Emerald Health Pharmaceuticals Important Notice

Emerald Health Pharmaceuticals Inc. (the Company) is currently engaged in an ongoing offering under Regulation A+ (Regulation A+) under the Securities Act of 1933, as amended. The offering will be made only by means of an offering circular. This presentation shall not constitute an offer to sell or the solicitation of an offer to buy, nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction. No money or other consideration is being solicited at this time, and if sent in response to these materials, it will not be accepted. No securities may be sold, and no offer to buy securities can be accepted and no part of the purchase price can be received for an offering under Regulation A+ except pursuant to an Offering Circular qualified by the U. S. Securities and Exchange Commission, and any such offer may be withdrawn or revoked, without obligation or commitment of any kind, at any time before notice of its acceptance given after the qualification date. A person's indication of interest in a Regulation A+ offering is non-binding and involves no obligation or commitment of any kind. Our most recent Offering Circular and periodic reports are available via this URL: https://emeraldpharma.life/sec-filings-2019/

Cautionary Note Regarding Forward-Looking Statements

TO THE EXTENT STATEMENTS CONTAINED IN THE FOLLOWING PRESENTATION ARE NOT DESCRIPTIONS OF HISTORICAL FACTS REGARDING THE COMPANY, THEY SHOULD BE CONSIDERED “FORWARD-LOOKING STATEMENTS,” AS DESCRIBED IN THE PRIVATE SECURITIES LITIGATION REFORM ACT OF 1995, THAT REFLECT MANAGEMENT’S CURRENT BELIEFS AND EXPECTATIONS. YOU CAN IDENTIFY FORWARD-LOOKING STATEMENTS BY WORDS SUCHAS “ANTICIPATE,” “BELIEVE,” “COULD,” “ESTIMATE,” “EXPECT,” “FORECAST,” “GOAL,” “HOPE,” “HYPOTHESIS,” “INTEND,” “MAY,” “PLAN,” “POTENTIAL,” “PREDICT,” “PROJECT,” “SHOULD,” “STRATEGY,” “WILL,” “WOULD,” OR THE NEGATIVE OF THOSE TERMS, AND SIMILAR EXPRESSIONS THAT CONVEY UNCERTAINTY OF FUTURE EVENTS OR OUTCOMES. FORWARD-LOOKING STATEMENTS CONTAINED IN THESE PRESENTATIONS INCLUDE, BUT ARE NOT LIMITED TO, STATEMENTS REGARDING: (I) THE SUCCESS AND TIMING OF OUR PRODUCT DEVELOPMENT ACTIVITIES AND CLINICAL TRIALS; (II) OUR ABILITY TO DEVELOP OUR PRODUCT CANDIDATES; (III) OUR PLANS TO RESEARCH, DISCOVER, EVALUATE AND DEVELOP ADDITIONAL POTENTIAL PRODUCT, TECHNOLOGY AND BUSINESS CANDIDATES AND OPPORTUNITIES; (IV) OUR ABILITY TO DEVELOP AND MANUFACTURE OUR PRODUCT CANDIDATES AND TO IMPROVE THE MANUFACTURING PROCESS; (V) OUR ABILITY TO ATTRACT AND RETAIN KEY SCIENTIFIC OR MANAGEMENT PERSONNEL; (VI) THE ANTICIPATED TIMING OF CLINICAL DATA AVAILABILITY; (VII) OUR ABILITY TO MEET OUR MILESTONES; (VIII) OUR EXPECTATIONS REGARDING OUR ABILITY TO OBTAIN AND MAINTAIN INTELLECTUAL PROPERTY PROTECTION; AND (IX) THE IMPACT OF CAPITAL MARKET CONDITIONS ON US. FORWARD-LOOKING STATEMENTS ARE SUBJECT TO KNOWN AND UNKNOWN FACTORS, RISKS AND UNCERTAINTIES THAT MAY CAUSE ACTUAL RESULTS TO DIFFER MATERIALLY FROM THOSE EXPRESSED OR IMPLIED BY SUCH FORWARD LOOKING STATEMENTS. UNDUE RELIANCE SHOULD NOT BE PLACED ON FORWARD-LOOKING STATEMENTS. WE UNDERTAKE NO OBLIGATION TO PUBLICLY UPDATE ANY FORWARD-LOOKING STATEMENTS. THE COMPANY’S INVESTIGATIONAL DRUG PRODUCTS HAVE NOT BEEN APPROVED OR CLEARED BY THE FDA. P.2 Emerald Health Pharmaceuticals

