First of all, I would like to take this opportunity to welcome you all to our R&D Day. R&D Day is an important annual event for the company. It has been the company's tradition to showcase our research and pipeline development and share our excitement with investors, experts, and our partners. Without further ado, I would like to take the first 15 to 20 minutes to set a stage for today's R&D presentation, and more specifically, discuss how to best position the company in this turbulent market to focus our resources on our key business priorities and deliver high-value milestones and catalysts. Now, what is the company's competitive advantage or differentiation? Over the years, we have successfully demonstrated that I-Mab's competitive advantage and differentiation is our R&D capability in the area of immuno-oncology. We have been focusing on global innovation to develop biologics with first-in-class, best-in-class potential. We have done well in this regard with multiple examples. Since 2016, we have created three waves of innovative programs or assets at different development stages. The first wave is represented by global frontrunner and differentiated monoclonal antibodies. The best examples include lemzoparlimab, our phase III-ready differentiated CD47 antibody, and uliledlimab, our differentiated CD73 antibody that is ready for phase III in 2023. The second wave is comprised of a novel bispecific antibody portfolio, leveraging our proprietary 4-1BB platform. The two most advanced bispecific antibodies are in phase I clinical trials in the U.S., and we expect others to follow. The third wave is comprised of even more innovative drug candidates such as messenger RNA-encoded therapeutic antibodies, cell-penetrating antibodies, and novel immune adjuvants, all of which are enabled by cutting-edge science and transformative technologies. As part of our strategy, we have been taking two steps to capitalize on our global innovation. The first step is to create value through a partnership with a global pharma for ex- China rights when our asset is validated in phase I or phase II clinical trial. Here, the best example is the lemzoparlimab, our CD47 antibody. We reached a global partnership deal with AbbVie for ex- China rights of lemzoparlimab. The deal size is around $2 billion with upfront of $180 million + $20 million. With multiple partnership deals, including the AbbVie deal, we have achieved two key goals. One is to provide validation for our global innovation, and the other is to successfully generated cash flow. The existing deals are expected to generate a cumulative $800 million in five years. We strive to continue to do more deals. The other step is to advance the assets through clinical development to market in China to realize the commercial value of our products. In the next three years, between 2023 and 2025, we expect to submit three potential PLAs followed by product launches. As a result of our innovation combined with in-licensing efforts, we have built innovative and globally competitive pipeline of 20 assets, mostly in phase II, phase III, and another 10 early stage assets. That is very rich pipeline. How will we prioritize and invest our resources in the value driver assets? Since the beginning of this year, we have been facing the same challenges as many other companies have faced in this market. How do we best position the company to not only survive, but also thrive in this turbulent market to continue strengthening our fundamentals? Here, I would like to briefly summarize our repositioning strategy in three aspects. The keywords here are prioritization and focus. The first aspect is about near-term commercialization of felzartamab, our CD38 monoclonal antibody for multiple myeloma, and eftan long-acting growth hormone for PGHD. For these two products, we will choose to partner with the leading domestic big pharma companies with proven commercialization capabilities with established sales forces and channels. We have already established a commercial partnership with Jumpcan, a market leader in the pediatric therapeutic area in China for eftan long-acting growth hormone. We have been working with them to prepare for the BLA and a subsequent product launch. We're in the process of contemplating a similar commercial partnership deal for felzartamab. With this partnership strategy, we're able to avoid draining significant resources into building a large sales force and a commercialization capability in this difficult time when our cash runway is essential. We must prioritize our resources in the developments of our high-value assets. That's the area we do best and have a competitive advantages. However, when the time comes to commercialize lemzoparlimab, and later other core products, we will always have the option to commercialize selected products on our own. That's what I mean by this hybrid model, which allows flexibility to maximize the value of our products. The second aspect is to prioritize our resources on the value driver assets in our pipeline. Our pipeline is rich, so we must focus. Through a systematic science and business review, we have placed our priority on six assets associated with 12 clinical trials. Some of them are ongoing, and some others are yet to start. With the progress to be made with these prioritized assets, we expect to do more BD deals to reinforce our strategy and extend our cash runway. The third aspect is to invest in our next-generation pipeline assets. This area is one of our core strengths. We're on the way to generating a novel portfolio of the next-generation programs to achieve four to five R&D or phase I clinical trials by 2025. It is worth mentioning that our current cash runway with cash on hand plus the expected milestone payments is three years and is sufficient to support our core business activities as I just laid out. Now I would like to expand further on the three key aspects of our business areas we