IGC US Equity☆

UNITED

STATES

SECURITIES

AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM

10-K

☒Annual report pursuant to Section13 or 15(d) of the Securities Exchange Act of 1934

For FiscalYear Ended March 31, 2025.

☐Transition report pursuant to Section13 or 15(d) of the Securities Exchange Act of 1934

For the transition period from to

Commission file number: 001-32830

IGC PHARMA, INC.

(Exact Name of Registrant as Specified in Its Charter)

(Address of Principal Executive Offices) (Zip Code)

(301) 983-0998

(Registrant’s telephone number, including

area code)

Securities registered pursuant to Section 12(b)

of the Act:

Common Stock IGC NYSE American LLC

Securities registered pursuant to Section 12(g)

of the Act: None.

Indicate

by check mark if the registrant is a well-known seasoned issuer, as defined in Rule 405 of the Securities Act. ☐ Yes ☑ No

Indicate

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

No

Indicate

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

Act of 1934 during the preceding 12 months (or for such shorter period that the registrant was required to file such reports), and (2)

has been subject to such filing requirements for the past 90 days. ☑ Yes ☐ No

Indicate

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

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

was required to submit such files). ☑ Yes ☐ No

Indicate by check mark whether the registrant

is a large accelerated filer, an accelerated filer, a non-accelerated filer, a smaller reporting company, or an emerging growth company.

See the definitions of “large accelerated filer,” “accelerated filer,” “smaller reporting company,”

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

Large accelerated filer ☐ Accelerated filer ☐

Non-accelerated filer ☑ Smaller reporting company ☑

Emerging growth company ☐

If an emerging growth company, indicate by check

mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting

standards provided pursuant to Section 13(a) of the Exchange Act. ☐

Indicate by check mark whether the registrant

has filed a report on and attestation to its management assessment of the effectiveness of its Internal Control Over Financial Reporting

under section 404 (b) of the Sarbanes-Oxley by the registered public accounting firm that prepared or issued its annual report. ☐

If securities are registered pursuant to Section

12(b) of the Act, indicate by check mark whether the financial statements of the registrant included in the filing reflect the correction

of an error to previously issued financial statements. ☐

Indicate by check mark whether any of those error

corrections are restatements that required a recovery analysis of incentive-based compensation received by any of the registrant’s

executive officers during the relevant recovery period pursuant to § 240.10D-1(b). ☐

Indicate by check mark whether the registrant

is a shell company (as defined in Rule 12b-2 of the Exchange Act). ☐

Yes ☑ No

The aggregate market value of the voting and non-voting

stock held by non-affiliates of the Registrant, as of September 30, 2024, the last business day of the Registrant’s most recently

completed second fiscal quarter, was approximately $29,724,689. Solely for the purposes of this disclosure, shares of common stock held

by executive officers and directors of the Registrant as of such date have been excluded because such persons may be deemed to be affiliates.

This determination of executive officers and directors as affiliates is not necessarily a conclusive determination for any other purposes.

83,891,586 shares of our common stock were outstanding

as of June 20, 2025.

DOCUMENTS INCORPORATED BY REFERENCE

None

IGC PHARMA, INC.

FORM 10-K

FOR THE FISCAL YEAR ENDED MARCH 31, 2025

TABLE OF CONTENTS

Page

PART I

Item 1. Business 5

Item 1A. Risk Factors 25

Item 1B. Unresolved Staff Comments 39

Item 1C. Cybersecurity 39

Item 2. Properties 40

Item 3. Legal Proceedings 40

Item 4. Mine Safety Disclosures 40

PART II

Item 6. [Reserved] 42

Item 7A. Quantitative and Qualitative Disclosures About Market Risk 51

Item 8. Financial Statements and Supplementary Data 51

Item 9A. Controls and Procedures 78

Item 9B. Other Information 78

Item 9C. Disclosure Regarding Foreign Jurisdictions that Prevent Inspections 78

PART III

Item 10. Directors, Executive Officers, and Corporate Governance 79

Item 11. Executive Compensation 85

Item 14. Principal Accountant Fees and Services 88

PART IV

Item 15. Exhibits and Financial Statement Schedules 91

Signatures 93

Table of Contents

FORWARD-LOOKING STATEMENTS AND IMPORTANT

FACTORS

This Annual Report

on Form 10-K and the documents incorporated in this report by reference contain “forward-looking statements” within the meaning

of federal securities laws. Additionally, we or our representatives may, from time to time, make other written or verbal forward-looking

statements. In this report and the documents incorporated by reference, we discuss plans, expectations, and objectives regarding our

business, financial condition, and results of operations. Without limiting the foregoing, statements that are in the future tense, and

all statements accompanied by terms such as “believe,” “could,” “project,” “expect,”

