Commercial, you know, knowledge sharing with the community oncologists. I think the uptake, they're getting more into the commercial and the government insurance and increased listing in the formulary listing. The uptake, I think, is going to be stronger because, you know, most of the prescription in the U.S. is pretty much in the late line setting. Because we have the third label, it also has an R agent, have a good, very good, efficacy and the safety profile. I think the penetration in the market, based on Takeda's experience, is going to be, you know, have a high confidence for the future. Yeah. Yeah, that's helpful. You know, strong growth in the U.S., maybe looking to the launch in Japan slash the EU. How are those launches going? Are you seeing a similar ramp to what you were seeing in the U.S.? Anything you can share there? Yeah, so, I mean, Takeda has a very strong footprint in Japan, right? But they're, even in the GI oncology, they have big place. So they're just have a pretty strong oncology GI presence there. So it is, you know, since the insurance coverage last year, November, the quarter over quarter growth has been pretty strong. According to this, Takeda's 2024 annual report, right, the latest quarter to, you know, over quarter increase is actually 78%. Last quarter, they get the $10.5 million revenue. The uptake in Japan is also on a very strong trajectory. In the EU, since we also only get the, you know, insurance coverage in Spain, with more countries also get the listing and the insurance coverage, the growth is going to also increase and take off. We are very hopeful, Takeda really take on a broader approach to increase the market capturing. Yeah. That's helpful. And maybe, you know, sort of forward looking, thinking about the market opportunity. I know there's been some recent developments in third line plus. I think CytomX had just had recent data. Sort of how do you see that competitive market developing? How do you, you know, continue to see yourself as an advantage? Yeah, so I think, you know, we actually had the luxury. We've been developing fruquintinib actually in China. There are a lot of investigator-initiated trials. They have more development combination with TAS-102. And certainly, you know, another combination with PD-1, for example. They are increasing the data readout. Also, Takeda is looking more at, you know, knowledge generation. Overall, you know, because of the safety and efficacy of the fruquintinib, the team both in the U.S. and China, for example, I think it is also maintaining the good opportunity, yeah, for us to grow in the future. Yeah. Yeah, that's great. Maybe switching to sovleplenib now. I think you guys had positive top line results for SAVANNAH in October, I want to say. Maybe remind us of those readouts and what you're looking forward to, for potential commercialization there. Yeah, so sovleplenib, you know, AstraZeneca actually presented the SAVANNAH trial at the ELCC in March. The data is actually very strong. It's really consistent with the previous in the MET amplified and overexpressed setting. They have a very strong ORR readout of 55% and also the PFS 7.5 months. The data is very consistent. You know, they actually have the discussion, right, with FDA because, for the, you know, the MET, for the EGFR resistant setting, right, you know, it is because of all these development, you know, with, you know, MARIPOSA-2 with our other available therapies. The discussion with FDA is, we'll wait for this, you know, the SAFFRON trial, which is the phase III trial, in order for us to, for the global submission. This is actually the, you know, update for the AstraZeneca development. Yeah. Sure. So maybe speaking to SAFFRON, sort of what bar are you looking for in these patients and how are you thinking about staging? Yeah, so, just, you know, for the information, SAFFRON is a, you know, global phase III trial. It is osimertinib plus sovleplenib versus chemotherapy in the MET overexpress and amplified patient population. This is the setting, you know, for the global registration. The bar, you know, what you mentioned here, you can look at this SAVANNAH data as one reference, right? If you can see the, you know, the response rate, the PFS, you know, it is a PFS-driven event for the primary endpoint. It is that reference. I want to also mention, right, the true bar here is also this is the only biomarker-selected patient population, right? We know just from the published data, the, you know, the previous, you know, early SAVANNAH trial really demonstrates MET overexpression amplification is a poor prognosis. You know, in this patient's actually is a, you know, the, the condition is actually quite poor. In that setting, when we look at the, you know, the control arm, right, I think that will really, you know, speaking out the bar, true bar here to, looking at the resistance setting, the standard of care how to