BIVI US Equity☆

UNITED

STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM

10-K

(Mark

One)

☒ANNUAL REPORT UNDER SECTION 13 OR 15(d) OF THE SECURITIES EXCHANGE ACT OF 1934.

FOR

THE FISCAL YEAR ENDED JUNE 30, 2023

☐TRANSITION REPORT PURSUANT TO SECTION 13 OR 15(d) OF THE SECURITIES EXCHANGE ACT OF 1934

For

the transition period from ____________to _____________

Commission

File Number: 001-39015

BIOVIE INC.

(Exact

name of registrant as specified in its charter)

(State or other jurisdiction of (I.R.S. Employer Identification Number)

incorporation or organization)

(Address of principal executive offices, Zip Code)

(Registrant’s telephone number, including area code)

Securities

registered pursuant to Section 12(b) of the Act:

Title of each class Trading Symbol(s) Name of each exchange on which registered

Securities

registered pursuant to Section 12(g) of the Act:

None

Indicate

by check mark if the registrant is a well-known seasoned issuer, as defined in Rule 405 of the Securities Act.

Yes

☐

No ☒

Indicate

by check mark if the registrant is not required to file reports pursuant to Section 13 or Section 15(d) of the Act

Yes

☐

No ☒

Indicate

by check mark whether the registrant (1) has filed all reports required to be filed by Section 13 or 15(d) of the Exchange Act during

the past 12 months (or for such shorter period that the registrant was required to file such reports), and (2) has been subject to such

filing requirements for the past 90 days.

Yes

☒

No ☐

Indicate

by check mark whether the registrant has submitted electronically every Interactive Data File required to be submitted pursuant to Rule

405 of Regulation S-T (§ 232.405 of this chapter) during the preceding 12 months (or for such shorter period that the registrant

was required to submit such files).

Yes

☒

No ☐

Indicate

by check mark whether the registrant is a large accelerated filer, an accelerated filer, a non-accelerated filer, a smaller reporting

company, or an emerging growth company. See the definitions of “large accelerated filer,” “accelerated filer,”

“smaller reporting company,” and “emerging growth company” in Rule 12b-2 of the Exchange Act.

Large Accelerated Filer ☐ Accelerated Filer ☐

Non-Accelerated Filer ☒ Smaller reporting company ☒

Emerging growth company ☐

If

an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying

with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☐

Indicate

by check mark if the registrant has filed a report on and attestation to its management’s assessment of the effectiveness of its

internal control over financial reporting under Section 404(b) of the Sarbanes-Oxley Act (15 U.S.C. 7362(b)) by the registered public

accounting firm that prepared or issued its audit report.

Yes

☐

No ☒

If

securities are registered pursuant to Section 12(b) of the Act, indicate by check mark whether the financial statements of the registrant

included in the filing reflect the correction of an error to previously issued financial statements. ☐

Indicate by check mark whether any of those error corrections are

restatements that required a recovery analysis of incentive-based compensation received by any of the registrant’s executive officers during the relevant recovery period pursuant to §240.10D-1(b). ☐

Indicate

by check mark whether the registrant is a shell company (as defined in Rule 12b-2 of the Exchange Act).

Yes

☐

No ☒

The

aggregate market value of the voting and non-voting common equity held by non-affiliates computed by reference to the price at which

the common equity was last sold, or the average bid and asked price of such common equity, as of the last business day of the registrant’s

most recently completed second fiscal quarter was $86,033,369.

There

were 36,803,768shares of the Registrant’s Class A Common Stock, $0.0001 par value per share, outstanding as of August 9, 2023.

DOCUMENTS

INCORPORATED BY REFERENCE

None.

BIOVIE

INC.

FORM

10-K INDEX

PART I

Item 1. Business 1

Item 1A. Risk Factors 15

Item 1B. Unresolved Staff Comments 30

Item 2. Properties 30

Item 3. Legal Proceedings 30

Item 4. Mine Safety Disclosures 30

PART II

Item 6. [Reserved] 31

Item 7A. Quantitative and Qualitative Disclosures About Market Risk 35

Item 8. Financial Statements and Supplementary Data 35

Item 9A Controls and Procedures 35

Item 9B. Other Information 36

Item 9C. Disclosure Regarding Foreign Jurisdictions that Prevent Inspections 36

PART III

Item 10. Directors, Executive Officers and Corporate Governance 37

Item 11. Executive Compensation 43

Item 14. Principal Accountant Fees and Services 54

PART IV

Item 15. Exhibits and Financial Statement Schedules 55

Item 16. Form 10-K Summary

(i)

BIOVIE

INC.

FORWARD-LOOKING

STATEMENTS

This

report contains forward-looking statements within the meaning of Section 21E of the Securities Exchange Act of 1934, and Section 27A

of the Securities Act of 1933. Any statements contained in this report that are not statements of historical fact may be forward-looking

statements. When we use the words “intends,” “estimates,” “predicts,” “potential,” “continues,”

“anticipates,” “plans,” “expects,” “believes,” “should,” “could,”

“may,” “will” or the negative of these terms or other comparable terminology, we are identifying forward-looking

statements. Forward-looking statements involve risks and uncertainties, which may cause our actual results, performance or achievements

to be materially different from those expressed or implied by forward-looking statements. These factors include our research and development

activities, distributor channel; compliance with regulatory impositions; and our capital needs. Although we believe that the expectations

reflected in the forward-looking statements are reasonable, we cannot guarantee future results, levels of activity, performance or achievements.

