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XPro1595 decreases development of amyloid beta and tau following TBI in murine model of Alzheimer’s disease Boca Raton, Florida, Dec. 22, 2022 (GLOBE NEWSWIRE) -- INmune Bio, Inc. (NASDAQ: INMB) (the “Company”), a clinical-stage immunology company focused on developing treatments that harness the patient’s innate immune system to fight disease in concert with Virgina Commonwealth University (VCU) and Barrow Neurological Institute have received a grant from the United States Department of Defense (DoD). The grant is titled: Novel solTNF inhibitor improves outcomes in a mouse model of TBI-induced AD. The funding covers a collaboration that studies the impact of traumatic brain injury (TBI) in the development of Alzheimer’s disease (AD) related pathology. These DoD funded studies are a collaboration between Dr. Kirsty Dixon, Associate Professor of Surgery and director of Surgery’s Neurotrauma Repair Laboratory at Virginia Commonwealth University, and Dr. Elliott Mufson, Professor of Neurobiology and the director of the Alzheimer’s disease research laboratory at Barrow Neurological Institute and INmune Bio. “This is a great example of collaboration for innovation,” said RJ Tesi MD, CEO of INmune. “Two stellar academic institutions combine with industry (INMB) and government (DoD) to answer an important medical question.“ TBI is a risk factor for developing AD, although reasons for this remains largely unknown. The ApoE4 allele is the strongest known risk factor for late onset AD, and the presence of human ApoE4 following TBI results in accumulation of AD pathology (soluble Aβ and tau/p-tau levels). Evidence suggests a role for soluble tumor necrosis factor (sTNF) and its receptor TNFR1 in the development of AD in patients with previous TBI, especially in individuals carrying the APOE4 allele. These studies will use XPro1595 to determine the contribution of ApoE4 and TBI on sTNF/TNFR1-induced hippocampal inflammation, AD pathology and dendritic spine plasticity, that collectively promote cognitive impairment. “Much of the neurologic damage after TBI is driven by neuroinflammation,” said Kirsty Dixon, PhD, associate professor in the Department of Surgery at the VCU School of Medicine. “This study aims to confirm that neuroinflammation caused by an acute neurologic injury has long-term consequences that contribute to dementia and that early intervention can prevent disability later in life.” "We know that traumatic brain injury can accelerate the onset of Alzheimer's disease, however little is known about the association between the two diseases," says Elliott Mufson, PhD, researcher at Barrow Neurological Institute. "This study is an important step toward helping us better understand the relationship between these disorders and to develop effective therapies." About INmune Bio, Inc. INmune Bio, Inc. is a publicly traded (NASDAQ: INMB), clinical-stage biotechnology company focused on developing treatments that target the innate immune system to fight disease. INmune Bio has two product platforms that are both in clinical trials: The Dominant-Negative Tumor Necrosis Factor (DN-TNF) product platform utilizes dominant-negative technology to selectively neutralize soluble TNF, a key driver of innate immune dysfunction and a mechanistic driver of many diseases. DN-TNF product candidates are in clinical trials to determine if they can treat cancer (INB03™), Mild Alzheimer’s disease, Mild Cognitive Impairment and treatment-resistant depression (XPro™). The Natural Killer Cell Priming Platform includes INKmune™ developed to prime a patient’s NK cells to eliminate minimal residual disease in patients with cancer. INmune Bio’s product platforms utilize a precision medicine approach for the treatment of a wide variety of hematologic and solid tumor malignancies, and chronic inflammation. To learn more, please visit . Forward Looking Statements Clinical trials are in early stages and there is no assurance that any specific outcome will be achieved. Any statements contained in this press release that do not describe historical facts may constitute forward-looking statements as that term is defined in the Private Securities Litigation Reform Act of 1995. Any statements contained in this press release that do not describe historical facts may constitute