Good morning and welcome to BeyondSpring's R&D Day. At this time, all participants are in a listen-only mode. Following management's prepared remarks and clinical experts' presentations, we will hold brief question-and-answer sessions. As a reminder, this call is being recorded today. It's now my pleasure to turn the call over to Shirley Liang from BeyondSpring. Ms. Liang, please go ahead. Thank you, everyone, for joining today's call. I would like to advise listeners that comments made on today's call may reflect forward-looking statements that are related to such matters as BeyondSpring's clinical and preclinical research and development activities and results, regulatory and commercial plans, industry trends, market potential, collaborative initiatives, and financial projections, among others. While management believes that its assumptions, expectations, and projections are reasonable in view of the currently available information, you are cautioned not to place undue reliance on these forward-looking statements. A company's actual results may differ materially from those discussed during this call for a variety of reasons, including those described in the forward-looking statements and risk factor sections of the company's 20-F and other filings with the SEC, which are available on the investor section of BeyondSpring's website. Joining us on today's call is Dr. Lan Huang, BeyondSpring Co-founder, Chairman, and Chief Executive Officer. Dr. Jun Lu, BeyondSpring Chief Scientific Officer. Dr. James Tonra, SEED Therapeutics President and Chief Scientific Officer. Dr. Trevor Feinstein, Director of Research and Oncologist at Piedmont Cancer Institute and Chair of the Lung Disease Group for the One Oncology Network. Dr. Steven Lin, Professor and Radiation Oncologist at MD Anderson Cancer Center. Dr. Alberto Chiappori, Senior Member of Oncology and Medicine for the Thoracic Oncology Program and Medical Oncologist at Moffitt Cancer Center. Please note that as the timing of this conference call overlaps with Dr. Feinstein's clinical hours, Dr. Feinstein has graciously prepared a prerecorded presentation and Q&A on the development of plinabulin in the Phase 3 anti-cancer study. As a reminder, all participants are welcome to use the Q&A feature on Zoom Webinar to ask questions during this call. After each clinical expert and senior management's presentation, a brief Q&A section will be followed to take questions from Zoom and the phone line. It is now my pleasure to turn the call over to Dr. Lan Huang. Lan. Thank you, Shirley. Good morning, everyone, and thank you for joining today's call. It is my pleasure to be here to share with you the latest development in, number one, advancing plinabulin, our first-in-class microtubule destabilizing DC or dendritic cell maturation agent, in clinical development in unmet medical needs, including anti-PD-1/PD-L1-failed cancer patients. Currently, anti-PD-1/PD-L1 has annual sales over $40 billion and around 60% fail, who have limited treatment options. And number two, SEED Therapeutics, our majority-owned subsidiary, which uses our proprietary targeted protein degradation, or TPD, molecular glue platforms for innovative drug discovery. We are grateful to have Eli Lilly as SEED investor and R&D collaboration partner, with upfront payments and up to $780 million milestone payments and tiered royalties for a number of targets. We have been developing plinabulin for over 15 years, and it has been used in over 700 cancer patients with good tolerability. Today, Dr. Feinstein will share the final and long-term overall survival data for our positive phase 3 study in second-line, third-line, non-small cell lung cancer patients with EGFR wild-type. Second, Dr. Lin will showcase our preclinical-to-clinical translation work and some promising activity of a triple IO radiation combination study in patients of various cancer types after immunotherapy failure. Following that, Dr. Chiappori will give an overview on the unmet medical needs in extensive-stage small cell lung cancer and briefly introduce our triple combination study with pembrolizumab and etoposide platinum chemotherapy in the first-line setting. I should also note that plinabulin is easy to use as an intravenous infusion, used once or twice in a chemo cycle. Finally, we have a strong patent portfolio and a protection to 2038 in 48 jurisdictions for plinabulin. Finally, we will have multiple phase I-II readouts in 2024 that can inform us of the next steps in designing pivotal randomized clinical studies beginning in 2025. This slide shows plinabulin's development timeline. Since its discovery and early clinical work done at Nereus Pharmaceuticals, in 2015, BeyondSpring initiated the first phase III study called DUBLIN-3 in combination with docetaxel, standard of care in EGFR wild-type, second-line, third-line, non-small cell lung cancer. In this very study, we quickly learned about plinabulin's ability to reduce docetaxel-induced neutropenia, which triggered phase II-III studies of plinabulin alone or in combination with G-CSF to manage high-grade neutropenia in breast cancer patients receiving the toxic TAC regimen. Meanwhile, we actively pursued mechanistic studies in collaboration with MD Anderson, Mass General Hospital, and University of Basel, and published two key articles in 2019, which showcased that plinabulin is a unique, truly binding and potent DC maturation agent that activates durable anti-cancer immune response. Follow-up translational work led by Dr. Lin at MD Anderson triggered multiple triple IO combination studies, including with PD-1 and radiation in 2021, or with Keytruda and chemotherapy in 2023. To go into briefly the mechanism of action on plinabulin, the co-crystal structure had been solved, which showed that plinabulin is indeed a unique tubulin binder with a unique plinabulin binding site distinct from other tubulin binders. Upon binding, plinabulin causes depolymerization of the microtubule, which in turn liberates the Rho guanine nucleotide exchange factor H1, which is GEF-H1, from microtubules. The immune defense protein GEF-H1, in turn, activates downstream signaling cascade of Rho, ROCK, and JNK, which can lead to direct cytotoxicity of cancer cells. But in dendritic cells, the signaling cascade leads to DC maturation and subsequent T cell activation to mediate immunogenic cell death. To understand how plinabulin can synergize with radiation or chemotherapy and anti-PD-1 agents to generate an optimal anti-tumor immune response, we can look at the cancer immune cycle diagram here and see that when there is tumor enzyme release induced by radiation or chemotherapy and then coupled with plinabulin's effect on DC maturation, this will further increase antigen presentation. This leads to increased priming of DCs as antigen-presenting cells migrate to tumor-draining lymph nodes and leads to greater anti-tumor specific T cell activation and an optimal systematic T cell response. Given plinabulin's mode of action as an immune chemotherapeutic agent, we believe that plinabulin is a potential add-on therapy to the current IO regimens to help address unmet medical needs in two potential regulatory paths. Number one, while PD-1/PD-L1 inhibitors have been approved for around 20 cancer indications with over $40 billion annual sales, around 60% of patients would eventually fail and contribute significant unmet medical needs in the second-line and third-line settings. In this patient population who have developed acquired resistance, PD-1 alone or in combo with other agents do not work. This is likely due to mutation in the antigen-presenting pathways and T cell exhaustion in the tumor microenvironment. plinabulin, as an easy-to-use APC inducer, could potentially fill the gap and help resensitize patients to PD-1+ chemo, which we are investigating in combination with Keytruda and docetaxel for second-line, third-line, non-small cell lung cancer. Second, in first-line settings, PD-1/PD-L1 inhibitors and chemotherapy doubles the anti-cancer efficacy of PD-1 but still carries a CIN or chemotherapy-induced neutropenia risk, especially for patients receiving high-risk chemo and for patients with preexisting risk factors who are prone to high-grade neutropenia. In this case, plinabulin addition may help generate a durable anti-cancer response by immune modulation and CIN reduction as being investigated in combination with keytruda and etoposide platinum for extensive-stage small cell lung cancer. This is an overview of plinabulin's clinical program. Other than the completion of 2 late-stage phase III studies plus the phase I portion of the