NYSE: IGC

During fiscal 2025, the Company
reassessed its reportable segment structure in connection with its strategic realignment toward Life Sciences. As a result, management
determined that the Company operates as a single reportable segment, focused on the vision to make the world free from Alzheimer’s.
Historically, the Company reported two operating segments: Life Sciences and Infrastructure. While the Infrastructure segment generated
revenues in fiscal 2024, it did not generate any revenues in fiscal 2025 and is no longer actively managed or evaluated as a discrete
operating segment by the Company’s Chief Operating Decision Maker. For more information, please refer to “Note 18 –
Segment Information”.

Our Drug Development Pipeline

IGC Pharma is on a mission to transform Alzheimer’s
treatment. We are building a robust pipeline of drug candidates, each targeting different aspects of the disease. Our product candidate
pipeline and anticipated milestones include the followings: -

Asset
Target Indication
Mechanism of Action
Development Stage
Key Milestones

IGC- AD1
Agitation in Alzheimer’s dementia
CB1 receptor partial agonist; reduces neuroinflammation and restores neurotransmitter balance
Phase 2 clinical trial (CALMA study)
Interim Phase 2 data analysis suggests cognitive improvements in the active treatment group versus the placebo group.

TGR-63
Early to moderate Alzheimer’s disease
Disrupts amyloid-beta (Aβ) plaque formation; crosses blood-brain barrier
Preclinical
Demonstrated favorable safety profile; advancing towards clinical trials

LMP
Alzheimer’s disease
Targets neuroinflammation, neurotransmitter imbalance, and inflammasome-3
Preclinical
Bioequivalence to IGC-AD1 anticipated in 2025

IGC-M3
Early-stage Alzheimer’s disease
Inhibits Aβ plaque aggregation
Preclinical
Toxicology studies planned for mid-2025

IGC-1C
Alzheimer’s disease and metabolic disorders
Targets tau protein phase separation; potential GLP-1 receptor agonist
Preclinical
Exhibits strong binding affinity to tau protein; potential for weight loss applications

IGC-1A
Metabolic disorders (e.g., type 2 diabetes, obesity)
Potential GLP-1 and GIP receptor agonist; CB1 receptor inverse agonist
Preclinical
Identified through AI modeling; toxicology and dosing studies underway

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This pipeline reflects IGC
Pharma’s strategic focus on addressing neurodegenerative diseases, particularly Alzheimer’s, through innovative mechanisms
targeting key pathological features like amyloid plaques and tau protein aggregation. Additionally, the expansion into metabolic disorders
showcases the versatility of our drug discovery platform, leveraging AI to identify promising therapeutic candidates.

The Company is also attempting
to harness the power of AI to develop early detection models, optimize clinical trials, and explore new applications for our drugs. Additionally,
our 31 patent filings, including for IGC-AD1, demonstrate our commitment to innovation and protecting our intellectual property.

Artificial Intelligence (AI)/Machine Learning (ML)

In our pursuit of innovation,
we leverage AI and ML. AI refers to the development of intelligent systems that can learn and act autonomously. ML is a branch of AI that
allows computers to learn from data without the need for explicit programming. This technology plays a role in our efforts and could allow
companies of our size to do what previously was the domain of much larger pharmaceutical companies. For instance, we are utilizing ML
by training transformers, a powerful neural network architecture, to analyze vast datasets from our Phase 1 and unblinded Phase 2 interim
clinical trial to identify patterns and optimize the clinical trial protocol for a potential Phase 3 trial. The AI model, for example,
has the potential to tell us if a particular neuropsychiatric scale that we used in Phase 1 and Phase 2 added valuable information to
the trial, and if it did not, we could remove that scale from a future Phase 3 trial, thus saving money and time in the overall trial
management. In the long term, with more data, the trained AI model could allow us to consider incoming patient signatures, such as scans,
symptoms, patient history, among others, and predict outcomes for our drug, including adverse effects, thus personalizing the delivery
of IGC-AD1, of which there can be no assurance.

Currently, the AI team is
working on developing a Multimodal Interpretable Transformer for Alzheimer’s Disease (MINT-AD). This tool aims to support clinicians
in real-world decision-making towards reducing Alzheimer’s false negatives and delayed diagnosis. We are developing MINT-AD for
three aims/phases: risk stratification for AD, cognitive decline prediction 2-5 years in advance, and deployment as a physician’s
tool.

We have collected and started
harmonizing a group of 32 worldwide databases that include longitudinal aging data, clinical and neuroimaging, and omics data. The databases
represent participants from various countries, with a large representation from North, Central, and South America, and Asia. A detailed
map of the databases is shown in Fig. 1.