• A clinical-stage biotechnology company developing first-in-class new chemical entities to treat diseases with unmet medical need

• Our technology has a unique multi-pronged mechanism of action, addressing validated targets for neurodegenerative, autoimmune, fibrotic & inflammatory diseases

• Preclinical studies demonstrate disease modification with the potential to reverse the progression of diseases which currently have no cure and cause significant morbidity and mortality

• Phase I completed successfully on our lead product candidate - Phase II initiation underway

WWW.EMERALDPHARMA.LIFE 3 Emerald Health Pharmaceuticals

Status: Private Headquarters: San Diego, CA, USA R&D: Córdoba, Spain

Focused on developing patented synthetic cannabinoid-derived drug candidates to treat diseases with unmet medical need

WWW.EMERALDPHARMA.LIFE 4 Emerald Health Pharmaceuticals: Key Highlights

Unique Strong IP & Strong Mechanism of Clinical Stage Significant Market Team Action Development

New Chemical Broad patent Phase 1 completed Experienced Entities (NCEs) protection with a on lead product biotech/pharma with the potential US$39B market candidate executives and for disease opportunity in the demonstrating globally- modification in first 4 targeted tolerability, safety, recognized clinical diseases with no diseases and dosing and scientific current cure flexibility advisors

WWW.EMERALDPHARMA.LIFE 5 Not for Distribution Development Roadmap

NOTE: In the scientific literature: EHP-101 = VCE-004.8 EHP-102 = VCE-003.2

WWW.EMERALDPHARMA.LIFE 6 Market Opportunity: ~$39B in the First Four Target Diseases

1Global Drugs Market Size, Market Share, Application Analysis, Regional Outlook, Growth Trends, Key Players, Competitive Strategies and Forecasts, 2017 To 2025 Research and Markets Report 2Parkinson's Disease Therapeutics Market Global Industry Analysis Size, Share, Growth ,Trends, and Forecasts, 2017 To 2025 Transparency Market Research Report 3Scleroderma Diagnostics and Therapeutics Market Global Industry Analysis, Size, Share, Growth, Trends, and Forecast 2017 - 2024 Transparency Market Research Report 4Opportunity Analyzer: Huntington's Disease Opportunity Analysis and Forecast to 2024 Research and Markets Report

WWW.EMERALDPHARMA.LIFE 7 The Technology: Patented NCEs Derived from CBD & CBG

• Cannabidiol (CBD) & Cannabigerol (CBG) have multiple positive physiologic effects through interaction with the endocannabinoid system (ECS)

• Research indicates they are: - Anti-inflammatory - Antioxidative - Neuroprotective - Analgesic - Anti-infective - Non-psychoactive

Source: https://carebydoctors.com/ailments-corresponding-cannabinoids/ WWW.EMERALDPHARMA.LIFE 8 The ECS Exists Throughout the Body

Distribution of CB1 Receptors

Receptors

Health benefits; CB1 Psychoactive effects

CB2 TRPV1 Health benefits; GPR55 FAAH No psychoactive effects

PPARs MALG TRPA1

WWW.EMERALDPHARMA.LIFE 9 Our Scientific and Pharmaceutical Approach

To improve on the positive health effects of CBD and CBG by modifying them to create enhanced new chemical entities

• EXPANDED receptor targeting

• FOCUSED on receptors that can treat diseases with unmet medical need

• DEVELOP composition of matter patented new chemical entities (NCEs)

• CREATE a strong IP portfolio

WWW.EMERALDPHARMA.LIFE 10 Cannabinoid Science: Rational Drug Design

Chemical modifications of the Synthetic CBD molecule create new targets and receptor binding

New, patented molecules

• Our drug discovery platform CB2 TRPV1 The Result: focuses on targets related • Totally synthetic NCEs to the ECS without binding GPR55 FAAH to CB1 receptors • Non-psychotropic • Targeted receptor activity • The goal: to affect targets PPARs MALG validated for various diseases TRPA1 • Potential for disease modification with unmet medical need • Composition of matter patents

WWW.EMERALDPHARMA.LIFE 11 Patents 14 patented CBD derivatives 16 granted, 22 pending, covering 25 molecules