forward-looking statements as that term is defined in the Private Securities Litigation Reform Act of 1995. Any forward-looking statements contained herein are based on current expectations but are subject to a number of risks and uncertainties. Actual results and the timing of certain events and circumstances may differ materially from those described by the forward-looking statements as a result of these risks and uncertainties. INB03™, XPro1595, and INKmune™ are still in clinical trials or preparing to start clinical trials and have not been approved by the US Food and Drug Administration (FDA) or any regulatory body and there cannot be any assurance that they will be approved by the FDA or any regulatory body or that any specific results will be achieved. The factors that could cause actual future results to differ materially from current expectations include, but are not limited to, risks and uncertainties relating to the Company’s ability to produce more drug for clinical trials; the availability of substantial additional funding for the Company to continue its operations and to conduct research and development, clinical studies and future product commercialization; and, the Company’s business, research, product development, regulatory approval, marketing and distribution plans and strategies. These and other factors are identified and described in more detail in the Company’s filings with the Securities and Exchange Commission, including the Company’s Annual Report on Form 10-K, the Company’s Quarterly Reports on Form 10-Q and the Company’s Current Reports on Form 8-K. The Company assumes no obligation to update any forward-looking statements in order to reflect any event or circumstance that may arise after the date of this release. INmune Bio Contact: David Moss, CFO (858) 964-3720 info@inmunenbio.com Investor Contact: Jason Nelson, Core IR (516) 842-9614 x-823

Parkinson’s disease (PD) patients treated with NE3107 for 28 days experienced a clinically meaningful increase in motor control.Additional data presented at the Clinical Trials in Alzheimer’s Disease (CTAD) conference showed that NE3107 enhanced cognition as measured by a variety of assessment tools. Furthermore, a large majority of patients with abnormal MRI scans before treatment showed improvement in one or more brain regions as seen from advanced functional MRI studies after 3 months of treatment with NE3107.NE3107 Appears to Impact Biomarkers of Aging-Related Disease States; Reduces Horvath DNA Methylation SkinBlood Clock by 3.3 years after 3 months of treatment. CARSON CITY, Nev., Dec. 07, 2022 (GLOBE NEWSWIRE) -- BioVie Inc., (NASDAQ: BIVI) (“BioVie” or the “Company”) a clinical-stage company developing innovative drug therapies for the treatment of advanced liver disease and neurological and neurodegenerative disorders, today issued the following letter to shareholders: Dear shareholders, The company has made significant progress with our clinical programs and released additional data within the last week. Thus, I wanted to send you this letter to summarize the large body of information we recently released. The key points to takeaway are: Parkinson’s disease (PD) patients treated with NE3107 for 28 days experienced a clinically meaningful increase in motor control.Additional data presented at the Clinical Trials in Alzheimer’s Disease (CTAD) conference showed that NE3107 enhanced cognition as measured by a variety of assessment tools. Furthermore, a large majority of patients with abnormal MRI scans before treatment showed improvement in one or more brain regions as seen from advanced functional MRI studies after 3 months of treatment with NE3107, and these improvements tended to vary directly with cognitive change.NE3107 appears to impact biomarkers of aging-related disease states and reduces Horvath DNA methylation SkinBlood clock by 3.3 years after 3 months of treatment. NE3107 enhances motor control The NM201 study (NCT05083260) is a double-blind, placebo-controlled, safety, tolerability, and pharmacokinetics study in Parkinson's disease (PD). This trial was launched with two design objectives: 1) the primary objectives are to demonstrate safety and the absence of adverse interactions of NE3107 with levodopa; and 2) the secondary objective is to determine if NE3107’s promotoric activity observed in nonhuman primates