For the first phase, we are
pretraining and finetuning state-of-the-art Large Language Models (LLMs) to extract intricate patterns in the data that uncover groups
of interacting risk factors for early detection. Our first efforts have focused on the longitudinal data due to its compatibility and
ease of use in LLMs. To input the data into language models, we are building prompts in two formats: semi-structured prompts made up by
the original variable names and their values, and descriptive prompts made up by tailored text for each database. Also, we are implementing
masked attention strategies to help the model focus on the data that is available for each database. By leveraging LLMs, we aim to enhance
interpretability, generalizability, and clinical usability. Regarding interpretability, we have tested adversarial attack approaches that
can help understand the decision-making of the model and expose wanted and unwanted behaviors in early stages. Additionally, to define
a training target, we have extracted cognitive scales so that the model identifies which risk factors impact the patient the most. Some
of the scales we have found across databases include the Mini-Mental State Examination (MMSE), the Community Screening Interview for Dementia
(CSI-D), and the Montreal Cognitive Assessment (MoCA). We are also working on incorporating clinical and imaging data, including MRI and
PET scans, and varied omics data, such as RNA sequencing, whole genome sequencing, and DNA methylations. Each group of data types will
be developed in modules and then integrated through a Mixture-of-Experts (MoE) architecture. Fig. 2 shows a general overview of our approach
with MoE. Our next steps will focus on finishing the harmonization process and incorporating the remaining databases. Once we have various
modules, we plan to train their ensemble in the MoE and test gating strategies to properly direct the input to the most appropriate expert.

So far, the first phase is
focused on the current cognitive state and the factors that have the most significant impact on that state. In the second phase, we want
to focus on understanding how cognitive abilities evolve over time and how modifiable risk factors lead to a positive or negative cognitive
trajectory. For this task, we will include datapoints throughout time, focusing on the importance of temporality and causality in the
data. Also, we can leverage strategies like chain-of-thought (CoT) in the transformer-based models from the previous phase to train the
models to understand how the reasoning behind a risk factor leads to the cognitive outcome. This strategy will be implemented with help
from experts that can provide examples of the analysis process on a case-by-case basis.

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In the last phase, we will
deploy the final model with insights from both previous phases to conduct further real-world validation and assess the impact of the model
in early detection and cognitive trajectory improvements.

Fig. 1: Overview of the database for MINT-AD

Fig. 2: MINT-AD architecture using MoE

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Our Strategy

Our goal is to develop product
candidates to diagnose and/or treat central nervous system disorders, such as Alzheimer’s disease and neurodegenerative conditions.
Key elements of our business strategy to achieve this mission include:

●

Advance Differentiated Therapies for High-Need
CNS Indications: - Subject to FDA approval and clinical trials, IGC Pharma is advancing IGC-AD1 as a potential treatment for
agitation in dementia due to Alzheimer’s disease—an area with limited effective therapies and significant unmet medical need.

●

Expand IGC-AD1’s therapeutic potential
to treat AD, subject to FDA approval: - Subject to FDA approval, IGC Pharma aims to broaden the clinical application of IGC-AD1 beyond
agitation to target core Alzheimer’s disease symptoms, contingent upon regulatory approval and support clinical data. Although there
can be no assurance, this expansion could significantly enhance the drug’s value and impact in addressing a major unmet medical
need.

●

Advance the development of TGR-63 as a potential
therapeutic for AD: - IGC Pharma is progressing TGR-63, a preclinical candidate designed to target amyloid-beta plaque formation,
a hallmark of Alzheimer’s pathology. This molecule represents a key component of the Company’s long-term strategy to diversify
its Alzheimer’s pipeline and address the disease at its biological core.

●
Publish scientific findings in peer-reviewed journals to strengthen clinical credibility and visibility: - IGC Pharma actively disseminates research through peer-reviewed publications to validate its scientific approach, enhance transparency, and support regulatory engagement. This strategy reinforces the Company’s reputation within the medical and investor communities and underpins the advancement of its drug development programs.

●
Allocate Capital to Enhance Shareholder Value: - IGC Pharma Inc. is committed to strategically allocating capital to enhance shareholder value by advancing its AD pipeline, optimizing operational efficiency, and maintaining a robust financial position.

We believe developing a drug
for both symptom and disease-modifying agents has less risk due to the need for expensive multi-year trials. However, there is considerable
upside and significant value creation to the extent we obtain a first-in-class advantage, of which there can be no assurance. If we were
to obtain a first-in-class advantage, such an advantage could result in significant growth if and when an approved drug such as IGC-AD1
launches.

We believe that additional
investment in clinical trials, AI, R&D, facilities, marketing, advertising, and the acquisition of complementary products and businesses
will be critical to the ongoing growth of the Life Sciences segment. Although there can be no assurance, we believe these investments
will fuel the development and delivery of innovative products that drive positive patient and customer experiences. We hope to leverage
our R&D and intellectual property to develop ground-breaking, science-based products that are proven effective through clinical trials,
subject to FDA approval. Although there can be no assurance, we believe this strategy can improve our existing products and lead to the
creation of new products that can provide treatment options for multiple conditions, symptoms, and side effects.

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Core business competencies and advantages

Our core competencies include:

●
a network of doctors, scientists with Ph.D. degrees, and intellectual property legal experts with a sophisticated understanding of drug discovery, research, FDA filings, intellectual protection, and product formulation;

●
knowledge of various cannabinoid strains, their phytocannabinoids profile, extraction methodology, and impact on various pathways;

●
knowledge of plant and cannabinoid-based combination therapies;

●
knowledge of research and development in the field;

●
approximately thirty-one (31) patent applications out of which our portfolio includes twelve (12) granted patents. For more information, please refer to Item I, “Business” of Part I;

●
facilities and a team with experience in manufacturing, marketing, and selling products. These competencies have enabled us to make progress on our business goals, specifically completing the Phase 1 clinical trial of IGC-AD1, which has the potential to positively impact on the lives of millions of patients suffering from the symptoms of Alzheimer’s disease, subject to FDA approval.