Molecules in our NCE Library

• Composition of matter and method of use patents

• Broad protection in the US, EU 11 patented CBG derivatives and many countries worldwide

• Protection to 2039

• Potential for multiple products and indications

WWW.EMERALDPHARMA.LIFE 12 The Unique Convergence of Cannabinoids, Science & Biology

Cannabinoids Science Other New Proprietary Cannabinoids Molecules CBG The EHP-101 EHP EHP-102 (VCE-004.8) Platform (VCE-003.2)

14 patented 11 patented CBD derivatives CBG derivatives

Patented CBD Derivatives (“4-series”) Patented CBG Derivatives (“3-series”)

EHP-102 EHP-101

Biology

WWW.EMERALDPHARMA.LIFE 13 Provides Many Therapeutics Opportunities

Neurodegenerative Inflammatory Auto-Immune

Lupus Parkinson’s disease Huntington’s disease Ulcerative Colitis / Crohn’s

Metabolic Cancer Fibrotic Diabetes Systemic Sclerosis (Scleroderma)

WWW.EMERALDPHARMA.LIFE 14 Lead Product Candidate: EHP-101 CBD A patented CBD derivative (NCE)

• Oral formulation

• Unique multi-pronged mechanism of action

• Preclinical proof-of-concept established EHP-101 • IND-enabling studies completed

• Phase I completed

• Phase II initiation underway

WWW.EMERALDPHARMA.LIFE 15 A Cannabinoid that is Not a Controlled Substance

The U.S. Drug Enforcement Administration (DEA) has determined that:

• VCE-004.8 (the active ingredient in EHP-101) is not a controlled substance

WWW.EMERALDPHARMA.LIFE 16 EHP-101: Designed for Targeted Mechanism of Action

Our strategy: Reduces neuroinflammation To improve on CBD’s PPARγ known positive effects Increases by creating a unique Neuroprotection new molecule that affects CB2 validated targets in MS: EHP-101 Improves - PPARγ survival and repair - CB2 - HIF HIF Promotes Remyelination PPARγ: Peroxisome proliferator-activated receptor gamma CB2: Cannabinoid receptor Type 2 HIF: Hypoxia inducible factor

WWW.EMERALDPHARMA.LIFE 17 EHP-101: Efficacy Demonstrated in Multiple Sclerosis

Efficacious in 4 validated MS models: EAE 1. Experimental Autoimmune Encephalomyelitis (EAE) 2. Theiler’s Murine Encephalomyelitis Virus (TMEV) 3. Cuprizone 4. Modified Cuprizone TMEV

Studies demonstrate:

• Significant improvement in clinical Cuprizone signs and clinical scores

• Stops neuroinflammation and demyelination Modified 0 8 10 12 14 16 18 20 22 24 26 Weeks of age Adult male C57BL/6 • Remyelination of Cuprizone Cuprizone/Rapamycin Demyelination 0 2 4 6 8 10 12 12+2 12+4 12+6 Remyelination Oral EHP-101 treatment Evaluation 5, 10, or 20 mg/kg/day

WWW.EMERALDPHARMA.LIFE 18 EHP-101: Efficacy Demonstrated in Multiple Sclerosis EHP-101 shows efficacy in all four validated MS models

Approved MS Drugs Attributes EAE TMEV Cuprizone Modified Cuprizone (effects in animal models)

Moderate Intense demyelination; demyelination; Relapsing-Remitting remyelination model MS stage Progressive MS model remyelination model MS model with 6w therapeutic with 2w therapeutic window window Reduced clinical severity and All approved self-injected, infused and ü ü oral MS drugs (EAE) neuropathology

Corticosteroids, Interferon beta (EAE & Reduced microglia Cuprizone); (EAE); activation and ü ü ü (EAE & Cuprizone); inflammation (EAE); Tecfidera: (EAE & TMEV); Immunosuppressors (EAE) Fingolimod (EAE & Cuprizone); Reduced lymphocyte Siponimod (EAE1); Tecfidera: (EAE & migration to CNS and ü ü TMEV); Immunosuppressors (EAE): immunosuppression (EAE): (EAE): (EAE) Neuroprotection and (Tecfidera) (EAE & reduced TMEV); Siponimod (EAE); Ocrelizumab ü ü (EAE); Alemtuzumab (EAE); demyelination Natalizumab (EAE)