MD Anderson triple combo study, we are expecting preliminary efficacy data for Study 303, which is plinabulin combination with Keytruda and docetaxel in second-line, third-line, non-small cell lung cancer patients who failed PD-1 inhibitors, and for Study 302, plinabulin combination with Keytruda and EP in first-line, extensive-stage small cell lung cancer patients, which could have preliminary data in the first half of 2025. As for the Study 303 data matures, we are looking as early as ESMO for release but may opt for other congresses in the second half of 2024. As you know, there are limited options for patients who failed PD-1/PD-L1 inhibitors, as PD-1 alone or in combo with other agents do not work for these patients. It is enlightening that Amtagvi, a TIL cell therapy developed by Iovance Biotherapeutics, recently was approved for melanoma that has not responded or stopped responding to an anti-PD-1 drug. Its estimated cost per dose is over $500,000, and its annual global sales could be over $1 billion by 2030. Therefore, we are actively developing plinabulin in IO combinations for these immune therapy-failed patients in broad indications, with the potential advantage that plinabulin is an easy-to-use intravenous injection agent with one dose per cycle. Now, it is my great pleasure to introduce Dr. Trevor Feinstein, who was our lead PI at Piedmont Cancer Institute for the DUBLIN-3 phase 3 study. Dr. Feinstein co-runs Piedmont Cancer Research Department and is director of research at Piedmont Cancer Hospital. He's actively involved in clinical trials focused on improved therapies for various cancers. Thank you for asking me to review the DUBLIN-3 study, which demonstrated plinabulin's improvement in overall survival in advanced non-small cell lung cancer. Despite improvements in advanced non-small cell lung cancer, we know that most patients will eventually progress. 70%-80% of patients will need additional lines of therapy. More treatment options are needed in this patient population. Currently, docetaxel is the mainstay treatment for second and third-line non-small cell lung cancer without a driver mutation. However, docetaxel-based treatments demonstrate limited efficacy and are associated with severe neutropenia. Other options for treatment include ramucirumab, which demonstrates a modest overall survival benefit when added to docetaxel. However, increased incidence of neutropenia. Pemetrexed demonstrates similar overall survival to docetaxel with less neutropenia. Although pemetrexed is most efficacious in non-squamous histology and is often used in treatment in earlier lines of therapy, multiple attempts to address treatment needs have been unsuccessful. Since the approval of nivolumab eight years ago, no new novel mechanism of action has been approved. Recent clinical trials have failed to demonstrate an improvement, including the SAPPHIRE, the CONTACT-01, LEAP-008, CANOPY-2, EVOKE-01, and the CARMEN-LC03. Recently, the LUNAR trial utilizing TTF fields demonstrated an overall survival benefit but no benefit in progression-free survival or response rate. The TROPION-Lung01 utilizing Dato-DXd showed only an interim overall survival benefit in non-squamous histology. Next. Presented here is the schema for the DUBLIN-3. This was a globalized, randomized, single-blinded, blinded to patients only, utilizing docetaxel and plinabulin versus docetaxel and placebo in patients with EGFR wild-type non-small cell lung cancer. Inclusion criteria included non-squamous and squamous non-small cell lung cancer, Stage IIIB and IV, patients with an ECOG performance status of 2 or less, progression during or after treatment with 1 or 2 treatment regimens including a platinum, must have had 1 measurable lung lesion, prior checkpoint inhibitor therapy was allowed. There was stratification by region: Asian versus non-Asian, prior lines: second or third line, ECOG performance status: 0 versus 1 and 2, and prior PD-1 or PD-L1 therapy. The primary endpoint was overall survival. Secondary endpoints included overall response rate, progression-free survival, percent of patients without severe neutropenia on day 8, months 24 and 36, overall survival rate, duration of response, Q-TWiST, proportion of patients who received docetaxel greater than 8 cycles, greater than 10 cycles, and greater than 12 cycles. There were 559 patients and randomization was 1-to-1 to docetaxel and plinabulin versus docetaxel and placebo. Docetaxel was dosed at 75 mg/m² on days 1 and plinabulin was dosed at 30 mg/m² on days 1 and 8. Next. Here are the baseline and disease characteristics of the DUBLIN-3. You'll find very similar characteristics in both the docetaxel and placebo and docetaxel and plinabulin in age, sex, ECOG performance status, region, and prior PD-1 or PD-L1 therapy. I would like to highlight the tumor histology that there is increased incidence of non-squamous histology in docetaxel and placebo and increased incidence of squamous histology in docetaxel and plinabulin. Next. plinabulin plus docetaxel met its primary endpoint with an improvement in median overall survival. Median overall survival improved from 9.4-10.5 months with an improved hazard ratio of 0.82. I would like to bring your attention to the tail of the survival curve. Here, plinabulin demonstrates a durable improvement in long-term overall survival. If you look at the right, we see that in years two and three that the survival rates are almost doubled with the addition of plinabulin. Here is an overall survival forest plot. Anything to the left demonstrates plinabulin was better than placebo. In all subgroups, plinabulin demonstrated a benefit irrespective of age, gender, race, ECOG performance status, PD-1 or PD-L1 therapy, second- or third-line therapy, and region of treatment. Specifically, I would like to highlight the greater benefit seen with non-squamous histology. Next. Histological assessment shows patients with non-squamous histology derived a greater benefit with plinabulin. The study did not stratify patients by histology. 55% of the patients had non-squamous histology in the plinabulin arm versus 63% in the control. Subset analysis demonstrated a significant survival benefit in non-squamous histology. Median overall survival was improved by 2.4 months with a hazard ratio of 0.76. Next. There was an improvement in overall survival benefit with more treatment cycles. The survival benefit became stronger with more treatment cycles. For example, in patients who received four or more cycles, the median overall survival improved from 13.5 months to 18.3 months. If patients received eight or more cycles, the median overall survival went from 19.3 months to 28.2 months. Although not meeting statistical significance, plinabulin demonstrated an improvement in duration of response. The median duration of response improved from six months to 8.3 months. Next. The use of plinabulin significantly reduced grade four neutropenia. plinabulin allowed patients to remain on docetaxel for a longer duration. Patients randomized to plinabulin had greater exposure to docetaxel. Next. Herein we present Q-TWiST. Q-TWiST is quality-adjusted time without symptoms of disease and toxicity. It incorporates quality and quantity of life. plinabulin added a 1.93 gain of Q-TWiST by adding it to docetaxel. A Q-TWiST greater than 18% is felt to be meaningful. plinabulin demonstrated a Q-TWiST of 18.4%. In KEYNOTE-010, pembrolizumab was compared to docetaxel and had a similar Q-TWiST benefit of 20%. Next. Most toxicities were manageable. There was an increase in hypertension with plinabulin. No patients discontinued due to hypertension. Hypertension was transient. Most hypertension resolved within 4-6 hours after the plinabulin infusion. The plinabulin group reported more gastrointestinal side effects versus the control group. In the study, the treatment protocol for plinabulin infusion time was increased from 30 minutes to 60 minutes. Also, prophylactic antidiarrhea drugs were administered. This reduced the incidence of grade 3-4 gastrointestinal side effects. Post-hoc analysis demonstrated use of G-CSF to treat neutropenia was lower in the plinabulin arm. The use of plinabulin reduced the incidence of leukopenia and neutropenia. Next. The addition of plinabulin as a single agent added to docetaxel improved overall survival with a more pronounced survival benefit in non-squamous histology. This treatment was well tolerated. Side effects were mitigated with changes in infusion time and antidiarrhea agents. There was an improvement in quality of life with reduced incidence of neutropenia. plinabulin allowed patients