NASDAQ: INM

3

Our
INM-901 is a proprietary small molecule, disease modifying drug candidate being developed as a potential treatment for Alzheimer’s
disease. INM-901 has multiple potential mechanisms of action as a preferential signaling agonist for both CB1 and CB2 receptors, as well
as impacting the peroxisome proliferator-activated receptor, or PPAR, signaling pathway. Combined, these mechanisms of action may offer
a unique treatment approach targeting several biological pathways associated with Alzheimer’s disease.

Outcomes
from our ocular research, based on the proprietary small molecule INM-089, indicate potentially promising neuroprotective effects in
the back of the eye, which may lead to the preservation of retinal function. Neuroprotection in dry AMD remains an unmet medical need
and a new treatment option may help solve this multifactorial disease.

We
have completed a Phase 2 clinical trial of INM-755 (cannabinol) cream studying its safety and efficacy in treating symptoms related to
EB. Results from the Phase 2 clinical trial showed a positive indication of enhanced anti-itch activity for INM-755 cream versus the
control cream alone in an exploratory clinical evaluation. We are also pursuing strategic partnership opportunities for INM-755 in EB
and other itch-related skin conditions.

Together
with BayMedica, our manufacturing capabilities include traditional approaches such as chemical synthesis and biosynthesis, as well as
a proprietary, integrated manufacturing approach called IntegraSyn. With multiple manufacturing approaches, we have sought to maintain
enhanced flexibility to select the most cost-effective method to deliver high quality, high purity Products and Product Candidates fit
for their intended uses. BayMedica’s commercial business specializes in the B2B commercialization of bulk rare, non-intoxicating
cannabinoids as raw materials for the Health and Wellness sector that are bioidentical to those found in nature.

Corporate
Information

We
were originally incorporated in the Province of British Columbia, under the Business Corporations Act (British Columbia) (the
“BCBCA”), on May 19, 1981 (the “Incorporation Date”), and we have undergone a number of executive management,
corporate name and business sector changes since such Incorporation Date, ultimately changing our name to “InMed Pharmaceuticals
Inc.” on October 6, 2014. Our principal executive offices are located at Suite 1445, 885 West Georgia Street, Vancouver, BC, V6C
3E8 and our telephone number is +1-604-669-7207. Our website is https://www.inmedpharma.com/. The information that is contained on, or
that may be linked to or accessed through our website, is not incorporated, in whole or in part, into this Annual Report in any respect.
We have included our website address in this Annual Report solely as an inactive textual reference.

Employees
and Human Capital

Our
management team is comprised of highly experienced pharmaceutical and biotechnology executives with successful track records in researching,
developing, gaining approval for and commercializing novel medicines to treat serious diseases. Each member of our management team has
20 to 30+ years of industry experience, including our Chief Executive Officer (“CEO”), Chief Operating Officer (“COO”),
Chief Financial Officer (“CFO”), General Manager and VPs of Preclinical Drug Development, Discovery Research, Chemistry,
Synthetic Biology and of Sales & Marketing. Together, this management team has covered the spectrum of pharmaceutical drug discovery,
preclinical research, formulation development, manufacturing, human clinical trials, regulatory submissions and approval, and global
commercialization of pharmaceutical and wellness products. Additionally, the management team has significant experience in company formation,
capital raises, mergers and acquisitions, business development, and sales and marketing in the pharmaceutical and other industries. Our
Board is constituted of individuals with significant experience in the pharmaceutical and biotechnology industries. As of September 12,
2025, inclusive of our management team, we had 13 full-time employees, and we also utilize the services of several consultants. None
of our employees are represented by a collective bargaining agreement, nor have we experienced any work stoppage. We believe that we
maintain strong relations with our employees.

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We
are committed to growing our business over the long-term. As a result of the competitive nature of the industry in which we operate,
employees have significant career mobility and opportunity, and as a result, the competition for experienced employees is great. The
existence of this competition, and the need for talented and experienced employees to realize our business objectives, underlies the
design and implementation of our compensation programs. At the same time, we seek to keep our approach to compensation simple and streamlined
to reflect the still relatively moderate size of the Company. We have, therefore, implemented compensation, leave and benefits programs
necessary to attract and retain the talented and experienced employees necessary to develop our business, including what we believe to
be competitive salaries, stock options awards to permanent employees (both upon initial hiring and on an annual basis thereafter), and
pay annual bonuses to permanent employees contingent on the achievement of corporate and/or personal objectives. We have developed an
Employee Handbook that contains all corporate policies and guidelines for professional behavior. Our policies and practices apply to
all employees, regardless of title. These guidelines include, among others, our Code of Business Conduct as well as our policies for
corporate disclosure, insider trading and whistle blower, all of which are posted on our website.

For
all current and future pharmaceutical Product Candidates we intend to submit new drug applications (“NDAs”) (or their international
equivalents) in most major jurisdictions, including the United States, either alone or with development/commercial partners.

Our
Business Strategy

Our
goal is to develop a pipeline of prescription-based Product Candidates targeting treatments for diseases with high unmet medical needs.

●
Develop and produce proprietary
small molecule Product Candidates for use in our drug development programs

●
Advance pharmaceutical
drug Product Candidates through preclinical and clinical development, thereby establishing important human proof-of-concept in multiple
therapeutic applications

These
activities are at various stages of development, including, with INM-901 (for the treatment of Alzheimer’s disease), INM-089 (for
the treatment of dry AMD) and INM-755 (for the treatment of symptoms related to EB). We have the internal capabilities to design and
execute, together with multiple external vendors, the preclinical experimentation and clinical studies required to advance pharmaceutical
drug candidates towards commercialization.

●
Actively seek avenues to
accelerate drug development via licensing, partnering or sale to external companies

We
do not currently have an internal organization for the sales, marketing and distribution of pharmaceutical products. With respect to
the commercialization of each Product Candidate, we may therefore rely on (i) a “go-it-alone” commercialization effort; (ii)
out-licensing to third parties; or, (iii) co-promotion agreements with strategic collaborators for our Product Candidates. The decision
to pursue a “go-it-alone” commercialization effort versus out-licensing to third parties will depend on various factors including,
but not limited to, the complexity of the Product Candidate and process, the expertise required and related cost of building any such
infrastructure for our Product Candidates. For INM-755 in EB, further advancement is contingent on identifying drug development and commercial
partnerships. The optimal commercial strategy for the INM-901 and INM-089 compounds will be evaluated in due course.

●
Expand portfolio and revenues
of Products into the existing distribution network and to end-product manufacturers of specialty health and wellness products

●
Develop cost effective
and scalable manufacturing processes for high quality Products and Product Candidates as APIs for our core internal drug candidate
pipeline and for licensing opportunities of non-core drug candidates.

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Our
Strengths

We
are a pharmaceutical drug development company as well as a developer and supplier of rare, naturally occurring cannabinoids that is focused
on commercializing important medicines to treat diseases with high unmet medical needs. Our key strengths include the following:

Experienced
executive team and board of directors with proven track records.

One
key critical success factor in the field of pharmaceutical drug development is the experience and skill set of the individuals leading
us. We have been successful in attracting and retaining executive and directors with extensive experience in all facets of the pharmaceutical
industry, including fundamental research and development, multiple manufacturing techniques, drug formulation, clinical trial execution,
regulatory approvals, pharmaceutical commercialization, company and capital formation, business development, legal, and corporate governance.
Our leadership team is well-poised to lead us through all facets of drug development and product commercialization, either internally
or externally via partnerships. It is this group of individuals that will help optimize our chances for success.

Scope
of research and robust pharmaceutical pipeline

Over
several years of dedicated research, we have built a robust pipeline of drug development candidates, including two preclinical programs
targeting Alzheimer’s (INM-901) and ocular diseases (INM-088 for glaucoma and INM-089 for AMD), as well as a completed Phase 2
study in dermatology (INM-755). The INM-089 and INM-901 preclinical programs offer a differentiated treatment approach using proprietary,
disease-modifying small molecules that target the CB1 and CB2 receptors, which management believes is a key strength of the Company.

Multiple
manufacturing approaches.

Our
management team believes that our combined manufacturing technologies provide us with a competitive advantage to utilize the most cost-efficient
methodology (i.e. chemical synthesis, biosynthesis and IntegraSyn) for the development and commercialization of new Products and Product
Candidates to a wide spectrum of market opportunities.

Early
mover status as a B2B supplier of non-intoxicating rare cannabinoids to the health and wellness sector.

As
demonstrated by the launch of several non-intoxicating rare cannabinoids into the health and wellness sector, the team at BayMedica has
substantial expertise in the commercial manufacturing scale-up to produce rare cannabinoids at large scale as well as extensive sales
and marketing expertise. This know-how is important to establishing an early-mover status and to maintain cost leadership with regards
to specific rare cannabinoids.

Diverse
portfolio of patent applications covering a spectrum of commercial opportunities.

Success
in pharmaceutical markets often rests with the strength of intellectual property, including patents, to protect our commercialization
interests. We have filed several patents on our novel findings and expect to continue to do so. The acquisition of BayMedica brought
several additional new patent families to bolster our manufacturing as well as drug development opportunities.

Research
and Development Pipeline of Therapeutic Drug Candidates

INM-901
for the Treatment of Alzheimer’s Disease (“AD”)

Traditionally,
Alzheimer’s disease has been defined by the buildup of amyloid beta (“Aβ”) plaques and neurofibrillary, also referred
to as tau protein, tangles within the brain, making it a central focus of neurological research for many years. However, more recently,
other factors such as neuroprotection and synaptic dysfunction are being recognized as contributors to disease progression.