behave. Another reference is actually we have announced the positive phase III trial in China, the SACHI trial, which is a similar setting, you know, EGFR resistant patient population, osi plus versus chemotherapy. And, you know, we have a top line readout. I'm actually very happy to say that the abstract, the paper will be presented at ASCO on June 1st. It's been selected as our presentation. That trial also shines some light about the true bar here, right? Because, you know, again, it's a control trial. In that kind of a setting, the data readout will really establish how to, you know, compare with the EG biomarker selected patient population, how the combination will, you know, work not only for the efficacy, but also the safety. Yeah. That's helpful. Maybe looking broader, I know you have SANOVO readouts as well. What patient population do you sort of see as the key driver for value with sovleplenib? Yeah, so SANOVO trial again is, you know, in the phase III trial in the, it is the front line setting, right? You know, in the MET selected patient population with overexpression, how the combination versus ops, versus osimertinib agent, right? The overall, we think this could be a very, you know, good opportunity for capturing the highest value. Again, the bar here as you see is osimertinib alone, as compared to, you know, people will think probably you compare with the [Fru-0 2] or, you know, the MARIPOSA trial as a bar there. Again, from the biology perspective, we think the MET overexpression patient population had a poor prognosis. The true bar is really the compare of a single agent in the more, you know, poor prognosis setting, how the combo will behave, not only in the safety, but also the efficacy perspective will truly define the final, you know, commercial value for this, for this setting. We do think that based on the biology, based on the data what we have for SACHI, this is going to be a good opportunity for the future value creation for this compound. Yeah. It's very helpful on sovleplenib. Maybe one more on surufatinib before going to sort of the wave two. Can you speak to maybe how you are improving brand awareness here and how you're thinking about gaining market share versus somatostatin analogs? Yes. For surufatinib, right, you know, we are actually the leading, you know, target therapy in the med setting, in a neuroendocrine setting, right? It is really based on the two global, two China phase III trial, to get approval in the SANET-p and SANET-ep. The market uptake is very strong. You know, there are multiple cohort analysis, post hoc analysis, even though it is not a direct comparison with the Sutent, but the overall survival and, you know, the efficacy perspective and also the safety really demonstrate surufatinib is a really good, well tolerated, and also efficacious treatment. We continue to, you know, generating new clinical data to really help our, you know, commercial colleagues to develop a new knowledge. So we have, you know, just published our, you know, the combined pooled analysis for SANET, SANET-ep trial, right? It just, you know, published in June issue of European Journal of Cancer and really demonstrate because, you know, at the termination of the trial, there's a large portion of patient population crossover from placebo to the treat R to, to the surufatinib R. And the data has shown is really pretty remarkable. We actually justify all these, you know, crossover effect, right, using different model. We consistently look at, you know, the hazard ratio, you know, versus original placebo group, you know, with the benefit is, and, you know, with hazard ratio 0.55-0.82 using different model, but consistently the overall survival is over 15 months. It is a very strong data. We continue to, you know, follow up the patient, get the data to our medical community, right, to really further demonstrate our leadership position in the neuroendocrine tumor space. We'll continue to be the leading brand in this setting. Yeah. That's helpful. Maybe moving to wave two for sovleplenib. Anything to specifically point out here for approval? You know, how are you thinking about building out capabilities for launch? Yeah. For sovleplenib, it is a Syk inhibitor. And, you know, we presented our data last year at the ESLIM-0 1 trial data at EHA last year. Then subsequently have a, you know, ASH updated data with a longer follow-up. The data is actually quite strong, right? If we look at the patients who have, you know, been in second line and above, patient population in ITP, we actually observed the durable overall response rate, 48%. At the ASH update, we also showed that durable response rate is at 51%. It is very strong data compared with all different modalities, right? The momentum is building up. In the, you know, during the regulatory review process, we actually look at the, you know, the GAD request. There is addressing the question, we