to receive increased treatment exposure to docetaxel. Hi, everyone. We now start our first Q&A segment. My name is Jun Lu and I recently took over the role of Chief Scientific Officer at BeyondSpring. My background is in cancer immunotherapy and small molecules. To supplement his audio presentation, Dr. Feinstein was also kind enough to offer his answers to a few questions we prepared for him. So, Dr. Feinstein, could you please help explain the small clinical benefits in median progression-free survival and overall survival in the DUBLIN-3 study? First, multiple studies have failed to demonstrate an improvement in progression-free survival and overall survival. plinabulin demonstrated a durable anti-cancer treatment response. There was a doubling of 2- and 3-year overall survival. Duration of response was longer and overall survival benefit was greater with more treatment cycles. Although the etiology is not known, it is thought plinabulin might induce maturation of dendritic cells, macrophages, and activated T- cells to develop a durable immune response. Furthermore, in all subgroups, overall survival had a hazard ratio less than one. plinabulin also reduced chemotherapy-induced neutropenia and improved quality of life. The next question is about in which treatment setting is plinabulin and a docetaxel combination potentially positioned within the current non-small cell lung cancer landscape? The treatment landscape of non-small cell lung cancer has rapidly changed in the last 10 years. Today, there are more targetable mutations which has changed earlier lines of therapy. However, most patients still need additional lines of therapy. Furthermore, PD-1 and PD-L1 inhibitors are the mainstay of non-driver mutation-driven non-small cell lung cancer. In the DUBLIN-3, PD-1 and PD-L1 stratification favor treatment with plinabulin. There are currently ongoing studies looking at the role of plinabulin combined with pembrolizumab which might open the door for earlier combinations. To summarize, plinabulin improved survival, improved quality of life, and reduced the incidence of neutropenia when combined with docetaxel in persons with advanced non-small cell lung cancer after failure of platinum-based therapy. This last question is about how much do you think that the DUBLIN-3 data would help the EGFR wild-type non-small cell lung cancer patients in the era of checkpoint inhibitors? Has the DUBLIN-3 study results been submitted to regulatory agencies? DUBLIN-3 is a positive study which is in final review of a leading medical journal for publication. In DUBLIN-3, about 20% of patients had received immune checkpoint inhibitors. Currently, there is an ongoing intent-to-treat study in non-small cell lung cancer patients who had failure of immune checkpoint inhibitors prior. The hope would be by adding p embrolizumab to plinabulin and docetaxel there would be a more robust clinical benefit. Thank you. Hello, good morning. I'm delighted to introduce to you Dr. Steven Lin, a physician scientist, radiation oncologist, and professor of thoracic malignancies at MD Anderson. It has been a great honor to have been working with Dr. Lin for the last seven years to understand plinabulin's DC maturation mechanism in preclinical models and then in human subjects, and also the journey to translate plinabulin into clinical settings for unmet medical needs. With that, I'm turning the podium to Dr. Lin. Dr. Lin. Thank you, Dr. Huang. The title of my presentation will be on anti-cancer immunity using plinabulin in combination with radiation and immune checkpoint inhibitors. I'll talk about this in the context of both preclinical data as well as actually that set the basis and the foundation for our phase one clinical trial that was conducted and completed here at MD Anderson. Next slide. We know that actually radiation in itself can actually stimulate an immune response and that can generate a systemic immune response in patients, particularly through the activation of dendritic cells. We know that radiation, along with other cytotoxic agents like chemotherapy, oncolytic viruses, etc., can induce and cause cytotoxicity of tumor cells. This can, in turn, release damage-associated molecular patterns or DAMPs to the tumor microenvironment. Those activate receptors on the surface of dendritic cells which, in turn, are activated and therefore migrate to draining lymph nodes. In these draining lymph nodes, there are a host of immune cells that, particularly the lymphocytes, NK cells, CD8 T- cells, CD4 T -cells. These, in turn, are the areas where tumor antigen processing occurs and presentation occurs, and this then, in turn, generates an anti-tumor immune response. And in a setting of radiation, sometimes, rarely can also induce a systemic immune response through the factor of activating dendritic cells and also T- cells. Next slide. So, whether radiation can induce a systemic immune response or an immunologic response has been seen in several studies. This is actually just an example of one, a trial that was actually completed a couple of years ago where they test the question whether if you just do radiation along with immune checkpoint blockade like durvalumab compared to just durvalumab alone, will you see a radiation immune response. So, they actually did this in a neoadjuvant setting before surgery. So, this is, it's a phase 2 study in patients with stage 1 - 3 resectable non-small cell lung cancer where they gave patients durvalumab alone in 30 patients versus adding some radiation to the primary site, however, not treating the mediastinum in this patient with stage 3 disease. What they found is actually compared to durvalumab, which only had a major pathologic response of 6% and 0% pathologic complete responses, if you just add radiation to the primary site, this induces a major pathologic response of 53% and a highly significant increase in improvement in pathologic complete response of 27%, suggesting that just adding radiation along with immunotherapy is promising to stimulate an immune response in particularly early-stage diseases. However, this may not hold for more advanced disease. Next slide. So, there was a phase 2 randomized trial combining or testing the question whether radiation in the setting of immune checkpoint blockade, in this case, with durva + or - tremelimumab, which is an anti-CTLA-4 agent, in patients with PD-1 refractory disease. Unfortunately, this trial was a negative study because the overall response rate was only 10% with a disease control rate of 30% in the combination arm, suggesting that in these patients who are multi-refractory, particularly in the metastatic non-small cell lung cancer patients who are refractory to previous PD-1 or PD-L1 agent, just the dual combination of effect approach using radiation with immunotherapy does not have a very good response compared to just the immunotherapy alone. Next slide. So, the question is, can we augment the effect of radiation in combination with immunotherapy? We believe, yes, by further activating dendritic cells. So, if you don't mind, there's some animation here. Just going to toggle through twice. Yes. So, radiation itself can, of course, like we talked about, can stimulate both the tumor cells as well as the tumor stroma to enhance pro-inflammatory cytokines as well as DAMPs. In combination with plinabulin, which is a dendritic cell active, very potent dendritic cell activator, this can promote a T- cell activation or significantly augment T- cell activation and generate a systemic anti-tumor response. In the setting of PD-1, PD-L1 agent, this can further augment the anti-tumor response. Next slide. So, we wanted to conduct this study to test this hypothesis, whether the triple combination, plinabulin along with radiation and anti-PD-1, PD-L1 agent, can further augment the systemic response. And our hypothesis is that the priming the system with radiation following, followed by plinabulin and anti-PD-1, PD-L1 agent, is safe and efficacious in immunotherapy progressing advanced malignancies. However, we do need to have some preclinical evidence to demonstrate that radiation priming followed by plinabulin could elicit an effective anti-tumor immune response. So, for this, we conducted some preclinical studies in my lab. Next slide. First, we want to test in vitro if there's an optimal sequencing of radiation with plinabulin that could optimally elicit the dendritic cell activation. We conducted the study both adding plinabulin before or after radiation. What we found very significantly and very clearly is that radiation before plinabulin is absolutely critical. If you actually