have prioritized. Firstly, in terms of the pipeline prioritization, here is what the prioritized pipeline looks like. We will focus our resources on these six high-value clinical stage assets to deliver key clinical and BD milestones. For the interest of time, I will leave it to Andrew, our head of R&D, to go into detailed discussion later in this presentation. Secondly, how will we maximize the commercial value of the two near-term products, namely felzartamab, our CD38 monoclonal antibody, and eftan long-acting growth hormone. For felzartamab, we have completed the registrational trial for third-line multiple myeloma treatment. The study met all the preset primary and secondary endpoints and is ready for BLA submission. For the second-line multiple myeloma treatment, we completed the patient enrollments in September last year. I want to emphasize that felzartamab is uniquely positioned as the only locally manufactured CD38 monoclonal antibody product to be more competitive in the China market, where the pricing pressure is very high. With the product advantages and local manufacturing, felzartamab's peak sales are estimated to reach CNY 2 billion. The other product for near-term commercialization is eftan long-acting growth hormone. The phase III clinical trial is on track. We already completed all patient enrollments in May 2020, and patients are being treated and evaluated. We expect to conclude the study by 2023. As shown on this slide, the current growth hormone market in China is dominated by short-acting daily injectables and is rapidly migrating to long-acting weekly injectables as the overall growth hormone market continues to grow. By 2030, the market share of long-acting growth hormone products is expected to surpass that of daily injectables. We are among the four players in this space, and eftan has a potential safety differentiation. We expect to have a significant market share of around 15%-25%, with expected peak sales between CNY 3 billion and CNY 5 billion. Last year, we reached a commercial partnership deal with Jumpcan. The commercial partnership is mainly based on profit sharing in addition to prearranged payments valued at $315 million, including upfront milestone payments. Jumpcan is a market leader in the pediatric therapeutic area in China, with extensive hospital networks and sales channels around the country. By partnering with Jumpcan, we'll be able to leverage their market leader position and quickly establish eftan's market position and penetration. Thirdly, I-Mab's pipeline is not a random collection of drug programs. It is designed strategically and driven by cutting-edge science. We're focused on potential best-in-class and first-in-class products. Our innovation comes in three waves. For monoclonal antibody portfolio, in addition to lemzoparlimab and uliledlimab, we have been working on new candidates to expand our monoclonal antibody portfolio. For our novel bispecific antibody portfolio, we have a significant progress, as some of the programs have already advanced to the clinic with exciting preliminary data. For the third wave, next generation drug candidates, although relatively early in discovery, new leads are emerging. I'd like to leave it to Andrew and Jerry, our CSO, to tell you more about these exciting programs later in their presentations. Now I'd like to move on to our expected deliverables in terms of milestones and catalysts in the second half of this year. On the clinical development front, we will initiate the planned phase III clinical trial for lemzoparlimab as a first-line MDS treatment. We have submitted the application package and are in process of communicating with the CDE. In addition, we expect to achieve a few new data readouts, including lemzoparlimab MDS phase II data at ESMO in September. Additional data readouts for uliledlimab phase II lung cancer trial, and a preliminary clinical data readouts for TJ-CD4B. Meanwhile, our BD negotiations are ongoing for uliledlimab, TJ-CD4B and a commercial partnership for felzartamab. Among the key corporate milestones on the right side of this slide, I would like to highlight one particular milestone we expect to complete shortly. That is the switch to a U.S. based auditing firm that is PCAOB compliant. With that, our 2022 financial report will be fully compliant with the HFCAA requirements and guidelines to mitigate the risk of being delisted as an ADR company. In parallel, we're continuing pushing forward with our dual listing plan. What will our pipeline look like by 2025? We expect to achieve three potential BLAs followed by product launches. Two active registrational clinical trials for lemzoparlimab and uliledlimab. Three to four critical phase II clinical trials. The ongoing efforts to generate the next generation drug candidates is expected to produce four to five new R&D or phase I clinical trials by 2025. In parallel, we also expect to complete more BD deals as the clinical development of multiple assets progresses with more data. Last but not least, I'm pleased to highlight that we have a strong management team that is up to challenges and committed to delivering key milestones and pipeline value. It's worth mentioning that the three of us, including myself, Andrew, and John, are all U.S. licensed physicians with extensive global trial experience in developing innovative drugs. We are confident that we have the best professionals with sophisticated leadership in all key positions to achieve the company's continuous success. Now, I would like to stop here and pass today's presentation to Andrew, our Head of R&D. Andrew. Thank you, Dr. Zang, for the introduction. I'm Dr. Andrew Zhu, President of the company. I want to join my colleagues in welcoming you to I-Mab 's 2022 R&D Day. Next, I will give you an overview of I-Mab's key clinical development and progress as we continue to strive to bring transformational medicines for our patients. Currently at I-Mab, we