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Our
early research demonstrating the neuroprotective capabilities of CB1 and CB2 agonists in the eye led us to investigate how such molecules
might play a role in protecting other neurons in the human body, potentially, impacting different diseases. To this end, we initiated
research on the neurons that are associated with the brain and how our proprietary CB1 and CB2 agonist drug candidates could affect neurodegenerative
diseases such as Alzheimer’s, Parkinson’s, and Huntington’s. In October 2023, InMed announced it had selected and would
be advancing a lead AD drug candidate, named INM-901, following positive results from several proof-of-concept studies. INM-901 is a
proprietary small molecule drug candidate. which, based on preclinical studies in well-characterized AD study models, may address multiple
pathologies related to AD progression. In these preclinical study models, INM-901 demonstrated neuroprotective effects, statistically
significant reduction in neuroinflammation, the ability to extend the length of neurites signifying enhanced neuronal function, and improvement
in behavior, cognitive function and memory. These early studies show the potential of INM-901 to reverse neuronal damage from AD and
potentially provide disease-modifying effects.

As
a small molecule compound, INM-901 may offer various modes of administration including oral delivery, which could overcome several limitations
associated with currently approved antibody therapies for AD, such as the high drug expenses, complicated and inconvenient drug administration
and its associated compliance and accessibility challenges.

INM-901’s
innate ability to safely cross the blood-brain barrier, promising preclinical studies, multifactorial mechanism of action and small molecule
profile offer a potentially attractive treatment option for AD.

Alzheimer’s
Disease Prevalence and Impact – A Major Medical and Societal Burden

Alzheimer’s
disease is a progressive neurodegenerative condition that predominantly afflicts the elderly, resulting in severe cognitive impairments.
It is a subset of dementia that impacts the part of the brain that controls memory and language and leads to increased morbidity and
mortality.

According
to the U.S. Alzheimer’s Disease Association, AD accounts for 60-80% of dementia cases and is the fifth leading cause of death for
people aged 65 and older. It’s estimated that 6.9 million Americans are living with AD, and it’s expected to grow to 12.7
million by 2050. About 1 in 9 people aged 65 and older has AD (10.7%), affecting 1 in 5 women and 1 in 10 men in their lifetime.

The
disease has a major medical and societal burden with health and long-term care costs valued at $360 billion. In addition to the cost
to the healthcare system, it’s estimated 11 million Americans are providing 18.4 billion hours of unpaid care valued at $350 billion
for people living with AD or other dementias, making it one of the costliest diseases to society.

Additionally,
the emotional and mental health burden on patients and their caregivers cannot be overstated.

Pathology
of Alzheimer’s disease

Alzheimer’s
disease is a complex neurodegenerative disease with multiple pathologies leading to its development and progression. Hallmarks of the
disease point to the toxicity and disruption of proteostasis caused by misfolded amyloid beta protein and neurofibrillary tangles or
tau tangles. Amyloid-beta is a naturally occurring protein in the brain, but when abnormal levels of amyloid-beta clump together to form
plaques, it causes damage to neuronal cell function resulting in AD.

The
focus of Alzheimer’s research has been traditionally centered around amyloid-beta plaques and tau protein, which play a crucial
role in stabilizing microtubules within neurons, supporting their structure and function. Increased activity of enzymes called tau kinase
causes the tau protein to misfold and clump, creating neurofibrillary tangles which disrupt the normal functioning of neurons. The stage
and severity of AD is associated with an abundance of tau tangles.

In
addition to these two aspects of Alzheimer’s disease, neuroinflammation and synaptic dysfunction are also recognized as contributors
to AD progression. Microglia, the brain’s immune cells, are involved in the removal of amyloid-beta and has been a focus of research
in neuroinflammation. Therapies targeting the modulation of microglial activity aim to reduce inflammation and protect neurons.

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Examples
of Current treatments in Neurodegenerative Diseases

Brand

Company

Mechanism
of Action

Status

Aducanumab
(Aduhelm™)

Biogen

Anti-amyloid beta target
both insoluble and soluble aggregates

Approved June 2021, discontinued
November 2024

Lecanemab
(Leqembi ®)

Biogen/ Eisai

Anti-amyloid beta, electively
binds to large, soluble Aβ protofibrils

Approved January 2023

Donanemab
(Kisunla™)

Eli Lilly

Anti-amyloid beta, target
pyroglutamated AB in plaques

Approved July 2024

Gantenerumab

Roche

Anti-amyloid beta, target
aggregated forms of AB including oligomers and plaques

Phase 3 failed November
2022

Remternetug
(LY3372993)

Eli Lilly

Anti-tau, O-GlcNAcase Inhibitor

Phase 3

BIIB080

Biogen

Anti-Tau, antisense oligonucleotide
(ASO)

Phase 2

Semorinemab

Genentech

Anti-tau

Phase 2 Failed

Currently
approved medications for AD generally fall into two main categories. The first category comprises drugs designed to address symptoms
related to memory and cognitive function. While these medications cannot halt the damage that AD inflicts on brain cells, they can help
alleviate or stabilize symptoms for a limited duration by influencing specific chemicals responsible for transmitting messages between
nerve cells in the brain. Essentially, these medications are aimed at preserving neurotransmitters. However, they do not replace the
deteriorating ones and thus do not impede the disease’s progression.

Until
recently, cholinesterase inhibitors and glutamate regulators were the only treatments available to people living with AD. These drugs
are intended to improve cognitive and behavioral symptoms and do not address the prevention or progression of the disease.

In
recent years, there has been a growing emphasis on developing disease-modifying treatments that target the underlying biology of AD.
One major focus of these research and development endeavors has centered on addressing the accumulation of amyloid plaques and the removal
of both these plaques and tau proteins. This approach aligns with the long-standing amyloid hypothesis, which posits that AD is triggered
by the buildup of (Aβ) in the brain. This accumulation leads to neuronal toxicity within the central nervous system, disrupting
neuronal and synaptic function, ultimately culminating in neuronal degeneration and cell death.

Since
2021, three disease-modifying treatments have been approved for the treatment of mild cognitive impairment due to Alzheimer’s disease.
All three treatments primarily address symptoms related to memory and cognitive function via the reduction of beta-amyloid plaques. Aduhelm™,
the first of these drugs to be approved by the FDA has since been discontinued by Biogen. These disease-modifying medications are aimed
at removing amyloid plaque build-up between the neurons in the brain; however, they do not restore or rebuild deteriorating neurons and
thus do not reverse Alzheimer’s disease progression. In addition, these treatments are related to some significant side effects,
including amyloid-related imaging abnormalities (“ARIA”) with edema (brain swelling), requiring brain scans once or twice
a year. The administration of these treatments, which include an intravenous infusion every 2-4 weeks, also presents a challenge.

Role
of CB1 and CB2 Agonists in Alzheimer’s disease:

Numerous
studies have indicated dysregulation of the Endocannabinoid System (“ECS”), which encompasses receptors, endocannabinoids,
and synthesizing/metabolizing enzymes, in various neurodegenerative conditions, notably AD. These investigations have unveiled the potential
of CB1 and CB2 agonists, both endogenous and synthetic, in mitigating the harmful effects of AD pathology. These CB1 and CB2 agonists
have been suggested to diminish Aβ toxicity, reduce tau hyper-phosphorylation, and suppress neuroinflammatory responses while curbing
the production of reactive oxygen species (“ROS”). As a result, they may enhance the survival of neurons in the aftermath
of Aβ aggregation.

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CB1
and CB2 agonists exert their biological effects through two primary membrane receptors, endogenous CB1 and CB2 receptors, which are widely
distributed in the central nervous system and peripheral tissues. Activation of CB1 has demonstrated its ability to alleviate neurotoxicity
in various AD models. Conversely, CB2 agonism and increased expression have been associated with the removal of Aβ by macrophages.

The
precise molecular mechanisms responsible for safeguarding specific neuronal populations remain elusive. However, several observations
support this concept:

a)
CB1 and CB2 agonists possess a capacity to exert broad effects on multiple molecular targets, including critical brain structures and
behavior;

b)
CB1 and CB2 agonists act not only through ECS receptors but also interact with other non-ECS receptors such as transient receptor potential
vanilloid 1, peroxisome proliferator-activated receptors (“PPARs”), and transcription factors such as nuclear factor kappa-light-chain-enhancer
of activated B cells (“NFkB”); and

c)
CB1 and CB2 agonists exhibit anti-inflammatory properties, modulate neurotransmitter release, and limit oxidative stress, collectively
contributing to the enhancement of neuronal viability.

AD
is a progressive neurodegenerative condition primarily driven by the toxicity and disruption of proteostasis caused by misfolded Aβ
protein. CB1 and CB2 agonists have emerged as promising agents capable of preserving neuronal integrity and functionality, offering a
potential strategy to slow down disease progression and enhance the quality of life for affected individuals. Furthermore, CB1 and CB2
agonists exhibit the capacity to mitigate neuroinflammation, shield against beta-amyloid-induced neurotoxicity, and mitigate neurodegeneration
in animal models of AD. Additionally, research has unveiled dysregulation of the ECS in the brains of AD patients, which could contribute
to the cognitive and behavioral symptoms associated with the disease.

INM-901
is highly lipophilic (dissolves in fats, oils and lipids) and can easily cross the blood-brain barrier, a capability that renders it
a promising candidate for pharmaceutical use in the treatment of neurological disorders.

The
use of CB1 and CB2 agonists in AD treatment holds great promise; however, further research is needed to fully understand the mechanisms
to develop safe and effective CB1 and CB2 agonists-based therapeutics.

