10-K
1
edsa_10k.htm
ANNUAL REPORT
edsa_10k
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, 2020
OR
☐ 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: 001-37619
EDESA BIOTECH, INC.
(Exact name of registrant as specified in its charter)
British Columbia, Canada N/A
100 Spy Court Markham, ON, Canada L3R 5H6
(Address of principal executive offices) (Zip Code)
Registrant’s telephone number, including area code: (289)
800-9600
Securities registered pursuant to Section 12(b) of the
Act:
Name of each exchange on which
Title of each class Trading Symbol registered
Common Shares, without par value EDSA The Nasdaq Stock Market LLC
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 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
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 whether the
registrant is a shell company (as defined in Rule 12b-2 of the
Act). Yes ☐ No ☒
As of March 31, 2020, the last business day of the
registrant’s most recently completed second fiscal quarter,
the aggregate market value of the registrant’s outstanding
common shares held by non-affiliates was approximately $8,422,972,
which was calculated based on 8,859,159 common shares outstanding
as of that date, of which 3,935,968 common shares were held by
non-affiliates at the closing price of the registrant’s
common shares on The Nasdaq Capital Market on such
date.
As of
December 2, 2020, the registrant had 10,523,087 common shares
issued and outstanding.
DOCUMENTS INCORPORATED BY REFERENCE: NONE
EDESA BIOTECH, INC.
ANNUAL REPORT ON FORM 10-K
Year Ended September 30,
2020
Table of Contents
Item Page
PART I
1. Business 4
1A. Risk Factors 15
1B. Unresolved Staff Comments 28
2. Properties 28
3. Legal Proceedings 28
4. Mine Safety Disclosures 28
PART II
6. Selected Financial Data 30
7A. Quantitative and Qualitative Disclosures About Market Risk 34
8. Financial Statements and Supplementary Data 34
9A. Controls and Procedures 34
9B. Other Information 35
PART III
10. Directors, Executive Officers and Corporate Governance 36
11. Executive Compensation 39
13. Certain Relationships and Related Transactions, and Director Independence 47
14. Principal Accounting Fees and Services 48
PART IV
15. Exhibits and Financial Statement Schedules 49
SIGNATURES 52
2
FORWARD-LOOKING STATEMENTS AND OTHER MATTERS
This Annual Report on Form 10-K contains certain forward-looking
statements within the meaning of Section 27A of the Securities Act
of 1933, as amended (the Securities Act) and Section 21E of the
Securities Exchange Act of 1934, as amended (the Exchange Act) and,
as such, may involve known and unknown risks, uncertainties and
assumptions. Forward-looking statements are based upon our current
expectations, speak only as of the date hereof, are subject to
change and include statements about, among other things: the
status, progress and results of our clinical programs; our ability
to obtain regulatory approvals for or successfully commercialize
any of our product candidates; our business plans, strategies and
objectives, including plans to pursue collaboration, licensing or
other similar arrangements or transactions; our expectations
regarding our liquidity and performance, including our expense
levels, sources of capital and ability to maintain our operations;
the competitive landscape of our industry; and general market,
economic and political conditions.
Forward-looking statements are those that
predict or describe future events or trends and that do not relate
solely to historical matters. You can generally identify
forward-looking statements as those statements containing the
words “anticipate,”
“believe,” “plan,” “estimate,”
“expect,” “intend,” “may,”
“will,” “would,” “could,”
“should,” “might,” “potential,”
“continue” or other similar expressions. You
should not rely on our forward-looking statements as they are not a
guarantee of future performance. There can be no assurance that
forward-looking statements will prove to be accurate because the
matters they describe are subject to assumptions, known and unknown
risks, uncertainties and other unpredictable factors, many of which
are beyond our control.