add plinabulin before radiation, you don't see this dendritic cell activation or synergy to activate dendritic cells. However, if you do radiation before plinabulin treatment, particularly about 1-3 hours before plinabulin treatment, you see a significant dendritic cell activation both in these markers that you see, MHC class II, CD80 and 86 markers, as well as CD40 marker, which are markers for dendritic cell activation. The positive control here is LPS, which is lipopolysaccharide, which is a bacterial antigen. It's positive control here to stimulate dendritic cells. What you can see here is that our in vitro data with radiation followed by plinabulin treatment, you can see even bigger response in this combination, even more than LPS as a positive control. Next slide. We also found that actually in what we do with this T- cell proliferation assay, which is a co-assay when you combine dendritic cells, these activate dendritic cells along with naive T- cells to see whether these dendritic cells will activate T- cells. You can see here on the bottom panel, if you just take your dendritic cells, naive dendritic cells, without any stimulation, the T- cell proliferation is only about 1.5%. However, if you actually trigger dendritic cell activation directly with radiation by itself, you see there is some dendritic cell activation. So, you see some T- cell proliferation of 9.6%. If you just add plinabulin alone without radiation, plinabulin itself has a pretty effective dendritic cell activation. So, you see T- cell proliferation increases 22%. However, it's really optimal when you combine radiation with plinabulin. You see a very high and a significant increase to 51% T- cell proliferation when you do the triple combination approach. Next slide. We also see that plinabulin itself not only can activate dendritic cells, but in vitro, we can see also increases PD-L1 expression on dendritic cells. This is well known actually in the literature in that the dendritic cell activation can stimulate PD-L1 activity. And it's the PD-L1 activity and expression on dendritic cells that drives immune suppression in tumors. So, therefore, it makes a lot of sense that we would like to combine not only plinabulin with radiation but also with anti-immune checkpoint blockade to further augment this and reduce and block these immune suppressive mechanisms as a result of dendritic cell activation. Next slide. So, in vivo, these are in vivo models now where we implanted two tumors, one on each flank of the animal. These are mice. One of the tumors, we radiated, and the other tumor on the other side, we observed to see whether there's going to be a systemic immune response. So, we're looking at both the primary tumor response but also looking at this systemic tumor response, which we call the abscopal response. So, if you actually look at the primary tumor response, you see there's a significant reduction in the primary tumor growth when you combine, when you do the triple combination approach compared to just radiation with a PD-1 agent. But however, this also you see this significant anti-tumor systemic response as well in the triple combination compared to just anti-PD-1 and radiation. Next slide. So, this is, again, a much broader and bigger experiment where we looked at all the different combinations with radiation alone, PD-1 agent, combining radiation with PD-1 agent, plinabulin with PD-1 agent, and the triple combination. You can see very clearly that this abscopal tumor, which is the non-radiated systemic tumor, is the one that actually responds best with the triple combination. Also, very significantly is that if you harvest these tumors and you look for dendritic cell activation, you see a significant MHC class II expression on these dendritic cells only in the triple combination compared to any other arms of the study. And you also see significant increases in T cell infiltration in these tumors, both in CD4 as well as CD8 in the triple combination arm. Next slide. So, we have basis now to suggest, to believe that plinabulin does enhance this cancer immunity cycle. However, particularly when you combine with radiation or any other cytotoxic agents, including chemotherapy, along with anti-PD-1. We know that the plinabulin sits at the gateway in this cancer immunity cycle in that radiation or chemotherapy first elicit tumor antigens. This can, in combination with plinabulin, can significantly increase dendritic cell activation and therefore can further trigger T cell proliferation activation, particularly in the setting of checkpoint blockade. Next slide. So, that's the basis and foundation of our phase 1, phase 1b, 2 clinical trial to test the question whether it's safe but also potentially efficacious to examine this triple combination approach of plinabulin, radiation, and immunotherapy. The patients that we enroll to this date, patients are any patient with any cancers that are progressing on prior standard of care anti-PD-1 or anti-PD-L1 agents. The patient must have at least one site to be treated with radiation and another site that's not radiated for a biopsy to take a look at translational studies to look at immune infiltration as well as dendritic cell activation. So, this is an open-label single-center study here done at MD Anderson. It's a 3+3 design. Also, we assess DLT within 30 days after receiving the triple combination treatment. So, you can see here by the schema is that at baseline, we collected both the tumor as well as any blood samples. The patients are treated with radiation first, just very much like our preclinical studies. Radiation is administered 1-3 hours before the drug delivery of plinabulin with anti-PD-1, PD-L1. Then two cycles later, before cycle 3, we also repeat the biopsy as well as blood draws to further look at translational studies. The primary endpoint is safety as well as overall response rate as well as the disease control rate. Next slide. This is the top-line data presented at SITC conference in 2023. We have screened 29 patients. 19 patients were treated. However, 11 patients with the best target lesion response were evaluable. You can see here by B here in the panel B is that a number of these patients had a response. Particularly, a couple of these patients had continued response even up to today, almost one year out from the initial therapy. These are heavily pretreated patients. Many of these patients have 14-16 lines of therapy before coming on this trial. You can see that on panel C, the overall response rate is 30% and the disease control rate is 80%, far exceeding our expectation of response in this triple combination compared to historical controls. In panel D is an illustration of one of our patients. You can see here is that one of the tumors is radiated. And you can see here by the dosimetry and plots, the site in the lymph node was radiated in the neck. And then we looked at other sites. The biopsy site was actually in the area in the mediastinum. You can see very clearly a dramatic response comparing before treatment on the PET scan. After cycle 3, day 1, you can see sorry, after 2 cycles of treatment, you can see a very clear systemic response in this patient, a very large partial response in this patient. Next slide. For translational studies, this is actually a blood draw for this patient. We see a very significant increase in both activated as well as CCR7-positive dendritic cells. CCR7-positive dendritic cells are the activated but also the migratory dendritic cells that go from the tumor to the draining lymph nodes to activate T cells. You can see a very significant increase in CCR7-positive dendritic cells in the peripheral blood as well as activated dendritic cells in both CD80 and CD83-positive dendritic cells. This also promotes pro-inflammatory monocytes in the blood in the patients who are responder patients. Also, you can see here on the plots on the right as well, significant increases in pro-inflammatory monocytes in the blood, particularly in the responder patients. Next slide. When we looked at intratumoral responses, when we did single-cell RNA sequencing of the tumor, both look at tumor cells as well as the immune microenvironment, we're able to see that in the responder patients, there's a significant increase in GEF-H1-positive dendritic cells. So, GEF-H1, as you heard from the introduction, these are the signaling pathways of plinabulin. You can see here is that only the responder group, you see there's significant increases in GEF-H1-positive dendritic cells in the responder group in DC3-positive as well as MoMac3-positive macrophages that are GEF-H1-positive