can be seen in humans. The trial met both objectives. Before study commencement and at multiple points throughout the 28-day trial, patients who did not receive PD medications for at least 8 hours overnight were observed using the Unified Parkinson’s Disease Rating Scale (UPDRS) first thing in morning (hour 0). Patients were then given medication and observed again using UPDRS at 1, 2, 3, 4, and 8 hours after drug administration. Part 3 of the UPDRS instrument assessed motor control. Patients treated with NE3107 and levodopa saw improvements of part 3 score on Day 28 compared to Day 0 that is 3+ points better than those treated with levodopa alone at the 2 and 3 hour marks. This level of superiority is considered by PD experts to be clinically meaningful.*Patients younger than 70 years old treated with NE3107 and levodopa experienced improvements that are roughly 6 points better than levodopa-treated alone. Patients younger than 70 years old represented roughly one-half of study participants.After 28 days of treatment, 63.6% of patients treated with levodopa alone experienced >30% improvement from Day 0 at the two-hour mark compared to 80% for NE3107+levodopa-treated patients and 88.9% of NE3107+levodopa patients under 70 years old. This pattern is also observed for other time periods.There were no drug-related adverse events. Full details from this trial will be presented at the upcoming AD/PD™ 2023 International Conference on Alzheimer’s and Parkinson’s Diseases to be held March 28-April 1, 2023 in Gothenburg, Sweden. This trial is primarily a safety and drug-drug interaction study that we expanded in hopes of finding an efficacy signal. The fact that this small trial showed this magnitude of therapeutic impact for NE3107 allows us to proceed with planning the Phase 3 program for discussion with the FDA. NE3107 enhances cognition The company supported an Investigator-Sponsored 2 trial (NCT05227820) to explore NE3107’s impact on biomarkers and brain imaging in mild cognitive impaired (MCI) and mild AD patients. Topline results were released on September 7, 2022, and the Principal Investigator’s team presented additional data at the CTAD annual conference, held in San Francisco, CA November 29 to December 2, 2022. These data showed the following among patients with MMSE>=20 (i.e., MCI and mild AD): Patients demonstrated enhanced thinking, memory, and function after three months of treatment with NE3107 compared to baseline as measured using multiple rating scales. Statistically significant improvements were observed using modified Alzheimer’s Disease Assessment Scale-Cognitive (ADAS-Cog12 scale, 2.2 points improvement, p=0.0173), the Clinical Dementia Rating scale (CDR, 0.11 point improvement, p=0.0416), and the Alzheimer’s Disease Composite Score (ADCOMS, 0.07 point improvement, p=0.0094).Improvements in inflammation (reduction in TNFa) correlated with improvements in cognition (R=0.59, p=0.0259).Patients experienced a reduction of CSF phospho-tau levels of -1.66 pg/mL (p=0.0343) and the ratio of p-tau to Ab42 by -0.0024 (p=0.0401). Among responders, the reduction in p=tau was -3.22 pg/mL (p=0.0027) and the ratio of p-tau to Ab42 was 0.0040 (p=0.0144).18 of 22 patients with abnormal baseline scans showed improvement in one or more brain regions as seen from advanced functional MRI studies.MCI and mild AD subjects with abnormal scans that improved after 3 months treatment also saw a -0.068 points improvement in their ADCOMS scores (p=0.0258). We believe AD pathology is driven by multiple factors. Amyloid beta (Ab) and phosphorylated tau (p-tau) have been the focus of the AD research community, but decades of research on dozens of agents have found inconsistent and modest decrements in the overall rate of cognitive and functional decline over a period of years. We believe in addition to Ab and p-tau, other factors such as inflammation, insulin resistance, metabolic dyshomeostasis, apoptosis, oxidative stress, and glucose utilization also play critical roles in AD etiology. Data show that NE3107’s ability to reduce TNFa (the major regulator of inflammation) is highly correlated to improvements in cognition. We hypothesize that the modulation of TNFa levels and its inflammatory activation lead to a multitude of changes among the many factors downstream from this master regulator, which collectively