have 20 assets in development and 10 at clinical stage. Today, I want to focus my discussion on our core assets with key milestones and near-term commercial partnerships highlighted, including felzartamab, a differentiated CD38 antibody where we expect to submit BLA for third-line multiple myeloma in 2022 or 2023. A BLA for second-line multiple myeloma in 2023 or 2024, and also looking at a potential commercial partnership. Eftansomatropin alfa is our long-acting growth hormone. We expect to submit a BLA for pediatric growth hormone deficiency in 2023 or 2024. In November of last year, we had announced a commercial partnership with Jumpcan, a top 100 Chinese pharmaceutical company specializing in the pediatric space. Lemzoparlimab, a differentiated CD47 antibody, and we expect to enter a phase III clinical trial in first-line MDS in 2022, and a phase III clinical trial in first-line AML in 2023. We are also working on advancing clinical trials for solid tumors and NHL. Our partnership with AbbVie was announced in September 2020. Next, uliledlimab, a differentiated CD73 antibody. We expect to enter a phase three trial in non-small cell lung cancer in 2023 and continue to work on other potential solid tumor indications. We continue to actively look for a global partner for uliledlimab. Efineptakin, a first-in-class long-acting recombinant interleukin-7 that is moving towards clinical trials in triple-negative breast cancer and other solid tumors. Finally, TJ-CD4B, a bispecific antibody targeting claudin 18.2 and 4-1BB. We're developing these indications for gastric cancer and pancreatic cancer, and it is one of our bispecific assets which may lead to a potential global partnership. I want to discuss each asset in more detail. First, let me start by focusing on felzartamab, a differentiated CD38 antibody. Considering the relevance of this therapeutic target, it is important to note there are approximately 20,000 new cases of multiple myeloma each year in Greater China, with approximately 125,000 multiple myeloma patients in China as of 2021. Meanwhile, the estimated biologics market for multiple myeloma in China is estimated at $800 million by 2030. Felzartamab is differentiated with a distinct profile, where it can be administered in an outpatient setting because of the shorter infusion time and lower infusion reaction rate. We have also demonstrated the good efficacy, including in elderly patients with multiple myeloma. Our CD38 antibody shares a similar mechanism of action as with other CD38 antibodies. It can deplete CD38-positive multiple myeloma cells via antibody-dependent cytotoxicity, also known as ADCC, and antibody-dependent phagocytosis, known as ADCP. However, the complement-dependent cytotoxicity effect was attenuated to mitigate the potential infusion reaction and other side effects. This slide summarizes our development progress in multiple myeloma, membranous nephropathy, and a potential new combination with lemzoparlimab. In multiple myeloma, our registrational third-line trial has met the primary endpoint of ORR and secondary endpoints, including PFS and OS. In second-line phase III trial examining the combination with lenalidomide and dexamethasone, patient enrollment was completed in the third quarter of 2021. In membranous nephropathy, our global partner has released the encouraging data showing a significant reduction of anti-phospholipase A2 receptor autoantibody level after one week of treatment. Finally, in our animal model of high-risk multiple myeloma, which was less responsive to CD38 antibody alone, the combination treatment with lemzoparlimab showed an enhanced antitumor efficacy, providing the rationale of exploring additional felzartamab-based combination. Felzartamab will potentially be the first locally manufactured CD38 antibody in China. To support the company's rapidly growing and manufacturing pipeline, we have made substantial progress in the construction of a state-of-the-art GMP manufacturing facility in Hangzhou, China. A process development laboratory in our phase I GMP manufacturing facility is already operational to handle CMC product needs. Three times 2,000 L production lines in place. The phase II commercial production facility is being constructed to accommodate up to nine times 6,000 L commercial production lines, and is on track to be completed by 2024. This manufacturing facility will allow for better market access in China while gaining cost advantages from being a locally manufactured product. Meanwhile, we continue to explore other potential commercial opportunities, including a hybrid commercialization model, to maximize the value of this product. In addition, we continue to assess other potential disease indications. Next is Eftansomatropin alfa, also known as TJ101. Our differentiated long-acting growth hormone. Eftansomatropin alfa is the only natural long-acting growth hormone in the proprietary fusion protein format, and that is a pure protein-based molecule. It's not chemically linked with PEG or other linkers. Its safety, tolerability, and efficacy have been well demonstrated in a phase II clinical trial in a European trial. As shown in the figure in the middle panel, weekly or bi-weekly treatment with Eftansomatropin alfa showed comparable efficacy to daily Genotropin injection. There are advantages to using a weekly versus daily injection for treatment of pediatric growth hormone deficiency. This includes improved patient compliance, with patients more likely to consistently take their treatment in a weekly or bi-weekly versus daily setting. We're also in the process of developing an auto-injector, which would also help with convenient use. This slide highlights the design of our phase III registrational, also known as TALLER trial. Patients with pediatric growth hormone deficiency would receive either eftansomatropin alfa at 1.2 mg/kg weekly or Norditropin at 0.034 mg/kg daily in a 2:1 ratio and continue