INM-901:
A Multi-factorial Approach to Treating Alzheimer’s disease

While
progress has been made recently in the development of new treatments for AD, there are no treatments addressing the multiple aspects
of this complex disease such as neuroinflammation, neuroprotection, synaptic dysfunction or the restoration of the damaged neurons –
factors that may help to restore brain function loss or reverse the damage caused by AD.

Preclinical
studies indicate that INM-901 may target multiple biological pathways. InMed has conducted several in vitro and in vivo
studies to test the pharmacological effects of INM-901 in well-characterized AD preclinical models.

Figure
1. Multiple Mechanisms of Action

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Figure
2. Neuroprotection of human neuronal cells

Phyto-cannabinoids
(“pCBx”) promote neuroprotection. (A) Amyloid peptide (Aβ, 5µM) induces cytotoxicity in SHSY5Y
cells. Aβ1-42 insult induced approximately ~45% cytotoxicity of the SH-SY5Y cells. (B) Concurrent exposure of Aβ
with pCBx at 5 µM and 10 µM concentrations protected cells from Aβ induced toxicity in a dose-dependent manner. Cell
viability was determined by MTT assay.

Figure
3. Neurogenesis of human neuronal cells

Cannabinoid
pCBx promotes neuritogenesis. Tuj1 Tubulins are building blocks of microtubules. As such, Tuj1 expression can reveal the fine
details of axonal structures and dendrites. Therefore, changes in Tuj1 expression can be directly correlated with neuronal health and
communication. (A) Photomicrographs illustrating Tuj1 expression in control and pCBx (5 and 10µM) treated cells. The formation
of extended neurites and arborization is evident upon pCBx treatment.

INM-901
demonstrates anti-inflammatory effects

Neuroinflammation
plays a key role in the progression of Alzheimer’s disease and is a hallmark of neurodegenerative disorders. INM-901 has demonstrated
the ability to reduce neuroinflammation in both in vivo and ex vivo models, reinforcing its potential as a disease-modifying
therapeutic candidate.

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In
a long-term (seven-month dosing) in vivo study, INM-901 demonstrated statistically significant, dose-dependent reductions in several
pro-inflammatory cytokines in plasma, including tumor necrosis factor alpha (“TNF-α”), interleukin-1 beta (“IL-1β”),
and interferon gamma (“IFN-γ”). In addition, INM-901-treated groups showed reduced plasma levels of neurofilament light
chain (“NfL”), a biomarker associated with neurodegeneration. mRNA analysis from brain tissue revealed reduced expression
of glial fibrillary acidic protein (“GFAP”), CD-33, and Toll-like receptor 2 (“TLR-2”), all of which are associated
with neuroinflammatory responses in Alzheimer’s disease.

Further
supporting these findings, an ex vivo study using lipopolysaccaride (“LPS”)-induced inflammation in animal brain tissue
demonstrated that INM-901 significantly reduced the expression of NLRP3, a key inflammasome marker, as well as the cytokines IL-6, IL-1β,
IL-2 and KC/GRO. These anti-inflammatory effects were observed in a dose-dependent manner and were statistically significant. The data
support INM-901’s direct anti-inflammatory activity independent of amyloid-beta or tau-related pathology.

INM-901
shows behavioral improvements in in vivo models

INM-901
treatment in the well-established 5xFAD AD mouse model led to improvement in cognitive function and memory, locomotor activity, anxiety-based
behavior, and sound awareness. InMed’s most recent study evaluated INM-901 using a longer treatment duration and subjects with
more advanced disease to validate and expand upon previous findings, which have demonstrated improvements in cognitive function, anxiety-related
behavior, and sensory responsiveness.

Summary
of INM-901 Iong-term 5xFAD study:

● Hippocampal
RNA Expression - Several genes associated with inflammation, the endocannabinoid system,
synaptic dysfunction and oxidative stress and apoptosis (cell death) were evaluated following
treatment. In some cases, INM-901 demonstrated a dose-dependent trend towards a return to
non-diseased baseline following treatment.

● Anti-inflammation
– Treatment with INM-901 resulted in a significant reduction in the inflammatory biomarkers
IFN-γ, TNF-α, IL-1β, KC-GRO, IL-2 and NfL, suggesting a dose-dependent therapeutic
effect in neuroinflammation.

● Immunohistochemistry
- Amyloid-beta immunoreactivity is reduced following INM-901 treatment in a dose-dependent
manner. The microtubule-associated protein 2 (“MAP2”) is a protein found in the
neurons, especially in the dendrites and is involved in neurite outgrowth and signal transduction
of the neurons, is partially restored with INM-901 treatment.

● Behavior
– Cognitive function, anxiety-related behavior, and sensory responsiveness were restored
or approaching normal following INM-901 treatment in diseased animals.

INM-901
Interacts with Specific Receptors in the Brain

Studies
of INM-901 demonstrate activity as a preferential signaling ligand for CB1 and CB2 and impacts the peroxisome proliferator-activated
receptors (“PPAR”) signaling pathway. Research indicates that activating CB1 and CB2 receptors may induce neuroprotective
effects and may help to protect brain cells from damage and death. Enhancing the activity of these receptors may help to slow down the
progression of the AD, in which neuronal cell death is a hallmark. Moreover, the activation of these receptors, along with other cellular
receptors, has also been shown to have an impact on neuroinflammation. As neuroinflammation is believed to contribute to the progression
of AD, targeting these receptors could help alleviate this inflammatory response.

INM-901
is a Proprietary Small Molecule Compound

INM-901
is a small molecule compound, one of several cannabinoid analogs developed by our scientists. Cannabinoids are small molecules known
to be highly lipophilic and can safely cross the blood-brain barrier, enabling the potential therapeutic modulation of brain signaling
and making them promising pharmaceutical targets for neurological diseases such as AD.

Small
molecule drugs have several advantages that contribute to their widespread use. Those advantages include oral administration (making
it convenient for patients to comply), good bioavailability (allowing these compounds to be efficiently absorbed), ability to cross the
blood-brain barrier (enabling therapeutic modulation in brain signaling), stability in storage and transport (ease of drug handling and
dose adjustment) and low-cost manufacturing.

Key
Outcomes from INM-901 Studies

In
Vitro Studies

● Treated
groups display neuroprotection and extended neurite length, a potential marker for improved
neuronal function. Neurites promote cell-to-cell communication, essential for brain signaling

● Treated
groups demonstrated dose- dependent cell survival and proliferation

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In
Vivo Studies

● Showed
a reduction in neurofilament light chain, marker of cellular damage

● Demonstrated
statistically significant, dose-dependent reductions in several pro-inflammatory cytokines
in plasma

● Showed
improvement in cognitive function and memory, locomotor activity, anxiety-based behavior,
and sound awareness

Ex
Vivo Studies

● Demonstrated
reduced levels of NLRP3 and IL-1β, two inflammasome markers increasingly implicated
in the pathogenesis of Alzheimer’s disease and other neuroinflammatory diseases.

● Treatment
resulted in a dose-dependent and statistically significant reduction in several key pro-inflammatory
markers, including IL-6, IL-1β, KC/Gro, and IL-2.

● Reduced
key pro-inflammatory markers, independent of amyloid-beta or tau pathology, signifying potential
to treat other dementia-related diseases.

INM-901
Next Steps

Research
& Development

●
Additional proof-of-concept
(“PoC”) studies are planned to further elucidate the various effects of INM-901 in AD disease

●
On-going Chemistry, Manufacturing
and Controls (“CMC”) activities for drug substance and oral drug product

●
On-going studies of receptor
interactions (mechanism of action (“MoA”)) and Distribution/Metabolism/Pharmacokinetics (“DMPK”)

●
Dose Ranging and other non-GLP studies, with GLP studies
to follow

● Seeking
business development partnerships

Key
Milestones

●
November 3, 2021 —
we announced the filing of an international patent application demonstrating neuroprotection and enhanced neuronal function using
a rare cannabinoid for the potential treatment of neurodegenerative diseases such as Alzheimer’s Disease, Parkinson’s
Disease, Huntington’s Disease and others. This Patent Cooperation Treaty (PCT) application, entitled “Compositions and
Methods for Treating Neuronal Disorders with Cannabinoids”, specifies a rare cannabinoid that may inhibit or slow the progression
of neurodegenerative diseases by providing neuroprotection in a population of affected neurons. Furthermore, the PCT application
also demonstrates the subject cannabinoid compound can also be used to promote neurite outgrowth, signifying the potential to enhance
neuronal function. The rare cannabinoid included in the PCT application is new to InMed’s portfolio.

●
November 16, 2022 —
we announced announces the launch of its neurodegenerative disease program (INM-900 series), investigating the effects of cannabinoid
analogs in diseases such as Alzheimer’s, Huntington’s and Parkinson’s. In addition, Dr. Ujendra Kumar of the Faculty
of Pharmaceuticals Sciences at UBC has been awarded an Alliance grant from NSERC, with InMed as the named industry partner. The funding
will support the research and development studies of InMed’s cannabinoid pharmaceutical candidates, investigating their potential
therapeutic effects in neurodegenerative diseases. The collaboration project is entitled “Pharmacological Characterization
of Phytocannabinoids and the Endocannabinoid System”.

●
June 1, 2023 — we
announced that results from a neurodegenerative disease study was presented in a scientific poster at the Canadian Neuroscience Meeting
in Montreal from May 28-31, 2023. The InMed sponsored research, entitled “Cannabinoids modulate cytotoxicity and neuritogenesis
in Amyloid-beta-treated neuronal cells”, demonstrated the ability of a specific rare cannabinoid (“pCBx”) in
our INM-900 series of potential candidates that reduces amyloid toxicity and tau protein expression while enhancing neuronal cell
growth and neuritogenesis markers in vitro, all considered to be important targets in the potential treatment of neurodegenerative
diseases such as Alzheimer’s.