Except

as may be required by applicable law, we do not undertake or intend to update or revise our forward-looking statements, and we assume

no obligation to update any forward-looking statements contained in this report as a result of new information or future events or developments.

Thus, you should not assume that our silence over time means that actual events are bearing out as expressed or implied in such forward-looking

statements. You should carefully review and consider the various disclosures we make in this report and our other reports filed with

the Securities and Exchange Commission that attempt to advise interested parties of the risks, uncertainties and other factors that may

affect our business.

All

statements other than statements of historical fact are statements that could be deemed forward-looking statements. The Company assumes

no obligation and does not intend to update these forward-looking statements, except as required by law. When used in this report, the

terms “BioVie”, “Company”, “we”, “our”, and “us” refer to BioVie, Inc.

(ii)

PART

I

ITEM 1. BUSINESS

Overview

BioVie

Inc. (the “Company” or “we” or “our”) is a clinical-stage company developing innovative drug therapies

for the treatment of neurological and neurodegenerative disorders and advanced liver disease.

Neurodegenerative

Disease Program

In neurodegenerative disease, the Company’s

drug candidate NE3107 inhibits inflammatory activation of extracellular single-regulated kinase (“ERK”) and Nuclear factor kappa-light-chain-enhancer

of activated B cells (“NFkB”) (e.g., tumor necrosis factor (“TNF”) signaling) that leads to neuroinflammation

and insulin resistance, but not their homeostatic functions (e.g., insulin signaling and neuron growth and survival). Both inflammation

and insulin resistance are drivers of Alzheimer’s disease (“AD”) and Parkinson’s disease (“PD”).

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). The Company is targeting primary completion

of this study in the fourth quarter of calendar year 2023.

In

December 2022, topline results were released from the Company’s Phase 2 study assessing NE3107’s safety and tolerability

and potential pro-motoric impact in PD patients. The NM201 study (NCT05083260) was a double-blind, placebo-controlled, safety, tolerability,

and pharmacokinetics study in PD participants treated with carbidopa/levodopa and NE3107. Forty-five patients with a defined L-dopa “off

state” were randomized 1:1 to placebo:NE3107 20 mg twice daily for 28 days. The trial was launched with two design objectives:

1) the primary objective was safety and a drug-drug interaction study (as requested by the U.S. Food and Drug Administration (“FDA”)) to demonstrate the absence of adverse interactions of NE3107 with levodopa; and 2) the secondary objective was to determine

if preclinical indications of promotoric activity and apparent enhancement of levodopa activity observed in a Parkinson’s disease

model in monkeys can be seen in humans. Both objectives of the study were met. Patients treated with NE3107 experienced greater motor

control.

The

Company provided the financial support and the use of our NE3107 formulated drug product for an open-label phase 2, Investigator-Initiated

Trial in mild cognitive impairment (“MCI”) and Mild AD, NCT05227820, conducted by (“The Regenesis Project”)

of Dr. Sheldon Jordan. The study received FDA authorization on December 12, 2021 and was designed to measure NE3107’s effect on cognition,

cerebral spinal fluid (“CSF”) and blood biomarkers, and neuro-imagining endpoints. Topline results were released September

7, 2022, and additional data was presented at the Clinical Trial in Alzheimer’s Disease (“CTAD”) annual conference in

December 2022. The data showed that three months of treatment with NE3107 in patients with MCI and mild AD enhanced cognition compared

to baseline, as measured using multiple rating scales, had improvement in daily function and improvements in inflammation correlated with

improved cognition. No drug-related adverse events were observed.

The

Company acquired the biopharmaceutical assets of NeurMedix, Inc. (“NeurMedix”), from a related party privately held clinical-stage

pharmaceutical company, in June 2021. The acquired assets included NE3107, a potentially selective inhibitor of inflammatory ERK signaling that, based on animal studies and Dr. Jordan’s study, is believed to reduce

neuroinflammation. NE3107 is a novel orally administered small molecule that is thought to inhibit inflammation-driven insulin resistance

and major pathological inflammatory cascades with a novel mechanism of action. There is emerging scientific consensus that both inflammation

and insulin resistance may play fundamental roles in the development of AD and PD, and NE3107 could, if approved by the FDA represent

a new medical approach to treating these devastating conditions affecting an estimated 6 million Americans suffering from AD and 1 million

Americans suffering from PD.

Inflammation-driven

insulin resistance is believed to be implicated in a broad range of serious diseases, and we plan to begin exploring these opportunities

in the coming months using NE3107 or related compounds acquired in the NeurMedix asset purchase. NE3107 is patented in the United States

(“U.S.”), Australia, Canada, Europe and South Korea.

1

Liver

Disease Program

In liver disease, our Orphan Drug candidate BIV201

(continuous infusion terlipressin), with FDA Fast Track status, has been evaluated in a U.S. Phase 2b study (NCT04112199) for the treatment

of refractory ascites due to liver cirrhosis. BIV201 is administered as a patent-pending liquid formulation. The study was closed before

full enrollment, without clinically meaningful adverse effects associated with BIV201 treatment and data that appeared to show that treatment

with BIV201 plus standard-of-care (“SOC”) resulted in a reduction in ascites fluid accumulation during treatment versus pre-treatment.

In June 2023, we requested guidance from the FDA regarding the design and endpoints for definitive clinical testing of BIV201 for the

treatment of ascites due to chronic liver cirrhosis.