only in the responder group. However, in the progressors, you don't see this increase at all. You do not even see a decrease in these cells, suggesting a target effect of plinabulin in the tumors. Next slide. So, we believe that the pplinabulin in combination with radiation and these immune checkpoint inhibitors does induce a very significant dendritic cell maturation and also potentially resensitizes these immunotherapy failure tumors to immune checkpoint blockade. So, we know that plinabulin is a unique tubulin binder and has a very distinct site other than other tubulin binders. And that in combination, it has a very strong preclinical proof of principle and concept that in combination with radiation, anti-PD-1 activate dendritic cells, stimulates T cell proliferation as well as activates and achieves an abscopal response. We now have clinical evidence of efficacy in at least 10 IO refractory patients. There's a greater than 50% disease control rate as well as durable responses in these heavily pretreated patients, suggesting a potential for clinical efficacy in this growing high unmet need patients who are IO refractory. So, there is now clinical evidence of immune activation. And these responding patients, particularly, exhibit early immune activation with DC maturation in that these IO effects, it goes across multiple cancer types, particularly non-small cell lung cancer, head and neck squamous cell carcinoma, as well as Hodgkin's lymphoma, indicating a broad clinical applicability of this triple combination approach. Next slide. So, this is actually so further, this can be further extrapolated to other agents, particularly cytotoxic chemotherapy. So, this is now an ongoing study, a phase 2 investigator-initiated study done in China in collaboration with Merck, where these patients with metastatic non-small cell lung cancer who are also progressing on anti-PD-1, PD-L1 monotherapy. And these patients are treated with chemotherapy with docetaxel along with plinabulin and pembrolizumab. We know for these patients, these PD-1, PD-L1 refractory patients, historically, the median progression-free survival is only 3-4 months with only an overall response rate of only 10%. So, therefore, we believe that in this combination with chemotherapy and PD-1 and plinabulin, we're going to see a much greater improvement in overall response rate that will exceed these historical controls. So, the overall primary endpoint is overall response rate but also a number of secondary endpoints. We believe that the fertility analysis has been completed and will be reported in one of the upcoming meetings. Next slide. I'll be happy, I believe this is the last slide. I'll be happy to take any questions. Thank you. At this time, we'll be conducting a question-and-answer session. If you'd like to ask a question over the Zoom platform, please type it into the Q&A pod. Over the phone, you may press star one to verbally ask a question. Once again, if you have any questions at this time on the Zoom platform, please type your questions into the Q&A pod. Over the phone, you may press star one to be placed into question queue. One moment, please, while we pull for questions. Once again, if there are any questions at this time, please type them into the Q&A pod on your screen. Okay. Thank you, Dr. Lin. Maybe I'll start with a question first. So, as far as the clinical evidence you have seen in the blood and also the tumor biopsy of those patients, how would you apply this in future studies to identify the sensitive cancer types as well as the responders? No, that's an excellent question. Thank you so much, Dr. Lu. Yeah, I think we were very, very thrilled, actually, somewhat unexpected to see that patients there are a number of patients that are responders. But more importantly, in the patients who are responders, we see that they are actually already primed for potential response through the GEF-H1 signature. We see that in the immune cells as well as not only in the tumors but more importantly, in the blood, that we can look at these dendritic cells and monocytes that are circulating in the blood, the GEF-H1 signature are already present in these patients. And these are the patients with the GEF-H1 signature are the patients who are responders to plinabulin combination, suggesting that this can be used as an effective biomarker to potentially preselect patients for efficacy. And therefore, this potentially can be used as a tumor-agnostic biomarker. So, not necessarily whether we can select for non-small cell lung cancer or head and neck cancers or Hodgkin's lymphoma, but potentially, we can just use this biomarker as a way to select patients to be a responder to this triple combination approach. Thank you, Dr. Huang. Thank you. There are no further questions at this time. Thank you very much, Dr. Lan. Now, we are turning to Dr. Alberto Chiappori from Moffitt Cancer Center. It is my great pleasure to introduce to you Dr. Chiappori, who has been involved in our early small cell lung cancer program. Dr. Chiappori currently serves as a senior member of the oncology and medicine for the thoracic oncology program at the Moffitt Cancer Center. He has been there since 2001 as a member of the thoracic oncology program. Now, the podium is yours, Dr. Chiappori. Thank you. Awesome. Awesome. Thank you very much, Dr. Huang. So, thank you very much for the kind introduction. Thank you for the invitation. Maybe we can just go straight to the next slide, please. So, many of you, I'm sure, know small cell lung cancer is what we consider a neuroendocrine carcinoma. Neuroendocrine carcinomas, although the nomenclature is changing a little bit or has changed recently, neuroendocrine carcinomas, in general, correspond to a spectrum of diseases that goes from diseases that are somewhat more indolent, "slow-growing," low-grade, to diseases that are much more aggressive, high-grade, and where the prognosis is quite dramatic. You can see that in the table there in the lower corner. The first group are considered the carcinoid tumors, typical and atypical. The second, the high-grade type of carcinomas, that's where small cell lung cancer falls down. That classification has a series of clinical characteristics that we will see on the next slide. So, typically, small cell lung cancer, as I said, is a disease that is high-grade and aggressive. Because of that, it is very rare that the disease is going to be detected in early stages. The majority of patients are detected once the cancer has already extended beyond the chest. That is why most of the time, the classification or the staging of the tumor, even though a TNM classification is available, the one most commonly used is the one that was developed many, many decades ago by the VA lung cancer system or lung cancer group, dividing them in limited stage and extensive stage, depending on whether the disease was limited to the chest or extended beyond the chest. And you can see some of the percentages there in the table. The next slide, please. The treatment of small cell lung cancer, extensive stage small cell lung cancer, basically has consisted of chemotherapy, first-line chemotherapy, characteristically a combination of etoposide and platinum, at least in the Western Hemisphere. In Japan, there have been studies showing that irinotecan may be superior to etoposide as a companion of the platinum core of the treatment. But that is something that has not been seen in Western countries or in the Western Hemisphere, certainly in the United States, as you can see again in the table on the right side of your panel. The responses are good. On average, the overall response falls within 50%-60% or 70%. However, those responses are short-lasting. As you can see, the two-year survival rapidly falls to less than 5% or, if you prefer, single digits. There is a median progression-free survival of 2-4 months and a median overall survival around 10 months, 9-11 months. Next slide. For decades, literally for decades, we never saw or we did not see or we failed to see any improvement in the outcomes of patients with extensive stage small cell lung cancer despite multiple attempts of manipulating chemotherapy. You can think of whatever way you could manipulate the chemotherapy, it was attempted, but it failed. However, as you can see here, more recently, 2018, probably for IMpower133, two studies now show the benefit of adding immunotherapy. IMpower133 added atezolizumab to chemotherapy and CASPIAN added durvalumab to chemotherapy in first-line treatment of extensive stage small cell lung cancer. Next slide, please. What was observed in both studies was