changed the excipient. We're actually generating more stability data to support the NDA submission. We're hoping the data can really get the approval. You know, we're aiming for later this year and hope the strong data is a new modality. We can really support, you know, our first immunology, you know, launch. I mentioned about tazemetostat is our EZH2 inhibitor, in-licensed from Ipsen. We actually got approval. So we build a hematology franchise in China. That also will help us do the pre-launch planning activity for the sovleplenib. Yeah. That's helpful. Maybe on ITP, I think, you know, in recent data you shared that there were no events, thromboembolic events in these patients. Can you speak to how meaningful that is for these patients? Is that something they're looking for? Yeah. So it is, you know, the thromboembolic event is a very, you know, well-established side effect profile for people, people RA because these agents have a continued stimulation of platelet production. So you can actually see overshoot the platelet. So that increased the risk of thromboembolic events. Some of it could be very disturbing because cerebral hemorrhage and all these can really have a, you know, very serious effect and sometimes linking to death, right? This is, you know, is a typical, you know, concern for the TPO-RA agent. For sovleplenib, because this is a different agent, it, you know, in, it's just, you know, the, we don't in the ESLIM-0 1 trial center, we don't see this platelet overshoot. So you, you actually increase the platelet, you know, prevented macrophage eating out the platelet, but also it's not overshooting like a TPO-RA. From those data we have seen, right? It just, there's just no thrombolytic event reported. So this is actually a key advantage, right? When the physician, particularly for a lot of ITP patients, you can see they have increased the thrombolytic risk. So the sovleplenib data is really, you know, provide is a, is a good opportunity in the setting, to have a reduced thrombolytic event, due to the mechanism of action. So it could be a key, potential advantage for this class molecule. Maybe one more question before we move to ATTC, which I know is a very interesting topic. I guess just, you know, what learnings have you had from initial data, you know, sort of experience that you're using for future development in autoimmune or other immune conditions? Yes. I think the, you know, we think Syk pathway is one of the important pathways for, you know, autoimmune disease, right? There are certainly other opportunities, right? If you look at the BTK inhibitor, also, you know, have the potentially broader application for the autoimmune disease. For us, I think the one key, at least some of the, you know, first of the indications we think about, there's certainly opportunity, probably the obvious one is secondary ITP because, you know, for a lot of autoimmune diseases like SLE, you know, antiphospholipid syndrome, you actually see this, you know, hyperactivated, anti, you know, thrombolytic status, right? We have seen in this setting, right, the French publication really showed the patients with APS, SLE, the standard of care is actually TPO-RA. If you look at a publication in those patients, right, secondary ITP, their thrombolytic event, reported incidence actually very high. It's over 20%. And some of them actually have a catastrophic, you know, thromboembolic event. It could be fatal. Right? This is obviously some of the setting, you know, using Syk inhibitor could potentially be, you know, ideal situation. That's certainly the development could be a potential. Yeah. Great. Maybe moving to, the ATTC platform, sort of a novel way of approaching things. How do you see the advantages, disadvantages versus ADCs or other antibody conjugates? Yeah. We recently reported, right, that, you know, our novel platform called Antibody -Targeted Therapy Conjugate, right, compared with the traditional ADC, which is, you know, the payload as a toxin, right? We think it's just actually been through several years of discovery, internal know-how and expertise, we are able to link in target therapy like a small molecule as a payload, through our linker technology, through our small molecule platform, have developed this ATTC platform. The concept here is really, you know, we observe a lot of these traditional ADCs, right? They are, you know, they've been reported scientifically. There are quite a few publications already out, even though with the newer payload in HER2, for example, in the different development setting, they actually observe the tumors. I mean, the patient with, you know, tumor with, oncogenic driver mutation, they actually tend to respond poorly. And, you know, there's a kind of a limitation we observe, right? Because if you look at the, you know, regardless the payload, the toxin payload, third generation or so, they pretty much have to, you know, it's