●
October 2, 2023 —
we announced the selection of a lead Alzheimer’s disease drug candidate, named INM-901, following positive results from several
proof-of-concept studies in a validated Alzheimer’s disease treatment model. InMed will be advancing INM-901, a cannabinoid
analog, in its pharmaceutical drug development program. In vitro Alzheimer’s disease studies showed that INM-901 treated
groups display neuroprotection and extended neurite length, a potential marker for improved neuronal function. INM-901 treated groups
in an in vivo Alzheimer’s disease model demonstrated improved behavioral, cognitive and memory outcomes in several Alzheimer’s
proof-of-concept studies.

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●
April 4, 2024 — we
announced additional preclinical data demonstrating INM-901’s positive pharmacological effects in the potential treatment of
Alzheimer’s Disease (“AD”). Additionally, the studies demonstrated INM-901 is a preferential signaling agonist
of the CB1and CB2 receptors and impacts the PPAR signaling pathway, reduced neuroinflammation and improved neuronal function, and
that mRNA data supports the observations made in the previously released behavior studies in locomotor activity, cognition and memory.

●
April 18, 2024 —
we announced the addition of Dr. David G. Morgan, a renowned leader in neurodegenerative disease to its Scientific Advisory Board
(“SAB”) reinforcing our commitment to advancing it’s INM-901 program in the treatment of Alzheimer’s disease.

● July
2024- we announced positive results from initial data sets from a long-term (7 months of
dosing) in vivo preclinical Alzheimer’s Disease (“AD”) study of INM-901
which confirms previously reported findings from a short-term (3 months of dosing) pilot
study. This long-term dosing study was conducted using the 5xFAD amyloidosis model with extended
dosing duration and increased sample size as compared to the short-term study. All assessments
of the INM-901-treated AD groups showed a positive trend towards behavior similar to the
untreated disease-free group, with most assessments demonstrating a clear dose response.
Furthermore, INM-901-treated AD groups achieved a statistically significant improvement in
certain behavior criteria in comparison to the placebo-treated AD groups.

● August
2024 - we confirmed INM-901 as an oral formulation that will be utilized in its development
programs for Alzheimer’s disease. Preclinical studies have demonstrated that INM-901,
a proprietary small molecule drug candidate, can be administered orally and achieve therapeutic
levels in the brain comparable to those obtained through intraperitoneal (“IP”)
injection, which is a common route of administration for preclinical investigation of neurodegenerative
diseases.

● October
2024 – We announced the appointment of Dr. Barry Greenberg to its Scientific Advisory
Board. Dr. Greenberg is the Director of the Alzheimer’s Disease Translational Center
and an Associate Professor in the Department of Neurology at the Johns Hopkins University
School of Medicine.

● October
2024 – we filed an additional international patent application, under the Patent Cooperation
Treaty (PCT), focused on the pharmaceutical composition and method of use for the proprietary
small molecule drug candidate INM-901 for treating neurodegenerative diseases, including
Alzheimer’s disease.

● January
2025 – we announced positive results from a long-term in vivo preclinical Alzheimer’s
Disease (‘AD’) study. In the study, INM-901 demonstrated a reduction in several
plasma and brain markers of neuroinflammation, a recognized contributor to Alzheimer’s
disease development and progression.

● June
2025 – we announced new preclinical data demonstrating that INM-901 significantly reduces
inflammation in ex vivo models of neuroinflammation, further supporting its potential
as a therapeutic candidate in Alzheimer’s disease. The study evaluated INM-901 in an
ex vivo model of lipopolysaccharide (LPS)-induced inflammation in animal brain tissue,
which is designed to induce a strong expression of pro-inflammatory cytokines IL-6, IL-1β,
IL-2, and KC/Gro and inflammasome marker NLRP3. Results demonstrated that INM-901 treatment
can reduce pro-inflammatory cytokines and may have a direct impact on neuroinflammation independent
of the influence of amyloid beta or tau aggregation. This study model offers insight into
INM-901’s potential therapeutic impact on brain inflammation that may underlie a broad
range of neurodegenerative diseases, including Alzheimer’s disease.

● July
2025 – we presented new preclinical data from its INM-901 program at the Alzheimer’s
Association International Conference (AAIC) 2025, the world’s leading forum for Alzheimer’s
disease (“AD”) and dementia research. Data was presented in a scientific poster
entitled, “Therapeutic Potential of INM-901 in Mitigating Alzheimer’s Disease
Pathology: Insights from a Long-term 5xFAD Mouse Model Study”. The Alzheimer’s
disease preclinical study measured hippocampal RNA expression, inflammatory markers, immunohistochemistry
and behavioral differences following long-term treatment with INM-901 and as compared to
healthy and to untreated diseased subjects in a well-established model.

INM-089
for the Treatment of Age-related Macular Degeneration (“AMD”)

Introduction

While
conducting the preclinical studies of a previous drug candidate, INM-088 in glaucoma, which involved comparing various naturally occurring
compounds including InMed’s proprietary small molecule candidates, it was discovered that one of InMed’s candidates was demonstrating
interesting pharmacological effects in the back of the eye. Further preclinical studies of this compound using AMD study models demonstrated
significant functional and pathological improvements. InMed has selected drug candidate INM-089, a proprietary small molecule analog
of INM-088, for further preclinical development in the potential treatment of dry AMD.

AMD
is a progressive eye disease that causes damage to the macula which affects a person’s central vision. AMD is common amongst the
elderly and is a leading cause of vision loss. Dry AMD is the most common form of AMD, accounting for 80% of AMD cases according to the
American Academy of Ophthalmology.

Until
recently, there were no approved pharmaceutical treatments for people with dry age-related macular degeneration. In 2023, the FDA approved
two new treatments which are complement inhibitors for advanced stages of dry AMD (called geographic atrophy (“GA”)).

In
vitro and in vivo studies of INM-089 have demonstrated neuroprotection of photoreceptors, improvement of the integrity of
the retinal pigment epithelium, a reduction in extracellular autofluorescent deposits (a hallmark of AMD), preservation of the retinal
function in the back of the eye and improvement in the thickness of the outer nuclear layer of the retina.

As
a small molecule, INM-089 is likely deliverable via various modes of administration, such as a topical eye drop or intravitreal injection
(“IVT”) formulations.

13

Pathology
of Age-related Macular Degeneration

AMD
is a progressive eye disease that causes damage to the macula which is part of the retina at the back of the eye. The macula controls
the sharp vision straight ahead of you, and damage to the macular affects a person’s central vision.

There
are two principal forms of AMD, atrophic (non-exudative) dry AMD and neovascular (exudative) wet AMD. Wet AMD constitutes about 10%-20%
of all cases of AMD and occurs when an abnormal blood vessel grows in or under the retina leading to central vision loss. Dry AMD is
the most common form affecting nearly 80%-90% of all patients with AMD. It is associated with the gradual loss of the outer nuclear layer
(“ONL”) photoreceptors and the retinal pigment epithelium (“RPE”) thinning, formation of drusen deposits, and
loss of the vessels in the retinal choriocapillaris. Advanced stage of dry AMD is characterized by GA at the center of the macula extending
through the outer neuroretina, RPE and choroid. GA is characterized by the atrophy of RPE, photoreceptors, choriocapillaris, and ONL.
The loss of functional RPE and photoreceptors in GA is not endogenously replaced and can result in complete sight loss.

AMD
is a leading cause of vision loss in adults

According
to the World Health Organization, 196 million people worldwide live with age-related macular degeneration. An estimated 19.8M Americans
aged 40+, about 12.6% of the population, suffer from AMD. While AMD does not cause complete vision loss, it affects central vision and
impairs one’s ability to perform daily tasks such as cooking, reading and driving.

As
the name suggests, aging is a strong risk factor for developing AMD. Adults aged 50 or older, smoke, have a diet of high saturated fat,
have cardiovascular disease or have a family history of AMD are more at risk of developing AMD. People of European ancestry are more
likely to develop AMD than Blacks, Hispanics or Asians. In addition, people with blue eyes have higher incidence rates of AMD than someone
with brown eyes.

Early
detection is key to slowing the progression of AMD. A sign of whether you might have AMD is when straight lines look wavy.

A
Major Unmet Medical Need for New AMD Treatments

Until
recently, there were no approved pharmaceutical treatments for people with dry age-related macular degeneration, which accounts for about
80%-90% of AMD cases.

In
2023, the FDA approved two new treatments which are complement inhibitors for advanced stages of dry AMD (or geographic atrophy). These
complement inhibitors are injected directly into the eye every one to two months.

Syforvre®
(pegcetacoplan), developed by Apellis Pharmaceuticals, was approved by the FDA in February of 2023 for the treatment of geography atrophy,
the late stage of dry AMD. Syforvre®, a C3 complement inhibitor, is injected into each eye every 25-60 days and reduces
the rate of lesion growth in the eye.

In
August 2023, the FDA approved Iveric’s Izervay® (avacincaptad pegol), a complement C5 inhibitor, which aims to reduce
an immune response that damages retinal cells. Similar to Syforvre®, the drug is approved for geographic atrophy and is
administered via intravitreal injection every month. According to the Alzheimer’s Association, these new complement inhibitor drugs
slow the development of GA by about 14%-20%, but do not improve eyesight, nor restore lost vision. Side effects of these new treatments
include inflammation, bleeding beneath the clear lining of the eye, blurred vision and fluid pressure, and some patients develop wet
AMD.

