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AVXL US Equity

Anavex Life Sciences Corp.Health Care · Biological Products, (No Diagnostic Substances) · CIK 1314052 · FY ends Sep 30
$3.39
+0.19 (+5.94%)
USD · as of 2026-08-19 · marketstack

AVXL · 10-K · period ended 2021-09-30

← all AVXL documents
filed 2021-11-24 · EDGAR original ↗

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UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM 10-K

(Mark One)

☒ ANNUAL

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

For

the fiscal year ended September 30, 2021

☐ 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: 001-37606

ANAVEX LIFE SCIENCES CORP.

(Exact name of registrant as specified in its

charter)

(Address of principal executive offices) (Zip Code)

Registrant’s telephone number, including

area code 1-844-689-3939

Securities registered under Section 12(b) of

the Act:

Common Stock, $0.001 par value AVXL NASDAQ Stock Market LLC

Title of each class Trading Symbol Name of each exchange on which registered

Securities registered pursuant to Section 12(g)

of the Act:

None

(Title of class)

Indicate

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

Yes ☒

No ☐

Indicate

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

Yes

☐ No☒

Indicate

by checkmark whether the registrant has (1) filed all reports required to be filed by Section 13 or 15(d) of the Securities Exchange

Act of 1934 during the preceding 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 and post such files).

Yes ☒

No ☐

Indicate

by checkmark 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 whether the registrant has filed a report on and attestation to its management’s assessment of the effectiveness

of its internal controls over financial reporting under Section 404(b) of the Sarbanes-Oxley Act (15 U.S.C. 7262(b)) by the registered

public accounting firm that prepared or issued its audit report.

Yes ☒

No☐

Indicate

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

Yes ☐

No ☒

State

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: $1,011,843,276 based on a price of $14.95 per share,

being the closing price of the registrant’s common stock on March 31, 2021.

Indicate

the number of shares outstanding of each of the registrant’s classes of common stock, as of the latest practicable date:

76,018,053 issued and outstanding as of November 19, 2021.

DOCUMENTS

INCORPORATED BY REFERENCE

None.

ii

TABLE OF CONTENTS

PART I 1

ITEM 1. BUSINESS 1

ITEM 1A. RISK FACTORS 22

ITEM 1B. UNRESOLVED STAFF COMMENTS 37

ITEM 2. PROPERTIES 37

ITEM 3. LEGAL PROCEEDINGS 37

ITEM 4. MINE SAFETY DISCLOSURES 37

ITEM 6 SELECTED FINANCIAL DATA 38

ITEM 7A QUANTITATIVE AND QUALITATIVE DISCLOSURES ABOUT MARKET RISK 43

ITEM 8. FINANCIAL STATEMENTS AND SUPPLEMENTARY DATA 43

ITEM 9A. CONTROLS AND PROCEDURES 65

ITEM 9B OTHER INFORMATION 65

PART III 66

ITEM 10 DIRECTORS, EXECUTIVE OFFICERS AND CORPORATE GOVERNANCE 66

ITEM 11. EXECUTIVE COMPENSATION 69

ITEM 14. PRINCIPAL ACCOUNTING FEES AND SERVICES 75

ITEM 15. EXHIBITS, FINANCIAL STATEMENT SCHEDULES 77

iii

Forward Looking Statements.

This Annual Report on Form 10-K includes

forward-looking statements. All statements other than statements of historical facts contained in this Annual Report on Form 10-K,

including statements regarding our anticipated future clinical and regulatory milestone events, future financial position, business

strategy and plans and objectives of management for future operations, are forward-looking statements. The words “believe,”

“may,” “estimate,” “continue,” “anticipate,” “intend,” “expect”

“should,” “forecast,” “could,” “suggest,” “plan” and similar expressions,

as they relate to us, are intended to identify forward-looking statements. Such forward-looking statements include, without limitation,

statements regarding:

● volatility in our stock and in the markets in general;

● the impact of the COVID-19 outbreak and its effect on us;

● our ability to generate any revenue or to continue as a going concern;

● our ability to obtain the support of qualified scientific collaborators;

● our ability to identify and obtain additional product candidates;

● our reliance on third parties in non-clinical and clinical studies;

● our ability to defend against product liability claims;

● our ability to safeguard against security breaches;

● our ability to comply with our intellectual property licensing agreements;

● our ability to defend against claims of intellectual property infringement;

● our ability to protect our intellectual property rights throughout the world;

● competition;

● the anticipated designs of our future clinical studies;

● the impact of fast track designation on receipt of actual FDA approval;

● our anticipated future cash position.

We have based these forward-looking

statements largely on our current expectations and projections about future events, including the responses we expect from the

U.S. Food and Drug Administration, (“FDA”), and other regulatory authorities and financial trends that we believe may

affect our financial condition, results of operations, business strategy, preclinical and clinical trials, and financial needs.

These forward-looking statements are subject to a number of risks, uncertainties and assumptions including without limitation the

risks described in “Risk Factors” in Part I, Item 1A of this Annual Report on Form 10-K. These risks are not exhaustive.

Other sections of this Annual Report on Form 10-K include additional factors which could adversely impact our business and financial

performance. Moreover, we operate in a very competitive and rapidly changing environment. New risk factors emerge from time to

time and it is not possible for our management to predict all risk factors, nor can we assess the impact of all factors on our

business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those

contained in any forward-looking statements. You should not rely upon forward-looking statements as predictions of future events.

We cannot assure you that the events and circumstances reflected in the forward-looking statements will be achieved or occur and

actual results could differ materially from those projected in the forward-looking statements. Except as required by applicable

laws including the securities laws of the United States, we assume no obligation to update or supplement forward-looking statements.