lead to improvements in neuronal health and cognition. We also recently announced that BioVie’s Phase 3 trial in AD has fully enrolled the targeted 316 patients and that the company is opting to increase study size to 400 due to our fast enrollment pace. The trial protocol specified enrolling at least 316 patients. The protocol also pre-specified the potential for a review when roughly 50% of the 316 enrolled patients have completed the study to determine if increasing enrollment of up to 400 patients might be desirable for the purpose of enhancing the probability of achieving statistical significance. The pace of enrollment increased dramatically in recent months, creating a situation where the Company finished enrolling all 316 patients before 50% of enrolled patients had completed the study. Thus, we decided that forgoing the interim analysis and continuing enrollment up to 400 patients is the best course for obtaining the strongest possible data set. We believe all 400 patients can be enrolled in the coming months and anticipate topline results will be available before the end of 3Q2023. By taking this step we believe we have enhanced our probability for success, and thus our ability to bring this hoped for innovation to the Alzheimer’s patient community. NE3107’s potential impact on Biomarkers of Aging-related Disease States As a part of the Phase 2 Alzheimer’s trial, blood samples were taken from the patients before and after 3 months of treatment with NE3107, and these samples were analyzed to assess NE3107’s potential to reduce inflammation and alter DNA methylation patterns associated with epigenetic biological clocks. Data shows that treatment with NE3107 for three months showed a reduction of 3.3 years (p=0.0021) using the Horvath DNA methylation SkinBlood clock. Furthermore, 19 out of the 22 patients experienced this reduction in the SkinBlood clock score. We are very excited by this initial finding and recognize that there is still much more to learn about the NE3107’s impact on the biomarkers of aging-related disease states and how this may affect disease progression, and we look forward to working with collaborators to answer questions such as whether the reversal will accumulate with longer treatment duration, the durability of the effect, and whether this translates to a reduced risk in diseases associated with aging. Let me explain by using an analogy. Our DNA provides the genetic code for everything in the body in much the same way that a music compact disc (CD) provides the code for its music content. With repeated use, the CD may become scratched and smeared with fingerprints, which affects the player’s laser’s ability to read and decode its content. Epigenetics is the study of how behavior (e.g., diet, exercise) and environment affect the way our genes work in addition to the genetic code itself (i.e., similar to the smearing and scratching of the CD). There’s an increasing body of evidence that signs of aging are epigenetic in nature.1,2 Perhaps the most studied area of epigenetics involves DNA methylation, which is the process of how methyl groups are added or removed from DNA and thus regulate the expression of various genes in our bodies.3 Many studies have shown that genes become over- or under-methylated as we age,4,5,6 thereby suggesting that the modulation of DNA methylation could enable the up- or down-regulation of specific genes and thus modulate the aging process. Dr. Steven Horvath, Professor of Human Genetics at the UCLA David Geffen School of Medicine and Professor of Human Genetics & Biostatistics at the UCLA Field School of Public Health, is a leading authority on the study of DNA methylation, and his research publications have been cited nearly 90,000 times in peer-reviewed articles. Professor Horvath studied a large number of datasets comprised of most tissue and cell types to create the first epigenetic clock (or “biological clock” to measure “biological age”) to measure the cumulative methylation of selected sites in the genome and how this could differ from a person’s “chronological age.” This finding that NE3107 may affect DNA methylation would be consistent with the understanding of its mechanism of action. NE3107 has been shown to modulate the expression of TNFa, which is considered to be the master regulator of inflammation.7 Inflammation