In
addition to the new complement inhibitors, there are surgical implants and ongoing clinical drug trials. An ophthalmologist may recommend
specific vitamins to slow the progression of AMD in its intermediate stage.

The
approval of complement inhibitors offers hope to people living with dry AMD, however, the modest effect, inconvenient drug delivery and
the increased risk of developing wet AMD may outweigh the benefit for some patients and their physicians. There remains a large unmet
medical need for more effective and convenient treatments for the large patient population affected by dry AMD.

Treatments
approved or in late-stage development for Geographic Atrophy (advanced dry AMD)

Brand

Company

Mechanism
of Action

Status

Syforvre®

Apellis Pharmaceuticals

Complement C3 inhibitor

Approved February 2023

Izervay®

Iveric

Complement C5 inhibitor

Approved August 2023

Tinlarebant

Belite Bio

Targets retinol binding
protein 4 (RBP4)

Phase 3

ANX007

Annexon Biosciences

Anti-C1q antibody

Initiating Phase 3

JNJ-1887/HMR59

Hemmera/ Janssen

Increase expression of
soluble form of CD59

Phase 2

IONIS-FB-LRx / RG6299

Ionis /Roche

Anti-sense complement factor
B inhibitor

Phase 2

Danicopan (ALXN2040)

Alexion

Complement Factor D inhibitor

Phase 2

14

Role
of CB1 and CB2 agonists in ocular disease

Mounting
scientific e is pointing to the neuroprotective effects of CB1 and CB2 agonists, supporting their therapeutic potential in ocular diseases
such as AMD and glaucoma, in which neuroprotection is key to preserving the nerve cells in the eyes and potentially slowing or reversing
eye damage. Several preclinical studies conducted by InMed in three of its drug development programs have consistently shown the neuroprotective
effects of naturally occurring CB1 and CB2 agonists and their analogs in well-recognized study models.

In
was during this research of INM-088 when InMed scientists observed the ability of a novel CB1 and CB2 agonist, now called INM-089, to
proactively protect the nerve cells in the back of the eye. As a result of this discovery, InMed launched the INM-089 drug development
program for the potential treatment of AMD.

INM-089:
Small molecule compound acting as a selective dual CB1 / CB2 agonist

CB1
and CB2 receptors are both part of the endocannabinoid system and are found throughout the body and are responsible for many homeostatic
functions. CB1 receptors are primarily located in the brain and central nervous system, while CB2 receptors are involved in modulating
neuroinflammation and immune responses. Activation of CB1 and CB2 receptors has been shown to have neuroprotective effects and protect
cells from damage and death.

INM-089
is a small molecule compound, one of several proprietary CB1and CB2 agonists discovered and developed by our team of scientists.

INM-089
in vitro and in vivo studies to date

Preclinical
studies of INM-089 demonstrate significant functional and pathological improvements in an AMD disease study model. Results from several
in vitro and in vivo studies demonstrate INM-089’s pharmacological effects in the potential treatment of dry AMD:

●
INM-089 provides neuroprotection
of retinal cells;

●
INM-089 improves the integrity
of the retinal pigment epithelium (“RPE”);

●
INM-089 reduces extracellular
autofluorescent (“AF”) deposits, including drusen, a hallmark of dry AMD;

●
INM-089 preserves photoreceptor
function and retinal cells in the back of the eye; and

●
INM-089 improves thickness
of outer nuclear layer (“ONL”) of the retina where photoreceptors are located.

Based
on widely accepted ocular research, the thickness of the outer nuclear layer is strongly correlated with photoreceptor preservation and
visual acuity.

15

INM-089
Study: Neuroprotective effects

INM-089
demonstrates neuroprotective effects in pressure-induced toxicity in vitro model in retinal ganglion cells in a dose-dependent
manner.

INM-089
Study: Photoreceptor Function Preservation

In
a light-induced toxicity in vivo AMD model, a single intravitreal injection was performed at the back of the eye to deliver either
INM-089, INM-088 or vehicle control. INM-089 outperforms INM-088 (‘CBN’ in the graph below) and vehicle control in preserving
photo-receptor function.

16

INM-089
Study: Autofluorescent Extracellular Deposit Level

In
a light-induced toxicity in vivo AMD model, a single intravitreal injection was performed at the back of the eye to deliver either
INM-089 or vehicle control. INM-089 reduced build-up of autofluorescent extracellular deposits, which causes damage to the macular. The
build-up of autofluorescent deposits such as drusen is a hallmark of dry AMD.

Selection
of intravitreal (‘IVT’) formulation for INM-089

InMed
selected an intravitreal (“IVT”) formulation for INM-089 as a drug candidate to be utilized in our ongoing development
program. InMed’s proprietary IVT formulation, combined with the INM-089 active pharmaceutical ingredient (“API”), has
been successfully delivered to the targeted area of the eye in preclinical studies in doses of up to 10 times the calculated safety margin
relative to the therapeutic dose level. This INM-089 IVT formulation will be used in the next stages of preclinical studies, including
GLP-enabling studies and subsequent stages of clinical development. Additionally, InMed completed a series of dose-ranging in vivo studies.
The information from the dose-ranging study will guide us in selecting the appropriate doses for the pivotal preclinical toxicology studies.

Intravitreal
injection has been the established method for the effective delivery of drugs to the back of the eye and remains the standard of care
among retinal specialists. Topical formulations, such as eye drops, face significant challenges in delivering highly lipophilic drugs
to this target tissue because the complex anatomy and protective barriers of the eye hinder effective drug permeation.

INM-089
Next Steps

Research
& Development

●
CMC activities for drug
substance and drug product scale up and supply

●
On-going studies of receptor
interactions (MoA) and DMPK

●
GLP studies to follow

17

INM-755
for the Treatment of Epidermolysis Bullosa (‘EB’)

Introduction

INM-755
(cannabinol, or ‘CBN’) cream is a proprietary, topical product candidate intended as a therapy in dermatological diseases.
The first clinical indication under development is treatment of symptoms related to EB. EB is a collective name for a group of genetic
disorders of connective tissues characterized by skin fragility leading to extensive blistering and wounding. It affects skin and mucous
membranes, particularly of the gastrointestinal tract, genitourinary and respiratory systems. EB is a debilitating disease affecting
a small proportion of people in the United States, thus earning it an orphan-disease status. The disease has no definitive cure, and
all current treatments are directed towards symptom relief. There are, however, a number of products, mainly gene therapies, currently
in clinical trials, in which a cure is being explored, according to several recent scientific publications. Our preclinical research
has identified a specific Product Candidate, CBN, that may prove beneficial to patients: first, by addressing certain key disease hallmarks
(which may include wound healing, infection, pain, inflammation, and itch); and second, by regulating the expression of various proteins
(keratins) that may compensate for reduced expression of others.

The
active ingredient in INM-755, CBN, is an agonist for both CB 1 and CB2 receptors, with a higher affinity for CB2, which means it should
have a greater effect on the immune system than on the central nervous system. The distribution of CB1 and CB2 receptors in sensory nerves
and inflammatory cells in the skin makes it an attractive pharmaceutical agent for dermal treatments in medical conditions characterized
by inflammation and pain.

Summary
of Completed Clinical Trials

Phase
1 Clinical Trials (Studies 755-101-HV and 755-102-HV)

A
regulatory application to support our first Phase 1 clinical trial in healthy volunteers with INM-755 (755-101-HV) was submitted November
4, 2019 and approved December 6, 2019 in the Netherlands. The initial Phase 1 clinical trial evaluated the safety, tolerability, and
pharmacokinetics of INM-755 cream in 22 healthy volunteers with normal, intact skin; the volunteers had cream applied once daily for
a period of 14 days. All subjects in this first clinical trial completed treatment and evaluations by March 27, 2020. Database completion
and data analyses were delayed by pandemic restrictions. Study results were reported November 25, 2020. A blinded interim safety review
from the first 16 subjects in this Phase 1 clinical trial were included in a regulatory application that was approved April 17, 2020,
for a second Phase 1 clinical trial of 8 healthy volunteers to test the local safety and tolerability of applying sterile INM-755 cream
to small wounds once daily for 14 days. As with the initial Phase 1 trial, the second clinical trial (755-102-HV) was conducted with
two different drug concentrations and a vehicle control. Enrollment began in early July 2020 and the clinical trial completed treatment
and evaluations at the end of September 2020. Study results were reported January 8, 2021.

Phase
2 Clinical Trial (Study 755-201-EB)

Regulatory
applications to support this global trial were filed for review by the National Competent Authorities and Ethics Committees in 8 countries
for 13 clinical sites. Approvals were obtained in all countries (Austria, France, Germany, Greece, Israel, Italy, Serbia, and Spain)
as of March 2022. Enrollment and patient treatment began in December 2021 and completed in April 2023.

18

The
goal of the Phase 2 study was to obtain safety and preliminary efficacy of INM-755 cream in treating symptoms and wound healing in patients
with EB, using a within-patient design in which matched index areas were randomized to INM-755 cream or vehicle (no drug) cream in a
blinded manner. A target of up to 20 patients were to be enrolled with treatment for 28 days, the longest period supported by nonclinical
toxicology studies.

No
single primary endpoint was set for the trial to allow for possible variations in presenting symptoms in each patient. These include
the presence of open wounds, wound pain associated with dressing changes, background wound pain, wound itch, and itch in non-wound areas.
To this end, InMed’s goal was to harvest data from the trial to evaluate the ability of INM-755 to treat chronic non-wound itch
and to heal wounds and treat associated pain and itch.