Background on Alzheimer’s Disease
(AD) Pathology

AD pathology can be divided
into two categories: familial or inherited AD and sporadic AD. The histopathology of early-onset familial AD and late-onset sporadic AD
is indistinguishable. Both forms of AD are characterized by extracellular amyloid-β (Aβ) plaques and intracellular tau-containing
neurofibrillary tangles (Gӧtz, et al., 2011). Simplistically, in normal brain functioning, a large protein called Amyloid Precursor
Protein (APP) is cleaved into smaller fragments called Aβ proteins. In a normal brain, these are subsequently broken down further
and cleared. However, in AD brains, these Aβ proteins are not broken down and cleared; they instead stick to one another and deposit
as inter-neuronal sticky plaque—that is, they deposit as plaque between neurons. In the brain, within a neuron, tau (τ) is a
key protein that holds together the transport scaffold. As an analogy, it is the brick-and-mortar of the highway over which nutrients
are transported within a neuron. In an AD brain, tau breaks down due to a process called hyperphosphorylation and is unable to hold the
transport highway. The breakdown results in neurofibrillary tangles (NFTs) and eventually leads to neuronal death.

The misfolded structure of
Aβ proteins, along with NFTs, generates a characteristic tendency for their aggregation (Chiti & Dobson, 2006) around damaged
or dead neurons and within cerebral vasculature in the brain. It manifests in memory loss followed by progressive dementia. It has long
been believed that Aβ1–40 (Aβ40) and Aβ1–42 (Aβ42) aggregates are the constituents of the insoluble plaques
that are characteristic of AD. This disease is also associated with neuroinflammation, excitotoxicity, and oxidative stress (Campbell
& Gowran, 2007; Rich, et al., 1995). However, the continuous aggregation of Aβ proteins along with hyperphosphorylation of tau
protein inside the cell, causing NFT formation, are generally accepted as the major etiological factors of the neuronal cell death associated
with the progression of Alzheimer’s disease (Octave, 1995; Reitz, et al., 2011; Pillay, et al., 2004). The two hallmarks of Alzheimer’s
are shown in Figure 3.

Figure
3: Hallmarks of Alzheimer’s

● Extracellular
Plaque: β-amyloid (Aβ)

● Tau
Neurofibrillary Tangles (NTFs).

Causes
loss of neurons & critical neuronal connections.

Also
linked to Alzheimer’s:

● Metabolism
disruption

● Mitochondrial
dysfunction

● Neuroinflammation

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Alzheimer’s affects
not only cognition but also mood and behavior, changes which increase in intensity as the disease progresses. Approximately 6.9 million
Americans aged 65 and older are living with Alzheimer’s dementia, according to the Alzheimer’s Association’s 2024 Facts
and Figures report. In 2025, it is estimated that 7.2 million Americans aged 65 and older have Alzheimer’s dementia, reflecting
the growing aging population. Alzheimer’s is the most common cause of dementia, accounting for an estimated 60% to 80% of cases.
Most individuals also have the brain changes of one or more other causes of dementia. This is called mixed pathologies, and if recognized
during life it is called mixed dementia. There are various symptoms associated with this medical condition, such as screaming, pacing,
biting, disrobing, excessive motor movements, physical aggression, and verbal aggression, among others. These behaviors make up clinical
agitation in dementia due to Alzheimer’s disease and it they make it very difficult for caregivers to manage their loved ones. Agitation
is associated with increased hospitalization and accelerated cognitive decline.

Symptoms of AD depend on the
stage of the disease: preclinical, mild, moderate, or severe. NPS, such as agitation, apathy, delusions, hallucinations, and sleep impairment,
are common accompaniments of dementia. Loss of functionality, including progressive difficulty in performing instrumental and basic activities
of daily living, is also seen with disease progression (Tang et al., 2019). There is a spectrum of behavioral disorders that can affect
patients with AD. These include agitation, anxiety, disturbance of the sleep cycle, depression, inappropriate sexual behavior, disinhibition,
and irritability, among others (Lyketsos, et al., 2011). These behavioral disturbances not only affect the patient’s quality of
life but also cause extreme emotional distress for the caregivers. These disturbances can become very difficult to manage, so most of
the time, combined therapy is used (Matsunaga et al., 2015). This can cause secondary undesirable effects, such as excessive sleepiness,
which diminishes the capability of the patient to be active and alert during the day; dizziness, which can increase the risk for falls
(Allan, et al., 2005); worsening of cognitive function, which in turn worsens functionality (Paterniti S, et al., 2002); and even death
due to cardiovascular complications (Qiu, et. Al., 2006).

Background on Agitation in Alzheimer’s
dementia

Agitation is a prevalent neuropsychiatric
symptom among individuals with Alzheimer’s disease, characterized by restlessness, aggression, and emotional distress. Studies indicate
that up to 80% of individuals with Alzheimer’s experience agitation during the course of the disease. Based on these figures, approximately
5.8 million Americans with Alzheimer’s may experience agitation in 2025. This substantial number underscores the critical need for
effective interventions targeting agitation to improve patient quality of life and reduce caregiver burden. Agitation is a behavioral
syndrome characterized by increased, often undirected, motor activity, restlessness, aggressiveness, and emotional distress. While there
can be no guarantee, we expect the Phase 2 trial to take between 12 and 18 months to complete, barring a variety of unknown factors.