Our actual results could differ materially and adversely from those
expressed in any forward-looking statements as a result of various
factors, some of which are discussed in this report in the Part I,
Item 1A. Risk Factors and elsewhere in this report. Risks and
uncertainties include, among others,
●
our ability to obtain funding for our operations;
●
our estimates regarding our expenses, revenues, anticipated capital
requirements and our needs for additional financing;
●
the timing of the commencement, progress and receipt of data from
any of our preclinical and clinical trials;
●
the expected results of any preclinical or clinical trial and the
impact on the likelihood or timing of any regulatory
approval;
●
the therapeutic benefits, effectiveness and safety of our product
candidates;
●
the timing or likelihood of regulatory filings and
approvals;
●
changes in our strategy or development plans;
●
the volatility of our common share price;
●
the rate and degree of market acceptance and clinical utility of
any future products;
●
the effect of competition;
●
our ability to protect our intellectual property as well as comply
with the terms of license agreements with third
parties;
●
our ability to identify, develop and commercialize additional
products or product candidates;
●
reliance on key personnel; and
●
general changes in economic or business conditions.
Except as required by law, we undertake no obligation to update
forward-looking statements.
As used in this Annual Report on Form 10-K, “Edesa,”
“the Company,” “we,” “us,” and
“our” refer to Edesa Biotech, Inc. and our consolidated
subsidiaries, except where the context otherwise
requires.
Our logo and other trademarks or service marks of Edesa Biotech,
Inc. appearing in this Annual Report on Form 10-K are the property
of Edesa Biotech, Inc. This Annual Report on Form 10-K contains
additional trade names, trademarks and service marks of other
companies. We do not intend our use or display of other
companies’ trade names, trademarks or service marks to imply
relationships with, or endorsement or sponsorship of us by, these
other companies.
All historical references to common shares, warrants and share
options outstanding prior to June 7, 2019 and the related exercise
prices in this Form 10-K have been adjusted to reflect the effect
of the one for six reverse split, effected at the close of market
on June 7, 2019.
3
PART I
Item 1.BUSINESS.
Overview
We are a biopharmaceutical company focused on acquiring, developing
and commercializing clinical-stage drugs for inflammatory and
immune-related diseases with clear unmet medical needs. Our two
lead product candidates, EB05 and EB01, are in later stage clinical
studies.
EB05
is a monoclonal antibody therapy that we are developing as a
treatment for Acute Respiratory Distress Syndrome (ARDS) in
COVID-19 patients. ARDS is a life-threatening form of respiratory
failure, and the leading cause of death among COVID-19 patients.
ARDS can be also caused by bacterial pneumonia, sepsis, chest
injury and other causes. Specifically, EB05 inhibits toll-like
receptor 4 (TLR4), a key immune signaling protein and an important
mediator of inflammation that has been shown to be activated by
SARS-COV2 as well as other respiratory infections such as
influenza. In multiple third-party studies, high serum levels of
alarmins (damage signaling molecules) that bind to and activate
TLR4 are associated with poor outcomes and disease progression in
COVID-19 patients. Since EB05 has demonstrated the ability to block
signaling irrespective of the presence or concentration of the
various molecules that frequently bind with TLR4, we believe that
EB05 could ameliorate TLR4-mediated inflammation cascades in ARDS
patients, thereby reducing lung injury, ventilation rates and
mortality. In November 2020, we initiated a Phase 2/Phase 3
clinical study of EB05 and are currently enrolling
subjects.
In addition to EB05, we are developing an sPLA2 inhibitor,
designated as EB01, as a topical treatment for chronic allergic
contact dermatitis (ACD), a common, potentially debilitating
condition and occupational illness. EB01 employs a novel,
non-steroidal mechanism of action and in two clinical studies has
demonstrated statistically significant improvement of multiple
symptoms in ACD patients. We initiated a Phase 2B clinical study
evaluating EB01 for chronic ACD in the fourth calendar quarter of
2019 and are currently enrolling subjects.
In addition to our current clinical programs, we intend to expand
the utility of our technologies and clinical-stage assets across
other indications.
Competitive Strengths
We believe that we possess a number of competitive strengths that
position us to become a leading biopharmaceutical company focused
on inflammatory and immune-related diseases,
including:
●
Validated technology and
drug development capabilities.We believe that the strength of our
technologies has been validated byfavorable clinical data from Phase 1 and
Phase 2 studies; and, our multiple arrangements with third parties
to develop and commercialize their clinical-stage drug
candidates.