While the active agent, terlipressin, is approved

in the U.S. and in about 40 countries for related complications of advanced liver cirrhosis, treatment of ascites is not included in these

authorizations. Patients with refractory ascites suffer from frequent life-threatening complications, generate more than $5 billion in

annual treatment costs, and have an estimated 50% mortality rate within 6 to 12 months. The U.S. FDA has not approved any drug to treat

refractory ascites.

The

BIV201 development program was initiated by LAT Pharma LLC. On April 11, 2016, the Company acquired LAT Pharma LLC and the rights to

its BIV201 development program. The Company currently owns all development and marketing rights to this drug candidate. Pursuant to the

Agreement and Plan of Merger entered into on April 11, 2016, between our predecessor entities, LAT Pharma LLC and NanoAntibiotics, Inc.,

BioVie is obligated to pay a low single digit royalty on net sales of BIV201 (continuous infusion terlipressin) to be shared among LAT

Pharma Members, PharmaIn Corporation, and The Barrett Edge, Inc.

Neurodegenerative

Disease Program

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 AD (NCT04669028). The study has co-primary endpoints looking at cognition using the Alzheimer’s Disease Assessment Scale-Cognitive

Scale (ADAS-Cog 12) and function using the Alzheimer’s Disease Cooperative Study-Clinical Global Impression of Change (ADCS-CGIC).

The program is fully enrolled and is targeting primary completion in the fourth quarter of the calendar 2023 year.

The Company supported a Phase 2 exploratory biomarker

study (Investigator-Initiated Trial in MCI and Mild Alzheimer’s Disease, NCT05227820) showing that patients treated with NE3107

experienced improved cognition as measured by a modified ADAS-Cog12 score, reduced TNF- a (i.e.,

inflammation) in a manner that’s correlated to improvements in cognition, reduced CSF p-tau levels and the ratio of p-tau to A b42,

and imaging findings suggestive of improved neuronal health. Despite the open-label nature of the exploratory study, the emerging data

and correlations provide encouraging signs of what we may see in the upcoming Phase 3 data reveal. The Phase 2 Study enrolled a total

of 23 patients – 17 patients with Mini-Mental State Examination (“MMSE”) scores greater than or equal to 20 (i.e., MCI

to mild AD) and 6 patients with MMSE <20 (i.e., moderate AD) – with an average age of 71.1 years. This open-label, single arm

study was designed to measure changes in cognition through verbal and visual test procedures and changes in biomarkers of AD and inflammation

that can be measured in cerebral spinal fluid (“CSF”), blood samples, and functional magnetic resonance imaging in patients

before and after treatment with 20 mg of NE3107 twice daily for 3 months. This data showed the following among patients with MMSE<20

(i.e., mild cognitive impairment and mild AD):

● No drug-related adverse events were observed.

Other potential NE3107 effects on biomarkers of

aging-related disease states were indicated. Blood samples were taken from the patients who participated in the investigator-initiated

Alzheimer’s Phase 2 trial before and after three months of treatment with NE3107, and these samples were analyzed to assess NE3107’s

potential to alter DNA methylation associated with epigenetic biological clocks. The resulting data for patients

treated with NE3107 for three months showed an average reduction of 3.3 years (p=0.0021) on the Horvath DNA methylation SkinBlood clock.

Furthermore, 19 out of the 22 patients experienced a reduction in the SkinBlood clock score.

2

In July 2023, the Company presented a poster detailing

the epigenetic basis for how its drug candidate NE3107 may have the potential to regulate methylation of specific genes in a manner that

significantly correlated with observed cognitive and biomarker improvements at the Alzheimer’s Associate’s International Conference

(AAIC) held in Amsterdam from July 16 through July 20, 2023.

The poster presentation titled Treatment-Induced

Epigenetic Modifications in MCI and Probable Alzheimer’s (Reading C, et al.), showed how patients with clinical dementia treated

with NE3107 for three months saw significant reductions in the level of DNA methylation, and that such reductions were, in some cases,

significantly correlated with observed improvements in various cognitive measures (e.g., ADAS-Cog11, CDR, ADCOMS, QDRS) and biomarkers

(including TNFα, CSF p-Tau/Aβ42, precuneus glutathione).

Inflammation has been shown to be associated with

the hypermethylation of our DNA,[1] which in turn has been shown to impact a wide range of diseases, including various forms

of cancers,[2] age-related cognitive impairment and dementia,[3] Parkinson’s disease,[4] cardiovascular

disease,[3,5] COPD and respiratory disease,[6] chronic kidney disease,[7] inflammatory bowel disease,[8]

sepsis,[9] and many others. The new data to be presented details how NE3107 may potentially change or affect the degree of

methylation of specific genes that are correlated with various markers of disease.

About

Inflammation and NE3107’s Mechanism of Action

Neuroinflammation,

insulin resistance, and oxidative stress are common features in the major neurodegenerative diseases, including Alzheimer’s Disease

(AD), Parkinson’s Disease (PD), frontotemporal lobar dementia, and Amyotrophic lateral sclerosis (“ALS”). NE3107 is

an orally bioavailable, blood-brain permeable, small molecule, with potential anti-inflammatory, insulin sensitizing, and ERK-binding

properties that may allow it to selectively inhibit ERK-, NFκB- and TNF-stimulated inflammation. NE3107’s potential to inhibit

neuroinflammation and insulin resistance forms the basis for the Company’s work testing the molecule in AD and PD patients.