We are currently developing
IGC-AD1 for the treatment of Agitation in Alzheimer’s dementia (AAD). There is only one FDA-approved pharmacological treatment for
the indication of AAD.

The National Institute on
Aging (NIA) at the National Institutes of Health (NIH) defines AD as an irreversible, progressive brain disorder that destroys memory
and thinking skills. AD is a progressive neurodegenerative disorder that manifests initially as forgetfulness, advancing to severe cognitive
impairment and memory loss. Emotional distress, aggressive behaviors, disruptive irritability, and disinhibition characterize agitation.
Agitation in Alzheimer’s dementia has been associated with increased caregiver burden, decreased functioning, earlier nursing home
placement, and death.

The NIA categorizes Alzheimer’s
in three stages- mild, moderate, and severe (NIA, 2019). Symptoms of mild Alzheimer’s can include wandering (getting lost, not remembering
the way home), trouble handling money and paying bills, repeating questions, and personality or behavior changes. As the disease progresses
to moderate, there is damage to the areas of the brain that control language, reasoning, sensory processing, and conscious thought. Patients
can have difficulty with multi-step tasks such as getting dressed. Behavioral problems, including hallucinations, delusions, paranoia,
and impulsive behavior, can also increase. When severe Alzheimer’s sets in, plaques and tangles spread throughout the patient’s
brain, and the brain shrinks significantly. People with severe Alzheimer’s are completely dependent on others for care. They cannot
communicate, and near the end of their life, they may be largely bedridden as the body shuts down (NIA, 2021).

Patients with AD are currently
treated with various medications, including antipsychotics, which have been considered the mainstay of treatment. These treatments, however,
are limited by safety concerns. Typical antipsychotics prescribed for agitation, aggression, or insomnia are associated with functional
decline in patients with AD, while studies indicate that atypical antipsychotics may be associated with increased rates of cerebrovascular
events and death in patients with dementia.

Currently, there are limited
options to help Alzheimer’s patients with agitation or relief the burden placed on their caregivers (Cheng, 2017).

Currently, IGC-AD1 is in a
Phase 2 clinical trial, and on March 20, 2024, and on November 14, 2024, IGC announced the “Positive Interim Results for IGC-AD1
in Reducing Alzheimer’s agitation” and “Additional Phase 2 Interim Results Highlighting Cognitive Benefits of IGC-AD1
for Alzheimer’s Treatment”, respectively. The interim data validates IGC-AD1’s potential as a transformative therapeutic
option with a large market opportunity in Alzheimer’s disease management, although there can be no assurance.

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IGC-AD1 as a Treatment for Agitation in Alzheimer’s
Dementia

Approximately 6.9 million
Americans aged 65 and older are living with Alzheimer’s dementia, according to the Alzheimer’s Association’s 2024 Facts
and Figures report. AAD is associated with an accelerated cognitive decline, increased caregiver burden, increased hospitalization, and
increased need for medication, all significantly diminishing the quality of life for patients. Current therapies carry black box warnings,
indicative of serious adverse reactions that may lead to death or serious injury. IGC-AD1 is designed to target AAD’s underlying
causes and address the unmet need for safe and effective therapy.

As illustrated in Figure 2,
neuroinflammation, neurotransmitter imbalance, and CB1 receptor dysfunctions are all associated with AAD (Yasuno et al., 2023; Manuel
et al., 2014). In addition, upregulation of inflammasome-3 has been shown to lead to neuroinflammation, consequently leading to aggressive
behavior (Yu et al., 2023). IGC-AD1’s formulation combines a CB1 receptor partial agonist with anti-neuroinflammatory properties
that help balance neurotransmitter imbalance and an inflammasome inhibitor that targets the upregulation of inflammasome-3.

The 146-patient IGC-AD1 Phase
2 trial, for which these interim results are presented, continues to enroll in the U.S. and Canada. As the interim results are based on
a small number of patients (n=26), there is no guarantee that the positive interim results will hold up as more patients are enrolled
in the trial. Learn more and find information about recruitment centers at https://clinicaltrials.gov/study/NCT05543681.

Figure 4: Damaged and Healthy Neurons

IGC-AD1 Clinical Trial Data

To the best of our knowledge,
the Company’s Phase 2 clinical trial of IGC-AD1 is the first human clinical trial using low doses of THC, in combination with another
molecule, to treat symptoms of dementia in Alzheimer’s patients. THC is a naturally occurring cannabinoid produced by the cannabis
plant. It is known for being a psychoactive substance that can impact mental processes in a positive or negative way, depending on the
dosage. THC is biphasic, meaning that low and high doses of the substance may affect mental and physiological processes in substantially
different ways. For example, in some patients, low doses may relieve a symptom, whereas high doses may amplify a symptom. IGC’s
trial is based on low dosing and controlled trials on patients suffering from Alzheimer’s disease.

We conducted a double-blind,
single-site, randomized, three-cohort, multiple-ascending dose (MAD) clinical trial (FDA IND Number: 146069, NCT04749563) using the investigational
new drug (IND) IGC-AD1. In this trial, we looked at safety, tolerability, neuropsychiatric symptoms, and pharmacokinetics, among others.
The trial concluded that all three dosing levels (once a day, twice a day, and twice a day) were safe, with no serious or life-threatening
events or deaths reported.