treatment for 42 weeks. The target sample size was 165 patients. We were very pleased that patient enrollment was completed on schedule in May 2022, despite the impact of COVID-related lockdown. Following the completion of the enrollment, final data from the TALLER trial is anticipated in 2023, followed by a BLA submission in either the fourth quarter of 2023 or the first quarter of 2024. We continue to develop the auto-injector in parallel. The next asset is our differentiated CD47 antibody, lemzoparlimab, which has attracted so much attention in the immuno-oncology field because of its potential as the best-in-class CD47 antibody and its leading position among the first CD47 antibody drugs potentially to be approved for hematologic malignancies. As stated before, lemzo is differentiated by design to minimize red blood cell binding while maintaining a high level of antitumor activity. This molecular differentiation has been validated pre-clinically and has translated clinical advantages that continue to be validated. The key factor behind lemzoparlimab's differentiation is related to a unique binding site of lemzoparlimab, also called glycoepitope on red blood cells. The unique glycosylation around the binding site of lemzoparlimab serve as a natural barrier to prevent lemzo from engaging RBC. This means that red blood cells are only minimally accessible by lemzo. By contrast, the binding site on tumor cells does not have similar glycosylation and is fully exposed, which explains why lemzo binds strongly to tumor cells and maintain its antitumor activity. Lemzoparlimab can uniquely distinguish tumor cells from red blood cells to avoid severe anemia that is commonly seen with other anti-CD47 molecules while still maintaining strong antitumor activity. Here you can see a summary of three generations of CD47 antibodies, including first generation magrolimab, second generation SRF231, and the third generation lemzoparlimab, by comparing their hemagglutination and RBC binding data respectively. As you can see, while magrolimab has both high hemagglutination and strong RBC binding, lemzoparlimab has no hemagglutination with minimal RBC binding activity. We believe the differentiated feature of lemzo has gained preliminary clinical validation, including the expected favorable safety profile with no priming dose required, less RBC-mediated sink effect, and promising antitumor activity across several clinical trials. In a systemic safety data review of over 190 patients who were treated with lemzoparlimab, either as monotherapy or in combinations, we have seen a compelling safety profile to date. Overall, the safety data from both the U.S. and China studies continue to be favorable when administered without a priming dosing regimen. MTD was not reached in any dose regimens. Mild TRA in solid tumors and NHL. Good safety profile in combination with azacitidine in AML MDS trial, and no grade 5 hematological TRAEs reported. In terms of efficacy of lemzoparlimab, three clinical trials are summarized here with the MDS and the phase II study to be finalized. Efficacy signals have been detected at higher dose cohort in monotherapy in patients with advanced and refractory solid tumors. In a smaller group of solid tumor patients who were previously treated with PD-1 based therapy, both PR and SD were detected. In another trial where lemzoparlimab is combined with rituximab for NHL, we observed encouraging early clinical efficacy. Of seven evaluable patients, CR rate reached 57% with an ORR at 71% and DCR at 100%. Finally, we have seen encouraging efficacy signal on lemzoparlimab combination therapy with AZA for newly diagnosed MDS, particularly for those with longer treatment duration, which will be discussed further. Here, I'd like to highlight our study design of lemzoparlimab in combination with AZA in first-line high-risk MDS. In our phase I dose escalation, we have escalated lemzoparlimab monotherapy in AML MDS from 1 mg per kg up to 30 mg per kg. In our phase II combination therapy in MDS cohort, lemzoparlimab was combined with AZA in newly diagnosed intermediate or high-risk MDS patients with the total target patient number at approximately 68 patients. Here, I'd like to highlight some high-level data from our phase II data of lemzoparlimab in combination with AZA in first-line high-risk MDS patients in China. In this treatment group, we have seen compelling safety with lemzoparlimab well-tolerated in combination with AZA, despite the more severe baseline features related to underlying disease in this cohort. We have also observed comparable efficacy to magrolimab with an ORR approaching 85% and a CR rate at 33%. We plan to present this detailed data set at the upcoming ESMO per the organizer's embargo policy. Additionally, as mentioned, we plan to initiate a phase III registration trial in the second half of 2022, and we have already submitted a communication package to CDE in the second quarter of 2022 to push this registration trial forward. As shown on this page, you can take a look at our global clinical development plan. Outside of China, we have partnered with AbbVie, who is spearheading global clinical efforts in several tumor types, including AML, MDS, where a triplet of lemzoparlimab in combination with AZA and venetoclax is being explored. In Greater China, AbbVie is leading the efforts in several tumor types, including in NHL, where lemzo will be combined with rituximab, in MDS and AML, where the combination with AZA is being explored. Our plan remains to initiate MDS registration trial in the second half of 2022, and we plan to have another phase III trial in AML in 2023. In solid tumors, we continue to explore the combination with toripalimab, and the enrollment remains on track. Importantly, I like to draw your attention to the addressable patient population of each of these indications. For example, in MDS, in China, there are 21,000 patients, where G7 nations have 