Thank you, David, and thank you to everyone joining our call. These are exciting times at INmune Bio. 2024 was a transitional year for our company. We believe this year will be a transformational year. In less than a hundred days, we expect to announce top-line data for our randomized, blinded, placebo-controlled Phase 2 trial using XPro to treat patients with early AD with inflammation. We call the trial ADO2 or MINDFuL. We have worked tirelessly to get to this point, and I must say hats off to the entire team at INmune Bio for reaching this major milestone. We can't wait to learn the results. INmune Bio's ADO2 Alzheimer's trial stands out from conventional approaches of treating Alzheimer's disease due to a focus on treating neuroinflammation as the primary driver of the disease. Rather than targeting plaques and tangles the dominant traditional targets of Alzheimer's drug development, we have targeted inflammation as the main driver. Because of the frustrating history of failed trials to treat Alzheimer's disease, we adopted a precision medicine approach for our Phase 2 program, that precision is first seen in patient selection. The ADO2 trial uses clinical biomarkers to match the patient's pathophysiology with XPro's mechanism of action that is XPro targets neuroinflammation. Therefore, we enriched the trial with 80 patients who have neuroinflammation driving their Alzheimer's disease. To our knowledge, ADO2 remains the only Alzheimer's trial using biomarkers other than amyloid or tau to guide patient selection. Next, we embraced EMACC as the primary endpoint of the trial. EMACC is designed to accurately test cognitive function in patients with early Alzheimer's disease. We don't understand why others embrace the use of cognitive test designed for staging patients with Alzheimer's disease or develop for use in patients with moderate -- to severe Alzheimer's disease as the primary endpoints for studies in patients with early Alzheimer's disease. Those measures of cognition are not designed to measure the clinical effectiveness of a therapy. EMACC is purpose-built objective test of cognitive function designed to be used in patients with early Alzheimer's disease with a dynamic range that allows the measure of worsening and improving cognitive function. Although the term precision medicine is most often used to define patient selection criteria in clinical trials, we believe EMACC provides a precision medicine measure to efficacy in Alzheimer's trials. The embrace of these novel approaches is based on solid preclinical data, compelling Phase I data and a belief that addressing the structural and pharmacological aspects of protocol design derisk the trial and improve the probability of success. By integrating inflammatory biomarkers to identify response to patients and utilizing a precise measure of cognitive response, INmune Bio’s hopes to do more than just slow cognitive decline. Our goal is to stop cognitive decline. If successful, we will challenge the longstanding amyloid-centric paradigm of Alzheimer's disease while supporting the perspective that Alzheimer's is an immunologic disease. Today, we are less than one hundred days away from reporting the results of ADO2. The trial enrolled 208 patients in eight countries. We worked to enroll the right patients into the trial, which resulted in enough screening nearly 800 patients. This seemingly simple process of patient screening is time was time-consuming, complicated and expensive, but one of the four important drivers of success in ADO2. The second and third drivers are the previously mentioned enrichment criteria used to select patients with neuroinflammation and the use of EMACC to precisely assess cognitive response. The final driver is EXPAREL, the drug. Success of this drug in patients with dementia caused by neuroinflammation may open a world of possibility for patients with neurologic disease because neuroinflammation is a common denominator in many difficult-to-treat CNS diseases. Also, in 2024, we completed the pivot to solid tumors with INmune, our NK cell targeting platform. Although INmune had interesting data in the treatment of hematologic diseases, we believe the future opportunities for INmune were greater by targeting and treating solid tumors. The CaRe PC trial using INmune to treat men with castrate resistant metastatic prostate cancers has made steady progress. We recently announced completion of dosing in the Phase 1 dose escalation part of the Phase I, Phase II trial and continue to dose patients in the Phase 2 part of the trial at the medium and high dose cohorts. As currently designed, we expect to complete dosing of patients with INmune during 2025. And we have promised that as data become available in those cohorts, because it is an open label trial, we will report it. CORDStrom is a 2025 event, but in fact, CORDStrom has been a quiet part of the new vial since 2018. Dr. Mark Liddell invented and perfected CORDStrom to support an NIHR-funded trial in the UK treating kids with intermediate to severe recessive dystrophic epidermolysis bullosa or RDEB. RDEB is a rare genetic disease caused by the mutation of the COL7A1 gene. The NIHR is the research arm of the United Kingdom's National Health Service. The INmune Bio team saw the clinical data on the use of cords drumming kids with RDEB for the first time in November of 2024. The data our compelling and provides INmune Bio with a unique in-licensing opportunity that is INmune Bio owns and invented and owns cords from the drug and GOSH, which is the Great Ormond Street Hospital for children, which is the largest pediatric hospital in the UK was the sponsor of the clinical trial and own the Mission EB Clinical Data. Mission EB is the name of the clinical trial that was performed at GOSH. Combining the two assets was necessary to generate value to the patients, caregivers and investors. INmune Bio in licensed the mission EB clinical data resulting in what we believe is a BLA-ready program that