Igc Pharma, Inc. · AMEX:IGC
Igc Pharma — Investor Presentation (February 2024)
41 slides from Igc Pharma's investor presentation, February 2024
Slide 1: February 2024 - NYSE American: IGC
February 2024. NYSE American: IGC
Slide 2: Safe Harbor
The matters discussed in this presentation include forward-looking statements about the business prospects of IGC Pharma, Inc. Forward-looking statements are often preceded by words such as believes, expects, anticipates, plans, will, goal, may, intends, assumes, or similar expressions. Forward-look
Slide 3: Company Overview
COMPANY OVERVIEW • Our focus is treating Alzheimer’s disease (AD) through our growing pipeline of five drug assets • Lead therapeutic candidate IGC-AD1 is currently in a 146-person Phase 2b trial for agitation in dementia due to Alzheimer’s. IGC-AD1 is a CB1r partial agonist that reduces neuroinflam
Slide 4: Alzheimer's Disease
ALZHEIMER’S DISEASE The global number of persons 1in 9 13.8 Million with AD dementia, prodromal AD, and preclinical AD were estimated at: 65+ yrs. Americans with • AD dementia: 32 million. Alzheimer’s by 20501 Americans with • Prodromal AD: 69 million. Alzheimer’s in 20231 • Preclinical AD: 315 mill
Slide 5: Investment Highlights
INVESTMENT HIGHLIGHTS Two Patented and three patent pending investigational drug candidates targeting Alzheimer’s All showing favorable pre-clinical attributes towards Alzheimer’s disease pathology IGC-AD1 is currently in Phase 2B with data milestones expected in mid-2024 Leading artificial intellig
Slide 6: Vertically Integrated Operations
VERTICALLY INTEGRATED OPERATIONS Potomac, MD. Vancouver, WA Colombia India Headquarters cGMP Manufacturing Licensed R&D facilities Analytics and Processing facility Constructed Significant Operational Barriers to Entry • Approved licenses • Licensed access to raw APIs • Phase 3 - ready manufacturing
Slide 7: AD Pipeline Overview
AD PIPELINE OVERVIEW ASSET PRECLINICAL PHASE 1 PHASE 2 PHASE 3 MILESTONE TARGETS neuroinflammation, neurotransmitter Interim Topline data IGC-AD1 imbalance, inflammasome-3 and AD pathology Second half 2024 TARGETS Aβ PLAQUES Tox study 2024 TGR-63 (Early- Moderate Stage Alzheimer’s) TARGETS neuroinfl
Slide 8: Agitation in Alzheimer's
AGITATION IN ALZHEIMER’S Agitation: excessive motor activity, verbal aggression, or physical aggression that is severe enough to impair personal relationships, social functioning, and/or daily activities1. Agitation starts early in AD and increases in severity as the disease progresses2. 7 6 % of Al
Slide 9: Our Solution
OUR SOLUTION The Promise of IGC-AD1 Two APIs that target 1) neuroinflammation, 2) neurotransmitter imbalance, 3) CB1r agonism and 4) inflammasome-3, all implicated in agitation in AD IGC-AD1 can potentially reduce agitation, and act on AD pathology (plaques, tangles) making it a significantly more p
Slide 10: Data from Preclinical Trial Results on Alzheimer's Cell Lines
DATA FROM PRECLINICAL TRIAL RESULTS ON ALZHEIMER'S CELL LINES Reduces two key hallmarks of Alzheimer's plaques and tangles (pTau): • Inhibits the aggregation of amyloid plaque • Reduces phosphorylated tau (pTau) • Enhances mitochondrial function • Non-toxic. Repeated low dosing over 48 hours is non-
Slide 11: Preclinical Data: Animal Model Memory Improved in AD Mouse Model
PRECLINICAL DATA: ANIMAL MODEL MEMORY IMPROVED IN AD (APP/PS1) MOUSE MODEL IGC- AD1 significantly improved times and fewer errors in a Morris Water Maze test than those in the control group in an Alzheimer's mouse model • The maze uses spatial cues for mice to navigate a swimming container full of s
Slide 12: IGC-AD1 Phase I Clinical Trial Data
IGC-AD1 PHASE I CLINICAL TRIAL, Safety, Tolerability, Agitation, NPS DATA No life-threatening or serious adverse Multiple Ascending Dose (MAD) study to evaluate events at any dosing level safety and tolerability of IGC-AD1 in participants with AD & NPS (Neuropsychiatric Symptoms) using the NPI (Neur
Slide 13: Data on Neuropsychiatric Symptoms Measured by NPI Scores
DATA ON NEUROPSYCHIATRIC SYMPTOMS MEASURED BY NPI SCORES Total NPI-12 score 35.0 ** 31.5 30.0 Results on Neuropsychiatric 25.0 ** Symptoms (NPS) 22.2 Measured by NPI-12 Average Total NPI 20.0 Baseline ** 16.0 Patients taking IGC-AD1 showed 14.8 * Day 15 15.0 an overall improvement in NPS 12.4 in all
Slide 14: Data on Agitation