As used in this Annual Report on Form

10-K, the terms “we,” “us,” “our,”, “Company” and “Anavex” mean Anavex

Life Sciences Corp., unless the context clearly requires otherwise.

iv

PART I

ITEM 1. BUSINESS

Overview and Strategy

Anavex Life Sciences Corp. is a clinical stage

biopharmaceutical company engaged in the development of differentiated therapeutics by applying precision medicine to central nervous

system (“CNS”) diseases with high unmet need. We analyze genomic data from clinical studies to identify biomarkers,

which we use to select patients that will receive the therapeutic benefit for the treatment of neurodegenerative and neurodevelopmental

diseases.

Our lead compound, ANAVEX®2-73,

is being developed to treat Alzheimer’s disease, Parkinson’s disease and potentially other central nervous system diseases,

including rare diseases, such as Rett syndrome, a rare severe neurological monogenic disorder caused by mutations in the X-linked

gene, methyl-CpG-binding protein 2 (“MECP2”).

We currently have two core programs and two

seed programs. Our core programs are at various stages of clinical and preclinical development, in neurodegenerative and neurodevelopmental

diseases.

The following table summarizes key information about our programs:

* = Orphan Drug Designation by the FDA;

Dashed lines indicate planned clinical studies

Anavex has a portfolio of compounds varying

in sigma-1 receptor (S1R) binding activities. The SIGMAR1 gene encodes the S1R protein, which is an intracellular chaperone protein

with important roles in cellular communication. S1R is also involved in transcriptional regulation at the nuclear envelope and

restores homeostasis and stimulates recovery of cell function when activated. In order to validate the ability of our compounds

to activate quantitatively the S1R, we performed, in collaboration with Stanford University, a quantitative Positron Emission Tomography

(PET) imaging scan in mice, which demonstrated a dose-dependent ANAVEX®2-73 target engagement or receptor occupancy

(RO) with S1R in the brain.

Source: Reyes S et al., Sci Rep. 2021 Aug 25;11(1):17150

Cellular Homeostasis

Many diseases are possibly directly caused

by chronic homeostatic imbalances or cellular stress of brain cells. In pediatric diseases like Rett syndrome or infantile spasms,

the chronic cellular stress is possibly caused by the presence of a constant genetic mutation. In neurodegenerative diseases, such

as Alzheimer’s and Parkinson’s diseases, chronic cellular stress is possibly caused by age-correlated buildup of cellular

insult and hence chronic cellular stress. Specifically, defects in homeostasis of protein or ribonucleic acid (“RNA”)

lead to the death of neurons and dysfunction of the nervous system. The spreading of protein aggregates resulting in a proteinopathy,

a characteristic finding in Alzheimer’s and Parkinson’s diseases that results from disorders of protein synthesis,

trafficking, folding, processing or degradation in cells. The clearance of macromolecules in the brain is particularly susceptible

to imbalances that result in aggregation and degeneration in nerve cells. For example, Alzheimer’s disease pathology is characterized

by the presence of amyloid plaques, neurofibrillary tangles, which are aggregates of hyperphosphorylated Tau protein that are a

marker of other diseases known as tauopathies as well as inflammation of microglia. With the SIGMAR1 activation through SIGMAR1

agonists like ANAVEX®2-73, our approach is to restore cellular balance, i.e. homeostasis. Therapies that correct

defects in cellular homeostasis might have the potential to halt or delay neurodevelopmental and neurodegenerative disease progression.

ANAVEX®2-73-specific Biomarkers

A full genomic analysis of Alzheimer’s

disease (AD) patients treated with ANAVEX®2-73 resulted in the identification of actionable genetic variants. A

significant impact of the genomic biomarkers SIGMAR1, the direct target of ANAVEX®2-73 and COMT, a gene involved

in memory function, on the drug response level was identified, leading to an early ANAVEX®2-73-specific biomarker

hypothesis. It is expected that excluding patients with SIGMAR1 identified biomarker variant (approximately 10%-20% of

the population) in prospective studies would identify approximately 80%-90% patients that would display clinically significant

improved functional and cognitive scores. The consistency between the identified DNA and RNA data related to ANAVEX®2-73,

which are considered independent of AD pathology, as well as multiple endpoints and time-points, provides support for precision

medicine clinical development of ANAVEX®2-73 by using genetic biomarkers identified within the study population

itself to target patients who are most likely to respond to ANAVEX®2-73 treatment in AD as well as indications

like Parkinson’s disease dementia (PDD) or Rett syndrome (RTT) in which ANAVEX®2-73 is currently studied.

Clinical Studies Overview

Alzheimer’s Disease

In November 2016, we completed a Phase 2a clinical

trial, consisting of PART A and PART B, which lasted a total of 57 weeks, for ANAVEX®2-73 in mild-to-moderate Alzheimer’s

patients. This open-label randomized trial met both primary and secondary endpoints and was designed to assess the safety and exploratory

efficacy of ANAVEX®2-73 in 32 patients. ANAVEX®2-73 targets sigma-1 and muscarinic receptors, which

have been shown in preclinical studies to reduce stress levels in the brain believed to restore cellular homeostasis and to reverse

the pathological hallmarks observed in Alzheimer’s disease. The Phase 2a trial demonstrated positive pharmacokinetic (PK)

and pharmacodynamic (PD) data, which established a concentration-effect relationship between ANAVEX®2-73 and study

measurements. These measures obtained from all patients who participated in the entire 57 weeks include exploratory cognitive and

functional scores as well as biomarker signals of brain activity. Additionally, the study appears to show that ANAVEX®2-73

activity is enhanced by its active metabolite (ANAVEX19-144), which also targets the sigma-1 receptor and has a half-life approximately

twice as long as the parent molecule.