The
Phase 2 Trial enrolled a total of 19 patients. Data from one patient were excluded from efficacy analyses due to a significant protocol
deviation. Of the 18 remaining patients whose data were considered reliable for clinical review, 17 were treated for chronic non-wound
itch and one patient was treated for wound-related itch. The remaining endpoints (pain, wound healing) could not be analyzed due to too
few enrollees with such symptoms.

Of
the 18 participants assessed, chronic itch improved by a clinically meaningful amount in 12 patients (66.7%), of whom:

●
6 patients (33.3%) had
the same level of itch improvement with INM-755 cream as with control cream;

●
5 patients (27.8%) treated
with INM-755 showed meaningful anti-itch activity beyond that of the control cream; and

●
1 patient (5.6%) showed
better itch reduction with the control cream.

In
summary, results from the Phase 2 clinical trial showed a positive indication of enhanced anti-itch activity for INM-755 cream versus
the control cream alone in an exploratory clinical evaluation. The results for non-wound itch were not statistically significant in this
small trial due, in part, to the clinically important anti-itch effect of the underlying control cream. We are, nevertheless, encouraged
by and satisfied with the INM-755 clinical data for non-wound itch treatment. That the majority of the assessed patients in the trial
showed clinically meaningful improvement in non-wound itch from the application of INM-755, be it with similar outcomes to the control
cream or better than the control cream, can be considered impressive.

Based
on the safety and efficacy data for treating non-wound itch in this EB study, as well as previous safety data from Phase 1 trials, we
are now seeking R&D and commercial partnership opportunities for any continued development of INM-755 cream. Continued development
of INM-755 cream will likely move beyond EB into broader indications involving chronic itch, with potentially much larger target populations
and commercial opportunities than offered solely by the EB indication.

Key
Milestones for the EB Program:

●
April 30, 2020 —
we announced clinical trial application approval in the Netherlands for Study 755-102-HV, a randomized, double-blind, vehicle-controlled
Phase 1 study designed to evaluate the safety and tolerability of INM-755 (two strengths) applied daily for 14 days on epidermal
wounds in 8 healthy volunteers.

●
November 25, 2020 —
we announced the top-line results of Study 755-101-HV (“Study 101”). Study 101 was a randomized, vehicle-controlled,
double-blind, Phase 1 trial, which examined the safety and tolerability of two strengths of INM-755 cream on intact skin in 22 healthy
adult volunteers over a 14-day treatment period. The Study 101 results indicate that INM-755 was safe and well-tolerated on intact
skin, caused no systemic or serious adverse effects. In addition, there were no subject withdrawals due to adverse events. Drug concentrations
in the blood were very low, as expected.

19

●
January 8, 2021 —
we announced the top-line results of Study 755-102-HV (“Study 102”). Study 102 was a randomized, double-blind, vehicle
controlled, single-center study, in 8 healthy adult volunteers to test the tolerability of 14 days of application of the INM-755
cream on epidermal wounds under treatment procedures designed to simulate wound care for Epidermolysis Bullosa (“EB”)
patients with open wounds. Results of Study 102 indicate that INM-755 cream was safe and well-tolerated on induced open epidermal
wounds, caused no systemic or serious adverse effects. In addition, there were no subject withdrawals due to adverse events. These
data from Study 101 and Study 102 support moving forward into clinical trials in patients with EB.

●
April 28, 2021 —
we announced that we filed Clinical Trial Applications (“CTAs”) in Austria, Israel and Serbia as part of a Phase 2 clinical
trial of INM-755 (cannabinol) cream in EB. Additional CTAs for 755-201-EB (the ‘201 study) will be submitted to National Competent
Authorities (“NCAs”) and Ethics Committees (“ECs”) in France, Germany, Greece, and Italy in the coming weeks.

●
September 30, 2021 —
we announced commencement of a Phase 2 clinical trial, the 755-201-EB study, of INM-755 (cannabinol) cream in the treatment of EB,
marking the first time cannabinol has advanced to a Phase 2 clinical trial to be studied as a therapeutic option to treat a disease.
The 755-201-EB study is designed to enroll up to 20 patients. InMed will evaluate the safety of INM-755 (cannabinol) cream and its
preliminary efficacy in treating symptoms and wound healing over a 28-day treatment period. All four subtypes of inherited EB; EB
Simplex, Dystrophic EB, Junctional EB, and Kindler Syndrome are eligible for this study.

●
July 25, 2022 — we
announced, based on the safety data of the first five adult patients who completed treatment with INM-755 CBN cream for the treatment
of symptoms in the Phase 2 clinical trial, an independent Data Monitoring Committee agreed it was safe to allow the enrollment of
adolescent patients, defined as persons aged twelve to seventeen.

●
March 28, 2023 —
we announced we had concluded enrollment of our Phase 2 clinical trial using investigational drug INM-755 cannabinol (“CBN”)
cream for the treatment of patients with EB. The Phase 2 study enrolled 19 of its targeted 20 patients.

●
June 22, 2023 — we
announced safety and efficacy results from the Phase 2 clinical trial (755-201-EB) for the treatment of symptoms in patients with
EB.

Next
Steps

We
believe INM-755 has potential for further advancement in the treatment of chronic itch and related conditions. However, progression of
the program will only occur in partnership with a suitable collaborator. To date, we have not been successful in our partnering efforts,
as we have deprioritized this initiative to focus resources on other corporate and business development opportunities.

Rare
Cannabinoid Products in the Health and Wellness Sector

BayMedica
has a revenue-generating commercial business unit that leverages our significant expertise in synthetic biology and chemistry to develop
efficient, scalable, and proprietary manufacturing approaches to produce high quality, regulatory-compliant, non-intoxicating rare cannabinoids
(“Products”) for consumer applications. BayMedica is currently commercializing Products as a B2B supplier to distributors
and manufacturers in the health and wellness sector, including nutraceuticals, cosmetics, functional foods and beverages, as well as
animal health markets. BayMedica currently has a robust portfolio of non-intoxicating Products including: cannabichromene (“CBC”),
cannabidivarin (“CBDV”) tetrahydrocannabivarin (“THCV”) and cannabicitran (“CBT”).

20

Following
the acquisition of BayMedica in 2021, a key priority in 2022 was accelerating commercial activities and building out a robust product
portfolio as a supplier of Products to the health and wellness sector. While there was slower than expected revenue growth in 2022, we
have seen increased demand through 2023 and the first half of 2024 due to better research of rare cannabinoids, companies and brands
looking for product innovation and effects-based outcomes, and the ability of companies like ours to reliably supply high quality and
consistent Products. During the financial year ended June 30, 2025, BayMedica achieved sales of approximately $4.9 million.

BayMedica
will continue to evaluate opportunities for potential structured supply arrangements and collaborations for the commercial business.
Sales and marketing efforts will remain focused on Products that contribute highest margins where BayMedica continues to hold a strong
competitive position.

Chemical
Synthesis-Derived Cannabinoids Commercialized by BayMedica

Cannabichromene
(CBC)

The
high cost of goods for rare / minor cannabinoids (e.g. CBC) extracted and purified from the plant made adoption of these more difficult
due to the cost of manufacture and cost to include in the final marketed product(s). Chemical synthesis has provided a consistent, scalable
approach to produce CBC and other minor cannabinoids at a highly competitive cost of goods with consistent batch to batch variability
and high purity of the cannabinoid. BayMedica has successfully manufactured and commercialized the rare cannabinoid CBC, for sale to
distributors into the health and wellness industry. The development of a scalable process for the manufacturing of CBC began in 2018
using well established chemical synthesis protocols.

In
2019, a Material Services Agreement was completed with a multinational contract research, development and manufacturing organization
(“Chemistry CDMO”) to facilitate the optimization and scale-up of BayMedica’s proprietary CBC manufacturing process
using commercially available starting materials sourced from various manufacturers. We scaled to a batch size of greater than 1kg by
calendar 2019 at which time we contracted a leading U.S. manufacturer to provide the final purification of CBC to greater than 95% purity.
This manufacturer also operates a North American based toll-processing facility with the capability to process from 10kg to metric ton
quantities of our crude CBC material under food-grade GMP conditions. By late 2019, our Chemistry CDMO had scaled the process to greater
than 10kg, and by year end 2019 to almost 30kg with final purification at the NA contractor. We commenced commercial sales of CBC in
November 2019.

Large
scale manufacturing of crude CBC began at our Chemistry CDMO in 2020 at >40kg. The emergence of the Covid-19 pandemic significantly
impacted sales beginning in calendar 2020. Large scale production continues with current batch sizes exceeding 200kg.

Cannabicitran
(“CBT”)

We
have developed a process for the efficient chemical synthesis of CBT through both in-house R&D efforts and via our Chemistry CDMO.
We began scaling this process and conducted downstream processing and purification trials in late calendar 2021. We received initial
purchase orders and commenced commercial sales of CBT in calendar 2022.

Cannabidivarin
(“CBDV”)

Beginning
in early 2021, BayMedica worked internally and with external parties to access and develop manufacturing technologies for the chemical
synthesis of the rare, non-intoxicating “varin” cannabinoid, CBDV. In calendar 2021, via a Chemistry CDMO, we successfully
scaled CBDV synthesis to commercial quantities. In April 2022, we commenced B2B sales of CBDV to the health and wellness sector. As of
fiscal 2023, a new source of CBDV was secured to provide a lower cost of goods replacement to the previously produced CBDV. Sales of
this CBDV were initiated in the second quarter of calendar 2024.