DATA ON AGITATION NPI Agitation Domain 5.0 4.7 4.5 4.3 4.2 4.0 Cohorts 1, 2,3 received IGC-AD1 once a day, twice a day and 3.5 three times a day respectively Average NPI Score 3.0 3.0 At three different doses, agitation 2.5 Baseline improved both clinically and Day 15 (EOT) 2.0 statistically (p<.05)
Slide 15: Ongoing IGC-AD1 Phase 2b
ON GOING IGC-AD1 PHASE 2b Placebo Controlled, Double Blind, Randomized, Multi Site Phase 2b protocol seeks to show that IGC-AD1 is effective, compared to placebo, in lowering agitation in participants with Alzheimer’s Objective • Evaluate if IGC-AD1 is superior to placebo in reducing agitation in a
Slide 16: AI-Integrated Trial
AI-INTEGRATED TRIAL IGC is partnered with leading Artificial Intelligence research center CINFONIA at the University of Los Andes Partnership aims to leverage deep learning algorithms and generative AI to analyze variations in disease signatures among patients, enabling IGC Pharma to identify indivi
Slide 17: TGR-63 Background
TGR-63 A PROMISING PATH-BREAKING MOLECULE • India-based Jawaharlal Nehru Centre for Advanced Scientific Research (JNCASR) created the TGR-63 molecule • IGC acquired exclusive rights to TGR-63 from JNCASR AD DRUG CANDIDATE 2 researchers in 2022 • Pre-clinical testing demonstrates that TGR-63 holds po
Slide 18: TGR-63: Mode of Action (PC12 cells)
TGR-63: Mode of action To study how TGR-63 can treat AD pathology and cognitive and behavioral symptoms, the AD-like environment was mimicked in vitro by exposing cultured PC12 and SHSY5Y cells to Aβ42. This resulted in the generation of cytotoxic aggregation species in the growth media. Aβ42 caused
Slide 19: TGR-63: Mode of Action
TGR-63: Mode of action • To understand the molecular mechanism underlying its ability to decrease plaque aggregates and increase neuronal viability, computational studies like molecular docking and molecular dynamics were performed. TGR-63 • These suggested that the molecular mode of action of TGR-6
Slide 20: Molecular Structures for TGR
Molecular Structures for TGR • Molecular structures that are candidates to modulate A𝛽42 aggregation and associated toxicity. • TGR-63 demonstrated higher capacity to inhibit A𝛽42 aggregation TGR-63 (A), higher capacity to dissolve Aβ42 aggregates (B) and increased PC12 cell viability (C) when…
Slide 21: The Promise of TGR-63: Reduction of Plaque in Mouse Model
The Promise of TGR-63: Reduction of Plaque in Mouse Model TGR-63 effectively reduced the amyloid burden in the mice cortex and hippocampus. WT DAPI AD +TGR63 +TGR63 DAPI OC DAPI OC Before administration TGR63 administration After administration AD/WT characterization Behavioral study Immunohistochem
Slide 22: TGR-63 Improved Behavior in a Mouse Model
TGR-63-Improved Behavior In a Mouse Model TGR-63 improved cognitive performance in APP/PS1 and Wild Type mice. The dose administered was 5 mg/kg body weight. Open field test TGR-63 treated mice had a lower locomotion in the field, indicating improved behavior. Adv. Therap. 2021, 4, 2000225 NYSE Amer
Slide 23: TGR-63 Improved Memory in a Mouse Model
TGR-63 Improved memory in a Mouse Model Novel object identification test Adv. Therap. 2021, 4, 2000225 TGR-63 treated mice had a higher exploration of the novel object. Morris Water Maze TGR-63 treated mice learned the location of the target and had less error rate than non treated mice.
Slide 24: TGR-63 to IGC-AD2 Timeline
TGR-63 TO “IGC-AD2” TIMELINE Early-Stage Preclinical FDA Review and Drug Preclinical Clinical Trials studies and Drug Post – Market Development studies (IGC-AD2) Monitoring Development Target Identified and Established the Licensing of TGR-63 Phase-2 Clinical Trial validated (JNCASR) Proof of Concep
Slide 25: First Mover Advantage with Intellectual Property
FIRST MOVER ADVANTAGE WITH INTELLECTUAL PROPERTY FOREIGN PATENT US-PATENTS TARGET DESCRIPTION PATENTS APPLICATIONS GRANTED GRANTED • Alzheimer's Disease (IGC-AD1) Composition & Method for treating CNS Disorders 7 1 1 • Alzheimer's Disease (IGC-AD1) Composition & Method for treating CNS Disorders 1 •
Slide 26: Senior Scientific Trial Team
SENIOR SCIENTIFIC TRIAL TEAM Dr. Varduhi Ghazaryan, MD, MPH Medical Director Dr. Saadia Shahnawaz, MD Medical Director Dr. Juan Manuel Orjuela, MD Scientific Neuropsychiatrist Management Jagadeesh Rao, PhD Principal Scientist Diego Rodriguez, PhD Senior Medicinal Chemist Evelyn Gutiérrez, Chem Eng.
