jay Olson with Oppenheimer.

Congrats on these impressive signals of efficacy and safety. Can you talk about the baseline levels of serum tryptase and the standard deviation you saw around those. It seems like there was 1 patient in the 120-milligram cohort with a relatively low baseline level of 3.6 nanograms per ml. Was that the same patient who did not achieve a response and also 1 of the 2 patients with grade 1 neutropenia? And would you consider enriching future study populations based on elevated serum tryptase at baseline?

Jay, thank you. Ed?

Yes. Thanks, Jay. I think, as I mentioned in the summary of the baseline demographics, this is a population which we think -- which we know represents a CIndU population. So we do see the majority of the patients within the bounds of normal tryptase. However, there are other patients who sometimes have higher levels of tryptase coming into the study. We don't think that impacts the results we're presenting here. With regards to the lower recording of tryptase again, that's very typical of this population. So don't see a concern here in the patients we brought in. And we had a very stringent inclusion/exclusion criteria for those patients coming into the study.

We have time for 1 more.

The next question comes from Emily Bodnar with H.C. Wainwright.

Congrats on the data. Maybe just a safety question for me. So you mentioned that you didn't see any cases of hair and skin color changes or hypersensitivity. But I'm curious if any of those may occur beyond the 6-week time period. I guess, just your confidence level that you wouldn't see that as you sort of go through the full 12 weeks?

Yes. Emily, thank you for the question. Again, we're really pleased by the safety profile that we've observed here. And I think to the question of -- it's one of -- an earlier question from Matt about the 6-week analysis, I think, is similarly consistent here is that by 4 weeks-ish, the drug is completely cleared from the system. And so we would not expect any late effects arising here. Ed, maybe you can provide some more background on that.

Yes. Thanks, Ron. Thanks, Emily, for the question. Yes, we are very pleased that we did not see hair color, skin color change, nor hypersensitivity reactions in the study, as you can imagine. That's going to be beneficial for patients who are administered briquilimab moving forward and also in our ongoing studies as well. I think what we are seeing with regards to the results is the opportunity for an optimal biologic dosing schedule here. And I think what Ron alluded to in his comments is the drug is being administered. It's doing its job to lower the mast cell burden, lowering that tryptase, but then also relieving the unnecessary or unwanted effects on those melanocytes with regards to hair and skin color change. And so the melanocytes have an opportunity in a -- without the c-Kit blockade to do its work to put the hair -- to put the color into the hair and to put the color into the skin. And so having this optimal biologic dosing in the future studies could be demonstrating an improved safety profile and avoid some of these safety liabilities. So in essence, after 6 weeks, we are really encouraged that we haven't seen these, and we'll continue to monitor those in our studies.

Thank you. In conclusion, again, 2024 is a transformational year for Jasper, now highlighted by clinical data demonstrating that briquilimab can drive substantial clinical benefit in chronic urticaria. We look forward to presenting the full SPOTLIGHT study results in the first half of next year, and the BEACON study, including the 180-milligram and 240-milligram dose level. So all patients in the BEACON study, the week of January 6. And on behalf of the entire Jasper team, thank you again for joining the call this morning.

The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.