Two consecutive trial extensions for the Phase

2a trial have allowed participants who completed the 52-week PART B of the study to continue taking ANAVEX®2-73,

providing an opportunity to gather extended safety data for a cumulative time period of five years. In August 2020, patients completing

these Phase 2a trial extensions were granted continued access to treatment with ANAVEX®2-73 through the Australian

Government Department of Health – Therapeutic Goods Administration (TGA) compassionate use Special Access Scheme.

A larger Phase 2b/3 double-blind, placebo-controlled

study of ANAVEX®2-73 in Alzheimer’s disease commenced in August 2018. The Phase 2b/3 study enrolled 509 patients

for 48 weeks, randomized 1:1:1 to two different ANAVEX®2-73 doses or placebo. The trial commenced in Australia;

and during fiscal 2020 additional regions were added in the United Kingdom, The Netherlands, Germany, and Canada. The ANAVEX®2-73

Phase 2b/3 study design incorporates genomic precision medicine biomarkers identified in the ANAVEX®2-73 Phase 2a

study. Primary and secondary endpoints will assess safety and both cognitive and functional efficacy, measured through Alzheimer’s

Disease Assessment Scale – Cognition (ADAS-Cog), ADCS-ADL and Clinical Dementia Rating – Sum of Boxes for cognition

and function (CDR-SB). The study completed enrollment in June 2021, exceeding the 450 patients enrollment target at 52 sites across

North America, Europe and Australia.

In October 2019, we initiated a long-term open

label extension study of ANAVEX®2-73, entitled the ATTENTION-AD study, for patients who have completed the 48-week

Phase 2b/3 placebo-controlled trial referenced above. This study is expected to last two years and will give patients the opportunity

to continue their treatment. Upon request by patients, caretakers and investigators, this extension study was extended by one further

year.

Rett Syndrome

In February 2016, we presented positive preclinical

data for ANAVEX®2-73 in Rett syndrome, a rare neurodevelopmental disease. The study was funded by the International

Rett Syndrome Foundation (“Rettsyndrome.org”). In January 2017, we were awarded a financial grant from Rettsyndrome.org

of a minimum of $0.6 million to cover some of the costs of a multicenter Phase 2 clinical trial of ANAVEX®2-73 for

the treatment of Rett syndrome. This award was received in quarterly instalments which commenced during fiscal 2018.

In March 2019, we commenced the first Phase

2 clinical trial in a planned Rett syndrome program of ANAVEX®2-73 for the treatment of Rett syndrome. The studies

are being conducted in a range of patient age demographics and geographic regions, utilizing a convenient oral liquid once-daily

formulation of ANAVEX®2-73.

The first Phase 2 study, which took

place in the United States, was completed in December 2020. This trial was a randomized double-blind, placebo-controlled safety,

tolerability, pharmacokinetic and efficacy study of oral liquid ANAVEX®2-73 formulation in 25 adult female patients

with Rett syndrome over a 7-week treatment period including ANAVEX®2-73-specific genomic precision medicine biomarkers.

The primary endpoint of the trial was safety. The dosing of 5 mg ANAVEX®2-73 was well-tolerated and demonstrated

dose-proportional PK (pharmacokinetics). All secondary efficacy endpoints of the trial showed statistically significant and clinically

meaningful, drug exposure-dependent response in the Rett Syndrome Behaviour Questionnaire (RSBQ) Total scores, when compared to

placebo, in the ITT cohort (all participants, p = 0.048). 66.7% of ANAVEX®2-73 treated subjects showed a statistically

significant improvement in drug exposure-dependent RSBQ response as compared to 10% of the subjects on placebo in the ITT cohort

(all participants, p = 0.011). ANAVEX®2-73 treatment resulted in a sustained improvement in Clinical Global Impression

Improvement (CGI-I) scores throughout the 7-week study, when compared to placebo in the ITT cohort (all participants, p = 0.014).

86.7% of ANAVEX®2-73 treated subjects showed a statistically significant CGI-I response, defined as sustained improvement

to treatment, as compared to 40% of the subjects on placebo in the ITT cohort (all participants, p = 0.014). Consistent with previous

ANAVEX®2-73 clinical trials, patients carrying the common form of the SIGMAR1 gene treated with ANAVEX®2-73

experienced stronger improvements in the prespecified efficacy endpoints.

The second Phase 2 study of ANAVEX®2-73

for the treatment of Rett syndrome, called the AVATAR study, commenced in June 2019. This study is taking place in Australia and

the United Kingdom using a higher dose than the U.S. based Phase 2 study for Rett syndrome. This randomized, placebo-controlled

study will evaluate the safety and efficacy of ANAVEX®2-73 in approximately 33 patients over a 7-week treatment

period including ANAVEX®2-73 specific precision medicine biomarkers. All patients who participate in the study will

be eligible to receive ANAVEX®2-73 under a voluntary open label extension protocol. The AVATAR study is expected

to read out topline data around year end 2021.

In July 2020, we commenced the third

study of ANAVEX®2-73 for the treatment of Rett syndrome, called the EXCELLENCE study. This Phase 2/3 study in pediatric

patients with Rett syndrome will evaluate the safety and efficacy of ANAVEX®2-73 in approximately 84 pediatric patients,

aged 5 to 18, over a 12-week treatment period incorporating ANAVEX®2-73 specific precision medicine biomarkers.

All patients who participate in the study will be eligible to receive ANAVEX®2-73 under a voluntary open label extension

protocol.

Parkinson’s Disease

In September 2016, we presented positive

preclinical data for ANAVEX®2-73 in an animal model of Parkinson’s disease, which demonstrated significant

improvements on behavioral, histopathological, and neuroinflammatory endpoints. The study was funded by the Michael J. Fox Foundation.