that, indeed, there was an improved survival when the checkpoint inhibitor, the PD-L1 inhibitor, atezolizumab for IMpower133 on the left and durvalumab for CASPIAN on the right were added to chemotherapy. And you can see that the improvement in survival was around two months in absolute median improvement, but that the improvement was statistically significant. And that is why, today, the standard of care for this group of patients that for decades was a combination of chemotherapy consisting of a platinum doublet, typically etoposide, has changed now to that same backbone chemotherapy plus the addition of atezolizumab or durvalumab, depending on the trial that you want to use to support your decision. Next slide, please. Even more important is the fact that this benefit from the addition of immunotherapy, at least this is representing data from the CASPIAN study with durvalumab, the most important thing, I think, is that this benefit seems to be a durable benefit in the sense that, as you can see, this is a Kaplan-Meier curve showing the three-year overall survival. And you can see in the blue curve, the three-year survival for those patients in the investigational arm at the time, the durvalumab plus chemotherapy arms, of 18%. Whereas in the chemotherapy group, what we would consider the traditional standard of care was only 6%. So again, a tripling of the three-year survival by the addition of durvalumab immunotherapy, PD-L1 inhibitor to chemotherapy. Next slide, please. Now, durvalumab and atezolizumab are not the only checkpoint inhibitors that have been tested in combination with chemotherapy. Nivolumab has been tested in a phase II study. pembrolizumab was also tested in a phase III study, KEYNOTE-604. Unfortunately, the results with pembrolizumab in this trial were not statistically significant, even though, as you can see, the numerical results and the hazard ratio were just obviously better. The statistical analysis showed that it barely, barely did not meet the endpoint required. Next slide, please. Unfortunately, despite the improvements that addition of immunotherapy presents to us, as we can see, inevitably, patients with extensive stage small cell lung cancer will develop recurrence. At the time of recurrence or relapse, you can, in general, recognize two groups of patients, those patients with resistant or refractory disease or, if you prefer, also typically called platinum-resistant patients, if the recurrence occurs within 90 days of the last dose of treatment, or those with sensitive relapse or platinum-sensitive disease, where those patients develop the recurrence more than 90 days after the last dose of chemotherapy. There are a few therapeutic implications for these two groups, but I think that those implications are somewhat limited in general terms. But just reflect, as the title of the presentation indicated, the number of unmet needs scenarios that we can recognize in patients with small cell lung cancer in general, extensive stage small cell lung cancer specifically, either those patients who are going to be treated in the first-line setting or patients that may receive treatment in the second-line setting or beyond. The next slide, please. I think that this was my last slide, but oh, no. So one of the ways or one of the attempts to address some of these unmet needs and following, to some extent, to a great extent, the preclinical data that has been reviewed previously, particularly by Steven and his work at MD Anderson, is that a study is now recruiting patients in China where plinabulin is being added to a combination of pembrolizumab and chemotherapy, etoposide and platinum, in the first-line extensive stage small cell lung cancer. This is a single-arm study. Basically, the question here is exactly the same question that has been asked in the prior presentations in regards to what is the benefit that plinabulin brings from the various mechanisms of action that this drug has to the standard combination that we nowadays use in first-line extensive stage small cell lung cancer. I think that this is basically my last slide. Next slide, please. Yes. Thank you very much. Thank you. Thank you, Thank you, Doctor. And once again, we'll be conducting a question-and-answer session. If you'd like to ask a question at this time, please type it into the Q&A pod on your screen. Or if you're connected via the phone, you can press star one to verbally ask a question. Once again, if you'd like to ask a question today, please type it into the Q&A pod on the bottom of your screen. One moment, please, while we pull for questions. Once again, if you do have a question today, please type it into the Q&A pod on the bottom of your screen. Or if you're connected via the phone, please press star one to verbally ask your question. Thank you, Dr. Chiappori. This is Jun. I'll start with a question. As you mentioned, extensive stage small cell lung cancer is aggressive and difficult to treat. Are there any subtype differences in response to chemoimmunotherapy in terms of median PFS and overall survival? That's an excellent question because one of the problems with small cell lung cancer is that exactly subtyping and subpopulations had never been previously recognized or identified. And we know how important that is from the parallels that we have seen over the last decade with non-small cell lung cancer. The good news is that recently, there have been some publications where different types of small cell lung cancer have been identified based on different expression levels of transcription factors. And the bottom line, or very, very, very, very, very quickly, these different subtypes sort of identify or can divide small cell lung cancer in these tumors that may have more neuroendocrine features versus less neuroendocrine features, the latter being a minority of patients but apparently being those who may be more sensitive to immunotherapy. There are some other biomarkers that are being potentially investigated that could relate to vulnerabilities that these different subtypes have or potentially may have, Schlafen 11 and a vulnerability with PARP inhibitors, for example, that has already partially been described and studied. But this is the field of development right now. This is the major area of interest in small cell lung cancer. Thank you, Doctor Chiappori. Thank you. If there are no further questions at this time, I'll turn the floor back over. Thank you very much, Dr. Chiappori. Now, I'm going to give you the presentation of our majority-owned subsidiary, SEED Therapeutics. BeyondSpring owns 60% at this moment. Joining me today is Dr. James Tonra, who's the President and CSO of SEED Therapeutics. I'm the CEO and also the co-founder of SEED. Next slide. Today, we are going to share with you the three-year exciting journey at SEED Therapeutics, which we specialize in target protein degradation, molecular glue, R&D. SEED is a global leader in the TPD space with deep expertise to address the key challenges, which is to select the right E3 for protein of interest. Why TPD is important? Because it can target 80% of disease-causing proteins currently are undruggable. All the top 20 large pharma are utilizing TPD platforms for innovative drug development. So second, we are also very grateful to the early validation and funding from Eli Lilly in the investment and also in the R&D collaboration. So for the investment, Lilly actually invested $10 million into SEED three years ago for around 20% of the company. In addition, they also preselected protein of interest. And we have R&D collaboration with Lilly with $10 million upfront and up to $780 million in milestone payment and also tiered royalty. And so far, we are very excited to report to you that we have already achieved three milestone payments with Lilly programs. And finally, SEED has a diversified and fast-evolving internal pipeline. So we have successfully translated our TPD platform into eight programs, six internal and two with Lilly in multiple indications, including oncology, neurodegeneration, immunology, and antiviral indications. And very importantly, for these eight programs, we have been using five novel E3s. Our lead program is the RBM39 oral degrader, which addresses the highly validated biology and targeting multibillion-dollar oncology market potential with the first-to-market and best-in-class profile. Our first human dose is targeted for the first half of 2025. Next slide. TPD is the new modality which could target 80% of disease-causing proteins, which are currently undruggable. Those include proteins which are unfolded or proteins which do not have a pocket, so