●
Novel pipeline
addressing large underserved markets.Our product candidates include novel
clinical-stage compounds and antibodies that have significant
scientific rationale for effectiveness. By initially targeting
large markets that have significant unmet medical needs, we believe
that we can drive adoption of new products and improve our
competitive position. For example, we believe that the novel,
non-steroidal mode of action of our sPLA2 technology will be
appealing alternatives for managing the symptoms of ACD and
hemorrnoids disease (HD). These diseases impact millions of people
in the United States and Canada, and can have significant effects
on patients’ quality of life and, in the case of many chronic
ACD patients and their employers, significant workplace-related
costs and limitations.
●
Intellectual property
protection and market exclusivity.We have opportunities to develop our
competitive position through patents, trade secrets, technical
know-how and continuing technological innovation. We have exclusive
license rights in our target indications to multiple patents and
pending patent applications in the United States and in various
foreign jurisdictions. In addition to patent protection, we intend
to utilize trade secrets and market exclusivity afforded to a New
Chemical Entity, where applicable, to enhance or maintain our
competitive position.
●
Experienced
leadership.Our
leadership team possesses core capabilities in dermatology,
infectious diseases, gastrointestinal medicine, drug development
and commercialization, chemistry, manufacturing and controls, and
finance. Our founder, Chief Executive Officer, Pardeep Nijhawan,
MD, FRCPC, AGAF, is a board-certified gastroenterologist and
hepatologist with a successful track record of building life
science businesses, including Medical Futures, Inc., which was sold
to Tribute Pharmaceuticals in 2015. In addition to our internal
capabilities, we have also established a network of key opinion
leaders, contract research organizations, contract manufacturing
organizations and consultants. As a result, we believe we are well
positioned to efficiently develop novel treatments for inflammatory
and immune-related diseases.
4
Our Business Strategy
We plan to develop and commercialize innovative drug products that
address unmet medical needs for large, underserved markets where
there is limited competition. Key elements of our strategy
include:
●
Rapidly develop EB05 as
a novel therapy for hospitalized COVID-19 patients.We intend to apply
our expertise in immune modulation and inflammation therapies and
clinical trial management to rapidly develop EB05 as a potential
treatment for ARDS. With potential investigational sites in
multiple jurisdictions, we believe there will be sufficient
patients available and that we can complete the study amid the
global health crisis. Should the antibody treatment demonstrate
promising results at the Phase 2 readout, we plan to continue with
a pivotal Phase 3 study, subject to funding and additional
regulatory approvals in certain
jurisdictions.
●
Establish EB01 as the
leading treatment for chronic ACD.Our goal is to obtain regulatory approval
for EB01 and commercialize EB01 for use in the treatment of ACD.
Based on promising clinical trial results in which patients treated
with EB01 experienced statistically significant improvements of
their symptoms with minimal side effects, we initiated a Phase 2B
clinical study evaluating EB01. The protocol includes a blinded
interim readout following the completion of the first part of the
Phase 2B study. In November 2020, we completed enrollment of more
than 50% of the patients planned for this part of a
study.
●
Selectively targeting
additional indications.In addition to our ARDS and ACD programs, we
plan to efficiently generate proof-of-concept data for other
programs where modulation of immune pathways or the inhibition of
sPLA2 activity may have therapeutic benefits. For example, we are
planning a proof-of-concept clinical study of our sPLA2 technology
as a potential treatment for patients with HD, subject to funding
and the resumption of normal, pre-pandemic operations at targeted
clinical sites.
●
In-license promising
product candidates.We
are applying our cost-effective development approach to advance and
expand our pipeline. Our current product candidates are in-licensed
from academic institutions or other biopharmaceutical companies,
and, from time to time, we plan to identify, evaluate and
potentially obtain rights to and develop additional assets. Our
objective is to maintain a well-balanced portfolio with product
candidates across various stages of development. In general, we
seek to identify product candidates and technology that represent a
novel therapeutic approach, are supported by compelling science,
target an unmet medical need, and provide a meaningful commercial
opportunity. We do not currently intend to invest significant
capital in basic research, which can be expensive and
time-consuming.