Additional data announced in October 2017 indicates that ANAVEX®2-73 induces robust neurorestoration in experimental

Parkinsonism. The encouraging results we have gathered in this model, coupled with the favorable profile of this compound in the

Alzheimer’s disease trial, support the notion that ANAVEX®2-73 is a promising clinical candidate drug for

Parkinson’s disease dementia.

In October 2020, we completed a double-blind,

randomized, placebo-controlled proof-of-concept Phase 2 trial with ANAVEX®2-73 in Parkinson’s Disease Dementia

(PDD), to study the effect of the compound on both the cognitive and motor impairment of Parkinson’s disease. The Phase 2

study enrolled approximately 132 patients for 14 weeks, randomized 1:1:1 to two different ANAVEX®2-73 doses, 30mg

and 50mg, or placebo. The ANAVEX®2-73 Phase 2 PDD study design incorporated genomic precision medicine biomarkers

identified in the ANAVEX®2-73 Phase 2a Alzheimer’s disease study.

Within this study ANAVEX®2-73

was safe and well tolerated in oral doses up to 50mg once daily. The results show clinically meaningful, dose-dependent, and statistically

significant improvements in the Cognitive Drug Research (CDR) computerized assessment system analysis. Treatment with ANAVEX®2-73

also resulted in clinically meaningful improvements as measured by the global composite score of Parkinson’s disease symptom

severity, MDS-UPDRS Total score on top of standard of care including dopaminergic therapy, levodopa and other anti-PD medications

after 14 weeks of treatment, suggesting ANAVEX®2-73’s potential global capability of slowing and reversing

symptoms that progress in Parkinson’s disease. The study confirmed the precision medicine approach of targeting SIGMAR1 as

a genetic biomarker in response to ANAVEX®2-73.

In January 2021, we announced we were

awarded a research grant of $1.0 million from The Michael J. Fox

Foundation for Parkinson’s Research (MJFF) to develop ANAVEX®2-73 for the treatment of Parkinson’s

disease. The award will explore utilization of PET imaging biomarkers to enable measurement of target engagement and pathway activation

of the sigma-1 receptor (SIGMAR1) with clinically relevant doses in people with Parkinson’s disease.

Frontotemporal Dementia

In July 2020, we commenced the First-in-Human

Phase 1 clinical trial of ANAVEX®3-71, which was previously granted orphan drug designation for the treatment of

Frontotemporal Dementia (FTD) by the FDA. ANAVEX®3-71 is an orally administered small molecule targeting sigma-1

and M1 muscarinic receptors that is designed to be beneficial for neurodegenerative diseases. In preclinical studies, ANAVEX®3-71

demonstrated disease-modifying activity against the major hallmarks of Alzheimer’s disease in transgenic (3xTg-AD) mice,

including cognitive deficits, amyloid and tau pathologies, as well as beneficial effects on mitochondrial dysfunction and neuroinflammation.

The Phase

1 clinical trial will be a prospective double-blind, randomized, placebo-controlled study. A total of at least 36 healthy male

and female subjects will be included. Single escalating doses of ANAVEX®3-71 will be administered in order to evaluate

the safety, tolerability, and pharmacokinetics (PK) of ANAVEX®3-71 and the effects of food and gender on its PK

in healthy volunteers. This study is expected to be followed by longer duration dosing including patients with FTD or other dementia

indications with unmet medical need, incorporating exploratory efficacy and disease biomarker measures.

Our Pipeline

Our research and development pipeline includes

ANAVEX®2-73 currently in three different clinical study indications, and several other compounds in different stages

of clinical and pre-clinical study.

Our proprietary SIGMACEPTORTM Discovery

Platform produced small molecule drug candidates with unique modes of action, based on our understanding of sigma receptors. Sigma

receptors may be targets for therapeutics to combat many human diseases, both of neurodegenerative nature, including Alzheimer’s

disease, as well as of neurodevelopmental nature, like Rett syndrome. When bound by the appropriate ligands, sigma receptors influence

the functioning of multiple biochemical signals that are involved in the pathogenesis (origin or development) of disease. Multiple

viruses including SARS-CoV-2 (COVID-19) induce cellular stress by intrinsic mitochondrial apoptosis and other related cellular

processes, in order to ensure survival and replication. Hence, it is possible that S1R could play a role in modulating the cellular

response to viral infection and ameliorate pathogenesis.

Compounds that have been subjects of our research

include the following:

ANAVEX®2-73 (blarcamesine)

ANAVEX®2-73 may offer a disease-modifying

approach in neurodegenerative and neurodevelopmental diseases by activation of sigma-1 receptors.

In Rett syndrome, administration of ANAVEX®2-73

resulted in both significant and dose related improvements in an array of behavioral paradigms in the MECP2 HET Rett syndrome disease

model. In addition, in a further experiment sponsored by Rettsyndrome.org, ANAVEX®2-73 was evaluated in automatic

visual response and respiration tests in 7-month old mice, an age at which advanced pathology is evident. Vehicle-treated MECP2

mice demonstrated fewer automatic visual responses than wild-type mice. Treatment with ANAVEX®2-73 for four weeks

significantly increased the automatic visual response in the MECP2 Rett syndrome disease mouse. Additionally, chronic oral dosing

daily for 6.5 weeks of ANAVEX®2-73 starting at ~5.5 weeks of age was conducted in the MECP2 HET Rett syndrome disease

mouse model assessed the different aspects of muscular coordination, balance, motor learning and muscular strengths, some of the

core deficits observed in Rett syndrome. Administration of ANAVEX®2-73 resulted in both significant and dose related

improvements in an array of these behavioral paradigms in the MECP2 HET Rett syndrome disease model.