Induction of Fingolimod (EAE & Cuprizone); remyelination ü ü ü

Reduction of NfL in Ocrelizumab and other anti-CD20 plasma ü mAbs (EAE) ✓ indicates positive EHP-101 efficacy response

WWW.EMERALDPHARMA.LIFE 19 EHP-101: Efficacy Demonstrated in Multiple Sclerosis

Efficacious in 4 validated MS models: Clinical Scores 1. Experimental Autoimmune Encephalomyelitis (EAE) 4 EAE+vehicle 2. Theiler’s Murine Encephalomyelitis Virus (TMEV) EAE+EHP-101 (1mg/kg) 3 3. Cuprizone Control (untreated): EAE+EHP-101 (5mg/kg)

4. Modified Cuprizone e EAE+EHP-101 (10mg/kg) r

o 2

c EAE+EHP-101 (20mg/kg) S

** • Mice are examined daily for clinical signs of MS 1 and disease scores were measured as follows: ** ** Treated: *** 0 ** 0 = no disease 0 10 20 30 *** days postinfection 1 = limb & tail weakness 2 = limb, tail & hind limb weakness Days Post-Infection (dpi) 3 = hind limb 4 = hind limb & front limb paralysis 5 = moribund and death. EHP-101 attenuates clinical severity and neuropathology, significantly ameliorating the clinical signs and progression of disease. Results • All animals are sacrificed at day 28 for expressed as mean ± SEM. **p<0.01, ***p<0.001 EAE + EHP-101 vs EAE + further analysis Vehicle (one-way ANOVA followed Tukey’s test).

WWW.EMERALDPHARMA.LIFE 20 EHP-101: Efficacy Demonstrated in Multiple Sclerosis

4 y t Efficacious in 4 validated MS models: i Histological s n ***

e 3 t n I

Analysis 1 a b

I 2

1. Experimental Autoimmune Encephalomyelitis (EAE) d ### e z i l a EAE + 1 m

2. Theiler’s Murine Encephalomyelitis Virus (TMEV) r EAEEHP- 101+ (20EHP mg/kg)-101 o CFACFA EAE EAE+ Vehicle+ Vehicle (20 mg/kg) N 3. Cuprizone 0 CFA EAE + EAE + 4. Modified Cuprizone Vehicle EHP-101 (20 mg/kg) 4

y *** t i s Iba1

Iba1 n e

EHP-101: t 3 n I ## P A

F 2 G

• d

Significantly reduces glial reactivity e z i l

a 1 m r o N 0 • Preserves structure CFA EAE + EAE + Vehicle EHP-101

GFAPGFAP Images are of thoracic spinal cord cross-sections of (20 mg/kg) 50 μm thick, in which immunofluorescence with 1.5 y t i s ### n

anti-Iba1, glial fibrillary acidic protein (GFAP), and e t n

I 1.0

myelin binding protein (MBP) were performed. The P

B *** M

d

quantification of each marker is shown as mean ± e z

i 0.5 l a m

SEM; significance was determined by one-way r MBP MBP o N ANOVA followed Tukey´s test. ***p<0.001 EAE + 0.0 Vehicle vs CFA; ##p < 0.01, ###p<0.001 EAE + CFA EAE + EAE + Vehicle EHP-101 EHP-101 vs EAE + Vehicle. (20 mg/kg)

WWW.EMERALDPHARMA.LIFE 21 EHP-101: Efficacy Demonstrated in Multiple Sclerosis

Efficacious in 4 validated MS models:

1. Experimental Autoimmune Encephalomyelitis (EAE) 2. Theiler’s Murine Encephalomyelitis Virus (TMEV) Clinical Scores 3. Cuprizone 4. Modified Cuprizone 2500 HACT 78 dpi 300 VACT 78 dpi ## 2000 # • General health conditions and motor function 200 were evaluated from day 60 (when animals 1500

showed their locomotor activity impaired) 1000 Time (sec) until 75 days post-infection Time (sec) 100 *** * 500 • Screening for locomotor activity (LMA) was 0 0 performed using an activity monitoring SHAM TMEV TMEV SHAM TMEV TMEV system coupled to a Digiscan Analyser + + + + VEH VCE-004.8 VEH VCE-004.8 • LMA data were collected for: horizontal EHP-101 attenuates clinical disease severity and ameliorates motor deficits. activity, as the total number of beam Actimeter test showed a significant reduction of the horizontal exploratory interruptions of horizontal area sensors, and activity (HACT) and of the vertical activity (VACT) of TMEV group at 78 dpi. vertical activity, as total number of beam *p<0.05 **p<0.01 TMEV+VEH vs Sham; #p<0.05 ##p<0.01 TMEV+VCE-004.8 interruptions in the vertical sensor vs TMEV+VEH. (Non-parametric Kruskal–Wallis test).