has been shown to be associated with hypermethylation of DNA,8 which in turn has been shown to impact a wide range of diseases, including various forms of cancers,9 age-related cognitive impairment and dementia,10 Parkinson’s disease,11 cardiovascular disease,10,12 COPD and respiratory disease,13 chronic kidney disease,14 inflammatory bowel disease,15 sepsis,16 and many others. I believe this encouraging finding that NE3107 may affect the biological markers associated with aging helps explain the results we have seen from our trials in Alzheimer’s and Parkinson’s, both diseases are associated with aging. NE3107 has shown the ability to modulate inflammation and insulin resistance by reducing TNFa, which leads to improvements in a series of downstream factors such as metabolic dyshomeostasis, apoptosis, oxidative stress, among others. NE3107’s impact on DNA methylation helps explain the magnitude and rapid pace of impact we see in the AD and PD trials. Overall, we are very excited with the progress of our clinical programs and the potential of advancing meaningful therapies for our patient communities. Over the course of 2022, we provided positive topline results from our AD and PD trials. Furthermore, we found that NE3107 has an unexpected impact on the biomarkers of aging-related disease states and how this may affect disease progression, which provides additional avenues of exploration for the molecule. We are also looking forward to an exciting 2023. With respect to additional data readouts, we start with the detailed presentation of our Parkinson’s data at the AD/PD™ 2023 International Conference on Alzheimer’s and Parkinson’s Diseases to be held March 28-April 1, 2023 in Gothenburg, Sweden. We look forward to providing data read out from our Phase 2 trial evaluating BIV201 in ascites in the first half of the year. And we eagerly anticipate reading out the Phase 3 potentially pivotal trial for NE3107 in Alzheimer’s Disease in 3Q2023. Given the efficacy signal detected in the Parkinson’s Phase 2 trial, we will start planning the next phase of the clinical development program for discussion with the FDA in anticipation of launching the Phase 3 for PD trials in 2023 as well. I hope you share our enthusiasm for how the programs are advancing and the potential for exciting catalysts over the next year. We thank you for your support. Cuong Do President & Chief Executive Officer About BioVie BioVie Inc. (NASDAQ: BIVI) is a clinical-stage company developing innovative therapies to overcome unmet medical needs in chronic debilitating conditions. In neurodegenerative disease, the Company’s drug candidate NE3107 inhibits inflammatory activation of ERK and NFkB (e.g., TNF signaling) that leads to neuroinflammation and insulin resistance, but not their homeostatic functions (e.g., insulin signaling and neuron growth and survival). Both are drivers of Alzheimer’s and Parkinson’s diseases. The Company is conducting a potentially pivotal Phase 3 randomized, double blind, placebo controlled, parallel group, multicenter study to evaluate NE3107 in patients who have mild to moderate Alzheimer's disease (NCT04669028) and is targeting primary completion in mid-2023. An estimated six million Americans suffer from Alzheimer’s. A Phase 2 study of NE3107 in Parkinson’s disease (NCT05083260) has completed and provided its topline data readout in December 2022. In liver disease, the Company’s Orphan drug candidate BIV201 (continuous infusion terlipressin), with FDA Fast Track status, is being evaluated in a US Phase 2b study for the treatment of refractory ascites due to liver cirrhosis with top-line results anticipated in mid-2023. BIV201 is administered as a patent-pending liquid formulation. The active agent is approved in the U.S. and in about 40 countries for related complications of advanced liver cirrhosis. For more information, visit http://www.bioviepharma.com/. Forward-Looking Statements This press release contains forward-looking statements, which may be identified by words such as "expect," "look forward to," "anticipate" "intend," "plan," "believe," "seek," "estimate," "will," "project" or words of similar meaning. Although BioVie Inc. believes such forward-looking statements are based on reasonable assumptions, it can give no assurance that its expectations will be attained. Actual results may vary