●
Capture the full
commercial potential of our product candidates.If our product candidates are successfully
developed and approved, we may build commercial infrastructure
capable of directly marketing the products in North America and
potentially other major geographies of strategic interest. We also
plan to evaluate strategic licensing arrangements with
pharmaceutical companies for the commercialization of our drugs,
where applicable, such as in territories where a partner may
contribute additional resources, infrastructure and
expertise.
Acute Respiratory Distress Syndrome (ARDS)
Acute
respiratory distress syndrome (ARDS) is a life-threatening form of
respiratory failure, and the leading cause of death among COVID-19
patients. In addition to virus-induced pneumonia, ARDS can be
caused by bacterial pneumonia, sepsis, chest injury and other
causes.
Specifically, ARDS
involves an exaggerated immune response leading to inflammation and
injury to the lungs that deprives the body of oxygen. ARDS is
classified as mild, moderate and severe by using an arterial
partial pressure of oxygen (PaO2) to fraction of inspired oxygen
(FIO2) threshold of 300, 200, and 100 mm Hg, respectively. For
moderate to severe cases, there are currently few meaningful
treatments, other than supplemental oxygen and mechanical
ventilation, and patients suffer high mortality rates. Prior to
COVID-19, ARDS accounted for 10% of intensive care unit admissions,
representing more than 3 million patients globally each year. ARDS
has historically affected approximately 200,000 patients each year
in the United States, resulting in nearly 75,000 deaths annually,
according to medical literature.
Countering the
exaggerated innate immune response in ARDS has been a key area of
interest among researchers. One of the most studied targets has
been Toll-like receptor 4 (TLR4) – a key component of the
innate immune system and an important mediator of inflammation.
Since TLR4 detects molecules found in pathogens and also binds to
endogenous molecules produced as a result of injury, it is a key
receptor on which both infectious and noninfectious stimuli
converge to induce a proinflammatory response. Specifically, TLR4
signaling activates leukocytes to secrete proinflammatory cytokines
(i.e., CXCL10, IL-6,
IFN-b, IL-1b, TNF-a), which under certain circumstances can result
in a “cytokine storm” – a severe immune reaction
in which the body releases too many cytokines into the blood too
quickly.
Such
upregulation of TLR4 and its associated cytokines has been observed
in SARS-CoV-2 as well as other respiratory infections such as
influenza. In multiple third-party studies, high serum levels of
alarmins, such as calprotectin and HMGB1(high mobility group
protein B1), that bind to and activate TLR4 are associated with
poor outcomes and disease progression in COVID-19 patients. In
addition, TLR4 inhibition (antagonism) prevents cytokine production
at a very early stage and has been shown to have a protective
effect. For example, in preclinical studies in mice, it was
demonstrated that administration of a TLR4 antagonist blocked
influenza-induced lethality and ameliorated virus-induced acute
lung injury. Antagonism of TLR4 has also been shown to modulate the
secretion of proinflammatory cytokines (IL-6, CRP, IFNb, TNF-a,
CXCL-10, IL8 and MIP-1b). Based on this data as well as previous
clinical results, we believe that the modulation of the TLR4
provides a compelling opportunity to treat ARDS.
5
EB05
Overview and Status
EB05 is a monoclonal antibody (mAb) that has been engineered to
alter inflammatory signaling by binding to and blocking the
activation of TLR4. Specifically, EB05 dampens TLR4 signaling by
blocking receptor dimerization (and subsequent intracellular
signaling cascades). The drug has demonstrated the ability to block
signaling irrespective of the presence or concentration of the
various molecules that frequently bind with TLR4, known as ligands.
Based on this broad mechanism of action, we believe that EB05 could
ameliorate TLR4-mediated inflammation cascades in ARDS patients,
thereby reducing lung injury, ventilation rates and mortality. EB05
has demonstrated the ability to resolve fever and stabilize heart
and breathing rates in human subjects that were injected with
lipopolysaccharide (LPS) – a potent inducer of the acute
systemic inflammation. In previous Phase 1 and Phase 2 clinical
studies, EB05 has demonstrated favorable safety and tolerability
profiles.
