Phase 2 Discovery, Inc.

Phase 1 trial enrolled all comers, with vast majority of patients having zero or very low MAGE-A4 expression IMC-C103C has a manageable safety profile and demonstrated signals of clinical activity The RECIST response rate was low in the population with zero or very low MAGE-A4 expression ctDNA reductions observed even at low MAGE-A4 expression OXFORDSHIRE, UK & CONSHOHOCKEN, PA & ROCKVILLE, MD, USA I December 08, 2022 I Immunocore Holdings plc (Nasdaq: IMCR), a commercial-stage biotechnology company pioneering the development of a novel class of T cell receptor (TCR) bispecific immunotherapies designed to treat a broad range of diseases, including cancer, autoimmune and infectious diseases, today presented data for IMC-C103C, a bispecific T cell engager targeting MAGE-A4, in patients with ovarian cancer. The Phase 1 data, presented in a poster at the ESMO Immuno-Oncology 2022 Congress, include 33 heavily pre-treated patients with ovarian cancer, who received doses of ≥ 90 mcg intravenously. This includes 16 new patients, and 17 patients previously reported at the ESMO Immuno-Oncology 2021 Congress, now with longer follow-up. All patients had platinum relapsed/refractory ovarian cancer (70% PARP inhibitors experienced) and were enrolled regardless of MAGE-A4 protein expression, which was analyzed retrospectively. Of the 33 patients, 39% (13/33) were MAGE-A4 negative as measured by immunohistochemistry (IHC), and 2 patients had an unknown H score. Of the 55% (18/33) MAGE-A4 positive patients, the majority had low expression (median score = 29 of 300), and only 2 had an H score > 150. The safety profile was consistent with that reported previously and the mechanism of action, i.e., T cell activation. No related AE led to treatment discontinuation or death. At the time of data cut-off, 32 patients were evaluable for response, with one additional patient (H score 21) still on treatment and not having had first tumor assessment​. Of the 17 evaluable MAGE-A4 positive patients, one had a durable Partial Response (PR), with a duration of 12.7 months, one patient who had a Stable Disease (SD) converted to an unconfirmed PR after the poster data cutoff date and is still ongoing, and 5 had SD. Reductions in ctDNA were observed in over half of ctDNA evaluable patients (12/22), including 7 with ≥ 50% reductions, and even in those with low or zero MAGE-A4 expression. “Immunocore has learned from tebentafusp that OS benefit and ctDNA reduction are observed in patients with both high and low total protein expression, while RECIST responses are enriched at higher protein expression,” said David Berman, Head of Research and Development of Immunocore. “The emerging IMC-C103C results, where most patients had either no or very low MAGE-A4 expression, are consistent with the RECIST and ctDNA reduction results reported for tebentafusp.” IMC-C103C is part of a co-development / co-promotion collaboration with Genentech, a member of the Roche Group under which Immunocore shares program costs and profits equally. Both companies are evaluating next steps for the IMC-C103C program. About Immunocore Immunocore is a commercial-stage biotechnology company pioneering the development of a novel class of TCR bispecific immunotherapies called ImmTAX – Immune mobilizing monoclonal TCRs Against X disease – designed to treat a broad range of diseases, including cancer, autoimmune, and infectious disease. Leveraging its proprietary, flexible, off-the-shelf ImmTAX platform, Immunocore is developing a deep pipeline in multiple therapeutic areas, including five clinical stage programs in oncology and infectious disease, advanced pre-clinical programs in autoimmune disease and multiple earlier pre-clinical programs. Immunocore’s most advanced oncology TCR therapeutic, KIMMTRAK, has been approved for the treatment of HLA-A*02:01-positive adult patients with unresectable or metastatic uveal melanoma (mUM) in the United States, European Union, Canada, Australia and the United Kingdom, having demonstrated an overall survival benefit in a randomized Phase 3 clinical trial in mUM, a cancer that has historically proven to be insensitive to other immunotherapies. SOURCE: Immunocore