“trend,” “estimate,” “forecast,” “assume,” “intend,” “plan,”

“target,” “anticipate,” “outlook,” “preliminary,” “will likely result,” “will

continue,” and variations of them and similar terms are intended to be “forward-looking statements” as defined by federal

securities laws. We caution you not to place undue reliance on forward-looking statements, which are based upon assumptions, expectations,

plans, and projections. In addition, our goals and objectives are aspirational and are not guarantees or promises that such goals and

objectives will be met. Forward-looking statements are subject to risks and uncertainties, including those identified in the “Risk

Factors” included in this report and in the documents incorporated by reference that may cause actual results to differ materially

from those expressed or implied in the forward-looking statements. Forward-looking statements speak only as of the date when they are

made. Except as required by law, we assume no obligation to update forward-looking statements to reflect events, circumstances, changes

in expectations, or the occurrence of unanticipated events after the date of those statements.

Forward-looking statements

are based upon, among other things, our assumptions with respect to:

● our disposal of non-core Company assets;

● our ability to maintain a stock listing on a national securities exchange;

● our ability to timely complete regulatory filings;

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● our financial performance;

● our ability to fund the costs of clinical trials and other related expenses;

● our ability to obtain and protect patents for the use of our formulations;

● our ability to successfully implement our strategy.

You should consider

the limitations on, and risks associated with, forward-looking statements and not unduly rely on the accuracy of predictions contained

in such forward-looking statements. As noted above, these forward-looking statements speak only as of the date when they are made. Moreover,

in the future, we may make forward-looking statements through our senior management that involve the risk factors and other matters described

in this report, as well as other risk factors subsequently identified, including, among others, those identified in our filings with

the SEC in our quarterly reports on Form 10-Q and our current reports on Form 8-K.

This document contains

statements and claims that are not approved by the FDA, including statements on hemp and hemp extracts, including cannabinoids. These

statements and claims are intended to be in compliance with federal and state laws.

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PART I

In this report, unless

the context requires otherwise, all references in this report to “IGC,” “the Company,” “we,”

“our,” and “us” refer to IGC Pharma, Inc., together with the subsidiaries identified

in Exhibit 21.1 of this Annual Report on Form 10-K. We exclude our investments and minority non-controlling interests, and any information

provided by them is not incorporated by reference in this report. They should not be considered part of this report.

ITEM 1. BUSINESS

Overview

IGC is a Maryland corporation

established in 2005 with a fiscal year ending on March 31, spanning a 52- or 53-week period. Please refer to Note 1, “Nature of

Operations” and Item 8 of this Annual Report on Form 10-K, for further information on business segments.

Our mission is to improve

the lives of individuals affected by Alzheimer’s disease by addressing both its symptoms and the disease. Our near-term focus is

on advancing IGC-AD1, our lead drug candidate currently in Phase 2 clinical trials targeting agitation in Alzheimer’s patients.

We are also investing in our early-stage pipeline of investigational therapies and exploring Artificial Intelligence (AI) powered models

designed to identify early markers of Alzheimer’s. We believe that combining scientific innovation with operational execution, including

leveraging our internal contract research organization, positions us to efficiently advance our pipeline toward commercialization, although

there can be no assurance thereof. Our long-term strategy is to build a portfolio of differentiated therapies that not only address symptomatic

needs but also target disease-modifying mechanisms, thereby creating sustainable value for patients, caregivers, and shareholders.

Our lead investigational drug,

IGC-AD1, has progressed through preclinical evaluations and a successful Phase 1 safety trial, and is currently being evaluated in a multicenter,

randomized, double-blind, placebo-controlled Phase 2 clinical trial, officially named “CALMA” (Calming Agitation in Alzheimer’s).

Interim data from this trial have demonstrated encouraging signs of efficacy, with patients receiving IGC-AD1 experiencing a statistically

significant reduction in agitation compared to placebo within the first 2-6 weeks of treatment. This reduction in agitation is particularly

notable as it could, although there can be no assurance, significantly improve patient care and represents a potential breakthrough in

managing Alzheimer’s-related agitation. In addition, IGC-AD1, Phase 2 clinical trial interim data also demonstrate a clinical and

statistically significant reduction in sleep disturbances among Alzheimer’s patients receiving the active medication compared

to placebo.

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

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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:

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:

● knowledge of plant and cannabinoid-based combination therapies;

● knowledge of research and development in the field;

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.

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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.

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

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)

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

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.

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