In March 2019, we commenced the first Phase

2 clinical trial in a planned Rett syndrome program of ANAVEX®2-73 for the treatment of Rett syndrome. This study,

which took place in the United States, was completed in December 2020, however two other clinical trials in Rett syndrome, the

AVATAR study and the EXCELLENCE study, are still underway. The studies are being conducted in a range of patient age demographics

and geographic regions, as more fully described above under Clinical Studies Overview – Rett Syndrome.

In May 2016 and June 2016, the FDA granted

Orphan Drug Designation to ANAVEX®2-73 for the treatment of Rett syndrome and infantile spasms, respectively. In

November 2019, the FDA granted to ANAVEX®2-73 the Rare Pediatric Disease (RPD) designation for the treatment of

Rett syndrome. The RPD designation provides priority review by the FDA to encourage the development of treatments for rare pediatric

diseases.

Further, in February 2020, the FDA granted

Fast Track designation for the ANAVEX®2-73 clinical development program for the treatment of Rett syndrome. The

FDA Fast Track program is designed to facilitate and expedite the development and review of new drugs to address unmet medical

needs in the treatment of serious and life-threatening conditions.

For Parkinson’s disease, data demonstrates

significant improvements and restoration of function in a disease modifying animal model of Parkinson’s disease. Significant

improvements were seen on all measures tested: behavioral, histopathological, and neuroinflammatory endpoints. In October 2020,

we completed a double-blind, randomized, placebo-controlled proof-of-concept Phase 2 trial with ANAVEX®2-73 in Parkinson’s

Disease Dementia (PDD), to study the effect of the compound on both the cognitive and motor impairment of Parkinson’s disease.

The Phase 2 study enrolled approximately 132 patients for 14 weeks, randomized 1:1:1 to two different ANAVEX®2-73

doses, 30mg and 50mg, or placebo. The ANAVEX®2-73 Phase 2 PDD study design incorporated genomic precision medicine

biomarkers identified in the ANAVEX®2-73 Phase 2a Alzheimer’s disease study.

The study found that ANAVEX®2-73

was safe and well tolerated in oral doses up to 50mg once daily. The results show clinically meaningful, dose-dependent, and statistically

significant improvements in the Cognitive Drug Research (CDR) computerized assessment system analysis. We anticipate conducting

further clinical trials of ANAVEX®2-73 in Parkinson’s disease dementia after submitting the results of the

study to the FDA to obtain regulatory guidance.

In Alzheimer’s disease (AD) animal models,

ANAVEX®2-73 has shown pharmacological, histological and behavioral evidence as a potential neuroprotective, anti-amnesic,

anti-convulsive and anti-depressive therapeutic agent, due to its potent affinity to sigma-1 receptors and moderate affinities

to M1-4 type muscarinic receptors. In addition, ANAVEX®2-73 has shown a potential dual mechanism which may impact

amyloid, tau pathology and inflammation. In a transgenic AD animal model Tg2576, ANAVEX®2-73 induced a statistically

significant neuroprotective effect against the development of oxidative stress in the mouse brain, as well as significantly increased

the expression of functional and synaptic plasticity markers that is apparently amyloid-beta independent. It also statistically

alleviated the learning and memory deficits developed over time in the animals, regardless of sex, both in terms of spatial working

memory and long-term spatial reference memory.

Based on the results of pre-clinical testing,

we initiated and completed a Phase 1 single ascending dose (SAD) clinical trial of ANAVEX®2-73. In this Phase 1

SAD trial, the maximum tolerated single dose was defined per protocol as 55-60 mg. This dose is above the equivalent dose shown

to have positive effects in mouse models of AD. There were no significant changes in laboratory or electrocardiogram (ECG) parameters.

ANAVEX®2-73 was well tolerated below the 55-60 mg dose with only mild adverse events in some subjects. Observed

adverse events at doses above the maximum tolerated single dose included headache and dizziness, which were moderate in severity

and reversible. These side effects are often seen with drugs that target CNS conditions, including AD.

In December 2014, a Phase 2a clinical trial

was initiated for ANAVEX®2-73, for the treatment of Alzheimer’s disease. The open-label randomized trial was

designed to assess the safety and exploratory efficacy of ANAVEX®2-73 in 32 patients with mild-to-moderate Alzheimer’s

disease. ANAVEX®2-73 is an orally available drug candidate that restores cellular homeostasis by targeting sigma-1

and muscarinic receptors. Preclinical studies demonstrated its potential to halt and/or reverse the course of Alzheimer’s.

The Phase 2a study met both primary and secondary objectives of the study.

In July 2018, we presented

the results of a genomic DNA and RNA evaluation of the participants in the Phase 2a study. More than 33,000 genes were analyzed

using unbiased, data driven, machine learning, artificial intelligence (AI) system for analyzing DNA & RNA data in patients

exposed to ANAVEX®2-73. The analysis identified genetic variants that impacted response to ANAVEX®2-73,

among them variants related to the Sigma-1 receptor (SIGMAR1), the target for ANAVEX®2-73. Results showed that study

participants with the common SIGMAR1 wild type gene variant, which is about 80 percent of the population worldwide, demonstrated

improved cognitive (MMSE) and the functional (ADCS-ADL) scores. The results from this evaluation have been used to establish a

precision medicine approach in subsequent clinical trials, since these signatures can now be applied to neurological indications

tested in clinical studies with ANAVEX®2-73 including Alzheimer’s disease, Parkinson’s disease dementia

and Rett syndrome.