28,000 patients. For AML, we have 38,000 patients in China, and there are 38,000 patients in the G7 nations. Finally, for NHL, China has 93,000 patients, where G7 nations have close to 180,000 patients. Finally, in addition to trials that are currently underway, we are also exploring novel combinations beyond PD-1 or PD-L1 in the treatment of patients with solid tumors. This includes a combination treatment with HER2 ADC in patients with either gastric or breast cancer, as CD47 is highly expressed in these tumors. As shown here, the combination with HER2 ADC with lemzoparlimab showed synergistic antitumor activity in HER2-positive models, providing the rationale for further clinical development in this setting. Similarly, a combination treatment with a KRAS inhibitor in non-small cell lung cancer model with KRAS G12C mutation also showed a synergistic antitumor effect. Next, I would like to discuss uliledlimab, another global frontrunner that we're developing for solid tumors. As previously reported, uliledlimab is differentiated by design to avoid the so-called hook effect. So what is hook effect? Simply put, the hook effect is characterized by an abnormal phenomenon that the drug molecule paradoxically loses its effect at higher doses. Uliledlimab's differentiation comes from a unique binding epitope at its C-terminus. We believe the differentiation give uliledlimab a better therapeutic window and more flexibility when combined with other antitumor drugs. In addition, uliledlimab has potential advantages over small molecules with a non-competitive inhibitory effect that is not blunted by high level of CD73 enzyme substrate abnormally accumulated in the tumor microenvironment, which would be expected for small molecule competitive blockers. Finally, we have observed stronger in vivo antitumor activity when combined with a PD-L1 antibody. Importantly, we observed a linear PK profile at doses of 5 mg per kg and above, and a steep PK/PD relationship that supports 20 mg per kg Q3 weeks as our RP2D. Complete CD73 inhibition and receptor occupancy saturation were achieved at a target C trough concentration of 30 mcg per mL and above. A population PK analysis indicates no difference between patients in China and the U.S., with an effective half-life of 18 days. We first observed encouraging antitumor activity in the initial phase I study in combination with atezolizumab. In this completed phase I study of uliledlimab in combination with atezolizumab for patients with refractory or recurrent solid tumors, among the 13 evaluable patients, an overall response rate was reached at 23%, with one complete response and two partial responses, and the disease control rate at 46%. For the one patient with a CR, this patient was a PD-1 naive patient with ovarian cancer who remained on this study for over 21 months as of now. For the two patients with PR, they were both non-small cell lung cancer patients. One has failed prior nivolumab, and the other one was PD-1 or PD-L1 naive. Of the three patients with stable disease, two patients had previously failed PD-1 or PD-L1 treatment. In this phase I study, we have also explored the possibility of CD73 as a potential predictive biomarker. Interestingly, the three responders all had baseline high CD73 expression. In contrast, almost all patients showed a strong and high prevalence of A2AR staining, with no significant difference in the expression level between the responders and non-responders. Here, we highlight the ongoing phase II clinical trial design in China of uliledlimab in combination with toripalimab, a PD-1 antibody developed by Junshi in China. Uliledlimab was administered with an entry weekly dose of 2 mg per kg and in monotherapy escalation up to 30 mg per kg every three weeks, and in combination up to 30 mg per kg of uli and 240 of toripalimab every three weeks. In dose expansion at the recommended phase II dose, which is 20 mg per kg every three weeks, we have actually explored five cohorts of patients. Cohort 1 represents patients with non-small cell lung cancer who failed standard of therapy but naive to a checkpoint inhibitor. Cohort 2 patients represent non-small cell lung cancer patients who failed standards of therapy, including prior checkpoint inhibitor. Cohort 3 represents non-small cell lung cancer patients who were either unsuitable or declined the standard therapy. Cohort 4 represents other solid tumor except non-small cell lung cancer. Finally, cohort 5 represents the platinum-resistant ovarian and other GYN cancers. With the accumulated compelling efficacy signal observed in cohort 3, we are currently focusing our efforts to expand the cohort 3 for further study. With data cutoff as of March 29 this year, encouraging efficacy signals were observed in cohort 3, advanced non-small cell lung cancer patients who were unsuitable for or declined standard chemotherapy treatment. In this cohort, most of the patients have stage 4 non-small cell lung cancer. About 80% in this cohort had low PD-L1 expression at baseline tumor samples, defined by the TPS score of 1%-49% or negative at TPS <1%. These patients were generally considered less responsive to PD-1 based therapy. For example, in the KEYNOTE-042 study, this population only had 17% ORR. Patients with negative TPS appear to be less likely to benefit from PD-1 based treatment. In our study, of 19 efficacy evaluable patients in this cohort, the response rate was 26% and a disease control rate at 74%, with 5 PR and 9 SD observed, with a median follow-up time of 3.3 months. Of note, in the COAST trial in stage III non-small-cell lung cancer patients, durvalumab monotherapy in the control arm demonstrated 17% ORR, while the combination of oleclumab combined with durvalumab showing a 30% ORR. We also explored a potential correlation between CD73 expression and clinical response in cohort 3. Baseline CD73 expression was measured in archival samples and were available in 18 