Thank you Sean, and good morning everyone. Over the next few minutes, I will review the recent progress and upcoming milestones of our clinical pipeline, starting with uliledlimab, or uli for short. Slide 7 begins the section on uli. Uli targets CD73, which is the rate-limiting enzyme critical for converting AMP, or adenosine monophosphate into the immunosuppressive metabolite, adenosine. Blocking CD73 allows anti-tumor immunity to proceed in the tumor microenvironment without the presence of an adenosine-induced immunological fog. We believe uli is differentiated given its superior pharmacokinetic properties versus other competitors, as demonstrated by its ability to completely inhibit CD73 activity without the hook effect that has been described for other drugs that target CD73 and may prevent them from achieving maximal inhibition of CD73. The illustrations on Slide 8 were created to show uli’s mechanism of action and how uli is differentiated from other CD73 antibodies. CD73 is activated when it is in a closed confirmation. We believe that uli’s differentiation comes from its ability to bind to the C-terminus of the enzyme to prevent the formation of the closed dimer. CD73 is a butterfly structure. It has two end termini and two C termini. Because one molecule of uli binds to two adjacent CD73 dimers on the C-terminus, it doesn’t exhibit the hook effect. In fact, our preclinical studies show that this approach completely inhibits CD73 in a dose-dependent manner. In contrast when looking at other compounds such as oleclumab, which binds to the end terminus of CD73, what can happen is that as concentrations of drug increase, the intermolecular bonds needed to inhibit 73 activity are harder to form because the antibodies bind to the end terminal binding sites with single valency, therefore intermolecular bonds are not formed as readily at high concentrations as at lower concentrations and inhibition of CD73 is paradoxically less at higher concentrations than at lower concentrations. This is not observed with uli in preclinical model systems. During this call, I will walk you through the three studies from the uli program. The first study is outlined on Slide 9. Data from this study presented at ASCO 2023 show that patients who had CD73 expression and a PD-L1 TPS score of greater than or equal to 1% experienced an objective response rate, or ORR of 63%. Patients with lower levels of CD73 expression had a lower ORR. The ORR in the CD73 high group is higher than that observed in Keynote 42, which tested pembrolizumab monotherapy in the same disease setting and with the same distribution of PD-L1 expression. These data suggest that tumors with high levels of CD73 expression will respond best to uli. In addition to providing important proof of concept data, the study also shows that the combination was well tolerated. Two-thirds of metastatic non-small cell lung cancer patients have tumors that express PD-L1 in less than 50% of cells. For them, the standard of care is a checkpoint inhibitor, or IO combined with chemotherapy. On Slide 10, we outline the clinical rationale for a combination study that will include uli plus IO plus chemotherapy. First, the addition of chemotherapy to IO monotherapy has extended the benefit of IO to patients whose tumors express low levels of PD-L1. Second, uli has a favorable toxicity profile that suggests that the four-drug combination could be tolerated. Third, published data show that chemotherapy can induce CD73 expression which could increase the likelihood of response to uli. Ultimately, non-small cell lung cancer is one of the most common and deadly cancer diagnoses globally and we believe that uli has the potential to improve upon currently available standard of care, whether that standard of care is IO monotherapy or IO plus chemotherapy. I-MAB has received FDA clearance to proceed with the study of uli plus pembro plus chemotherapy, and we expect to dose the first patient in the first half of 2025. In the previous slide, we laid out the rationale for the four-drug combination study. This is an important study because we believe it could help define the regulatory path for uli in the future. We intend to enroll patients who are eligible for first-line treatment of locally advanced or metastatic non-small cell lung cancer. The study is randomized against IO plus chemo standard of care and is designed to evaluate two different uli dose levels. Importantly, CD73 expression will be assessed retrospectively. The primary endpoint is objective response rate with standard secondary endpoints of progression-free survival, duration of response, and overall survival all stratified by PD-L1 expression. This study includes a small dose escalation lead-in with an N=6. Dosing is expected to begin in the first half of 2025. Once safety is assessed in the lead-in, patients will be randomized in a two-to-one ratio against standard of care, assessing uli with two different dose levels. In this slide, we believe it’s important to share not only uli’s upcoming milestones but the adenosine pathway as a whole, given its promise in the immuno-oncology space. We have prepared this chart to put the upcoming clinical milestones for uli into context with other CD73 programs. On the top of the chart, we have summarized three milestones for the ongoing and planned studies in our program, including the first patient dosed in the randomized Phase II study of uli plus pembro plus chemo I just described. We expect to be able to provide a read-out from this study in the second half of 2026. Additionally, we highlight upcoming progression-free survival, or PFS data from the uli plus toripalimab randomized Phase II study ongoing in China only in the second half of 2025. This study is being