materially from those expressed or implied by the statements herein due to the Company's ability to successfully raise sufficient capital on reasonable terms or at all, available cash on hand and contractual and statutory limitations that could impair our ability to pay future dividends, our ability to complete our pre-clinical or clinical studies and to obtain approval for our product candidates, to successfully defend potential future litigation, changes in local or national economic conditions as well as various additional risks, many of which are now unknown and generally out of the Company's control, and which are detailed from time to time in reports filed by the Company with the SEC, including quarterly reports on Form 10-Q, reports on Form 8-K and annual reports on Form 10-K. BioVie Inc. does not undertake any duty to update any statements contained herein (including any forward-looking statements), except as required by law. For Public/Press Relations Inquiries: Dennis Consorte(201) 344-9648dennisconsorte@gmail.com For Investor Relations Inquiries: Bruce Mackle Managing Director LifeSci Advisors, LLC bmackle@lifesciadvisors.com *Horvath K. doi.org/10.1016/j.parkreldis.2015.10.006 1Oberdoerffer P Nat Rev Mol Cell Biol 2007, 8:692–702.2Campisi J J Gerontol A Biol Sci Med Sci 2009, 64A:175–178.3Moore L Neuropsychopharmacology vol 38, pages23–38 (2013)4Fraga MF Ann N Y Acad Sci 2007, 1100:60–74.5Christensen BC PLoS Genet 2009, 5:e10006026Horvath S Genome Biol 2012, 13:R977Jang et al. Int J Mol Sci. 2021 Mar; 22(5): 27198Stenvinkel P doi: 10.1111/j.1365-2796.2007.01777.x9Wang Z Nucleic Acids Research, 2020, Vol. 48, No. 510Sugden K Neurology 2022;99:e1402-e141311Tang X DOI: 10.1002/mds.2915712Tabaeia S Artificial Cells, Nanomedicine, and Biotechnology, 47:1, 2031-204113Qiu W Am J Respir Crit Care Med Vol 185, Iss. 4, pp 373–381, Feb 15, 201214Rysz C Int. J. Mol. Sci. 2022, 23(13), 710815Kraiczy J Mucosal Immunology volume 9, pages 647–658 (2016)16Rump K Sci Rep 9, 18511 (2019)

Novel antibody, TB006, demonstrated improvements in cognition and function and was well tolerated in a one-month Phase 1b/2 trial in mild to severe Alzheimer’s disease (AD) patientsTB006 also demonstrated improvements in PET and MR imaging, consistent with dissolution of toxic amyloid plaque shown in preclinical studiesOngoing open-label extension study with more than 100 participants is generating long-term safety and efficacy data FOSTER CITY, Calif., Dec. 06, 2022 (GLOBE NEWSWIRE) -- TrueBinding Inc. a clinical-stage biotherapeutics company focused on pioneering the development of innovative monoclonal antibodies for the treatment of some of the most challenging neurodegenerative diseases and other serious diseases, highlighted the unique method of action (MOA) of TB006, an investigational monoclonal antibody against Galectin-3 (Gal-3) for the treatment of mild to severe AD, at the recent 15th Clinical Trials on Alzheimer’s Disease (CTAD) Conference. Aβ, p-Tau and other pathogenic factors are not considered toxic when they exist as monomers; however, when they are aggregated and become oligomers, they become very toxic, which leads to neuronal death and neuroinflammation. Gal-3 has been shown to play a detrimental role in AD pathology by promoting the aggregation of Aβ, p-Tau, Apo-E4 and other pathogenic factors. In preclinical studies, TB006, a humanized monoclonal antibody, was shown to block Gal-3 and dissolve the toxic aggregates, which reversed disease progress in animal models of AD. “Our monoclonal antibody, TB006, targets Gal-3, which acts as a glue and has a role in the formation of toxic protein oligomers that compromise normal neuronal function in the brain and leads to disease progression,” said Dongxu Sun, Ph.D., chief executive officer of TrueBinding. “Unlike other antibodies in development that target the components of the aggregates, TB006 is unique in that it targets what may be the key nucleating factor for the aggregates to inhibit its activity. We are encouraged by the early clinical data and look forward to advancing our understanding of TB006 and its potential to improve cognition and functioning with an ambitious goal of potentially reversing the course of AD.” Dr. Sun continued, “Our Phase 1b/2 proof-of-concept trial demonstrated the potential of TB006 to improve cognition and function