patients. We observed positive clinical signals in PD-L1 low or negative patients and a potential correlation between tumor CD73 expression and clinical response. In our study, seven out of 18 patients or 39%, had a high expression of CD73 using 35% as cutoff. In the seven patients with high CD73 expression, four patients had PR and another three with SD, with a disease control rate of 100%. In contrast, in the 11 patients with low CD73 expression, only one PR was observed. Here, we would like to highlight our current clinical development plan for uliledlimab. In China, we plan to focus on and expand the cohort 3 in non-small-cell lung cancer patients to further evaluate the clinical efficacy and continue to evaluate CD73 expression as a potential predictive biomarker. In parallel, we are developing a standardized companion diagnostic kit to be employed in our future phase III clinical trial. Additionally, we are working closely with external leading lung cancer experts as we plan to initiate a pivotal phase III registration trial in China of uliledlimab in combination with a PD-1 antibody in selected non-small-cell lung cancer patients. We are working diligently to design the protocol to commence this study in 2023. In the U.S., we are planning to initiate a new phase II clinical trial to explore the therapeutic potential of uliledlimab in other cancer types and beyond combination with PD-1 or PD-L1 inhibitor. Finally, I would like to discuss TJ-CD4B, a bispecific antibody targeting claudin 18.2 and 4-1BB. This is our conditional 4-1BB agonist with strong potency and with the potential to reduce systemic toxicity. Prior development of 4-1BB agonists have encountered significant challenges. In the case of urelumab, while good efficacy was observed, this agent has shown significant hepatotoxicity precluding its further development. In the case of utomilumab, while the safety was favorable, up to 10 mg/kg, marginal efficacy was observed. With our I-Mab's-developed 4-1BB platform, we hope to develop a class of agents using the 4-1BB platform, and that will retain the antitumor potency, but also having the good safety profile. This platform exploits the potential cross-linking by the tumor-associated antigen shown on the right side. The conditional T cell activation upon TAA engagement was made possible because in the periphery, the 4-1BB in the T cells cannot be clustered and therefore cannot be activated. However, in the tumor microenvironment, upon binding to the TAA, the T cell will be activated, and the 4-1BB will be clustered. The local immune activation in the tumor microenvironment will minimize the systemic toxicity, including hepatic toxicity. We hope this platform will allow us to explore the development of multiple therapeutic targets with different targets. As a first example, we have developed a bispecific antibody using this platform and targeting claudin 18.2. While claudin 18.2 is a competitive target with multiple therapeutic modalities being developed, including monoclonal antibody and ADC, CD3-Bi, and CAR T, we believe our bispecific antibody has the unique advantage. As highlighted in this figure, while monoclonal antibody has good safety profile, their clinical efficacy so far has been marginal. In contrast, while CAR T, ADC, and CD3-Bi have the potential to be more efficacious, they have the potential of significant toxicities as well. Our CD4B molecule has the potential of maintaining good antitumor activity while having good safety profile. This slide highlights the phase I design and further clinical development program of TJ-CD4B. In the dose escalation phase, the agent was dose escalated from 0.3 mg per kg up to the current dose at 8 mg per kg. When we reach the range of potential therapeutic efficacy, starting at 5 mg per kg up to 12 mg per kg, we will actually have a small cohort to select patients with claudin 18.2 positive expression. Once we reach the RP2D, we will expand to a larger patient cohort with either gastric patients or pancreatic and cholangiocarcinoma patients. Our phase I program has actually proceeded very smoothly. Dose escalation in solid tumors in U.S. and dose expansion of claudin 18.2 positive patients in both U.S. and China. As of June 20th, five dose cohorts has completed enrollment, with 16 subjects dosed. So far, no grade 2 and above TRAEs observed and no DLTs. Dose-dependent exposure with accumulation at c-twelve, suggesting potential longer dose interval. PD biomarker analysis indicating the dose-dependent and sustained T cell activation. We have also observed preliminary antitumor activity. This slide highlights the PK profile on the left. As you can see, exposure increased with elevated dose. Accumulation of c- twelve was observed starting at 1 mg per kg. On the right, preliminary PD biomarker analysis indicate dose-dependent increase in soluble 4-1BB. Sustained increase in soluble 4-1BB at 3 mg per kg and above was observed, indicating long-lasting T cell activation. Finally, I want to demonstrate an index subject, and this is a patient with metastatic esophageal adenocarcinoma who has failed the standard three lines of prior therapy, including FOLFOX in combination with nivolumab, FOLFIRI in combination with nivo, and paclitaxel in combination with ramucirumab. The baseline biomarker analysis indicating claudin 18.2 expression at 10%. This subject was dosed at 5 mg per kg every 2 weeks with CD4B. Patient tolerated treatment well. At eight weeks of treatment, an unconfirmed PR was observed, and at 18 weeks, a confirmed PR was observed, and this patient is currently continuing the treatment. Now, I'd like to turn to Dr. Jerry Wang, my colleague and also the CSO at I-Mab, to further discuss our preclinical pipeline. Thank you, Andrew, for the introduction. Dear scientists, medical professionals, investors, and partners, I'd like to welcome you all to I-Mab's 2022 R&D Day. I am Jerry Wang, Chief Scientific Officer for