Slide 27: Senior Scientific Advisors
SENIOR SCIENTIFIC ADVISORS Prof. Chuanhai Cao, PhD Professor of Pharmaceutical Science Inventors Prof. T Govindaraju, PhD, FRSC. Professor - Bioorganic Chemistry Dr. L. Elliot Hong, MD Professor Psychiatrist Dr. James Saunders, PhD Ret. Professor, Molecular Biology Scientific Advisors Jeffrey L. Cum
Slide 28: Potential to Drive Significant Value
POTENTIAL TO DRIVE SIGNIFICANT VALUE NORTH AMERICA AND EUROPE ITEM Year 1 Year 2 Year 3 Individuals with AD 15M 15M 15M Agitation in AD (76%) 11M 11M 11M %adoption of drug (IGC- 3% 5% 10% AD1) Annual Price/Patient of drug $2,400 $2,400 $2,400 Estimated Revenue $0.8B $1.3B $2.6B Key Market Factors No
Slide 29: Estimated Public Company Valuations During Trials
ESTIMATED PUBLIC COMPANY VALUATIONS DURING TRIALS • Public. • Year shows year when the company was in the clinical stage that is mentioned. Assumptions • Estimated valuation is the valuation at the time the company was closest to Phase entered the Phase that is mentioned. • Current Market valuation
Slide 30: Initiating Coverage with BUY and $2.75 Target
Initiating Coverage with BUY and $2.75 Target (~ $167m valuation) https://ascendiant.com/
Slide 31: Thank You
THANK YOU igc@imsinvestorrelations.com
Slide 32: Additional Information
(EIGCPHARMA ADDITIONAL INFORMATION
Slide 33: Caregiver Testimonial
Caregiver Testimonial From our Phase 1IGC-AD1 study “I want to tell you a story that brought incredible joy to me. We participated in your Phase 1Clinical trial in Puerto Rico. After about a week of medication, one day I came home to find that she had made dinner and was dancing to music that she en
Slide 34: Pre-clinical Studies: Detailed Scientific Results
aN Pre-clinical studies: Detailed scientific results
Slide 35: AB Production
AB Production Aggregation AB Monomers APP Levels Spatial Memory Neurotoxicity The API in IGC-AD1 reduces AB40 peptide production and AB42 aggregation in Alzheimer's cell lines. AB40 Production AB42 Aggregation petit Ot / —a— Aggregate THC 0.25nM —e—THC 2.5nM & = 6 P= rey 5 3 2 a ° z a < 6 a 24 Time
Slide 36: AB Production
AB Production , iacrouction AB Monomers APP Levels Spatial Memory Percentage (%) of AB monomers In Alzheimer’s cell lines, |GC-AD1 increased AB monomers and decreased AB aggregation in a dose-dependent I manner. Monomer Aggregation THC100nM THC 10nM 5 = re) c 6 ea a < xe} ae ny = s o x
Slide 37: APP Levels
ear an seainaner The APIs in IGC-AD1 did not reduce Amyloid Precursor Protein (APP) levels in Alzheimer’s cell lines. APP modulates cell growth, motility, and survival; it is cut to create small fragments such as the AB peptide that eventually deposit as plaque. 2 ca ® s 15 z & ez 1 + faa) a 0.5 a w
Slide 38: AB Production: Memory Improved in Alzheimer's Mice Model
AB Production & Aggregation Starting position _ No improvement in memory perfomance = sa Hidden platform Improved spatial memory performance Nature Protocols. 2006; 1: 848-858; Int. J. Mol. Sci. 2022, 23, 2757 AB Monomers APP Levels Spatial Memory Neurotoxicity Memory Improved in Alzheimer’s Mice Mo
Slide 39: AB Production: MTT Assay for Cell Viability
AB Production a ageregation AB Monomers APP Levels Spatial Memory Neurotoxicity MTT assay for cell viability Over 48 hours, repeated low-dose exposure to the API in IGC-AD1 was not toxic to Alzheimer's cells (N2a/ARPPsWe cells). = S = o c o ac] 1 2 z Q fe) 0.25nM THC Concentration Representation of
Slide 40: Two APIs That Target Multiple Pathways
TWO APIs THAT TARGET MULTIPLE PATHWAYS Focused on relieving pathological alteration due to agitation in AD Agitation in AD Treatment with IGC-AD1 Deficient in CB1 receptor function increases agitation animals1 ; CB1 activity at earlier AD stages is higher in Partial agonist targets CB1 receptor hipp
Slide 41: Preclinical Data
PRECLINICAL DATA https://igcpharma.com/igc-ad1/#results