in patients with Alzheimer’s disease with a short one-month weekly treatment regimen. Improvements in patient cognition and function were seen as early as 15 days after the first treatment, and continued through day 36, only diminishing once we stopped treatment with TB006. Notably, this efficacy was observed across the patient population, whose disease severity ranged from mild to severe. Beyond the quantitative clinical measures we track, we’ve also received an overwhelming number of touching personal stories from participating physicians and caregivers about the dramatic improvement in symptoms of trial participants and the hope they have for a safe and effective treatment for this debilitating disease.” “There is an immense need for disease modifying treatments that can help the more than 6.5 million patients diagnosed with Alzheimer’s disease in the U.S,” said Malisa Agard, MD, principal investigator, Conquest Research. “Unfortunately, our existing treatment options are quite limited, so I was excited to review the data from the TB006 trial. Despite it being early-stage data, it gives me a great deal of hope in the potential of TB006 to help the millions of patients who are suffering now and, additionally, the millions more who are likely to develop this disease in the future.” Data from the Phase 1b/2 trial presented at CTAD and more information on the promising mechanism of action of novel antibody TB006 can be found on the TrueBinding website at www.truebinding.com. In the Phase 1b/2 trial, administration of TB006 versus placebo reduced the Clinical Dementia Rating-Sum of Boxes (CDR-SB*) score, a patient and caregiver combined assessment, after just one month treatment. Through day 104, the data showed a treatment difference of 63 percent versus placebo, which represents a score change of -0.44 points (p=0.08); indicating a trend toward improvement in clinical function of patients in the analysis of the Intent-to-treat (ITT) population. Of note, at Day 36 TB006 versus placebo significantly improved not only Mini Mental State Examination (MMSE**) scores by 1.02 points (p=0.02), but also the percentage of responders (one or more points reduction of CDR-SB from the baseline, p=0.016). In addition, treatment with TB006 resulted in patient improvements across a range of disease severity, including within the difficult-to-treat moderate and severe patient population. In addition, TB006 significantly reduced Aβ 42 plasma levels and reduced amyloid plaques, further evidence of an impact on the underlying disease. TB006 was safe and well tolerated through the observation period of 3.5 months. There were no treatment-related serious adverse events and no imaging-related abnormalities (ARIA). The most common adverse event (AE) was infusion reaction. The trial was a seamless Phase 1b/2 double-blinded, placebo controlled, multicenter study conducted at 15 active sites in the U.S. to assess the safety and short-term efficacy of TB006 in 157 patients with mild to severe AD. Patients who met clinical diagnostic criteria for AD and had a screening MMSE <24 with no confounding neurologic or psychiatric disease were eligible. Amyloid positivity was not required for study participation. In the Phase 1b portion, three groups (140 mg, 420 mg, 1,000 mg) of eight patients received either weekly TB006 or placebo infusions in sequential ascending fashion for one month. In the Phase 2 portion, participants were randomized (1:1) to receive either TB006 (1,000 mg) or placebo weekly for one month. Other endpoints were the MMSE, neuropsychiatric inventory (NPI), CDR battery and plasma and imaging (MRI/PET) biomarkers. Cognition testing was performed at baseline and on days 15, 36, 64 and 104. Safety assessments were conducted at each visit. An ongoing open-label extension study assessing monthly injections of TB006 at 4,000 mg in over 100 participants is generating long-term safety and efficacy data, with initial, interim data expected in the first quarter of 2023. A longer-term, 12-month, randomized, placebo-controlled Phase 2b trial is planned. * CDR-SB is a numeric scale used to quantify the various severity of symptoms of dementia. Based on interviews of people living with AD and family/caregivers, qualified healthcare professionals assess cognitive and functional performance in six areas: memory, orientation, judgment