WWW.EMERALDPHARMA.LIFE 22 EHP-101: Efficacy Demonstrated in Multiple Sclerosis Histological Analysis A SHAM TMEV + VEH TMEV + VCE-004.8 SHAM TMEV + VEH Efficacious in 4 validated MS models: TMEV + VCE-004.8 1. Experimental Autoimmune Encephalomyelitis (EAE) 2. Theiler’s Murine Encephalomyelitis Virus (TMEV) 3. Cuprizone B SHAM 4. Modified Cuprizone TMEV + VEH TMEV + VCE-004.8 EHP-101:

• Reduces microglial reactivity & infiltration of C inflammatory cells • Preserves myelin structure

Images shown are thoracic-lumbar spinal cord cross-sections 30 μm thick; immunofluorescence with anti-Iba1 (A), anti-CD4 (B), H-E (C), and Neurofilament H staining, (D), with immunohistochemistry was performed. Treatment reduces the number of CD4+T cells and cell infiltrates (C, arrows) and a causes a significant D TMEV + VEH TMEV + VCE-004.8

decrease in microglial reactivity (A). Quantifications are shown as means ±SEM, TMEV + VEH and significance was determined by Kruskal-Wallis non-parametric test. TMEV + VCE-004.8 ***p<0.001 vs Sham; ##p<0.01 ###p<0.001 vs TMEV + VEH. Scale bar: 150 μm (A), 100 μm (C and E). ***p<0.001 unpaired two-tailed Student´s t test (D).

WWW.EMERALDPHARMA.LIFE 23 EHP-101: Efficacy Demonstrated in Multiple Sclerosis

Histological Efficacious in 4 validated MS models: Analysis 1. Experimental Autoimmune Encephalomyelitis (EAE) 2. Theiler’s Murine Encephalomyelitis Virus (TMEV) 3. Cuprizone 4. Modified Cuprizone

ab bc CTRL CPZ 6W CTRL CPZ 6W MBP Corpus Callosum Cryomyelin

CPZ 6+1W + CPZ 6+1W + Cortex CPZ 6+1W EHP101 (20 mg/kg) CPZ 6+1W EHP101 (20 mg/kg)

Effect of EHP-101 treatment on remyelination in CPZ-induced demyelination. (a) Histological study of myelin by Cryomyelin staining in corpus callosum MBP

Cryomyelin and quantification of the mean intensity is shown (c). (b) Significant recovery of myelin staining is shown by immunofluorescence studies of myelin basic CPZ 6+2W + CPZ 6+2W + CPZ 6+2W EHP101 (20 mg/kg) CPZ 6+2W EHP101 (20 mg/kg) protein (MBP) in cortex and quantification of MBP immunoreactivity is represented (d). Data represents the mean ± SEM, and significance was determined by one-way ANOVA followed Tukey´s test. ***p<0.001 CPZ 6W or CPZ 6W + 1 or CPZ 6W + 2 vs Control; ###p<0.001 CPZ 6W +1 + EHP-101 MBP

Cryomyelin vs CPZ 6W +1, †††p<0.001 CPZ 6W +2 + EHP-101 vs CPZ 6W +2.

WWW.EMERALDd PHARMA.LIFE e 24

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0 N 0.0 CTRL CPZ + 20 + 20 CTRL CPZ + 20 + 20 6W 6W CPZ 6 + 1W CPZ 6 + 2W CPZ 6 + 1W CPZ 6 + 2W EHP-101: Efficacy Demonstrated in Multiple Sclerosis

Efficacious in 4 validated MS models:

1. Experimental Autoimmune Encephalomyelitis (EAE) Histological 2. Theiler’s Murine Encephalomyelitis Virus (TMEV) Analysis 3. Cuprizone c d 4. Modified Cuprizone y

y 8

t 6 t i i

a b s s *** CTRL CPZ 6W CTRL CPZ 6W n n e

e *** t

t ***

6 n n *** I ** I

4

*** P 1 ## A a F b

I 4

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d Iba1 GFAP d e e z

i 2 z l i l a 2 a m r

CPZ 6+1W + CPZ 6+1W + m r CPZ 6+1W EHP101 (20 mg/kg) CPZ 6+1W EHP101 (20 mg/kg) o o N