Parallels exist between AD and

PD, among them activated microglia driving inflammation, involvement of TNFα, oxidative stress, protein misfolding, mitochondrial

dysfunction, and insulin resistance. In preclinical and clinical studies, NE3107 reduced inflammation and enhanced insulin sensitivity,

both of which are important to PD pathology. Preclinical studies in marmoset monkeys have shown NE3107 administered alone to be as pro-motoric

as levodopa, underscoring the apparently critical role of inflammation in expression of PD motor symptoms. When NE3107 was administered

with levodopa, the combination improved motor control better than either drug alone. Furthermore, in the marmoset study, NE3107 reduced

the severity of levodopa induced dyskinesia (“LID”) concurrent with pro-motoric benefit and decreased neurodegeneration, preserving twice

as many dopaminergic neurons compared to control.

Alzheimer’s

Disease

Alzheimer’s

disease (AD), which affects an estimated 6 million Americans, is a neuroinflammatory and neurodegenerative condition characterized by

progressive deterioration of cognitive function and loss of short-term memory and executive function. Cognitive tests quantifying AD

severity have been exhaustively developed. Formal diagnosis of AD has historically been dependent on the presence of extraneuronal amyloid

beta (Aβ) plaques, which can only be observed at autopsy or with the aid of sophisticated radioimaging techniques. However, diagnostic

methods have recently been approved that quantify Aβ in peripheral blood and correlate well with imaging results. Aβ plaques

can also be found in people without apparent AD symptoms, which has cast doubt about the role of Aβ as the central mediator of disease

pathology.

Scientific

investigations in the past twenty years have provided strong evidence that inflammation, type 2 diabetes (T2D), and inflammation-driven

insulin resistance are drivers of AD. The link between these factors and cognitive impairment are described by relatively new terms,

type 3 diabetes and metabolic-cognitive syndrome.

2 Wang Z Nucleic Acids Research, 2020, Vol. 48, No. 5

5 Tabaeia S Artificial Cells, Nanomedicine, and Biotechnology, 47:1, 2031-2041

8 Kraiczy J Mucosal Immunology volume 9, pages 647–658 (2016)

3

A large body of evidence supports inflammation

as a primary driver of pathology in AD. The major inflammation signaling node, NFkB, and the cytokine tumor necrosis factor (TNF) are

important initiators of inflammatory signaling in AD pathology. NE3107 is believed to inhibit extracellular signal regulated kinase (ERK)/NFkB

activation and TNF production stimulated by inflammatory mediators, such as lipopolysaccharide. Inhibition of NFkB activation and TNF

production from this type of stimulation has broad potential implications for reduction of pathological peripheral and central nervous

system (CNS) inflammatory signaling in AD, which include reduction of inflammation-driven insulin resistance, decreased inflammatory cell

infiltration into the CNS, and decreased microglia activation. Reduction of systemic inflammation and inflammation-driven insulin resistance

are also predicted to have beneficial effects on hypothalamus-pituitary-adrenal (HPA) axis dysregulation and hippocampal dysregulation

of cortisol secretion that are consequences of adipose inflammation and insulin resistance, and are known to promote cognitive impairment,

and are also forward-feeding for insulin resistance.

Inflammation, insulin resistance, and associated

metabolic dysregulation in the brain contribute to Aβ oligomerization and aggregation, phospho-tau formation, reduced neuron survival

stimulus, and a forward-feeding cycle of neuronal energy deficit and oxidative stress, causing neuronal dysfunction (cognitive impairment)

and neurodegeneration. We believe NE3107’s combination of anti-inflammatory and insulin sensitizing activity has the potential to

disrupt this forward-feeding cycle of AD pathology.

Insulin has a major role in metabolic regulation

and neuron survival, while insulin resistance and T2D are closely linked to AD pathology. Insulin signaling is involved in synaptic plasticity,

learning, and memory. Exogenous insulin enhances cognition in normal and cognitively impaired subjects. Insulin resistance is linked to

cognitive impairment.

The multifactorial influence of insulin signaling

on neuron survival and cognition suggests that correction of insulin signaling deficits with NE3107 in the target population may provide

significant benefits on both cognition and disease progression. Additional rationale for targeting metabolic dysregulation with NE3107

has come from recent work showing that peripheral insulin resistance promotes insulin resistance and senescence in the CNS.

There is also an extensive literature on the complex

role of adipose tissue inflammation in systemic inflammation, insulin resistance, hypothalamus-pituitary-adrenal axis (HPA) dysregulation

and chronic cortisol excess in cognitive impairment in AD. Obesity and inflammation are closely linked in expanding adipose tissue, where

the production of inflammatory cytokines and increased cortisol are driven though up-regulation of 11β-hydroxysteroid dehydrogenase

type 1 and adipocyte mineralocorticoid receptor activation. Inflamed adipose tissue interacts with the HPA axis and hippocampus to increase

systemic cortisol, and promote hippocampal inflammation through chronically elevated cortisol, which freely penetrates the blood-brain

barrier. Hyperglycemia (secondary to insulin resistance) exacerbates adrenal cortisol production and promotes forward feeding of inflammation

and HPA-hippocampal dysregulation.

Systemic inflammation from inflamed adipose and

associated mononuclear cells, promotes CNS inflammation with associated cognitive decline and neurodegeneration. We believe NE3107’s

anti-inflammatory activity against systemic/adipose inflammation and factors that dysregulate cortisol secretion, such as hyperglycemia,

has the potential to decrease cognitive impairment and neurodegenerative mechanisms that have been linked to cortisol excess.