conducted by our collaborator in China, TJ Bio, who holds the right to uli in China. On the bottom of the chart, we summarize expected Phase I/II milestones for four other CD73 programs. We believe the positive results from other programs will help further validate the adenosine pathway, specifically CD73 as a target, and that our approach for patient selection using CD73 expression as well as uli’s ability to completely inhibit CD73 could represent a differentiated advantage. Next I’d like to turn givastomig on Slide 13. Givastomig, or giva is a bispecific antibody that is designed to target Claudin 18.2, a tumor-associated antigen found on solid tumors, especially gastric cancers. The bispecific antibody combines with Claudin 18.2 binding domain, where Claudin 18.2 is expressed, and 4-1BB which conditionally activates T-cells in the tumor microenvironment. Moreover, we believe giva is differentiated by its ability to bind to Claudin 18.2 even in tumors with very low levels of 18.2 expression. Slide 14 provides an opportunity to highlight giva’s bispecific design properties and the monotherapy data that may position it as a best-in-class Claudin 18.2 4-1BB biospecific antibody. Initial Phase I monotherapy data reported at the ESMO 2023 meeting showed encouraging monotherapy results in patients with gastric cancers whose tumors had progressed or were refractory, including those with low levels of Claudin 18.2 expression. Based on the data from the Phase I monotherapy results, we initiated a combination study of giva plus nivolumab plus chemotherapy in the first half of 2024. Bristol Myers Squibb is supplying nivolumab under a clinical collaboration and supply agreement. Top line data from the study are expected to read out in the second half of 2025. In the meantime, I-MAB plans to present new top line data from the Phase I monotherapy dose expansion study in patients with gastric cancers whose disease has progressed after previous treatment at ESMO 2024. Moving to Slide 15, investors often ask about other Claudin 18.2 programs in development and how giva compares to zolbetuximab, or zolbe. In response, we have prepared this comparative slide. On the left side of the chart, we have summarized several parameters from the giva Phase I monotherapy data presented at ESMO 2023 related to Claudin 18.2 expression and clinical outcomes. On the right-hand columns, we summarize published Phase I data and Phase II data from zolbe. While the table does not represent data from a head-to-head study, I believe it highlights the strength of potential differentiation of giva. This data highlights giva’s ability to treat patients even with low levels of Claudin 18.2 expression. For example, zolbe did not show a response in its Phase I study when Claudin 18.2 was expressed at 1+ or greater in at least 1% of cells. When Claudin 18.2 parameters were tightened to 2+ or greater staining in 50% of cells, zolbe monotherapy results appeared inferior to giva monotherapy results. These data support our view that giva has best-in-class potential and could be combined with frontline standard of care nivo plus chemo in gastric cancer. Lastly, I’d like to turn to ragistomig on Slide 16. Ragistomig, or ragi is a bispecific antibody in development to treat advanced solid tumors that are refractory to checkpoint inhibitors. The bispecific antibody was designed to provide anti PD-L1 activity and 4-1BB driven T-cell activation in a single molecule using the same 4-1BB technology design as giva. The combination of an FC-silent antibody with condition 4-1BB engagement is intended to optimize the compound for safety, including the potential for lower hepatotoxicity compared to traditional 4-1BB agonists. Localized activation of 4-1BB in the tumor microenvironment is intended to enhance anti-tumor immunity and reinvigorate exhausted T-cells while mitigating liver toxicity and systemic immune responses. Slide 17 provides a snapshot of early Phase I dose escalation and dose expansion data presented at ASCO 2024 by our collaborator, ABL Bio. The study enrolled 53 patients with advanced or relapsed solid tumors, 44 of whom were evaluable at the time of the presentation. The majority of patients had at least three prior lines of treatment. Top line Phase I results demonstrated an ORR of 27%, including six partial responses, one complete response, and a clinical benefit ratio of 69%. Seventy-one percent of patients who responded had received prior checkpoint inhibitors. The complete response was observed in a heavily pre-treated ovarian cancer patient who had received seven prior lines of therapy. We are encouraged by the results from the study because of the early clinical signs of efficacy. Enrolment in selected indications and different dose schedules is ongoing. Slide 18 provides a snapshot of the safety profile. While increased liver enzymes where the most common treatment-emergent adverse event, none of the transanimated salivations were accompanied by increases in bilirubin, the so-called Hy’s Law. Patients with grade 3 increases in liver enzymes improved with corticosteroid treatment and no cytokine release syndrome was reported. The combination of ragi’s early efficacy and manageable safety profile is encouraging, and enrollment in the Phase I study continues. Slide 19 provides a recap of the pipeline. In summary, we are encouraged by the early clinical data for uli, giva and ragi. We believe that each agent has a unique and differentiated mechanism of action and a manageable safety profile. We are excited to be on the cusp of clinical milestones for each program, including an upcoming data release at ESMO 2024 where we will share Phase I dose expansion monotherapy data. Now I will hand the call over to Joe for the financial overview.