On December 1, 2021, IGC submitted
the Clinical/Statistical Report (CSR) to the FDA on its Phase 1 trial titled “A Phase I Randomized Placebo-Controlled MAD Study
to Evaluate Safety and Tolerability of IGC-AD1 in Subjects with Dementia Due to Alzheimer’s Disease.” The already disclosed
data is presented here for a better understanding of the safety profile of IGC-AD1. The data presented here is not exhaustive and represents
a small portion of the data submitted to the FDA.

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Phase 1 Primary Endpoint: Safety & Tolerability

Safety and tolerability (S&T)
were assessed by recording both solicited and non-solicited Adverse Events (AEs). The solicited AEs, assessed daily, were somnolence,
falls, dizziness, asthenia, suicidal ideation, hypertension, psychiatric symptoms, and paradoxical nausea. All AEs were graded as mild,
moderate, severe, life-threatening, and serious (SAE). In the phase 1 trial, a) there were no SAEs, b) no life-threatening AEs, and c)
no deaths.

Phase 1 Secondary Endpoints: Neuropsychiatric Inventory (NPI)

Neuropsychiatric Symptoms
(NPS) such as agitation/aggression, depression, anxiety, elation/euphoria, apathy, disinhibition, irritability, delusions, hallucinations,
aberrant motor behavior, sleep disorders, and appetite/eating disorders are prevalent in patients who have AD (Phan et al., 2019). NPS
in Alzheimer’s is a significant burden on patients and caregivers, and at some point in the progression of Alzheimer’s disease,
more than 97% of patients suffer from at least one symptom. The Neuropsychiatric Inventory (NPI) is a scale that measures the severity
of each symptom and establishes both individual symptom scores as well as an overall NPI score. Separately, the NPI also scores caregiver
distress (NPI-D). The NPI is used by about 50% of neurologists to assess and treat Alzheimer’s patients (Fernandez et al., 2010).

In the Phase 1 trial conducted
on patients with AD, we measured changes in NPS as assessed by the NPI as well as caregiver distress as assessed by the NPI-D. In the
Phase 1 trial (N=10), seven received the active medication, and at baseline, they had agitation scores between two and twelve. The three
Cohorts shown in Table 1 received the medication once a day (qd), twice a day (bid), and three times a day (tid). We measured and analyzed
the change in the mean NPI score for agitation between Day 1 and Day 10 and between Day 1 and Day 15 for all three cohorts.

●As shown in the Table 1, our
analysis shows Cohort 2 (bid) had the largest absolute change in the mean agitation score between Day one and Day ten (53% drop, p=.085)
as well as between Day 1 and Day 15 (67% drop, p=.05).

Table 1: NPI (Agitation) analysis for each
of the three cohorts

Domain
Cohort
1 (n=7) qd
Cohort
2 (n=6) bid
Cohort
3 (n=5) tid

NPI
(Agitation)
Baseline
Day
Day
Baseline
Day
Day
Baseline
Day
Day

Day
0
10
15
Day
0
10
15
Day
0
10
15

Mean
Score
4.7
3.3
3
4.3
2.1
1.5
4.2
3.2
1.4

Mean
Change
-
1.4
1.7
-
2.2
2.8
-
1
2.8

Mean
Change%
-
37%
48%
-
53%
67%
-
23%
67%

p-values
-
0.058
0.045
-
0.085
0.05
-
0.29
0.045

According to the NPI, a reduction
of 4 points or 30% in the score is considered clinically meaningful (Cummings et al., 1994). In addition, we used a paired 2-tailed t-test
with 9 degrees of freedom to assess the statistical significance of the decrease in the overall NPI agitation domain. As seen in Table
1, the NPI score for Agitation in Cohort 2 at day 15 shows a reduction of 67% (p = .05). Based on this study the dosing of twice
a day or bid was selected for the Phase 2 trial.

IGC-AD1 Phase 2 Clinical Trial Update

IGC Pharma launched a Phase
2 trial with a protocol titled “A Phase 2, Multi-Center, Double-Blind, Randomized, Placebo-controlled, trial of the safety and efficacy
of IGC-AD1 on agitation in participants with dementia due to Alzheimer’s disease” (clinicaltrials.gov, Identifier: CT05543681).
The trial treatment duration is 6 weeks, with the intervention, IGC-AD1 or placebo, administered twice a day. The study is powered to
include 146 Alzheimer’s patients; as a superiority trial with parallel groups, half of the participants will receive a placebo,
and the other half will receive IGC-AD1. The primary and secondary endpoints are the mean change in agitation scores from baseline, compared
to placebo, as assessed by the Cohen-Mansfield Agitation Inventory (CMAI) in Alzheimer’s patients after 6 weeks of treatment and
the mean change in CMAI scores after 2 weeks of treatment, respectively. Agitation is rated at the trial site, at baseline, week 2, and
week 6, by a trained practitioner using the CMAI, a scale designed and widely used to measure agitation in Alzheimer’s dementia
(AAD) in clinical trials.

The IGC-AD1 Phase 2 is an
ongoing clinical trial that continues to enroll. IGC-AD1 is an oral liquid formulation administered twice daily (bid) for six weeks with
no placebo run-in and titration to full dose over two days. To date over 1,000 oral doses have been administered, with no dose-limiting
adverse events observed, highlighting the safety profile of IGC-AD1. The Investigational product targets different pathways implicated
in AAD, including CB1 receptor dysfunction, neuroinflammation and neurotransmitter imbalance. The investigational drug contains THC, the
principal psychoactive cannabinoid found in Cannabis, as one of two active pharmaceutical agents.