Our
Phase 2/3 protocol has been approved in Canada. We have also
received approved for the Phase 2 portion of our study in the
United States. The company is currently enrolling patients at U.S.
and Canadian hospitals.
As
planned, our Phase 2/Phase 3 study is an adaptive, multicenter,
randomized, double-blind, placebo-controlled trial to evaluate the
efficacy and safety of EB05 in adult hospitalized COVID-19
patients. We expect to enroll approximately 316 patients. Patients
will be intravenously infused with EB05 or placebo.
Standard-of-care COVID-19 treatment will be given to all patients.
The total follow-up duration of each patient will be 28 days.
Should the drug treatment demonstrate promising results at the
Phase 2 readout, the protocol allows for enrollment to continue as
a pivotal Phase 3 study in Canada. In the U.S., we expect to have
an end of Phase 2 meeting with the U.S. Food and Drug
Administration (FDA) to finalize the Phase 3 protocol.
Previous Phase 1 and Phase 2 Clinical Studies of EB05
In a randomized, double blind, placebo-controlled, PK/PD guided
Phase 1 study, 60 healthy volunteers were given escalating, single
intravenous infusion of EB05 in the absence and presence of an in
vivo LPS challenge. Forty-eight (48) subjects were exposed to
escalating doses between 0.001 to 15 mg/kg in Part 1 of the study.
The highest dose of EB05 displayed a pharmacological effect
(defined by 80% inhibition of cytokine after ex vivo LPS challenge)
lasting up to 14 weeks. Twelve (12) subjects were exposed to an in
vivo LPS challenge (2 ng/kg) in Part 2 of the study. Of these, 3
received EB05 at a dose of 0.01 mg/kg and 9 at a dose of 0.25
mg/kg. No safety signals were identified after administration up to
a dose of 15 mg/kg.
In a previous Phase 2 clinical study, EB05 was administered to 57
rheumatoid arthritis patients and demonstrated a favorable safety
and tolerability profile. Patients received intravenous infusions
of EB05 at 5mg/kg every 2 weeks for a total of 6 doses. EB05
blocked cytokine release after ex vivo LPS challenge, with full
effect from a dose of 1 mg/kg onwards. The duration of inhibition
of cytokine release was dependent on the dose and lasted up to 14
weeks at a dose of 15 mg/kg. The pharmacological effects of EB05
after the ex vivo and in vivo LPS challenges were comparable. At a
dose of 0.25 mg/kg, EB05 prevented the laboratory and clinical
changes induced by an in vivo LPS administration, up to 22 days.
LPS effects were fully recovered between 22 and 40 days after EB05
administration.
Allergic Contact Dermatitis
Contact dermatitis is one of the most common occupational and
work-related skin conditions in the United States. The disease can
be either irritant contact dermatitis or ACD. Together, these
conditions have been estimated to cost up to $2 billion annually as
a result of lost work, reduced productivity, medical care and
disability payments. Based on published reports and U.S. insurance
claims data, we estimate that there are more than 2.5 million
people in the United States with ACD, including more than 1 million
people who have chronic ACD. Since primary care physicians do not
always distinguish between irritant and allergic contact
dermatitis, a potentially larger undiagnosed patient population may
also be present.
ACD is caused by an allergen interacting with skin and usually
occurs on areas of the body that have been directly exposed to the
environment, with a high prevalence on the hands and face. Common
allergens associated with ACD include plants, metals, plastics and
resins, rubber additives, dyes, biocides, and various cosmetics.
The disease is characterized by inflammation, erythema (redness),
pruritus (itchiness), and blistering of the skin. Inflammation can
vary from mild irritation and redness to open sores, depending on
the type of irritant, the body part affected and the degree of
sensitivity. ACD can become chronic if not treated or if the
causative allergen is not removed. In many chronic cases, the
causative allergen is unknown or difficult to avoid (as an example,
the allergen is present in the workplace).
