INmune Bio Inc.

Greetings, and welcome to the ImmuneBio second quarter 2022 earnings call. At this time, all participants are in a listen-only mode. A question and answer session will follow the formal presentation. If anyone should require operator assistance during a conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. A transcript will follow within 24 hours of this conference call. At this time, it is my pleasure to introduce Mr. David Moss, co-founder and chief financial officer of ImmuneBio. David, the floor is yours.

Thank you, Doug, and good afternoon, everybody. We thank you for joining us for the call for ImmuneBio's second quarter 2022 financial results. With me on the call is Dr. RJ Tessie, CEO and co-founder of ImmuneBio, who will provide a business update on our DNTNF platform. and Dr. Mark Liddell, Chief Scientific Officer and Co-Founder, who will provide an update on our NK Cell Priming Platform. Before we begin, I remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause action results to differ materially from those in such forward-looking statements. Please see the forward-looking statements disclaimer on the company's earnings press release as well as the risk factors in the company's SEC filings, including our most recent quarterly filing with the SEC. There's no assurance of any specific outcomes. Undue reliance should not be placed on forward-looking statements which speak only after the date they are made, as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, ImmuBio disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances. Now, I'd like to turn the call over to Dr. RJ Tessie, co-founder and CEO of Immu. RJ.