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Pre-Specified Interim Results

An experienced third party
conducted a protocol pre-specified interim analysis, mean changes from baseline were analyzed using a mixed-effects model for repeated
measures (MMRM). Findings showed that patients taking IGC-AD1, on average, experienced a significant reduction in agitation scores compared
to those on placebo, and the positive effects were observed as early as week two of the trial. Interim results will be discussed in the
following sections.

IGC-AD1 Trial Interim Primary and Secondary
Endpoints Results

The primary objective is to
assess the efficacy of IGC-AD1 in AAD after six weeks of treatment using the CMAI scale. The secondary objective is to assess IGC-AD1
efficacy and early response in AAD using also the CMAI scale, after 2 weeks of treatment.

Based on the CMAI interim
results shown in Table 2 below, IGC-AD1 demonstrated a clinical and statistically significant agitation reduction compared to placebo
in patients with AD, indicating strong therapeutic potential and meeting the primary endpoint. The CMAI least-squared (LS) mean difference
at week 6 was -10.46 (95% CI: -20.53 to -0.40) with a Cohen’s d effect size of 0.79 (p= .042), indicating a large and significant
IGC-AD1 effect over placebo. Cohen’s d is a standardized statistical effect size that describes the magnitude of the difference
between two groups, taking into account the variability in outcomes.

Based on the interim results,
the secondary endpoint was also met; the data demonstrates a clinically significant reduction, approaching statistical significance, in
agitation in Alzheimer’s at week two compared to placebo. CMAI LS mean difference at week 2, assessing early response, was -12.19
with an ES of 0.79 (p= .071). The ES, similarly, to the primary endpoint, indicates a large magnitude of difference between the active
and placebo groups.

Table 2:- Interim CMAI Results for Week
2 and Week 6

Week 2
Week 6 (EOT)

Scale
LS Mean Change (95% CI)
p value
Cohen’s d
LS Mean Change (95% CI)
p value
Cohen’s d

CMAI
-12.19 (-25.52, 1.14)
.071
0.79
-10.46 (-20.53, -0.4)
.042
0.79

IGC-AD1 Clinical Trial Interim Data Demonstrates
Significant Reduction in Sleep Disturbances

As part of an interim analysis,
the Company observed statistically and clinically significant reductions in sleep disturbances, as measured by the Neuropsychiatric Inventory
(NPI-12) Sleep Subscale. At week 2, patients receiving the active medication experienced a 71% reduction in sleep disturbance (p = 0.012),
which improved further to 78% at week 6 (p = 0.02), compared to placebo. These findings suggest that IGC-AD1 may reduce the frequency
and/or severity of nighttime behavioral disturbances, an underrecognized but impactful symptom affecting up to 44% of individuals with
AD.

Figure 5: - Shows the clinically and statistically
significant decrease in the frequency and/or severity of sleep disturbances (B) for the active group versus the placebo group (A) as measured
by the NPI Sleep Subscale.

Sleep disturbances are known
to exacerbate cognitive and behavioral symptoms in AD and are a common contributor to caregiver distress and early institutionalization.
The ability to improve sleep quality represents an important potential therapeutic benefit, as enhanced sleep has been linked to reduced
amyloid-beta accumulation and slower disease progression in preclinical studies.

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Beyond its implications in Alzheimer’s care,
sleep disorders affect over 30 million Americans and are associated with increased risk for cognitive decline and cardiovascular disease.
If the sleep-related benefits of IGC-AD1 are confirmed in larger clinical trials, the candidate may address a significant unmet need within
the broader global sleep aid market, which is projected to exceed $100 billion by 2030.

Previously reported data from
the ongoing Phase 2 trial also demonstrated notable reductions in agitation, further supporting IGC-AD1’s potential as a multi-targeted
therapy for managing neuropsychiatric symptoms in AD. The Company anticipates additional data readouts from the CALMA trial in late 2025,
including further analysis of sleep-related outcomes.

In parallel, IGC Pharma plans
to initiate future studies evaluating IGC-AD1 as a disease-modifying therapy, reflecting the Company’s strategic commitment to advancing
innovative, mechanism-driven treatments for central nervous system disorders.

Existing Treatments for Agitation in Alzheimer’s
Dementia

In May 2023, the U.S. Food
and Drug Administration (FDA) approved the first medication for the treatment of AAD, Brexpiprazole, an atypical antipsychotic, with a
boxed warning. This approval followed a significantly larger 12-week Phase 3 trial, which showed a CMAI LS mean difference from baseline
at week 12, between active treatment and placebo of -5.32 with a Cohen’s d effect size of 0.35, and a p-value of 0.003 (Lee et al.,
2023).

Regulatory Environment for IGC-AD1

IGC-AD1 is currently made
from federally legal hemp In addition, IGC-AD1 contains the federally legal amount of THC as defined in the 2018 Farm Bill. Therefore,
IGC-AD1 is federally legal based on the amount of THC in the formulation and the origin of the THC. The Company grew hemp under a license
in the state of Arizona. Manufacturing IGC-AD1 from hemp is an extremely inefficient process requiring vast amounts of hemp to manufacture
the investigational medication. The regulatory landscape appears to be changing in that the U.S. government is seeking to reschedule THC
from Schedule 1 to Schedule 3. The Company use hemp to manufacture IGC-AD1 , which is egal. The Company has received permission from the
regulators to conduct the IGC-AD1 Phase 2 trial in the U.S., Canada, and Colombia.