people cannot design kinase inhibitors such as TKIs. Next slide. Our co-founders of SEED are really the pioneers in the field, including Dr. Hershko, who is the Nobel Prize winner, who won the Nobel Prize in 2004. He actually discovered the E1, E2, E3 ubiquitin system almost 50 years ago. So in addition, Professor Michele Pagano, another co-founder in SEED, who currently is the head of biology and molecular pharmacology at NYU, really started looking into the ubiquitin biology starting from almost 30 years ago. But I'm very fortunate to be another co-founder of SEED. In 1999, I saw the first E3 ligase structure, which is the HECT domain E3. And in addition, Professor Ning Zheng, who is the HHMI professor at the University of Washington, he saw the other RING finger E3 in 2002. So with all of us, we really understood how to use the right E3 for protein of interest. The field really had a renaissance in 2010 to 2014 when the field discovered that Revlimid is a molecular glue to target for the multiple myeloma after its peak sales at over $10 billion. So with that discovery, we understood that we really need to activate E3 ligases for protein of interest, which can target many indications and which give us tremendous potential for unmet medical needs. Next slide. So in addition to the scientific co-founders in SEED, we also have a league of balanced board members and also the expert translator, starting from Doctor James Tonra, who is the President and CSO of SEED. And he has over 20 years of drug discovery experience. He has brought 5 NDAs to the market. And he worked at Regeneron, Millennium, ImClone, Kadmon, and also BeyondSpring. So under James' leadership, we have successfully translated our TPD platform into 8 pipeline assets, 6 internal, and 2 with Lilly. In addition, we're also under the guidance of premier board members, including Mr. Ko-Yang Tao, who brings 50 years of experience in the legal system. He first taught at Harvard and Yale Law School. He was the former Eisai board member. Eisai is a leading CNS disease drug company. In addition, he was also general counsel at the World Bank. Next to him is Doctor Linus Lin. He came from Eli Lilly, from Eli Lilly's investment. So with Doctor Lin, he was the general manager of Lilly China R&D Center. Currently, he's the global head of Lilly Chorus, which conducts clinical studies for innovative drugs. And if Lilly sees something good, he will help Lilly to purchase those assets. And finally, we have Mr. Jackson Tai, who brings 50 years of experience in finance and also risk management. Jack was a senior partner at J.P. Morgan for 26 years. He was also the CEO and chairman of DBS Bank in Singapore. When he was a board member, he acted as a board member for Eli Lilly for 10 years, 15 years at Mastercard, 7 years at HSBC. Jack really is instrumental to bring us risk management and sound governance in the company and also to help us to elevate us to commercial success. Next slide. In the last three years, we also have built our infrastructure and also organization. We have a 10,000 sq ft lab space at King of Prussia, Pennsylvania. In addition, we also have a league of experienced and highly dedicated scientists at SEED Labs. These scientists had many years' experience in developing innovative drugs, including over 40 IND filings and over 12 drug approvals. Next slide. Controlled protein degradation is a validated pathway for novel drug discovery. We're very glad that the PROTAC, which is what you could call TPD 1.0 companies, has already achieved rapid advancement in novel drug discovery, including a drug from Arvinas already entering phase 3 studies. Major companies in the PROTAC space, including Arvinas and Kymera, are already achieving very high commercial success with over $2 billion market cap. But we believe that there's still some limitations with PROTAC because PROTAC is a bifunctional molecule, and it's very large, usually over 500,000, so potentially limiting its cell availability. And it does require a high affinity to both ends, which is the E3 and also the protein of interest. It requires the pocket in both proteins. And currently, it's very much E3-centric, which includes two important E3s, Cereblon and VHL. But with molecular glue development, we believe that we have a few advantages here because molecular glue is a much smaller molecule, which is usually less than 500,000, so it's more drug-like. And in addition, it does not require the high affinity on both sides. So it could target protein which is unfolded, such as Tau, or protein without a pocket. And it could be a protein substrate-centric. So we can utilize multiple E3s for protein of interest. So that gives us a lot more room to play for protein substrates. Next slide. So SEED is considered one of the leading companies using our TPD platform to develop molecular glue. We're very honored to be featured at a recent Nature Biotechnology review article in March, as you see here. And what sets SEED apart is really our special technology platform, which can identify the right E3 for protein of interest. Next slide. Currently, we use a multidimensional and a proprietary platform for E3 selection, which includes three components. We can select those three components in one or two for protein of interest, depending on the protein. It's very much tailor-made for the protein of interest. First, on the left, this is a structure-based quasi-interface analysis platform. As you see, there are over 600 E3s in the cell. There's only two classes of E3. One is the HECT domain E3, which I solved almost 25 years ago. Another is the RING finger E3, which Professor Ning Zheng solved. We basically covered the whole E3 structural space. We can use in silico screening to find the right E3, which has the right structural complementarity to the protein of interest. In addition, we also have a Lumid patented technology platform, which can identify the right E3 near the protein of interest in live cell. And finally, with Ning's revolutionary discovery, we require a basal interaction of the E3 receptor with the protein of interest. So before we go into the high-throughput screening, we require the in vitro assay to see that the E3 ligase we selected actually do have basal and weak interaction with the protein of interest. And we have an algorithm to calibrate that. Next slide. So utilizing our TPD platforms, we are taking a two-pronged approach to tackle both novel and known E3 ligases. And so far, we have been translating them into pipeline assets. First is the Tau, which is designing the best molecular glue against known E3s. So the program we are using here is the RBM39 oral degrader, which we are using, a known E3, which is called DCAF15. So this program has already advanced into IND candidate. And we expect to have first human dosing early next year, first half of 2025, in multiple oncology indications. In addition, we also have this powerful platform, which can select novel E3s for any protein of interest. And here you can see the example is a Tau. Tau is an unfolded protein. And for Tau, we have selected a novel E3, which is highly expressed in the brain. And we have identified its binding before we go into the HTS and also mono-ubiquitination of this novel E3 with Tau. So currently, Tau program is advancing very rapidly. We expect to have IND candidate by the end of 2025. Next slide. So we're very delighted to share with you that in the last three years, we had a very productive development history. So not only Lilly's project has advanced nicely, we have achieved three milestone payments with Lilly's two programs. The two programs Lilly had were very difficult. One is a 3,000-amino acid protein with an unfolded region. Another is the membrane protein. So it is very difficult, but it's our team's effort and also the power of our platform, which have allowed us to achieve three milestones with Lilly programs. In addition, as you see below, not only we built infrastructure and also the organization, we also have moved our program fast forward, as you see here, just to give you a speed sense. For the Tau program, from selecting Tau as a target to the cell activity, it only took us around six months. Next slide. So as you see, our TPD platform could be very powerful. So far, we have translated our platform into eight pipeline assets, six internal, two with Lilly, in multiple indications, including oncology, neurodegeneration, immunology, and also antiviral, which underscores the technology's versatility and scalability. Next slide. So the TPD field is really a high-valued field. This novel therapeutic modality is highly valued by