very difficult or almost impossible to combine with the chemotherapy. It's just primarily it's due to the additive effect of the toxicity of the chemotherapy. The ATTC platform not only helps us to address a patient population with a key driver mutation, but also, you know, has the advantage potentially to really combine with the other therapy, chemotherapy or so, target therapy or so, particularly in the early line setting. We think this ATTC platform will provide a novel opportunity to have potentially broader patient population coverage and also compete in the, using an add-on approach in early line setting. Yeah. Maybe on that broader patient population, can you speak to sort of which patients maybe benefit from this, you know, platform the most? Yeah. So, you know, I think, you know, when we develop ATTC activity, I think the antigen part selection, you know, what we actually select all these, we have clearly, clearly select these antigen, the antibody have a broader antigen coverage. And also we select the antibody part, which has been proven at the function, antibody activity. And also with, very carefully selected, target therapy payload, again, we start to looking all the pathway activity, selecting a higher frequent, you know, targets, you know, for these oncogenic drivers. So we combine these together. We think these have a broader coverage of patient population. Not only for target, for with oncogenic drivers, this is a potentially more efficacious therapy, but also, reduce the toxicity because it's more targeted. You, because these combination, you actually bypass some of these traditional therapeutic window for systemically oral therapy for target therapy. It has a more precision-driven kind of approach to, you know, to inhibit a tumor growth. From our perspective, it's easy for patients with oncogenic driver with the, you know, specific antigen expression tumor type. These will have an opportunity to have a better opportunity to compare with the traditional ADC. Also, because these target therapy payload, some of them is actually involved in the critical pathway for the oncogenic pathway. Even some, even non-mutated tumor, because this critical pathway inhibition, it also will respond to the therapy. In the clinical setting, we think, you know, in the driver, you know, oncogenic driver mutated patient tumors, right? Patient population will have a good response. Even in the frontline setting, because of its combination of the chemo and also some of the key pathway inhibition, the ATTC will have an opportunity to have a broader coverage and, on the tumor suppression. Yeah. Looking forward to initial data, what's sort of the key things you're looking for, you know, sort of as a green light or key point of de-risking that this platform works? Is it tolerability? Is it early responses? Is it dosing window? Yeah. So from our preclinical work, we actually have a very good proof of concept, right? We have the target therapy payload. We actually have some very successful, you know, preclinical data, right? Even the target therapy ATTCs, you give a single dose, you have a sustained tumor inhibition, you know, two weeks, three weeks. Also, you know, when you compare with the antibody alone, payload alone, or antibody plus payload, we have a more sustained tumor inhibition. That gives us confidence. This is, you know, in the practical setting, it works well. The true proof of concept, right, certainly will be in the clinical setting. That is why we are gearing up, you know, to have our first ATTC to enter the clinical trial later this year. Really the clinical proof of concept, we want to execute to really, you know, have a clinical proof of concept. ATTC is a novel therapeutic modality, for border tumor coverage in a, in a new setting. Yes. Maybe just one quick question, since I know we're close on time. I think you guys have over $800 million in cash. Sort of how do you see that being deployed? Is it mostly in development of ATTCs, trials, commercialization? Yes. I think we are in a very good, you know, cash position, right? Last year we have over $800 million. We are also divesting our SHPL asset. We are actually in a very fortunate position to really utilize those cash to really advance our ATTC platform development because this is what we think. If it is successful, it will be a brand new platform, generate multiple assets. Not only for us to push the clinical development to have a clinical proof of concept, but also we will invest in the next generation novel ATTC. For example, bisphenic acid antibody, newer payload to really accelerate our new platform development. That investment will really create shareholder value for the company. Yeah. Yeah, that's helpful. I think we're coming up on time, but I want to thank you for the great conversation and looking forward to hearing the updates coming up. Thank you, Matt. Yeah, appreciate our opportunity.