Immunocore presents ovarian cancer expansion data for ImmTAC® candidate IMC-C103C targeting MAGE-A4 Phase 1 trial enrolled all comers, with vast majority of patients having zero or very low MAGE-A4 expression IMC-C103C has a manageable safety profile and demonstrated signals of clinical activity The RECIST response rate was low in the population with zero or very low MAGE-A4 expression ctDNA reductions observed even at low MAGE-A4 expression (OXFORDSHIRE, England & CONSHOHOCKEN, Penn. & ROCKVILLE, Md, 08 December 2022) Immunocore Holdings plc (Nasdaq: IMCR), a commercial-stage biotechnology company pioneering the development of a novel class of T cell receptor (TCR) bispecific immunotherapies designed to treat a broad range of diseases, including cancer, autoimmune and infectious diseases, today presented data for IMC-C103C, a bispecific T cell engager targeting MAGE-A4, in patients with ovarian cancer. The Phase 1 data, presented in a poster at the ESMO Immuno-Oncology 2022 Congress, include 33 heavily pre-treated patients with ovarian cancer, who received doses of ≥ 90 mcg intravenously. This includes 16 new patients, and 17 patients previously reported at the ESMO Immuno-Oncology 2021 Congress, now with longer follow-up. All patients had platinum relapsed/refractory ovarian cancer (70% PARP inhibitors experienced) and were enrolled regardless of MAGE-A4 protein expression, which was analyzed retrospectively. Of the 33 patients, 39% (13/33) were MAGE-A4 negative as measured by immunohistochemistry (IHC), and 2 patients had an unknown H score. Of the 55% (18/33) MAGE-A4 positive patients, the majority had low expression (median score = 29 of 300), and only 2 had an H score > 150. The safety profile was consistent with that reported previously and the mechanism of action, i.e., T cell activation. No related AE led to treatment discontinuation or death. At the time of data cut-off, 32 patients were evaluable for response, with one additional patient (H score 21) still on treatment and not having had first tumor assessment​. Of the 17 evaluable MAGE-A4 positive patients, one had a durable Partial Response (PR), with a duration of 12.7 months, one patient who had a Stable Disease (SD) converted to an unconfirmed PR after the poster data cutoff date and is still ongoing, and 5 had SD. Reductions in ctDNA were observed in over half of ctDNA evaluable patients (12/22), including 7 with ≥ 50% reductions, and even in those with low or zero MAGE-A4 expression. “Immunocore has learned from tebentafusp that OS benefit and ctDNA reduction are observed in patients with both high and low total protein expression, while RECIST responses are enriched at higher protein expression,” said David Berman, Head of Research and Development of Immunocore. “The emerging IMC-C103C results, where most patients had either no or very low MAGE-A4 expression, are consistent with the RECIST and ctDNA reduction results reported for tebentafusp.” IMC-C103C is part of a co-development / co-promotion collaboration with Genentech, a member of the Roche Group under which Immunocore shares program costs and profits equally. Both companies are evaluating next steps for the IMC-C103C program. ## About Immunocore Immunocore is a commercial-stage biotechnology company pioneering the development of a novel class of TCR bispecific immunotherapies called ImmTAX – Immune mobilizing monoclonal TCRs Against X disease – designed to treat a broad range of diseases, including cancer, autoimmune, and infectious disease. Leveraging its proprietary, flexible, off-the-shelf ImmTAX platform, Immunocore is developing a deep pipeline in multiple therapeutic areas, including five clinical stage programs in oncology and infectious disease, advanced pre-clinical programs in autoimmune disease and multiple earlier pre-clinical programs. Immunocore’s most advanced oncology TCR therapeutic, KIMMTRAK, has been approved for the treatment of HLA-A*02:01-positive adult patients with unresectable or metastatic uveal melanoma (mUM) in the United States, European Union, Canada, Australia and the United Kingdom, having demonstrated an overall survival benefit in a randomized Phase 3 clinical trial in mUM, a cancer that has historically proven to be insensitive to other immunotherapies. Forward Looking Statements This press release contains “forward-looking statements” within the meaning of the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Words such as “may,” “can,” “will,” “believe,” “expect,” “plan,” “anticipate,” and similar expressions (as well as other words