ANAVEX®2-73

data presented met prerequisite information in order to progress into a Phase 2b/3 placebo-controlled study. On July 2, 2018, the

Human Research Ethics Committee in Australia approved the initiation of our Phase 2b/3, double-blind, randomized, placebo-controlled

48-week safety and efficacy trial of ANAVEX®2-73 for the treatment of early Alzheimer’s disease. Clinical

trial sites in Canada, the United Kingdom, the Netherlands and Germany were also added. This Phase 2b/3 study design incorporates

inclusion of genomic precision medicine biomarkers identified in the ANAVEX®2-73 Phase 2a study. The Phase 2b/3

study, which has completed enrollment, randomized 1:1:1 to either two different ANAVEX®2-73 doses or placebo, commenced

in October 2018.

Preclinical data also validates ANAVEX®2-73

as a prospective platform drug for other neurodegenerative diseases beyond Alzheimer’s disease, Parkinson’s disease

or Rett syndrome, more specifically, epilepsy, infantile spasms, Fragile X syndrome, Angelman syndrome, multiple sclerosis and,

more recently, tuberous sclerosis complex (TSC). ANAVEX®2-73 demonstrated significant improvements in all of these

indications in the respective preclinical animal models.

In a study sponsored by the Foundation for

Angelman Syndrome, ANAVEX®2-73 was assessed in a mouse model for the development of audiogenic seizures. The results

indicated that ANAVEX®2-73 administration significantly reduced audiogenic-induced seizures. In a study sponsored

by FRAXA Research Foundation regarding Fragile X syndrome, data demonstrated that ANAVEX®2-73 restored hippocampal

brain-derived neurotrophic factor (BDNF) expression to normal levels. BDNF under-expression has been observed in many neurodevelopmental

and neurodegenerative pathologies. BDNF signaling promotes maturation of both excitatory and inhibitory synapses. ANAVEX®2-73

normalization of BDNF expression could be a contributing factor for the positive data observed in both neurodevelopmental and neurodegenerative

disorders like Angelman and Fragile X syndromes.

Preclinical data presented also indicates that

ANAVEX®2-73 demonstrates protective effects of mitochondrial enzyme complexes during pathological conditions, which,

if impaired, are believed to play a role in the pathogenesis of neurodegenerative and neurodevelopmental diseases.

Preclinical data on ANAVEX®2-73

related to multiple sclerosis indicates that ANAVEX®2-73 may promote remyelination in multiple sclerosis disease.

Further, data also demonstrates that ANAVEX®2-73 provides protection for oligodendrocytes (“OL’s”)

and oligodendrocyte precursor cells (“OPC’s”), as well as central nervous system neurons in addition to helping

repair by increasing OPC proliferation and maturation in tissue culture.

In March 2018, we presented preclinical data

of ANAVEX®2-73 in a genetic mouse model of tuberous sclerosis complex (“TSC”). TSC is a rare genetic

disorder characterized by the growth of numerous benign tumors in many parts of the body with a high incidence of seizures. The

new preclinical data demonstrates that treatment with ANAVEX®2-73 significantly increases survival and reduces seizures.

ANAVEX®3-71

ANAVEX®3-71 is a clinical drug

candidate with a novel mechanism of action via sigma-1 receptor activation and M1 muscarinic allosteric modulation, which has been

shown to enhance neuroprotection and cognition in Alzheimer’s disease models. ANAVEX®3-71 is a CNS-penetrable

potential disease modifying treatment for cognitive impairments. It is highly effective in very small doses against the major Alzheimer’s

hallmarks in transgenic (3xTg-AD) mice, including cognitive deficits, amyloid and tau pathologies, and also has beneficial effects

on inflammation and mitochondrial dysfunctions. ANAVEX®3-71 indicates extensive therapeutic advantages in Alzheimer’s

and other protein-aggregation-related diseases given its ability to enhance neuroprotection and cognition via sigma-1 receptor

activation and M1 muscarinic allosteric modulation.

A preclinical study examined the response of

ANAVEX®3-71 in aged transgenic animal models and showed a significant reduction in the rate of cognitive deficit,

amyloid beta pathology and inflammation with the administration of ANAVEX 3-71. In April 2016, the FDA granted Orphan Drug Designation

to ANAVEX®3-71 for the treatment of Frontotemporal dementia (FTD).

During pathological conditions ANAVEX®3-71

demonstrated the formation of new synapses between neurons (synaptogenesis) without causing an abnormal increase in the number

of astrocytes. In neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease, synaptogenesis is believed

to be impaired. Additional preclinical data presented also indicates that in addition to reducing oxidative stress, ANAVEX®3-71

demonstrates protective effects of mitochondrial enzyme complexes during pathological conditions, which, if impaired, are believed

to play a role in the pathogenesis of neurodegenerative and neurodevelopmental diseases.

In July 2020, we commenced the first Phase

1 clinical trial of ANAVEX®3-71, with focus on the treatment of Frontotemporal Dementia (FTD) and other

dementia indications with unmet medical need. The study is more fully described above under Clinical Studies Overview

– Frontotemporal Dementia.

ANAVEX®1-41

ANAVEX®1-41 is a sigma-1 receptor

agonist. Pre-clinical tests revealed significant neuroprotective benefits (i.e., protects nerve cells from degeneration or death)

through the modulation of endoplasmic reticulum, mitochondrial and oxidative stress, which damages and impairs cell viability.

In addition, in animal models, ANAVEX®1-41 prevented the expression of caspase-3, an enzyme that plays a key role

in apoptosis (programmed cell death) and loss of cells in the hippocampus, the part of the brain that regulates learning, emotion

and memory. These activities involve both muscarinic and sigma-1 receptor systems through a novel mechanism of action.