0 N 0 CTRL CPZ + 20 + 20 CTRL CPZ + 20 + 20 6W 6W Iba1 GFAP CPZ 6 + 1W CPZ 6 + 2W CPZ 6 + 1W CPZ 6 + 2W

Impact of EHP-101 on microglia and astrocyte activation in acute CPZ-induced demyelination. CPZ 6+2W + CPZ 6+2W + (a) A decrease on cuprizone-induced microgliosis is detected by immunofluorescence studies CPZ 6+2W EHP101 (20 mg/kg) CPZ 6+2W EHP101 (20 mg/kg) of Iba1 in corpus callosum and quantification is shown (c). (b) Astrogliosis was determined by immunofluorescence studies of GFAP in corpus callosum and quantification of intensity is shown (d). Data represents the mean ± SEM, and significance was determined by one-way GFAP Iba1 ANOVA followed Tukey´s test. ***p<0.001 CPZ 6W or CPZ 6W + 1 or CPZ 6W + 2 vs Control; **p<0.01 CPZ 6W + 2 vs Control; ##p<0.01 CPZ 6W +1 + EHP-101 vs CPZ 6W +1.

WWW.EMERALDPHARMA.LIFE 25 EHP-101: Efficacy Demonstrated in Multiple Sclerosis

Histological Efficacious in 4 validated MS models: Analysis 1. Experimental Autoimmune Encephalomyelitis (EAE) 2. Theiler’s Murine Encephalomyelitis Virus (TMEV) 3. Cuprizone Remyelinated 4. Modified Cuprizone

• Significant increase in density of myelinated axons vs. control with oral EHP-101 (10 and 20 mg/kg/day)

• Significant difference between 10 mg/kg/day and 20 mg/kg/day relative to 5 mg/kg/day

• Result: EHP-101 promotes remyelination of axons in brain white matter

WWW.EMERALDPHARMA.LIFE 26 EHP-101: Other Opportunities

• Metachromatic • Multiple sclerosis • • Acute disseminated encephalomyelitis • Inflammatory/ Myelin Immune • Paraneoplastic • Adrenomyeloneuropathy disorders Disorders • Rheumatoid arthritis • Globoid cell (Krabbe) • Systemic lupus erythematosus leukodystrophy • Behcet’s disease • Alexander’s disease • Sjorgen’s disease • Canavan disease

• B12 deficiency • Human Immunodeficiency Virus • Central pontine Toxic/ Demyelinating • Progressive multifocal myelinolysis metabolic Infectious leukoencephalopathy disorders diseases • Lyme disease • Carbon monoxide Disorders (CNS) • Neurosyphilis • Radiation • Human T-cell leukemia virus-1 • Posterior reversible encephalopathy syndrome

Demyelination associated to • Sarcoidosis Granulomatous ischemic or diseases • Wegener granulomatosis Traumatic Brain Neonatal • Lymphoid granulomatosis injury intracranial hemorrhage

WWW.EMERALDPHARMA.LIFE 27 EHP-101: Systemic Sclerosis (SSc) – a Form of Scleroderma

Chronic, systemic autoimmune disease causing fibrosis of skin and internal organs

• Life-threatening orphan disease

• No SSc-specific approved drugs

• Current drugs are not effective and have toxicities

• Lung fibrosis is a common cause of death (~60% mortality in 10 years)

WWW.EMERALDPHARMA.LIFE 28 EHP-101: Why Systemic Sclerosis/Scleroderma?

Inhibition of collagen EHP-101 MoA targets scleroderma synthesis

Inhibition of ERK • PPARγ and CB2: extensively studied activation molecular targets for the treatment of CB2 scleroderma* Fibroblast migration decrease

• Combined effect on PPARγ, CB2 EHP 101 PPARγ Myofibroblast and HIF have not been described for differentiation other types of marketed drugs Anti-inflammatory activity in vivo • Pre-clinical proof-of-concept has been established in relevant animal models Anti-fibrotic activity HIF in vivo

Vascular protection and regeneration *Minghua et al, Tavarares et al, Akhmetshina et al, Del Rio et al