the company. In this section, I will lead the overview on our discovery and the preclinical programs. I would like to re-emphasize our goal of translating cutting-edge science into innovative drugs to specifically address areas of unmet medical need. To achieve this goal, we focused on three waves of discovery to generate potential first-in-class and best-in-class assets. The first wave is monoclonal antibodies or fusion proteins with unique differentiation, including the existing programs such as felzartamab, lemzoparlimab, uliledlimab, and eftansomatropin alfa, all of which have been in phase II or registration stage. Besides, we are also developing some novel monoclonal antibodies that target the driver immune checkpoint pathways and are designed to synergize with the existing clinical assets as combo therapies. The second wave is bispecific antibodies, including CD4B, C64B, L14B, L1IF, and L1T6. All of which have been in phase I or IND-enabling stage. These assets are designed to target specific cancers such as ovarian, gastric, and pancreatic cancer or treat PD-1 or PD-L1-resistant cancers by turning cold tumor to hot tumor. The third wave is super antibodies that were enabled by new technologies and formatted with novel modalities. Most programs are now in the preclinical stage. Among them, immune adjuvant is a focus area which is designed to prime and amplify immune response in tumor by different cytokine adjuvants such as efineptakin alfa and other new assets. With regard to the third wave super antibodies, we aim to enable the next wave of drug discovery through four new modalities. Masking technology, whereby Probody was conditionally activated in tumors. mRNA technology, whereby therapeutic antibodies are produced in body by encoded mRNA. Alphabody technology, whereby intracellular targets were hit by cell-penetrating antibodies. Artificial intelligence technology with antibody discovery accelerated by AI. Our bispecific antibody portfolio is positioned to turn cold tumor to hot tumor through activating the immune cells within tumor microenvironment. The portfolio can be divided into two categories. The first category is immune cell engager bispecific antibodies, as exampled by conditionally activated 4-1BB bispecifics. For example, CD4B and C64B to treat specific cancer types such as gastric, pancreatic, and ovarian cancers, which were normally not sensitive to PD-1 or PD-L1 therapy. Here, I would like to further highlight CD4B, a novel claudin 18.2, 4-1BB bispecific antibody, which is a global first-in-class asset and has already shown a favorable safety PK/PD profile and a promising efficacy signal from an ongoing phase I clinical study, as previously presented. CD4B is composed of a highly potent claudin 18.2 IgG with stronger binding affinity than zolbetuximab, even in claudin 18.2 low-expressing tumors. At the C-terminal, a unique 4-1BB single-chain Fv was conjugated, which could activate 4-1BB signaling only when this bispecific antibody engaged with claudin 18.2 positive tumor cells, leading to a reduced systemic and delivered toxicity. Due to the specific expression profile of claudin 18.2, CD4B is designed to treat patients with gastric and pancreatic cancer. A multi-regional phase I clinical trial in both U.S. and China is ongoing for this asset, which is co-developed with ABL Bio. As shown in the chart here, TJ-CD4B treatment induced a durable in vivo anti-tumor activity with localized immune activation. After the first tumor challenge, treatment of CD4B reached a significant tumor growth inhibition with six out of seven mice achieved complete tumor free when compared to other claudin 18.2 mono, 4-1BB mono, and combo therapies. We further rechallenged the mice with a lethal dose of tumor cells that had already undergone complete tumor regression after CD4B treatment. All the mice reject the rechallenged tumor, indicating a strong memory response induced by the treatment. Analysis of tumor-infiltrating lymphocytes showed a substantial increase of CD8 T cells and a ratio of CD8 to Treg cells by CD4B treatment, suggesting a localized immune activation in tumor. C64B is another 4-1BB-based bispecific in our pipeline. Claudin 6 is overexpressed in patients with ovarian and testicular cancer. C64B is composed of a claudin 6 IgG, which has strong and selective binding to claudin 6-positive tumor cells. Similar to CD4B, this bispecific antibody also works through claudin 6-dependent conditional 4-1BB activation. Meanwhile, C64B adopts a wild-type IgG1 to retain the competent Fc effector function to enhance the claudin 6-positive tumor cell depletion. C64B is now at the IND-enabling stage and planned for IND submission in 2023. C64B is specifically designed to treat ovarian and testicular cancers. As shown in the chart, claudin 6 is selectively overexpressed in most patients with ovarian and testicular germ cell cancer, while there is minimal expression in normal tissues. Although there are only three amino acid difference between claudin 6 and claudin 9, our antibody can selectively bind to claudin 6 over claudin 9, reducing the unwanted off-target toxicity since claudin 9 is known to have a broader expression pattern than claudin 6. By using the humanized 4-1BB model, where MC38 tumor cells expressing human claudin 6 was engrafted, C6 4B induced a strong anti-tumor activity in a dose-dependent manner. C6 4B treatment at a dose of 4.5 mg/kg result in the complete tumor regression for all the mice. Correspondingly, we also found a dose-dependent increase of CD8-positive T cells in tumor after C6 4B treatment, confirming the claudin 6-dependent 4-1BB activation at tumor site. The second category of bispecific portfolio is PD-L1 based bispecific antibodies, which are designed to treat PD-1 or PD-L1 resistant cancer patients by co-targeting immune activation pathways such as 4-1BB, TIGIT, or interferon alfa and tumor-derived PD-L1 inhibitory pathway to