all the 20 large pharma. As you see here, the financial value for those programs is very high, even at the preclinical stage, with Merck and Bayer acquiring Peloton and Vividion for over $1 billion at the preclinical stage and with recent deals between Genentech and other companies with upfront of $35 -$60 million and up to $1 billion in the milestone payment. When the asset actually goes into the pre-IND/IND stage, the upfront increases to $100 -$300 million in recent cases, such as the BMS-O rum recent case. Finally, if the drug goes into the early phase 2, the financial value even goes higher, like the recent Arvinas and Pfizer deal, which is basically around $1 billion for early phase 2 asset. Next slide. So to summarize, we believe that SEED is very differentiated in all the TPD biotech companies. First is we are target-centric. So basically, we can select the right E3 for protein of interest. And how do we identify the right E3? And because of our scientific team and also our TPD powerful platform, and currently, we have already shown our outcome in using 5 novel E3s for 8 proteins of interest over the last 3 years. Finally, we also have an engine which can highly effectively translate our TPD platform into the pipeline assets under James's leadership. In the end, I also want to say that our company also uses a two-pronged approach to have a de-risk revenue model. We do prioritize our R&D partnership with large pharma. Not only does it give us validation for our platforms, but also it awards us with upfront and milestone payment. In parallel, we also speedily develop internal programs so that we can bring shareholder value to our investors. Next slide. With that, we can open to questions. Thank you. Once again, if you have any questions, please type them into the Q&A pod on your screen. Or if you're on the phone, you may press star one to verbally ask a question. Once again, if you have any questions at this time, please press star one to verbally ask your question over the phone. Or over the Zoom, you can type your question into the Q&A pod on the bottom of your screen. One moment, please. We'll be pulling for questions. Before the audience asks some questions, let me first start with this question, James. SEED is very differentiated from other companies. Probably you can elaborate a little more on SEED's differentiation in the TPD platform and its drug development. Yes, sure. SEED is particularly target-centric rather than E3-centric like most of the other molecular glue companies. SEED is therefore not focusing on building a platform around a specific E3 ligase tool. But SEED has built and is applying a breakthrough platform to select the right E3 ligase from the greater than 600 E3 ligases that are in the human genome to target specific proteins that are well validated to cause human disease. Well, thank you, James. Can you also describe the next major evaluation inflection points for SEED? Yes. The next major value inflection milestone for SEED will be safety, target engagement, and efficacy data from the first RBM39 degrader clinical trial that is projected to start dosing patients in the middle of 2025. Okay. Thank you. And finally, does SEED operate independently from BeyondSpring? Yes, certainly. Operational and other decisions are made by SEED employees and the SEED board of directors independent of BeyondSpring. Okay. Thank you very much, James. So Dr. Lin, if you are still on, probably. I'm still on. We can just ask you a quick question from one of the audience. Yes. Mr. Panaka. His question is, what are your next steps to establish efficacy of the triple-combo strategy? Yes. I wrote in my—maybe I'm not sure if it's a direct reply. But for the rest of the audience, yeah, we will need to certainly expand on this, I think, very interesting but early data. But we would target these refractory patients, but also potentially adding in preselection based on the GEF-H1 signature. I think that'll be a very important whether planned, maybe initial phase two, but then potentially phase three as well. But then kind of phase two to evaluate whether that GEF-H1 signature does indeed predict for these responder patients before considering just kind of a more tissue-agnostic approach. And that will really open up a lot of these patients with these stage four patients with a very huge unmet need. And then also, of course, to test this triple combination approach, but then maybe in the initial phase 2, but also potentially a seamless phase 3 randomized trial design. Thanks. Yes. Thank you so much, Dr. Lin. It has been such a pleasure and a privilege to work with you for the last seven years. We hope to bring plinabulin to millions of patients with comorbid needs together with you. Thank you. Me too. Yeah. Thank you. Thank you. Thank you very much. There are no further questions at this time. I'd like to turn the floor back over to Dr. Huang for closing remarks. Thank you, everyone, for joining today's call. So let me just summarize. I think we're very excited about plinabulin's effects in DC maturation because it is serving as a bridge between the tumor antigen and also T cells. And potentially, by combining with PD-1 and chemoradiation or ADC, and also so it could potentially resensitize patients who failed PD-1, PD-1. This is truly unmet medical needs. And hopefully, plinabulin can add to the tools for oncologists. But very importantly, the combination usually also requires good safety. So as you heard from Dr. Feinstein, plinabulin adding to docetaxel actually can dramatically reduce neutropenia. So not only have we seen this CIN benefit in the Phase 3 study, but also we have seen this in five other clinical studies. So I think this is an additional safety benefit for the plinabulin in combination with chemo or ADC. So combining all this together, in the last 15 years, we have accumulated safety data in over 700 cancer patients, which serves as a very good safety foundation for us to build our triple IO combination strategy strong for these highly unmet medical needs patients. Next slide. So I hope you will stay tuned and look forward to our potential data readout for the 303 study, expected to be the second half of 2024, and also the first-line small cell lung cancer study, which is the study 302, expected to be the first half of 2025. Okay. Next slide. So in summary, I think we have showed you two very important programs at BeyondSpring. One is plinabulin, and there are multiple data points which are going to be released in the second half of this year and also early next year. This could be very transforming data for plinabulin and also for these truly unmet medical needs patients. Secondly is for SEED Therapeutics. I think in the last 3 years, we have already validated our TPD platform with multiple assets in development, oncology, neurodegeneration, immunology, and also in antiviral indications. And we also have proven ourselves in achieving 3 milestones with our partner, Eli Lilly. So with all of that, we believe that BeyondSpring could have a transforming year this year and also coming into 2025. We hope you can stay tuned with our progress. And I really appreciate all of your support over the years. Thank you very much, and have a nice day. Okay. So if I can answer one of the attendees' questions regarding SEED and Lilly's collaboration. So the question is, is the Eli Lilly collaboration exclusive, or is SEED open to other collaborations? And secondly, is there a plan to unlock the value of SEED to BeyondSpring shareholders? So if I can ask the first question. So the Eli Lilly collaboration is not exclusive. So Lilly actually gave us multiple targets. And for those multiple targets, then we cannot work with other companies. But since there are thousands of protein targets in the cell, so with SEED's platform, which is scalable and versatile, we can also work with other large pharma on their targets. So this is not exclusive. And then we are in deep discussions with other potential additional partners as well. So the second question is, can SEED be opened up to other BeyondSpring shareholders? So BeyondSpring is a public company, so you can buy freely on the public market. And as you know, BeyondSpring is owning around 60% of SEED. SEED currently is a private company, so it has its own financing strategies. Owning BeyondSpring is owning a part of SEED. This is the benefit. Thank you. Thank you. We've reached the end of our question-and-answer session. Ladies and gentlemen, that does conclude today's webcast. You may disconnect your lines at this time and have a wonderful day. We thank you for your participation today.