Parkinson’s

Disease

The Company completed its Phase 2 study assessing

NE3107 in Parkinson’s disease patients in the fourth quarter of calendar year 2022. The NM201 study (NCT05083260) was a double-blind,

placebo-controlled, safety, tolerability, and pharmacokinetics study in Parkinson’s disease (PD) participants treated with carbidopa/levodopa

and NE3107. Forty-five patients with a defined L-dopa morning “off state” were randomized 1:1 to placebo:NE3107 20 mg twice

daily for 28 days. The trial was launched with two design objectives: 1) the primary objective was safety and a drug-drug interaction

study (as requested by FDA) to demonstrate the absence of adverse interactions of NE3107 with levodopa; and 2) the secondary objective

was to determine if preclinical indications of promotoric activity and apparent enhancement of levodopa activity observed in a PD model

in monkeys can be seen in humans. Both objectives were met. Highlighted results of the study were:

4

Neuroinflammation and activation of brain microglia,

leading to increased proinflammatory cytokines (particularly TNF) that play a pivotal role in PD, which affects an estimated 1 million

Americans. Multiple daily administrations of levodopa (converted to dopamine in the brain) is the current standard of care treatment for

this movement disorder, but prolonged daily administration leads to side effects of uncontrolled movements called levodopa-induced dyskinesia,

commonly referred to as LID. Recent evidence demonstrates that daily administration of levodopa further increases neuroinflammation, microglia

activation, and TNF inflammatory damage in neurons.

We

have shown in a mouse model of PD that NE3107 decreases inflammation and TNF in the brain and increases neuron survival (Nicoletti, 2012

Parkinson’s Disease 969418.) In this neurotoxin induced model, NE3107 decreased clinical signs of disease and neuronal death compared

to placebo treated mice.

An

unpublished study in a neurotoxin induced marmoset model of Parkinson’s disease reported that administration of NE3107 decreased

movement abnormalities that are the clinical signs of the disease. In the same study, NE3107 in combination with levodopa had a stronger

effect on clinical signs of disease than levodopa or NE3107 alone, while marmosets treated with NE3107 developed less LID. NE3107-treated

monkeys also exhibited neuroprotective activity that promoted the survival of twice as many neurons in the substantia nigra (primary

region of the brain that degenerates to cause parkinsonism) as monkeys treated with placebo. The results from the marmoset study suggest

that NE3107 may decrease clinical signs of disease in humans (improve motor function), which if true could enable a straightforward clinical

development strategy to test NE3107 in PD patients needing promotoric therapy.

If

approved as a promotoric agent, NE3107 would provide a non-dopaminergic alternative to Parkinson’s patients, and an opportunity

to significantly delay the need to start levodopa therapy. This could represent a first step toward supplanting levodopa as the primary

PD therapy, and in addition to delaying the emergence of LID, could also imply a slowing of disease progression, the most important and

still unmet objective of PD drug development.

5

Liver Cirrhosis Program

BioVie’s orphan drug candidate BIV201 (continuous

infusion terlipressin) represents a novel approach to the treatment of ascites due to chronic liver cirrhosis. Ascites is a common complication

of advanced liver cirrhosis involving the accumulation of large volumes of fluid in the abdomen, often exceeding five liters, due to liver

and kidney dysfunction. The FDA has never approved a drug to treat ascites, and once patients reach the refractory stage the estimated

one-year survival rate is only approximately 50%[10]. BIV201 is a continuous infusion of terlipressin, a drug used in over

40 countries to treat related complications of liver cirrhosis (Type 1 hepatorenal syndrome and bleeding esophageal varices) that was

recently approved in the U.S. but is not approved in Japan. With the novel room temperature stable formulation in a pre-filled syringe,

BIV201 could potentially provide a superior terlipressin drug delivery system throughout the world. The goal of BIV201 therapy is to interrupt

the ascites disease pathway, thereby halting the cycle of accelerated fluid generation in ascites patients.

In a series of interactions between June

2019 and April 2020, representatives of BioVie and the FDA communicated regarding the design and endpoints for the Phase 2 study (NCT04112199).

In June 2021, the Company initiated a Phase 2

study (NCT04112199) designed to evaluate the efficacy of BIV201 (terlipressin, administered by continuous infusion for two 28-day treatment

cycles) combined with standard-of-care (“SOC”), compared to SOC alone, for the treatment of refractory ascites. The primary

endpoints of the study are the incidence of ascites-related complications and change in ascites fluid accumulation during treatment compared

to a pre-treatment period.

In March 2023 the company announced enrolment

was paused and that data from the first 15 patients treated with BIV201 plus SOC appeared to show a 34% reduction in ascites fluid during

the 28 days after treatment initiation compared to the 28 days prior to treatment (p=0.0046). This improvement was significantly different

from those patients receiving SOC treatment. Patients who completed the treatment with BIV201 experienced a 53% reduction in ascites fluid

(p=0.001), which was sustained during the three months after treatment initiation as compared to the three-month pre-treatment period

(43% reduction, p=0.06).

In June 2023, the Company requested guidance from

the FDA regarding the design and endpoints for definitive clinical testing of BIV201 for the treatment of ascites due to chronic liver

cirrhosis. FDA accepted the request and intends to send written comments in the third quarter of calendar year 2023.