TGR-63 and Alzheimer’s disease

TGR-63 was licensed from the
Jawaharlal Nehru Centre for Advanced Scientific Research in India and developed by Prof. T Govindaraju, who designed several naphthalene
monoimide compounds and compared their capacity to inhibit Aβ aggregation, their cytotoxicity, and their neuronal rescue capacity,
in which TGR-63 excelled.

Researchers at the Jawaharlal
Nehru Centre for Advanced Scientific Research (JNCASR), in India, conducted approximately 10 years of research on Naphthalene Monoimide
(NMI) compounds and the activity of NMI compounds on neurotoxicity associated with AD.

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In Alzheimer’s patients,
neurotoxicity is linked to beta-amyloid (Aβ) plaques and Neuro Fibrillary Tangles (NFT). JNCASR’s research based on Alzheimer’s
cell lines identified one lead NMI molecule, TGR-63, from a family of NMI molecules with the potential to reduce amyloid beta (Aβ)
plaques. Further, they demonstrated that the molecule reduces cognitive decline in a transgenic mouse model of Alzheimer’s. Their
results were published in Advanced Therapeutics under the title “Naphthalene Monoimide Derivative Ameliorates Amyloid Burden
and Cognitive Decline in a Transgenic Mouse Model of Alzheimer’s Disease” on January 28, 2021.

Pursuant to the signed agreement
dated March 28, 2022, IGC Pharma (through Hamsa Biopharma India Pvt. Ltd.) acquired exclusive intellectual property rights to the molecule,
which it intends to pursue as a potential new drug candidate, subject to further study, research, and development. IGC Pharma is conducting
human trials with IGC-AD1, which is currently being tested as a symptom-modifying agent in Alzheimer’s dementia. TGR-63, on the
other hand, could act as a potential disease-modifying agent to expand the Company’s pursuit of a drug that can treat AD.

Figures 6 and 7: - Show the destabilization
of Aβ plaques and Aβ42 peptide with the help of TGR-63.

Computational Studies: A Plausible Mode of Action

Figure 6: In silico analysis demonstrated
that TGR-63 molecular design enables it to interact with amyloid aggregates, disrupting various types of bonds. This destabilizes plaque’s
structure, facilitating their breakdown.

(*Adv. Therap. 2021, 4 2000225).

Figure 7: TGR-63 also shows high
affinity for the Aß42 peptide, compromising its tertiary structure and promoting the formation of globular non-toxic structures
that can be metabolized.

(*Adv. Therap. 2021, 4 2000225).

Pre-clinical studies of TGR-63

TGR-63 is a patent-pending
molecule designed to disrupt the structure of the amyloid beta (Aβ) plaque, one of the key hallmarks of AD, associated with neuronal
toxicity and cognitive decline. TGR-63 targets plaques by inhibiting the aggregation of Aβ42 peptides and destabilizing their tertiary
structure.

Specifically, the pre-clinical
research on TGR-63 showed the following:

Impact on plaque levels:
Studies in PC12 and SHSY5Y cell lines grown in an AD-like environment have showed TGR-63’s ability in decreasing Aβ plaque
levels, leading to an increase in 26% neuron viability (neuronal rescue). TGR-63’s potential as a treatment for AD was further evaluated
in a genetically modified mouse model mimicking Alzheimer’s amyloid pathology. In that assay, the group treated with TGR-63, compared
to the vehicle-treated group, showed a 78% and 85% reduction in the cortical and hippocampal amyloid load, respectively, demonstrating
its potential to alleviate amyloid burden. Figure 5 shows the reduction of the amyloid burden by TGR-63 in the APP/PS1 AD mouse model.

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Figure 8: Reduction of the amyloid burden
by TGR-63 in the APP/PS1 AD phenotypic mice model. A) Visualization of amyloid plaques in the half hemisphere: Confocal microscopy images
of coronal section of WT, AD mice, and TGR-63 treated AD mice brain. B) Reduction of cortical and hippocampal amyloid burden by TGR-63
treatment: Higher magnification images of vehicle and TGR-63 treated mice (WT and AD) brain sections to visualize and compare the Aβ
plaques deposition in the cortex and hippocampus areas. C, D) Quantification of Aβ plaques: The amount of Aβ plaques (%area)
deposited in different regions (cortex and hippocampus) of vehicle and TGR63 treated mice (WT and AD) brain was analyzed. Data represent
mean ± SEM, number of mice = 3 per group (*p < 0.05). Scale bar: 20 µm. (*Adv. Therap. 2021, 4 2000225).

Behavioral Impact: During the investigation,
two groups of APP/PS1 mice undertook an Open-Field (OF) test, a behavioral assessment designed to measure aberrant behavior, stress and
coping responses, and emotional state, among others, in rodent models. The mice in the APP/PS1 group that received TGR-63 treatment showed
a 43% reduction in their overall movement within the test area (p<.0001), a 59% reduction in movement within the central zone of the
test area (p<.01), and a 55% reduction in entries to the center zone compared to the untreated group (p<.05). These are shown in
Figure 6. The results from these multiple tests indicate that TGR-63 treatment helped to improve in their anxious-like and aggressive-like
behaviors compared to the group that did not receive the treatment, normalizing emotional and behavioral responses in the mouse model,
reinforcing its potential as a promising treatment.