21

Tetrahydrocannabivarin
(“THCV”)

As
part of the R&D into manufacturing techniques to synthesize and produce CBDV, we also began researching and developing processes
to convert CBDV to the non-intoxicating rare cannabinoid THCV. In conjunction with our Chemistry CDMO and our in-house team, we developed
a robust pilot-scale process that produces THCV. We have now developed a purification process to produce the finished THCV material.
We began scale-up of our novel process with this CDMO in the first quarter of calendar 2022 and commenced sales in second half of calendar
2022. A new, more cost-effective, manufacturing approach for the supply of THCV was initiated in calendar 2023 with initial sales in
the third quarter of calendar 2023. We will continue to assess further initiatives to reduce cost of goods for THCV.

Analogs
of Cannabinoids / New Chemical Entities (“NCE”)

In
addition to the natural cannabinoids above, we have leveraged our expertise in pharmaceutical chemistry and biosynthesis to produce a
number of novel cannabinoid analogs and variants of pharmaceutical interest.

In
the field of pharmaceutical drug development, the term analog is used to describe structural and functional similarity between an original
(or parent) molecule and one that has been somewhat modified. While any company researching a naturally occurring compound, like cannabinoids,
cannot own a patent on the molecule itself for commercial exclusivity, a modified molecule, which has certain structural and pharmacological
similarities with the original compound, can be patented. As well, modifications of the original molecule (ie, the analog) can be designed
to confer certain improvement in activity of the parent, such as an elevation of the desired physiological effects, a decrease in unwanted
side effects, improvement in aspects related to drug delivery to targeted tissues, etc., or a combination of these targeted outcomes.
We have filed patents covering numerous structural additions and modifications of the naturally occurring cannabinoids. Each individual
modification to each individual cannabinoid represents a NCE which can be patented. If issued, this patent family will confer market
exclusivity to us for the analogs that we intend to develop into pharmaceutical Product Candidates, license, partner or sell to interested
external parties.

Notable
Milestones:

●
May 21, 2015 —
we commenced the development of our biosynthesis process for the manufacturing of cannabinoids through a research collaboration with
Dr. Vikramaditya Yadav from the Department of Biological and Chemical Engineering at the University of British Columbia under a project
titled “The Metabolic Engineering of yeast and bacteria for synthesis of cannabinoids and Cannabis derived terpenoids”.
On May 31, 2017, we signed a Technology Assignment Agreement with the University of British Columbia whereby we retain sole worldwide
rights to all patents emergent from the technology under development in exchange for a royalty of less than 1% on sales revenues
from products utilizing cannabinoids manufactured using the technology (the “1% royalty”) and a single digit royalty
on sub-licensing revenues. On May 15, 2018, we extended our Collaborative Research Agreement with the University of British Columbia
for an additional three years, which expired in 2021. Other than the 1% royalty, we do not have any ongoing financial commitments
under these arrangements with the University of British Columbia.

●
February 2019 —
we entered into a separate process development collaboration by way of a Master Service Agreement with the Almac Group (UK)(“Almac”),
a seasoned GMP pharmaceutical Contract CDMO. Almac was initially tasked to develop a down-stream purification process to support
the fermentation optimization activities at the National Research Council of Canada. In addition, we also engaged Almac to assist
in the development of an “alternative” manufacturing process for cannabinoids which integrates the best available technologies
across the spectrum of pharmaceutical drug production. This process is now referred to as IntegraSyn. In May 2020, we announced our
working relationship with Almac on an integrated approach to augment current biosynthesis-based methods for cannabinoid production.
The companies have been engaged in developing a streamlined cannabinoid manufacturing process, specifically optimizing the upstream
cannabinoid assembly processes as well as downstream purification processes, to achieve cost-efficient, GMP-grade active pharmaceutical
ingredients for prescription-based cannabinoid medications. Almac is an international, privately-owned organization which has grown
organically over the past five decades now employing over 5,600 highly skilled personnel across 18 facilities including Europe, the
United States and Asia. We retain all rights to this new process while Almac retains certain rights-of-first refusal on the production
and supply of certain precursors, or starting materials, for this alternative process.

22

Other
Milestones Include:

●
September 2020 —
we announced the filing of a PCT patent application as part of a growing portfolio of intellectual property related to the IntegraSyn
manufacturing approach for producing low-cost, pharmaceutical-grade cannabinoids (refer to “Intellectual Property”, immediately
below).

●
April 2021 — we announced
that the IntegraSyn cannabinoid manufacturing approach has achieved a level of 2g/L cannabinoid yield, a milestone that signals commercial
viability and supports advancement to large-scale production in the coming months. Having achieved a 2g/L yield level, we will now
focus on manufacturing scale-up to larger batch sizes while continuing process and enzyme optimization, targeting increased cannabinoid
yield and further reducing the overall cost of goods. In parallel, we continue to prepare the manufacturing process to be Good Manufacturing
Practice (“GMP”)-ready for pharmaceutical quality production.

● April,
2022 We announced the publication of a patent application in North America for several cannabinoid
analogs. This patent application has broad claims directed to their molecular structure,
uses and methods of manufacturing. The patent application entitled, “Cannabinoid Analogs
and Methods for their Preparation”, describes several new cannabinoid-related chemical
compounds that have not been previously described.

● January
2025 – we were granted an international Patent Cooperation Treaty (‘PCT’)
patent in the first of several jurisdictions where the patent has been filed. Titled “Cannabinoid
analogs and methods for their preparation”. This patent protects the use of several
proprietary small molecule compounds and methods of their preparation, including the drug
candidates screened for InMed’s Alzheimer’s disease and dry age-related macular
degeneration programs.

Intellectual
Property

A
patent is a monopoly granted by a government for a period of up to 20 years. A patent provides an enforceable legal right to prevent
others from exploiting an invention being a product, device, system, substance, process or method in the country of grant. For an invention
to be patentable, it must be novel, involve an inventive step and useful at the time of filing the initial patent application for that
invention. At 18 months from the initial patent application, the detailed description of the invention is published. In order to secure
patent protection, a patent application is filed with the patent office in each country of interest, the application is considered under
the patent laws of that country, and a patent will issue if the application meets the patentability criteria of that country. After a
patent expires or lapses, anyone can then use the invention.

The
grant of a patent does not guarantee validity, and a patent may be challenged by third parties at a patent office by re-examination in
some countries or through the courts by revocation proceedings. The grant of a valid patent does not mean that the invention may be exploited
in a given country without infringing third party intellectual property rights in that country.

The
owner of a patent has the exclusive right to prevent others from making, selling, importing or otherwise using the patented invention
for the life of the patent. Patent infringement occurs when someone makes, hires, uses, imports or sells the patented invention, or a
product made by a patented method, or offers to do these things, within the country covered by the patent without the permission of the
owner of the patent.

Adequate
protection of intellectual property is a means to ensure that we can commercialize our intellectual property and reduce the likelihood
of imitation by competitors. We intend to utilize patents available to protect our IP wherever commercially realizable. In addition,
we also rely on trade secrets and process know-how to protect our intellectual property. While we cannot patent the naturally occurring
individual cannabinoids used in our Products and Product Candidates, there are a number of other approaches to protect our inventions.
These include:

●
patents on individual or
combinations of cannabinoids that provide novel methods for treating diseases;

●
cannabinoid delivery technology,
formulations designed specifically to increase the safety and efficacy of drug treatments; and

●
manufacturing processes
for cannabinoids.

The
patent methodologies listed above will be designed with the intention to maximize the protection of our multi-faceted approach to developing
novel cannabinoid medicines. We typically file patent applications in US, Canada, European Union (“EU”) and other selected
commercially significant foreign jurisdictions.

23

InMed
Patent Portfolio – August 2025

Subject
Matter

Scope

Ownership/
Origin

Filing
Status /

Filing Date

Patent
Reference Number –

Patent
Nos.

Earliest
Potential/

Patent
Expiry2

Jurisdictions
- Status

Metabolic
engineering of E. coli for the biosynthesis of cannabinoid products

Manufacturing Process

InMed, UBC1

PCT Application

filed 09/05/2018

WO2019/046941

AU 2018329232

US 12077802

2038

Granted: AU, US Pending:
CA, EP, JP

Compositions
and methods for biosynthesis of terpenoids or cannabinoids in a heterologous system

Manufacturing Process

InMed, UBC1

PCT Application

filed 3/6/2020

WO2020/176998

JP (patent no. TBD)

2040

Pending: AU, CA, EP,

JP (allowed), SG, US

Ocular
drug delivery formulation

(Hydrogel)

Formulation, Use

InMed

PCT Application

filed 05/08/2018

WO2018/205022

AU 2018266262

EP 3621656

IN 426267

JP 7323458

SG 11201910450S

US 12083229

2038

Granted: AU, EP, IN, JP,
SG, US

Pending: CA

Compositions
and methods for use of cannabinoids for neuroprotection

Use

InMed

PCT Application

filed 04/24/2020

WO2020/215164

IL (patent no. TBD)

JP 7633179

2040

Granted: JP Pending: AU,
CA, CN, EP,

IL (allowed), MX, SG, US, ZA

Topical
formulations of cannabinoids and use thereof in the treatment of pain

Formulation, Use

InMed

PCT Application

filed 09/21/2018

WO2019/056123

US 12357604

2038

Granted: US

Pending: EP

Use
of topical formulations of cannabinoids in the treatment of epidermolysis bullosa and related connective tissue disorders

Use

InMed

PCT Application

filed 05/04/2017

WO2017/190249

AU 2017260706

IL 262702

JP 7054691

JP 7342183

US 12042479

2037

Granted: AU, IL, JP, JP,
US

Pending: CA, EP,

Compositions
and methods for treating neuronal disorders with cannabinoids

Use

InMed

PCT Application

filed 10/21/2022

WO 2022/082313

2041

Pending: AU, CA, CN, EP,
IL, JP, MX, US

Compositions
and Methods for Use of Cannabinol Compounds in Neuroprotection

New Chemical Entity, Composition,
Use

InMed

PCT Application

filed 5/8/2024

PCT/US2024/028445

2043

Pending:

PCT (National stage application filings due April/May 2026)

Cannabinoids
Compounds and Methods for Treatment

Composition, Use

InMed

PCT Application

filed 10/23/2024

PCT/US2024/052535

2043

Pending:

PCT (National stage application filings due April/May 2026)

Cannabinoid
analogs and methods for their preparation

New Chemical Entity; Manufacturing
Process

InMed

PCT Application filed 10/31/2019

WO2020/092823

MX 417531

2039

Granted: MX Pending: AU, CA, CN,
EP, IL, IN, IN, JP, US

PCT
= Patent Cooperation Treaty. Members in this treaty includes over 150 countries including USA, Canada, Europe and others. Patents typically
expire 20 years from their filing dates, if granted, the patent expiry may be extended by patent agencies and/or health regulatory authorities.