Thank you, David. Thank you, everyone, for joining the call. As usual, I will arrange my remarks to highlight the key takeaways for the first quarter and subsequent period and provide updates on our platform programs. I will review developments in EXPRO, then hand the call to Mark Liddell, ImmuneBio CSO, who will speak about recent developments in Incmune before David discusses financial results, upcoming milestones, and we move to Q&A. You are all aware that we received a clinical hold letter from the FDA. The clinical hold relates to manufacturing issues. The new expo is manufactured by KVI at their Boulder facility, a different manufacturing site than the previous expo batches. The triple challenge of a new company manufacturing a first-in-class therapy at a new manufacturing site all contributes to the FDA's caution. We are working with the FDA to answer their CMC questions. We are not willing yet to give a timeline to resolving this hold. At this point, we have not changed our timelines for reporting top-line results on MCI and mild AD trials. This decision is being continuously evaluated. If the hold persists for longer than anticipated, it will affect the timing of the top-line data readout. EXPRO for the treatment of ADI is our flagship program. The Phase II program in patients with mild ADI is enrolling patients in the Australia program. I remind you that ADI as capital A, capital D, and small i is Alzheimer's disease caused by neuroinflammation. EXPRO targets neuroinflammation. We use enrichment criteria to enroll patients who have neuroinflammation driving their dementia. We believe this is one of the reasons that we learned so much from our Phase I trial, and I have confidence in the outcomes of our Phase II trial. This simple strategy allows us to design smaller, shorter trials, and we believe in the U.S. this still allows us to have a market target of 40% of patients with mild Alzheimer's disease. There may be more, but we believe at least 40% will meet our enrollment criteria. We will initiate the Phase II MCI trial once we have resolved the clinical hold. To our knowledge, we are the only company that has separated the development of therapies, development of strategies for the treatment of mild Alzheimer's disease and MCI. Most trials treat something they called early AD, which is an artificial construct or combination of mild Alzheimer's disease plus MCI. We believe two trials is more informative and less risky. While on the topic of how ImmuneBio's AD programs differ from others, I remind you we're using EMAC as the primary cognitive endpoint. EMAC, early Alzheimer's disease MCI cognitive composite, is a validated scale designed to detect cognitive changes in patients with mild AD or MCI. This sensitive instrument is purpose-built for these patients. We are doing this call from San Diego while attending AAIC, the Alzheimer's Association International Conference, which is the largest Alzheimer's disease conference in the world. The world of AD drug development is changing rapidly. Immune Bio is leading the change of innovation in Alzheimer's disease. At this meeting, we are witnessing a drift away from targeting amyloid and tau towards other therapeutic strategies. And I'm happy to say that neuroinflammation and glial dysfunction are a frequent topic. The use of biomarkers such as those used in our Phase I trial and deployed in our innovative Phase II programs are gaining acceptance and seeing broader use. There is no question that the use of biomarkers will improve our ability both at ImmuneBio and by the field at large to bring novel therapies patients with Alzheimer's disease faster and with less risk. Expro has uses beyond the treatment of AD. We will start a Phase II trial in patients with treatment-resistant depression soon after the mild AD and MCI trials are underway in the U.S., We are performing IND enabling preclinical studies in ALS. All of our CNS programs have received support in the form of non-diluting funding from the Alzheimer's Association, the National Institute of Mental Health, and the ALS Foundation, respectively. The common denominator of these CNS indications is destructive neuroinflammation caused by immune dysfunction. In our opinion, neuroinflammation drives the core pathology of synaptic dysfunction and nerve cell death that is a requirement of cognitive loss. Our successful phase one program showed that EXPRO safely decreases neuroinflammation, improves synaptic function, decreases nerve cell death, and promotes remyelination. In the patients with mild AD, we saw a positive clinical response. Immune Bio believes that the synaptic connections can be stored. Degenerating axons can be made healthy and remyelinated. when the brain's immune system is normalized and controlled by Expro. The phase two studies are designed to answer these questions. The clinical hold will delay the initiation of the phase two trial in Expro for treatment-resistant depression. The NIMH gave us a $2.9 million grant, and the trial design is consistent with our CNS drug development philosophy. We will enroll patients with peripheral biomarkers of inflammation, including elevated CRP, use functional MRI, a neuroimaging biomarker, to evaluate the activity of a pathway in the brain tied to both depression and inflammation. This is a six-week, double-blind, placebo-controlled study. It is unique. The primary outcome measures are functional connectivity measured by MRI, but we will also be measuring other biomarkers and clinical outcomes. Finally, on the preclinical front with EXPRO, during the second quarter, we presented preclinical data demonstrating that EXPRO promotes remyelination at the junction of the white and gray matter in animals with multiple sclerosis. This work was presented at the third European Conference on Neuroinflammation and provides mechanistic insight into the remyelination we saw in patients in our ADI trial. Finally, in commune, as we... We consider Incommune, our proprietary NK cell priming platform, a novel pseudokine that binds to NK cells and induces many of the same effects in NK cells as others achieve with a complex cocktail of cytokines. Based on new data, this statement understates the power of Incommune to alter NK cell function in patients with cancer. Incommute transforms resting NK cells into cancer-killing memory-like NK cells in the patient. To make these cancer-killing memory-like NK cells with cytokine, you need a complex cytokine triplet. of IL-12, 15, and 18, these cytokines complicate both manufacturing and the care of cancer patients because of cost and off-target side effects, common to many cytokine treatments. In contrast, cytokine-primed NK cells only activates NK cells as well-tolerated without any medication and, in fact, can be given as an outpatient treatment. The memory-like NK cells present after NK treatment may be better at killing cancer cells in the TME, or the tumor microenvironment of solid tumors. The increased fitness of NK cells is due to an upregulation of mitochondrial proteins. I remind you that mitochondria are the engines of the cell and are essential for NK survival. And we believe this increased fitness may be the cause of the extended therapeutic persistence. of memory like NK cells in inkimmune-treated patients. Mark Liddell will provide more details on the patients in a moment, but to our knowledge, inkimmune priming is the only NK therapy reporting improved functional mitochondrial function and therapeutic persistence lasting more than 100 days. These observations, combined with the data presented on the ability to of incoming to prime NK cells that thrive in the conditions of the tumor microenvironment, including hypoxia, has driven our strategy to pivot our development program towards solid tumors. I've said enough for now. I'm going to turn it over to Mark Liddell, Chief Scientific Officer of INCUMIN. Mark.