Figure 9 Behavioral Tests

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Impact on memory: The
cognitive impact of TGR-63 was assessed using two renowned behavioral tests, the Novel Object Recognition (NOR) Test and the Morris Water
Maze (MWM), conducted on APP/PS1 genetically modified Alzheimer’s mice.

During the NOI Test, mice
were familiarized with two identical objects, followed by exploration of both novel and familiar objects after 24 and 48 hours, to establish
the discrimination index (DI). AD mice displayed a significantly lower DI (-3, p<0.0001, 24h; -7, p<0.0001, 48h) compared to wild-type
(WT) mice (+49, 24h; +43 48h), indicating impaired long-term memory formation, while AD mice treated with TGR-63 exhibited an improved
DI (+50, p<0.0001; +38, p<0.001), indicative of healthy long term memory formation and successful memory retrieval.

In the MWM test, the time
to reach a platform hidden in a pool for four training days showed a remarkable improvement for the TGR-63 treated AD model compared to
the AD-vehicle group, indicating enhanced spatial memory, as demonstrated by a significant reduction (~60% reduction; p < 0.05) in
the time required by the TGR-63 treated AD mice to locate the hidden platform, exhibiting a similar behavior to healthy mice. The results
of the novel recognition test and the MWM are shown in Figures 7 and 8 respectively.

Figure 10: In the Novel Object Recognition test, mice treated with TGR-63 showed increased exploration of a new object over a familiar one, indicating enhanced learning capacity. (*Adv. Therap. 2021, 4 2000225).

Figure 11: During the Morris Water Maze test, mice treated with TGR-63 exhibited improved spatial memory, with decreased latency in finding the target compared to the untreated group. (*Adv. Therap. 2021, 4 2000225).

Contract Research Organization (CRO) and Clinical
Trial Software

The IGC-Pharma Electronic
Data Capture system (IGC-EDC) is a secure and user-friendly data management software designed to collect clinical trial data in electronic
format. The software incorporates rigorous security measures that help IGC to protect data and ensure compliance with regulatory requirements
and industry standards. This format is designed for our clinical trials, especially our Phase 2 trial. The EDC system is designed to store
and organize handwritten source documents, including medical history, concomitant medications, laboratory results, neuropsychiatric scale
scores, adverse events, vital signs, safety calls, and demographics, among others. The system allows users to generate data reports that
will be used for data analysis and generate computational models to simulate the effects of our investigational drug IGC-AD1 on participants’
outcomes.

At IGC Pharma, we recognize
the significance of operational excellence and cost management in clinical trials. One major cost driver in conducting trials is the expense
associated with engaging CROs. These costs can significantly impact the overall budget of a trial. To address this challenge and optimize
trial costs, we have established an internal CRO, including proprietary software, that we believe sets us apart from the traditional approach
of outsourcing. We believe this strategic move should enable us to reduce the costs associated with clinical trials compared to relying
on external CROs, although there can be no assurance.

Intellectual Property

IGC Pharma, is committed to
building a strong and defensible intellectual property (IP) portfolio that supports our strategic focus on neurodegenerative diseases
and related therapeutic areas. Our IP strategy is centered on securing exclusive rights to proprietary technologies, inventions, and product
candidates through the development, acquisition, and licensing of patents and related protections both in the United States and internationally.

We actively seek to protect
our innovations by filing patent applications that cover novel methods, compositions, and uses associated with our investigational drug
candidates, formulations, and related technologies. Our patent strategy is designed to cover key elements of our research and development
efforts, particularly in the fields of AD, epilepsy, pain management, and other central nervous system (CNS) disorders. In addition to
patent protection, we intend to leverage data exclusivity, market exclusivity, and patent term extensions, where applicable, to maximize
the commercial potential and lifecycle of our assets, although there can be no assurance thereof.

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Our commercial success depends in part on our
ability to:

●Obtain
and maintain strong patent and proprietary protection;

●Protect
our trade secrets and proprietary know-how;

●Secure
necessary licenses for third-party intellectual property;

●Enforce
our rights against infringement; and

●Operate
without infringing valid, enforceable third-party patents.

We aim to commercialize our intellectual property
through multiple channels:

1.Pharmaceutical products are subject to U.S. Food and Drug Administration (FDA) approval. Our lead candidate,
IGC-AD1, is currently in a Phase 2 clinical trial for treating agitation in AD. We are also developing TGR-63, a pre-clinical candidate
with potential disease-modifying effects in Alzheimer’s.

2.Branded wellness and lifestyle products, offered through retail and online distribution channels, in compliance
with applicable federal, state, and local laws.

3.Partnerships and licensing agreements with third parties to accelerate product development and market
entry.

We hold exclusive rights
to all patents filed with the U.S. Patent and Trademark Office (USPTO). In Fiscal 2017, we acquired exclusive rights to data and a patent
application from the University of South Florida (USF), and following Fiscal 2022, we acquired similar exclusive rights from the Jawaharlal
Nehru Centre for Advanced Scientific Research (JNCASR).

While patent registration
is a key component of our business strategy, we cannot guarantee that all provisional or non-final patent applications will result in
granted patents. Please refer to