1
UBC is a co-inventor and
has assigned all commercial rights to InMed in exchange for a royalty of less than 1% on sales revenues from products utilizing cannabinoids
manufactured using the technology and a single digit royalty on any sub-licensing revenues.

24

BayMedica
Patent Portfolio – August 2025

Subject
Matter

Scope

Ownership/
Origin

Filing
Status /

Filing Date

Patent
Reference Number

Earliest
Potential/

Patent
Expiry2

Jurisdictions

Recombinant
production systems for prenylated polyketides of the cannabinoid family

Manufacturing Process

BayMedica

PCT Application

filed 05/10/2018

WO2018/209143

AU 2018265408

US 10837031

US 11555211

MX 411852

2038

Granted: AU, US, US, MX

Pending: AU, CA, CN, EP, IN

Preparation
of cannabichromene and related cannabinoids

Manufacturing Process

BayMedica

PCT Application

filed 12/23/2020

WO2021/133989

US (patent no. TBD)

2040

Pending: CA, CN, EP, IN,
JP,

US (allowed)

Genetically
modified yeast for the production of cannabigerolic acid, cannabichromenic acid and related cannabinoids

Manufacturing Process

BayMedica

PCT Application

filed 01/20/2021

WO2021/150636

2041

Pending: CA, CN, EP, IN,
JP, US

Acyl
activating enzymes for preparation of cannabinoids

Manufacturing Process

BayMedica

PCT Application

filed 01/20/2022

WO2022/159589

2042

Pending: CA, EP, IN, JP,
US

PCT
= Patent Cooperation Treaty. Members in this treaty includes over 150 countries including USA, Canada, Europe and others. Patents typically
expire 20 years from their filing dates, if granted, the patent expiry may be extended by patent agencies and/or health regulatory authorities.

As
of July 2025, we have a total of thirteen patent families covering the following areas:

●
Six patent families covering
novel methods for treating diseases including two for our INM-755 program (WO/2017/190249 and WO/2019/056123), one for our INM-088
program (WO/2020/215164), two for treating neurodegenerative diseases for our INM-901 program (WO/2022/082313, PCT/US2024/052535)
and one for our INM-089 program (PCT/US2024/028445). If these patents applications are granted and all maintenance fees or annuities
are paid, these patents are expected to expire in 2037-2043. In some situations, the patent may be eligible for adjustment or extension
of the patent terms due to delay in the patent office during the prosecution phase. The expiration date above does not include the
adjustments or extensions;

●
Eight patent families covering
manufacturing process for cannabinoids of interest (WO2019/046941, WO2020/176998, WO2018/209143, WO2020/092823, WO2020/102430, WO2021/133989,
WO2021/150636 and WO2022/159589). If these patents applications are granted and all maintenance fees or annuities are paid, these
patents are expected to expire in 2038-2042. In some situations, the patent may be eligible for adjustment or extension of the patent
terms due to delay in the patent office during the prosecution phase. The expiration date above does not include the adjustments
or extensions; and

●
One patent family covering
a delivery technology for the ocular program (WO/2018/205022).

25

If
these patents applications are granted and all maintenance fees or annuities are paid, these patents are expected to expire in 2038.
In some situations, the patent may be eligible for adjustment or extension of the patent terms due to delay in the patent office during
the prosecution phase. The expiration date above does not include the adjustments or extensions.

The
Patent Cooperation Treaty (“PCT”) is an international patent law treaty, which provides a unified procedure for filing patent
applications to protect inventions in each of its member states. There are 151 member countries within the PCT, enabling near-global
patent coverage through successful patent prosecution in the U.S., Japan, Europe, Canada, Australia, New Zealand, China, Brazil, Russia,
India and many other countries. We have several filed patent applications currently either in the provisional stage or PCT stage of review
as shown above. None have been granted to date. We retain the full commercial rights to all of these patents with any exceptions noted
in the above table.

Government
Regulations

The
research, development, testing, manufacture, quality control, packaging, labeling, storage, record-keeping, distribution, import, export,
promotion, advertising, marketing, sale, and reimbursement of pharmaceutical products are extensively regulated by governmental
authorities in the United States and other jurisdictions. The processes for obtaining regulatory approvals in the United States and in
foreign countries and jurisdictions, along with compliance with applicable statutes and regulations and other requirements, both pre-approval
and post-approval, require the expenditure of substantial time and financial resources. The regulatory requirements applicable to product
development, approval and marketing are subject to change, and regulations and administrative guidance often are revised or reinterpreted
by the agencies in ways that may have a significant impact on our business.

Licensure
and Regulation of Biological Products in the United States

In
the United States, the FDA regulates human drugs under the Federal Food, Drug, and Cosmetic Act (the “FDCA”) and, in the
case of biological products, also under the Public Health Service Act, and their implementing regulations. The failure to comply with
the applicable U.S. requirements may result in the FDA’s refusal to approve any pending applications or delays in development and
may subject an applicant to administrative or judicial sanctions, such as issuance of warning letters, or the imposition of fines, civil
penalties, product recalls, product seizures, total or partial suspension of production or distribution, and injunctions and/or civil
or criminal prosecution brought by the FDA and the U.S. Department of Justice or other governmental entities. The FDA must approve all
product candidates, including the Product Candidates, for therapeutic indications before they may be marketed in the United States.

Other
U.S. Healthcare Laws and Regulations

In
the United States, biopharmaceutical manufacturers and their products are subject to extensive regulation at the federal and
state level, such as laws intended to prevent fraud and abuse in the healthcare industry. These laws, some of which apply only to approved
products, include: (i) federal false claims, false statements, and civil monetary penalties laws prohibiting, among other things, any
person from knowingly presenting, or causing to be presented, a false claim for payment of government funds or knowingly making, or causing
to be made, a false statement to get a false claim paid; (ii) federal healthcare program anti-kickback law, which prohibits, among other
things, persons from offering, soliciting, receiving, or providing remuneration, directly or indirectly, to induce either the referral
of an individual for, or the purchasing or ordering of, a good or service for which payment may be made under federal healthcare programs
such as Medicare and Medicaid; (iii) the federal Health Insurance Portability and Accountability Act of 1996 (“HIPAA”), which,
in addition to privacy protections applicable to healthcare providers and other entities, prohibits executing a scheme to defraud any
healthcare benefit program or making false statements relating to healthcare matters; (iv) the FDCA, which among other things, strictly
regulates marketing, prohibits manufacturers from marketing such products prior to approval or for off-label use, and regulates the distribution
of samples; (v) federal laws that require pharmaceutical manufacturers to report certain calculated product prices to the government
or provide certain discounts or rebates to government authorities or private entities, often as a condition of reimbursement under government
healthcare programs; (vi) federal transparency law, which requires pharmaceutical companies to report certain payments to healthcare
providers; (vii) state laws and regulations analogous to the above; and (viii) laws and regulations prohibiting bribery and corruption
such as the U.S. Foreign Corrupt Practices Act (“FCPA”) (as defined below), which, among other things, prohibits U.S. companies
and their employees and agents from authorizing, promising, offering, or providing, directly or indirectly, corrupt or improper payments
or anything else of value to foreign government officials, employees of public international organizations or foreign government-owned
or affiliated entities, candidates for foreign public office, and foreign political parties or officials thereof. Violations of these
laws are punishable by criminal and/or civil sanctions, including, in some instances, exclusion from participation in federal and state
health care programs, such as Medicare and Medicaid. Ensuring compliance is time consuming and costly. Similar healthcare laws and regulations
exist in the EU and other jurisdictions, including reporting requirements detailing interactions with and payments to healthcare providers
and laws governing the privacy and security of personal information.

U.S.
Privacy Law

In
the U.S., there are numerous state and federal laws and regulations governing the security and privacy of personal information. Additionally,
state and federal regulators have begun to pay more attention to companies’ data processing activities. At the state level, laws
require companies to safeguard personal information and take action in the event of a data breach (e.g., notifying governmental authorities
and data subjects). State attorney generals have been active in using their consumer protection authority to investigate companies’
data security practices. A number of states have passed laws governing data privacy and many others have similar legislation under consideration.
Although many of these laws contain exceptions for certain health data, these exceptions are not comprehensive. All of these laws give
rights to residents in their states and require businesses to take certain actions with respect to those rights (similar to the General
Data Protection Regulation (“GDPR”) in effect in the EU, but with notable differences). At the federal level in the United
States, the Federal Trade Commission has been active in using its Section 5 authority to bring enforcement actions against companies
for deceptive or unreasonable data processing activities.

26