Preclinical data presented also indicates that

ANAVEX®1-41 demonstrates protective effects of mitochondrial enzyme complexes during pathological conditions, which,

if impaired, are believed to play a role in the pathogenesis of neurodegenerative and neurodevelopmental diseases.

ANAVEX®1066

ANAVEX®1066, a mixed

sigma-1/sigma-2 ligand is designed for the potential treatment of neuropathic and visceral pain. ANAVEX®1066 was

tested in two preclinical models of neuropathic and visceral pain that have been extensively validated in rats. In the chronic

constriction injury model of neuropathic pain, a single oral administration of ANAVEX®1066 dose-dependently restored

the nociceptive threshold in the affected paw to normal levels while leaving the contralateral healthy paw unchanged. Efficacy

was rapid and remained significant for two hours. In a model of visceral pain, chronic colonic hypersensitivity was induced by

injection of an inflammatory agent directly into the colon and a single oral administration of ANAVEX®1066 returned

the nociceptive threshold to control levels in a dose-dependent manner. Companion studies in rats demonstrated the lack of any

effects on normal gastrointestinal transit with ANAVEX®1066 and a favorable safety profile in a battery of behavioral

measures.

ANAVEX®1037

ANAVEX®1037 is designed for

the treatment of prostate and pancreatic cancer. It is a low molecular weight, synthetic compound exhibiting high affinity for

sigma-1 receptors at nanomolar levels and moderate affinity for sigma-2 receptors and sodium channels at micromolar levels. In

advanced pre-clinical studies, this compound revealed antitumor potential. It has also been shown to selectively kill human cancer

cells without affecting normal/healthy cells and also to significantly suppress tumor growth in immune-deficient mice models. Scientific

publications highlight the possibility that these ligands may stop tumor growth and induce selective cell death in various tumor

cell lines. Sigma receptors are highly expressed in different tumor cell types. Binding by appropriate sigma-1 and/or sigma-2 ligands

can induce selective apoptosis. In addition, through tumor cell membrane reorganization and interactions with ion channels, our

drug candidates may play an important role in inhibiting the processes of metastasis (spreading of cancer cells from the original

site to other parts of the body), angiogenesis (the formation of new blood vessels) and tumor cell proliferation.

Our compounds are in the pre-clinical and clinical

testing stages of development, and there is no guarantee that the activity demonstrated in pre-clinical models will be shown in

human testing.

We continue to identify and initiate discussions

with potential strategic and commercial partners to most effectively advance our programs and realize maximum shareholder value.

Further, we may acquire or develop new intellectual property and assign, license, or otherwise transfer our intellectual property

to further our goals.

Our Target Indications

We have developed compounds with potential

application to two broad categories and several specific indications. including:

Central Nervous System Diseases

Cancer

Competition

The drug discovery and development industry

is very competitive, characterized by rapid advancements in technology, where protection of proprietary advancements is essential.

Any product candidates that we may successfully develop and commercialize, may compete with existing therapies, or new therapies

that may become available in the future. Our commercial opportunities could be reduced or eliminated if our competitors develop

and commercialize products that are more effective, have fewer side effects, are more convenient or are less expensive than any

products that we may develop.

Our approach to the treatment of Alzheimer’s

disease and other CNS diseases differs from our competitors. Our platform may offer a disease-modifying approach in neurodegenerative

and neurodevelopmental diseases by activation of sigma-1 receptors. When activated by SIGMAR1 agonists, such as ANAVEX®2-73,

SIGMAR1 reduces cellular stress before and after RNA gene transcription. Studies confirm the predictive biomarker of response established

through SIGMAR1 mRNA expression. Because of its role in maintaining neuronal homeostasis, sigma receptors show significant promise

as viable targets for therapeutic molecules in an effort to treat Alzheimer’s disease and other CNS diseases and disorders,

including Parkinson’s disease and Rett syndrome, by restoring healthy gene expression.

At this time, our competitors are primarily

other biomedical development companies that are aiming to discover and develop compounds to be used in the treatment of Alzheimer’s

disease and other CNS diseases, and those companies already doing so. We also face competition from academic institutions and government

agencies, both in the United States and abroad.

Our competitors may have significantly

greater financial resources, an established presence in the market, expertise in research and development, manufacturing, preclinical

and clinical testing, may be in the process of obtaining regulatory approvals and marketing of approved products. These competitors

also compete with us in recruiting and retaining qualified scientific and technical personnel, establishing clinical study sites

and patient registration for clinical studies, as well as in acquiring or developing technologies complementary to, or necessary

for, our programs. Smaller or early-stage companies may also prove to be significant competitors, particularly through collaborative

arrangements with large and established companies.

For additional discussion of the risks

related to competition, see Item 1A “Risk Factors.”

Patents, Trademarks and Intellectual

Property

We hold ownership or exclusive rights

to fifteen U.S. patents, sixteen U.S. patent applications, and various PCT or ex-U.S. patent applications relating to our drug

candidates, methods associated therewith, and to our research programs.

We own one issued U.S. patent entitled

“ANAVEX®2-73 and certain anticholinesterase inhibitors composition and method for neuroprotection” claims

a composition of matter of ANAVEX®2-73 directed to a novel and synergistic neuroprotective compound combined with

donepezil and other cholinesterase inhibitors. This patent is expected to expire in June 2034, absent any patent term extension

for regulatory delays. We own three issued U.S. patents each with claims directed to crystalline forms of ANAVEX®2-73.