6

Our proprietary novel liquid formulation of terlipressin

in a prefilled syringe is designed to improve convenience for outpatient administration and avoid potential formulation errors when pharmacists

reconstitute the current powder version of terlipressin. To date, analytical testing results have confirmed room temperature stability

of the prefilled syringe in storage for 18 months, with the potential for up two years stability. Room temperature storage presents a

key product differentiation versus terlipressin products in countries where the drug is approved. To the best of the Company’s knowledge,

all other terlipressin products sold globally must be stored under refrigeration and there is no prefilled syringe format of terlipressin

available for treating patients in these countries. BioVie has also filed a Patent Cooperation Treaty (“PCT”) application

covering our novel liquid formulations of terlipressin (international patent application PCT/US2020/034269, published as WO2020/237170)

and we plan to seek patent protection in at least the U.S., Europe, China, Japan and other jurisdictions.

BIV201 (continuous infusion terlipressin) has

the potential to improve the health of thousands of patients suffering from life-threatening complications of liver cirrhosis due to hepatitis,

nonalcoholic steatohepatitis (“NASH”), and alcoholism. The FDA has granted Fast-Track status and Orphan Drug designation for

the most common of these complications, ascites, which represents a significant unmet medical need. Patients with cirrhosis and ascites

account for an estimated 116,000 U.S. hospital discharges annually, with frequent early readmissions. According to the HCUP Nationwide

Readmissions Database 2016, those requiring paracentesis (removal of ascites fluid) experience an average hospital stay lasting eight

days incurring over $86,000 in medical costs. This translates into a total potentially addressable ascites market size for BIV201 therapy

exceeding $650 million based on Company estimates. The FDA has never approved any drug specifically for treating ascites. For patients

with refractory ascites the mean one-year survival rate is only 50% (Bureau et al. 2017). BIV201 has also received Orphan Drug

designation for hepatorenal syndrome (“HRS”). Patients with refractory ascites often progress to HRS which is the onset of

kidney failure and requires emergency hospitalization.

The BIV201 development program began at LAT Pharma

LLC. On April 11, 2016, we acquired LAT Pharma LLC and the rights to its BIV201 development program and currently own all development

and marketing rights to the product candidate. We and PharmaIN, LAT Pharma’s former partner focused on the development of new modified

product candidates in the same therapeutic field but not including BIV201, have agreed to pay royalties equal to less than 1% of future

net sales of each company’s ascites drug development programs, or if such program is licensed to a third party, less than 5% of

each company’s net license revenues. On December 24, 2018, we returned our partial ownership rights to the PharmaIN modified terlipressin

development program and simultaneously paid the remaining balance due on a related debt. PharmaIN’s rights to our program remain

unchanged.

About Ascites and Liver Cirrhosis

Cirrhosis is a leading cause of death in the U.S.

The condition results primarily from hepatitis, alcoholism, and fatty liver disease linked to obesity. Ascites is a common complication

of advanced liver cirrhosis, involving kidney dysfunction and the accumulation of large amounts of fluid in the abdominal cavity.

The Need for an Ascites Therapy

With no medications approved by the FDA specifically

for treating ascites, an estimated 40% of patients die within two years of diagnosis. Certain drugs approved for other uses such as diuretics

may provide initial relief, but patients may fail to respond to treatment as ascites worsens. This represents a critical unmet medical

need, reflected by the Fast Track designation granted to BIV201 by the FDA as a treatment for ascites refractory to or intolerant of diuretic

therapy. U.S. treatment costs for liver cirrhosis, including ascites and other complications, are estimated at more than $5 billion annually.

7

The

Ascites Development Pathway

Most

experts agree that ascites develops through a sequence of events illustrated by the above diagram. High blood pressure in the vein that

supplies blood to the liver, called “portal hypertension,” occurs as increasing liver damage (fibrosis) impedes blood flow

through the liver. This causes vasodilation and blood pooling in the central or “splanchnic” region of the body and

low blood volume in the arteries. The decrease in effective blood volume activates a signaling pathway (“neurohormonal systems”)

which tells the kidneys to retain large amounts of salt and water in an effort to increase blood volume. Ultimately the retention of

excess sodium and water leads to the formation of ascites as these substances “weep” from the liver and lymph system and

collect in the patient’s abdomen.

The

BIV201 Proposed Mechanism of Action

BIV201

is being developed with the goal of alleviating portal hypertension and correcting splanchnic vasodilation, thereby increasing effective

blood volume and reducing the signals to the kidneys to retain excess salt and water. If successful, BIV201 could halt the

cycle of accelerating fluid generation in ascites patients and reduce the need for the frequent and painful paracentesis procedures many

of these patients currently require.

8

Future

Possible BIV201 Indications

Based on international investigative studies of

the active agent in BIV201, terlipressin, we believe our drug candidate has potential future applications in other life-threatening conditions

due to liver cirrhosis. Securing marketing approvals for any of these new uses will require well-controlled clinical trials to satisfy

the FDA and/or other countries’ regulatory requirements, none of which have commenced at this time. The Company continues to evaluate

other indications for the use of terlipressin continuous infusion. BioVie will discuss such indications if and when selected for testing.

Intellectual Property

BIV201

BioVie relies on a combination of patent, trade

secret, other intellectual property laws (such as FDA data exclusivity), nondisclosure agreements, and other measures to protect our proposed

products. We require our employees, consultants, and advisors to execute confidentiality agreements and to agree to disclose and assign

to us all inventions conceived during the workday, using our property, or which relate to our business. Despite any measures taken to

protect our intellectual property (IP), unauthorized parties may attempt to copy aspects of our products or to obtain and use information

that we regard as proprietary.