6
The immune mechanisms involved in ACD are well documented. During
the initial contact with the offending allergen, the immune system
is sensitized. Upon subsequent contact, a delayed-type
hypersensitivity reaction (Type IV) occurs at the point of contact
between the skin and the allergen. As a cell-mediated response, the
immune reaction primarily involves the interaction of T cells with
antigens rather than an antibody response. More specifically, ACD
involves an exogenous substance binding a cell surface protein to
form a hapten that is recognized as a foreign antigen by the immune
system. Haptens are known to signal through toll-like receptors, a
family of receptors involved in the innate immune system
recognizing pathogens, leading to the induction of pro-inflammatory
cytokines such as interleukin (IL)-1b. EB01 has been shown in
preclinical studies to inhibit the production of pro-inflammatory
cytokines induced via toll-like receptor signaling (IL-1b, IL-6,
IL-8, MIP-1a, and TNFa), suggesting that EB01 may address the
underlying disease mechanism of ACD.
Current Treatments
Generally, dermatologists view chronic ACD from both a duration and
recurrence perspective, considering how often and how long symptoms
persist. Chronic disease affects patients over a prolonged period,
typically greater than six months or even years. These chronic
patients have either frequent intermittent exposure or continuous
exposure. Since inflammation in ACD is driven by external exposure
to an allergen, the severity of ACD does not necessarily correlate
with body surface area, as is often the case with other
dermatological diseases.
Current treatment plans begin by attempting to identify and remove
exposure to the allergen. However, the offending allergen(s) is
frequently not identified, and even when it is, avoiding exposure
is often not possible (e.g., present in the workplace), according
to our market research. To our knowledge, there are no drug
treatment options specifically indicated for ACD. As such,
physicians must utilize agents approved for other dermatological
conditions. Topical corticosteroids are the most commonly used
therapeutic intervention for ACD but cannot be used continuously
since they have well-known side-effects including skin thinning,
stretch marks, acne, testicular atrophy, nosebleeds, stinging,
burning and dryness. Other topical treatments for ACD include
immunomodulators such as topical calcineurin inhibitors. However,
these are less efficacious than topical corticosteroids and have an
FDA “black box warning” for risk of malignancies.
Systemic corticosteroids can be used for acute control of severe
cases of ACD but have safety concerns including
hypothalamic-pituitary-adrenal axis suppression, growth suppression
and loss of bone-density, thereby limiting the utility of steroids
for treating chronic disease. Finally, patients may be treated with
systemic immunomodulators, which have a series of “black box
warnings” and associated safety issues. Systemic therapies
also need to be tapered off each time the physician wants to patch
test allergens to identify the source of a patient’s
ACD.
EB01
Overview and Status
EB01 is a topical vanishing cream containing
a novel, non-steroidal anti-inflammatory compound. EB01 exerts its
anti-inflammatory activity through the inhibition of certain
pro-inflammatory enzymes known as secretory phospholipase 2, or
sPLA2. These enzymes are secreted by immune cells
upon their activation and produce arachidonic acid via phospholipid
hydrolysis, which, in turn, initiates a broad inflammatory cascade.
The sPLA2 enzyme family plays a key role in
initiating inflammation associated with many diseases, and we
believe that targeting the sPLA2 enzyme family with enzyme inhibitors will
have a superior anti-inflammatory therapeutic effect because the
inflammatory process will be inhibited at its inception rather than
after inflammation has occurred.
In October 2019, we initiated patient enrollment for a multi-center
Phase 2B clinical study evaluating EB01 as a monotherapy for
patients with moderate to severe chronic ACD. The double-blind,
vehicle-controlled study will primarily evaluate the safety and
efficacy of EB01 in ACD patients. Investigators will also evaluate
symptom reduction, quality of life and dose-relationships among
various strengths of EB01 cream as secondary and exploratory
measures. We plan to perform a blinded interim analysis following
the completion of the first cohort to determine the total number of
patients for the second part of the study. The sample-size adaptive
protocol contemplates up to 166 total subjects.
In April 2020, we filed a protocol amendment with the FDA. The
amendment provides for, among other changes, a reduction in the
number of in-person office visits, allowances for remote telehealth
appointments and other procedural updates to simplify enrollment