The first of these three patents claims crystalline forms of ANAVEX®2-73, dosage forms and compositions containing

crystalline ANAVEX®2-73, and methods of treatment for Alzheimer’s disease using them. This patent is expected

to expire in July 2036, absent any patent term extension for regulatory delays. The second of these three patents claims pharmaceutical

compositions containing a crystalline form of ANAVEX®2-73, and methods of treatment for Alzheimer’s disease

using the compositions. This patent is expected to expire in June 2037, absent any patent term extension for regulatory delays.

The third of these three patents claims pharmaceutical compositions containing a crystalline form of ANAVEX®2-73,

and methods of treatment for Alzheimer’s disease using the compositions. This patent is expected to expire in June 2037,

absent any patent term extension for regulatory delays. We also own two issued U.S. patents for seizure treatment. The first of

these two patents claims methods and dosage forms for treating seizures, the dosage forms containing a low-dose anti-epilepsy drug

combined with either: (i) ANAVEX®2-73 and its active metabolite ANAVEX®19-144; or (ii) ANAVEX®19-144.

The second of these two patents further claims a combination seizure treatment involving administration of an anti-epilepsy drug

combined with (i) ANAVEX®19-144, or (ii) ANAVEX 19-144® and ANAVEX 2-73®. Both patents

are expected to expire in October 2035, absent any patent term extension for regulatory delays. We also own two issued U.S. patents

with claims directed to treating neurodevelopmental disorders. These patents claim methods for treating a neurodevelopmental disorder

or multiple sclerosis by administering ANAVEX®2-73, ANAVEX®19-144, and/or ANAVEX®1-41

(another sigma receptor ligand similar to ANAVEX®2-73), or compositions thereof. Both patents are expected to expire

in January 2037, absent any patent term extension for regulatory delays. In addition, we own one issued U.S. Patent with claims

directed to methods of treating melanoma with a compound related to ANAVEX®2-73. This patent is expected to expire

in February 2030, absent any patent term extension for regulatory delays. We also own an issued U.S. patent that claims crystalline

forms of ANAVEX®19-144, dosage forms and compositions containing the crystalline forms of ANAVEX®19-144,

and methods of treatment for Alzheimer’s disease. This patent is expected to expire in July 2036, absent any patent term

extension for regulatory delays. Further, we own one issued U.S. Patent with claims directed to methods of treating cardiac dysfunction

with ANAVEX®2-73 . This patent is expected to expire in July 2038, absent any patent term extension for regulatory

delays.

We also own two issued U.S. patents

related to ANAVEX®1066. The first of these two patents claims methods for treating or preventing pain using (+)

ANAVEX®1066 isomer. The second patent claims methods for treating or preventing pain using (-) ANAVEX®1066

isomer. Both patents are expected to expire in November 2036, absent any patent term extension for regulatory delays.

For ANAVEX®2-73, ANAVEX®19-144,

ANAVEX®1-41, and ANAVEX®1066, we also have granted or pending applications in Australia, Canada,

China, Europe, Japan, and Hong Kong, which are expected to expire after 2035.

With regard to ANAVEX®3-71,

we own exclusive rights to two issued U.S. patents with claims respectively directed to the ANAVEX®3-71 compound

and methods of treating various diseases including Alzheimer’s with the same. These patents are expected to expire in April

2030, and January 2030, respectively, absent any patent term extension for regulatory delays. We also own exclusive rights to related

patents or applications that are granted or pending in Australia, Canada, China, Europe, Japan, Korea, New Zealand, Russia, and

South Africa, which are expected to expire in January 2030.

We also own other patent applications

directed to enantiomers, crystals, formulations, uses, and patient selection methods that may provide additional protection for

one or more of our product candidates.

We regard patents and other intellectual

property rights as corporate assets. Accordingly, we attempt to optimize the value of intellectual property in developing our business

strategy including the selective development, protection, and exploitation of our intellectual property rights. In addition to

filings made with intellectual property authorities, we protect our intellectual property and confidential information by means

of carefully considered processes of communication and the sharing of information, and by the use of confidentiality and non-disclosure

agreements and provisions for the same in contractor’s agreements. While no agreement offers absolute protection, such agreements

provide some form of recourse in the event of disclosure, or anticipated disclosure.

Our intellectual property position,

like that of many biomedical companies, is uncertain and involves complex legal and technical questions for which important legal

principles are unresolved. For more information regarding challenges to our existing or future patents, see “Risk Factors”.

Government regulation

Government authorities in the United

States, at the federal, state and local levels, and other countries extensively regulate, among other things, the research, development,

testing, manufacture, quality control, approval, labeling, packaging, storage, record-keeping, promotion, advertising, distribution,

marketing and export and import of products such as those we are developing. A new drug must be approved by the FDA through the

NDA process before it may be legally marketed in the United States. We are subject to various government regulations in connection

with the development of our pipeline.

U.S. Drug Development and Regulation

In the United States, the FDA regulates drugs

under the federal Food, Drug, and Cosmetic Act and its implementing regulations (“FDCA”). 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 U.S. requirements at

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

or judicial sanctions. These sanctions could include the FDA’s 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.

Once a drug candidate is identified for development,

it enters the preclinical testing stage. Preclinical tests include laboratory evaluations of product chemistry, toxicity and formulation,

as well as other preclinical studies. An Investigational New Drug application (“IND”) sponsor must submit the results

of the preclinical tests, together with manufacturing information and analytical data, to the FDA as part of the IND. The sponsor

must also include a protocol detailing, among other things, the objectives of the first phase of clinical trials, the parameters

to be used in monitoring the safety of the trial, and the effectiveness criteria to be evaluated should the first phase lend itself

to an efficacy evaluation. Some preclinical testing may continue even after the IND is filed. The IND automatically becomes effective

Source: SEC EDGAR (public domain) · 10-K for the period ended 2021-09-30, filed 2021-11-24 · accession 0001731122-21-002062

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