BIV201 was awarded Orphan Drug Designations in

the U.S. for the treatment of hepatorenal syndrome (received November 21, 2018) and treatment of ascites due to all etiologies except

cancer (received September 8, 2016). We also filed a PCT application covering our novel liquid formulations of terlipressin (international

patent application PCT/US2020/034269, published as WO2020/237170) and are seeking patent protection in at least the U.S., Europe, China,

Japan and other jurisdictions. Also, we own U.S. Patent 11,364,277, which is directed to a method of treating ascites with BIV201, and

we are pursuing similar patent coverage in Japan, Europe, and China.

9

NE3107 and related compounds

As

of August 15, 2023, we have fifteen (15) issued U.S. patents, six (6) pending U.S. patent applications, one (1) pending U.S. PCT application

and six (6) issued foreign patents directed to protecting NE3107 and related compounds and methods of making and using thereof. The U.S.

patents and pending patent applications and their projected expiration dates are provided below.

Title Patent Application Number Patent Number Expiration Date

Methods for the Treatment of Mild Cognitive Impairment 63/374631 pending —

Methods for the Treatment of Mild Cognitive Impairment 63/498703 pending —

Assay and Methods for Drug Discovery 63/479973 pending —

Methods for the Treatment of Biological Aging 63/381521 pending —

Methods for the Treatment of Biological Aging 63/508856 pending —

** Foreign counterparts issued in Europe and Japan expire 6/5/2029.

Government

Regulation

Government

authorities in the United States, at the federal, state and local level, and in other countries extensively regulate, among other things,

the research, development, testing, manufacture, quality control, approval, labeling, packaging, storage, record-keeping, promotion,

advertising, distribution, post-approval monitoring and reporting, marketing and export and import of products such as those we are developing.

Any pharmaceutical candidate that we develop must be approved by the FDA before it may be legally marketed in the United States and by

the appropriate foreign regulatory agency before it may be legally marketed in foreign countries.

United

States Drug Development Process

In

the United States, the FDA regulates drugs under the Federal Food, Drug and Cosmetic Act, or FDCA, and implements regulations. Drugs

are also subject to other federal, state and local statutes and regulations. Biologics are subject to regulation by the FDA under the

FDCA, the Public Health Service Act, or the PHSA, and related regulations, and other federal, state and local statutes and regulations.

Biological products include, among other things, viruses, therapeutic serums, vaccines and most protein products. The process of obtaining

regulatory approvals and the subsequent compliance with appropriate federal, state, local and foreign statutes and regulations require

the expenditure of substantial time and financial resources. Failure to comply with the applicable United States requirements at any

time during the product development process, approval process or after approval, may subject an applicant to administrative or judicial

sanctions. FDA sanctions could include refusal to approve pending applications, withdrawal of an approval, a clinical hold, warning letters,

product recalls, product seizures, total or partial suspension of production or distribution, injunctions, fines, refusals of government

contracts, restitution, disgorgement or civil or criminal penalties. Any agency or judicial enforcement action could have a material

adverse effect on us.

10

The

process required by the FDA before a drug or biological product may be marketed in the United States generally involves the following:

● FDA review and approval of the NDA or BLA.

The

lengthy process of seeking required approvals and the continuing need for compliance with applicable statutes and regulations require

the expenditure of substantial resources. There can be no certainty that approvals will be granted.

Clinical

trials involve the administration of the drug or biological candidate to healthy volunteers or patients having the disease being studied

under the supervision of qualified investigators, generally physicians not employed by or under the trial sponsor’s control. Clinical

trials are conducted under protocols detailing, among other things, the objectives of the clinical trial, dosing procedures, subject

selection and exclusion criteria, and the parameters to be used to monitor subject safety. Each protocol must be submitted to the FDA

as part of the IND. Clinical trials must be conducted in accordance with the FDA’s good clinical practices requirements. Further,

each clinical trial must be reviewed and approved by an independent institutional review board, or IRB, at or servicing each institution

at which the clinical trial will be conducted. An IRB is charged with protecting the welfare and rights of trial participants and considers

such items as whether the risks to individuals participating in the clinical trials are minimized and are reasonable in relation to anticipated

benefits. The IRB also approves the informed consent form that must be provided to each clinical trial subject or his or her legal representative

and must monitor the clinical trial until it is completed.

Human

clinical trials prior to approval are typically conducted in three sequential phases that may overlap or be combined:

Post-approval

studies, or Phase 4 clinical trials, may be conducted after initial marketing approval. These studies are used to gain additional

experience from the treatment of patients in the intended therapeutic indication and may be required by the FDA as part of the approval

process.

11

Progress

reports detailing the results of the clinical trials must be submitted at least annually to the FDA and written IND safety reports must

be submitted to the FDA by the investigators for serious and unexpected adverse events or any finding from tests in laboratory animals

that suggests a significant risk for human subjects. Phase 1, Phase 2 and Phase 3 clinical trials may not be completed

successfully within any specified period, if at all. The FDA or the sponsor or its data safety monitoring board may suspend a clinical

trial at any time on various grounds, including a finding that the research subjects or patients are being exposed to an unacceptable

health risk. Similarly, an IRB can suspend or terminate approval of a clinical trial at its institution if the clinical trial is not

being conducted in accordance with the IRB’s requirements or if the drug or biologic has been associated with unexpected serious

harm to patients.