overcome the resistance mechanism. TJ-L14B is the most advanced asset in this PD-L1 based bispecific antibody category. It is composed of an anti-PD-L1 IgG, which is designed to target PD-L1 positive tumor cells and block PD-L1 and PD-1 interaction. In the meantime, a 4-1BB single chain Fv was conjugated at the C-terminus to induce the PD-L1 dependent 4-1BB stimulation. This unique structure also ensured an optimal immune synapse formation between PD-L1 positive tumor cells and a 4-1BB positive T cells to maximize T cell activation. As supported by the recent clinical data of Genmab PD-L1 4-1BB bispecific antibody, which showed preliminary efficacy in non-small cell lung cancer patients who progressed on prior immune checkpoint inhibitor therapy. L14B is positioned to treat PD-1 or PD-L1 resistant cancer patients. This asset is co-developed with ABL Bio and are currently in an ongoing phase I trial in U.S. As shown in this slide, L14B showed an enhanced in vitro T cell activation as compared to PD-L1 4-1BB mono treatment or a combo treatment of both. Additionally, superior in vivo antitumor activity was also observed in the treatment of L14B, which yielded complete tumor regression for almost all the mice when compared to mono and combo treatments. TJ-L1IF is another PD-L1-based bispecific antibody, which is composed of an anti-PD-L1 nanobody homodimer conjugated with engineered interferon alfa cytokine. The PD-L1 arm serves as both a tumor-targeting engager and a functional blocker, whereas the interferon arm serves as a potent immune adjuvant to activate multiple effector immune cells to elicit synergistic effects with PD-L1 blockade for tumor control. Systemic delivery of high dose interferon alfa will cause dose-limiting toxicities. In addition to arming tumor targeting PD-L1 antibody with interferon alfa to achieve local delivery in tumor, a Probody strategy was also adopted to mask interferon alfa activity via a tumor-specific cleavable linker to further reduce systemic toxicity. The masked inactive format will convert to an active form in tumor, where the mask was efficiently cleaved by tumor overexpressed protease. L1IF is also designed to treat PD-1 or PD-L1 resistant cancers. This asset is currently at the preclinical stage, and we aim to submit IND in 2023. We intentionally used a PD-L1 resistant colon cancer model to evaluate the antitumor activity of L1IF. The data here showed that as opposed to the minimal effect, about 3% tumor growth inhibition by Tecentriq monotherapy and a marginal effect, about 35% tumor growth inhibition by Tecentriq and interferon alfa combo therapy respectively. Treatment of L1IF at 3 mg/kg achieved a remarkable antitumor effect by 76% tumor growth inhibition. After the first dose of treatment, we found the active form of the drug was quickly detected and accumulated in tumor tissue, but not in the periphery, confirming the local delivery and conversion of active interferon alfa at tumor site. As an important component of our third wave of innovative drug discovery, we aim to build a diversified immune adjuvant portfolio based upon engineered cytokine enabled by cutting-edge technologies that can complement our monoclonal and bispecific antibody portfolio to enhance antitumor immunity. This portfolio is comprised of cytokine fusions and immunocytokines. For cytokine fusions including TJ107, TJAJ1, TJAJ2, and et cetera. The molecules are engineered to extend half-life with FC fusion and detune the binding affinity and potency for better safety and efficacy with site-specific mutation. For immunocytokine, including TJ-L1IF, TJIC1, and et cetera. The molecules are engineered to conjugate masked cytokines to tumor or immune cell targeting antibody to achieve prolonged half-life, minimal systemic toxicity, and enhanced activity by selective tumor targeting. Here, we highlight four molecules and summarize their characteristics as examples of our novel immune adjuvant portfolio. Efineptakin alfa, which targets IL-7, is currently in a phase II clinical trial. It is designed to specifically activate naive and memory CD4 and CD8 T cells with no effect on Tregs. The differentiation of this asset stems from the use of hyFc to mediate its half-life extension. Efineptakin alfa has a great potential to combine with PD-1 or PD-L1 and CAR T therapies for cancer treatment. TJ-L1IF, which targets interferon alfa, is in the preclinical stage. It is designed to activate both innate and adaptive immune cells, including dendritic cells, M1 macrophages, and the CD8 T cells. The differentiation of this asset stems from the pro-cytokine strategy for tumor site activation. TJ-L1IF can be the potential combo partner of CD47, CD73, and PD-1 antibody. TJAJ1, which targets IL-18, is in the preclinical stage. It is designed to stimulate tumor attacking CD8 positive T cells and NK cells. The differentiation of this asset stems from the engineering of a natural IL-18 protein to be IL-18BP decoy resistant. TJAJ1 can potentially combine with PD-1 or PD-L1 T-cell or NK cell engager bispecific antibody. Last but not least, TJAJ2, which targets GM-CSF, is also in the preclinical stage. It is a potent and a clinically validated cytokine adjuvant to stimulate dendritic cell and M1 macrophages. We also adopt pro-cytokine strategy for this asset to achieve tumor site activation and increase therapeutic window. It has the potential to be an optimal combo partner of CD47 and a macrophage engager bispecific antibody. Thank you all for taking the time to listen, and I hope that today's discussion was helpful. With that, we'd like to thank everyone, all of our stakeholders, for taking the time to dial in to I-Mab's 2022 R&D Day today. Please note that there'll be no Q&A session on today's call. If anyone does have any questions, please reach out to your local investor relations representative. They'll be able to answer any questions you have. Thank you again to everyone dialing in.