and problem solving, community affairs, home and hobbies, and personal care. The total score of the six areas is the score of CDR-SB, and CDR-SB is also used as an appropriate item for evaluating the effectiveness of therapeutic drugs targeting the early stages of AD. **The Mini Mental State Examination (MMSE) is a tool that can be used to systematically and thoroughly assess mental status. It is an 11-question measure that tests five areas of cognitive function: orientation, registration, attention and calculation, recall, and language. About Alzheimer’s DiseaseAlzheimer’s disease (AD) is a chronic progressive neurodegenerative brain disorder. AD is the leading cause of dementia among older adults, affecting as many as 55 million patients worldwide1 with an incidence expected to increase as the global population ages. AD is a type of dementia that begins with mild memory loss but eventually symptoms can become severe enough to affect other cognitive abilities that are required for daily living. Major pathological hallmarks of AD include the formation of toxic oligomers in the brain involving the major proteins: amyloid beta (Aβ) peptides and phospho-tau, alpha synuclein, and ApoE4. Galectin-3 (Gal-3), an endogenous protein that is found at abnormally high levels in the brains of AD patients, has been shown to play a key role in AD pathology.2 Gal-3 is involved in the sustained release of proinflammatory molecules, such as cytokines and chemokines which contribute to the toxic environment in the brain that drives the progression of AD2. Gal-3 binds to Aβ peptides, p-Tau and other amyloid proteins, and acts as a glue, causing these proteins, which normally exist as monomers, to bind and form toxic oligomers. These oligomers cause plaque deposits in the brain, inflammation, and direct toxicity to intact neurons; thereby resulting in cognition defect symptoms in AD patients. While there is currently no known cure for AD, Gal-3 inhibition may provide a multi-pronged approach to the treatment of AD. About TB006TB006 is a humanized monoclonal antibody that, based on preclinical data and early clinical studies, has the potential to improve cognition and functioning of patients with Alzheimer’s disease (AD). In pre-clinical evaluations, Galectin-3 was shown to intrinsically promote the aggregation of Aβ and pTau proteins. In AD in vivo model studies, TB006 showed promising capabilities in significant reduction of the aggregation of Aβ/Tau proteins and neuroinflammation, and significant improvement of cognitive performance, which show potential therapeutic effect of TB006 in addressing underlying pathology and ameliorating the course of AD. Human safety of TB006 was established in a single, escalating dose safety and tolerability study, where doses of up to 5000 mg were safe and well tolerated. In a Phase 1b/2 proof-of-concept trial in mild to severe AD patients, TB006 demonstrated statistically significant improvements in cognition and functioning. TB006 is currently being evaluated in a Phase 2 open-label extension trial in patients with AD and in a Phase 2 trial in patients with acute ischemic stroke. About TrueBinding, Inc. TrueBinding Inc. is a clinical-stage biotherapeutics company focused on pioneering the development of innovative monoclonal antibodies for the treatment of some of the most challenging neurodegenerative diseases, including Alzheimer's disease (AD), as well as stroke, oncology and other serious diseases. The company is focused on rapidly advancing its lead drug candidate, TB006, a humanized monoclonal antibody targeting Galectin-3, that is being evaluated in a Phase 2 open-label extension trial in patients with AD and in a Phase 2 trial in patients with acute ischemic stroke. For more information, visit www.truebinding.com. Contacts: Dongxu Sun, PhDChief Executive Officerdsun@truebinding.com650.847.1117 References: World Health Organization . Geneva, Switzerland: World Health Organization; 2021. Fact sheets of dementia [Internet] [cited 2022 Apr 13]. Available from: https:// www.who.int/news-room/fact-sheets/detail/dementia.Boza-Serrano, A., Ruiz, R., Sanchez-Varo, R. et al. Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer’s disease. Acta Neuropathol. 2019; 138:251–273. DOI:10.1007/s00401-019-02013-z https://pubmed-ncbi-nlm-nih-gov.libproxy1.nus.edu.sg/31006066/