or expressions referencing future events or circumstances) are intended to identify forward-looking statements. All statements, other than statements of historical facts, included in this press release are forward-looking statements. These statements include, but are not limited to, statements regarding the therapeutic potential and expected clinical benefits of our product candidates, including overall survival benefit; expectations regarding the development of Immunocore’s pipeline and the design, progress, timing, scope and results of Immunocore’s existing and planned clinical trials; and statements regarding Immunocore’s collaboration with Genentech. Any forward-looking statements are based on management’s current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements, many of which are beyond the Company’s control. These risks and uncertainties include, but are not limited to, the impact of worsening macroeconomic conditions and the ongoing and evolving COVID-19 pandemic on Immunocore’s business, strategy, clinical trials, financial position and anticipated milestones, including Immunocore’s ability to conduct ongoing and planned clinical trials; Immunocore’s ability to obtain a clinical supply of current or future product candidates, or commercial supply of KIMMTRAK or any future approved products, including as a result of supply chain disruptions, the COVID-19 pandemic, the war in Ukraine or global geopolitical tension; Immunocore’s ability to obtain and maintain regulatory approvals for its product candidates; Immunocore’s ability to develop, manufacture and commercialize its product candidates; Immunocore’s ability and plans in continuing to establish and expand a commercial infrastructure and to successfully launch, market and sell KIMMTRAK and any future approved products; Immunocore’s ability to successfully expand the approved indications for KIMMTRAK or obtain marketing approval for KIMMTRAK in additional geographies in the future; the delay of any current or planned clinical trials, whether due to the COVID-19 pandemic, patient enrollment delays or otherwise; Immunocore’s ability to successfully demonstrate the safety and efficacy of its product candidates and gain approval of its product candidates on a timely basis, if at all; competition with respect to market opportunities; unexpected safety or efficacy data observed during pre-clinical studies or clinical trials; actions of regulatory agencies, which may affect the initiation, timing and progress of Immunocore’s clinical trials or future regulatory approval; Immunocore’s need for and ability to obtain additional funding, on favorable terms or at all, including as a result of worsening macroeconomic conditions such as rising inflation and interest rates, volatility in the capital markets and related market uncertainty, the COVID-19 pandemic, the war in Ukraine and global geopolitical tension; Immunocore’s ability to obtain, maintain and enforce intellectual property protection for KIMMTRAK or any product candidates it is developing; clinical trial site activation or enrollment rates that are lower than expected; and the success of Immunocore’s current and future collaborations, partnerships or licensing arrangements. These and other risks and uncertainties are described in greater detail in the section titled "Risk Factors" in Immunocore’s filings with the Securities and Exchange Commission, including Immunocore’s most recent Annual Report on Form 20-F for the year ended December 31, 2021 filed with the Securities and Exchange Commission on March 3, 2022, as well as discussions of potential risks, uncertainties, and other important factors in the Company’s subsequent filings with the Securities and Exchange Commission. All information in this press release is as of the date of the release, and the Company undertakes no duty to update this information, except as required by law. CONTACT: Immunocore Sébastien Desprez, Head of CommunicationsT: +44 (0) 7458030732 E: sebastien.desprez@immunocore.com Follow on Twitter: @Immunocore Consilium Strategic Communications (corporate and financial)Mary-Jane Elliott/ Chris Welsh/Jessica HodgsonT: +44 (0)203 709 5700E: Immunocore@consilium-comms.com Investor Relations Clayton Robertson, Head of Investor RelationsT: +1 (215) 384-4781E: clayton.robertson@immunocore.com

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)