has already been awarded or from drug status and rare pediatric disease designation. CORDStrom differentiates itself from other approved therapies for RDEB by providing a systemic disease modifying approach rather than focusing on local wound management. Many of you know that the wounds that don't heal are one of the major problems of this debilitating disease. We are not discounting the importance of those therapies, but RDEB affects every organ system in the body except the brain. Topical wound therapies while providing important local benefits do not address problems in the eyes, problems eating and elsewhere in the body. These many problems require systemic disease-modifying therapy. CORDStrom is an allogeneic pooled umbilical cord-derived mesenchymal strong cell platform delivered intravenously, excuse me. CORDStrom is a systemic therapy that aims to modulate inflammation, promote wound healing, reduce the debilitating itch, pain, and scarring that exacerbate RDEB in the skin, the esophagus, the eyes, and beyond. The patient Caregiver interviews provides some of the most interesting information or data from the blinded randomized mission EB trial. Those are best heard by listening to the webinar that in which Professor Anna Martinez reports the responses from the trial that's available on our website. The impact of courts from therapy on patients, quality of life seems clear. We believe this program is on a rapid path to the market where it will fulfil an unmet clinical need in kids with this desperately debilitating and ultimately lethal disease. While we love our cell therapy programs, we understand that ADO2 top-line data is the catalyst everyone, including ourselves are looking forward in the near term. At our core Immune Bio is a CNS company focused on Alzheimer's disease. We have built this company around our XPro platform and analysis and a hundred days away from the results of the trial. In the Phase 2 trial in Alzheimer's patients with biomarkers of inflammation. I reiterate, we will provide top-line results for the trial in June. I don't know exactly what date in June the top-line data will release. There are too many moving parts, but it will be June. Also, there is no industry-wide definition of what top line data make means. Our definition is simple, the data will provide unequivocal evidence of the impact of EXPAREL on the treatment and the clinical, and the response of those clinical symptoms of patients with early Alzheimer's disease with biomarkers of information. This means we will provide a robust package of cognitive, clinical and functional data from patients treated with EXPAREL in the trial. From these data, we will provide an answer to the question, does treating early Alzheimer's disease in patients with biomarkers of inflammation with EXPAREL safely alter the trajectory of their cognitive decline? There are four important aspects in the statement I just made. The trial is in Early AD. We are not studying patients with moderate or severe disease. Early AD patients are the same group that virtually everyone studies, including the approved anti-amyloid drugs. We are enrolling patients with biomarkers of inflammation. That is this is not an all comers trial, but a precision medicine trial enriched with early Alzheimer patients that have neuroinflammation. Three of the four enrichment criteria are biomarkers of peripheral inflammation, not central inflammation. This first makes them easy to obtain in peripheral blood, but importantly, experts agree that peripheral inflammation causes central inflammation that drives the Alzheimer's disease because EXPAREL treats both peripheral and central inflammation, it should stop disease in the brain and eliminate the fuel that feeds progression of the disease. Safety is paramount when treating elderly patients with Alzheimer's. As of today, there have been no unscheduled neuroimaging studies, no emergency MRIs, there have been no deaths and the number of infections can be treated on one hand. This is a remarkable history in a group of patients that averages 73 years old. Thus far, EXPAREL has shown to be safe in that target population. Finally, I chose the word trajectory of their cognitive decline carefully. Currently approved therapies slow the rate of cognitive decline. And realistically, we need to be as good as the currently approved therapies to claim success, but we have higher aspirations. Our goal is to halt disease progression or halt cognitive decline rather than the slow the progressive decline. We believe the results of this trial will challenge the longstanding plaques and tangle disease paradigm of Alzheimer's disease, providing a fresh perspective on the treatment of the Alzheimer's disease as an immunologic disease. We hope the first day of EXPAREL therapy is the last day of cognitive decline in patients with Early AD. We will know soon if this lofty aspiration is realized. We are confident. While we remain very optimistic about the upcoming results from ADO2, we believe bigger changes are afoot. Positive results will create a paradigm shift for the treatment of Alzheimer's disease and other CNS diseases, where neuroinflammation, often ignored and untreated, is finally recognized as an element of many of these diseases. And we now have a tool for to add to the physician’s armamentarium. For instance, neuroinflammation plays important roles of dementia associated with FTD, Parkinson's disease, traumatic brain injury, stroke, depression and beyond. Chronic inflammation is the driver of many diseases of aging and if we achieve our expected results targeting the immune dysfunction of lymphoma aging becomes a reality. 2024 was a major, year of major accomplishments in all our programs. Great progress is made in the clinic with our legacy programs. The addition of CORDStrom has added a third therapeutic platform to the company that should accelerate our timeline to becoming a commercial entity. I turn it back to David to go over the financials.