Concurrent

with clinical trials, companies usually complete additional animal studies and develop additional information about the chemistry and

physical characteristics of the drug or biologic as well as finalize a process for manufacturing the product in commercial quantities

in accordance with cGMP requirements. The manufacturing process must be capable of consistently producing quality batches of the drug

or biological candidate and, among other things, must include methods for testing the identity, strength, quality and purity of the final

drug or biologic. Additionally, appropriate packaging must be selected and tested and stability studies must be conducted to demonstrate

that the drug or biological candidate does not undergo unacceptable deterioration over its shelf life.

U.S.

Review and Approval Processes

The

results of product development, preclinical studies and clinical trials, along with descriptions of the manufacturing process, analytical

tests conducted on the chemistry of the drug or biologic, proposed labeling and other relevant information are submitted to the FDA as

part of an NDA or BLA requesting approval to market the product. The submission of an NDA or BLA is subject to the payment of substantial

user fees; a waiver of such fees may be obtained under certain limited circumstances.

The

FDA reviews all NDAs and BLAs submitted before it accepts them for filing and may request additional information rather than accepting

an NDA or BLA for filing. Once the submission is accepted for filing, the FDA begins an in-depth review of the NDA or BLA.

After

the NDA or BLA submission is accepted for filing, the FDA reviews the NDA to determine, among other things, whether the proposed product

is safe and effective for its intended use, and whether the product is being manufactured in accordance with cGMP to assure and preserve

the product’s identity, strength, quality and purity. The FDA reviews a BLA to determine, among other things, whether the product

is safe, pure and potent and the facility in which it is manufactured, processed, packaged or held meets standards designed to assure

the product’s continued safety, purity and potency. In addition to its own review, the FDA may refer applications for novel drug

or biological products or drug or biological products which present difficult questions of safety or efficacy to an advisory committee,

typically a panel that includes clinicians and other experts, for review, evaluation and a recommendation as to whether the application

should be approved and under what conditions. The FDA is not bound by the recommendations of an advisory committee, but it considers

such recommendations carefully when making decisions. During the approval process, the FDA also will determine whether a risk evaluation

and mitigation strategy, or REMS, is necessary to assure the safe use of the drug or biologic. If the FDA concludes that a REMS is needed,

the sponsor of the NDA or BLA must submit a proposed REMS; the FDA will not approve the NDA or BLA without a REMS, if required.

Before

approving an NDA or BLA, the FDA will inspect the facilities at which the product is to be manufactured. The FDA will not approve the

product unless it determines that the manufacturing processes and facilities are in compliance with cGMP requirements and adequate to

assure consistent production of the product within required specifications. Additionally, before approving an NDA or BLA, the FDA will

typically inspect one or more clinical sites to assure compliance with cGMP. If the FDA determines the application, manufacturing process

or manufacturing facilities are not acceptable it will outline the deficiencies in the submission and often will request additional testing

or information.

12

The

NDA or BLA review and approval process is lengthy and difficult and the FDA may refuse to approve an NDA or BLA if the applicable regulatory

criteria are not satisfied or may require additional clinical data or other data and information. Even if such data and information is

submitted, the FDA may ultimately decide that the NDA or BLA does not satisfy the criteria for approval. Data obtained from clinical

trials are not always conclusive and may be susceptible to varying interpretations, which could delay, limit or prevent regulatory approval.

The FDA will issue a “complete response” letter if the agency decides not to approve the NDA or BLA. The complete response

letter usually describes all of the specific deficiencies in the NDA or BLA identified by the FDA. The deficiencies identified may be

minor, for example, requiring labeling changes, or major, for example, requiring additional clinical trials. Additionally, the complete

response letter may include recommended actions that the applicant might take to place the application in a condition for approval. If

a complete response letter is issued, the applicant may either resubmit the NDA or BLA, addressing all of the deficiencies identified

in the letter, or withdraw the application.

If

a product receives regulatory approval, the approval may be limited to specific diseases and dosages or the indications for use may otherwise

be limited, which could restrict the commercial value of the product. Further, the FDA may require that certain contraindications, warnings

or precautions be included in the product labeling. In addition, the FDA may require Phase 4 testing which involves clinical trials

designed to further assess a product’s safety and effectiveness and may require testing and surveillance programs to monitor the

safety of approved products that have been commercialized.

Orphan

Drug Designation

Under

the Orphan Drug Act, the FDA may grant orphan designation to a drug or biological product intended to treat a rare disease or condition,

which is generally a disease or condition that affects fewer than 200,000 individuals in the United States, or more than 200,000 individuals

in the United States and for which there is no reasonable expectation that the cost of developing and making a drug or biological product

available in the United States for this type of disease or condition will be recovered from sales of the product. Orphan product designation

must be requested before submitting an NDA or BLA. After the FDA grants orphan product designation, the identity of the therapeutic agent

and its potential orphan use are disclosed publicly by the FDA. Orphan product designation does not convey any advantage in or shorten

the duration of the regulatory review and approval process.

If

a product that has Orphan designation subsequently receives the first FDA approval for the disease or condition for which it has such

designation, the product is entitled to orphan product exclusivity, which means that the FDA may not approve any other applications to

market the same drug or biological product for the same indication for seven years, except in limited circumstances, such as a showing

of clinical superiority to the product with orphan exclusivity. Competitors, however, may receive approval of different products for

the indication for which the Orphan product has exclusivity or obtain approval for the same product but for a different indication for