WWW.EMERALDPHARMA.LIFE 29 EHP-101: Efficacy Demonstrated in SSc BLM + Control BLM BLM + RGZ (5mg/kg) VCE-004.8 (20mg/kg;ip) Efficacy in validated bleomycin (BLM) scleroderma model

• Prevents dermal thickening BLM + BLM + BLM + BLM + • Prevents collagen accumulation and VCE-004.8 (5 mg/kg) VCE-004.8 (10 mg/kg) VCE-004.8 (25 mg/kg) VCE-004.8 (50 mg/kg) macrophage accumulation

• Prevents lung fibrosis

• Prevents blood vessel fibrosis 2 *** 1,8

• Increases skin vascular markers 1,6 ## 1,4

1,2 ### ### ### ### 1 thickness Effects of EHP-101 on fibrotic skin: Images show Masson´s trichrome staining 0,8 ##

Fold ## ## (upper panel) and their respective quantification of skin from BLM-treated mice 0,6 # (lower panel). Values expressed as mean ± SEM. ***p<0.001, *p<0.05 versus 0,4 *** 0,2

control group; #p<0.05, ##p<0.01, ###p<0.001 versus BLM group. 0 Control BLM BLM + RGZ BLM + BLM + BLM + BLM + BLM + (5 mg/kg) VCE-004.8 VCE-004.8 VCE-004.8 VCE-004.8 VCE-004.8 (5 mg/kg) (10 mg/kg) (25 mg/kg) (50 mg/kg) (20 mg/kg;ip) WWW.EMERALDPHARMA.LIFE 30 EHP-101: Efficacy Demonstrated in SSc

Efficacy in validated bleomycin (BLM) scleroderma model

• Prevents dermal thickening

• Prevents collagen accumulation and macrophage accumulation

• Prevents lung fibrosis

• Prevents blood vessel fibrosis

• Increases skin vascular markers

Upper panel: collagen staining by picrosirius red dye. Lower panel: immunostaining of skin sections and quantification for the macrophage specific marker F4/80 (indicated with arrows). Values are expressed as mean ± SEM. ***p< 0.001 versus control group; # p<0.05, ##p<0.01, ###p<0.001 versus BLM group.

WWW.EMERALDPHARMA.LIFE 31 EHP-101: Efficacy Demonstrated in SSc

A A BLM + Efficacy in validated bleomycin (BLM) Control BLM RGZ (5mg/kg) scleroderma model 5 *** 4 ###

3 ### ### ### • Prevents dermal thickening 2 BLM + BLM + BLM + EHP-101 (5 mg/kg) EHP-101 (10 mg/kg) EHP-101 (25 mg/kg) 1 Ashcroft score (A.U.) • Prevents collagen accumulation and 0 BLM - + + + + + macrophage accumulation RGZ (mg/kg) - - 5 - - - EHP-101 (mg/kg) - - - 5 10 25 • Prevents lung fibrosis B B BLM + BLM • Prevents blood vessel fibrosis Control RZG (5 mg/kg) 100µm • Increases skin vascular markers 60 ***

40 ### ### ### ## (A) Representative lung images with Masson’s trichrome (% area) (% 20

staining (left panel). Comparison of the Ashcroft score BLM + BLM + BLM + Collagen content EHP-101 (5 mg/kg) EHP-101 (10 mg/kg) EHP-101 (25 mg/kg) among the experimental groups (right panel). (B) Images 0 of collagen staining by picrosirius red dye (left panel) BLM - + + + + + RGZ (mg/kg) - - 5 - - - and their quantification (right panel). Values are EHP-101 (mg/kg) - - - 5 10 25 expressed as mean ± SEM. ***p<0.001 versus control group; ##p<0.01, ###p<0.001 versus BLM group.

WWW.EMERALDPHARMA.LIFE 32 EHP-101: Efficacy Demonstrated in SSc

Efficacy in validated bleomycin (BLM) scleroderma model

• Prevents dermal thickening A • Prevents collagen accumulation and macrophage accumulation C • Prevents lung fibrosis B • Prevents blood vessel fibrosis

• Increases skin vascular markers

(A) Prevents BLM-induced collagen accumulation around blood vessels. Representative images of Masson’s trichrome stained skin sections showing collagen around blood vessels (indicated with frames - left panels). Quantification of collagen accumulation in skin (right panel). (B) Immunoflourescence labelling of TNC (green fluorescence) in control, BLM+vehicle and BLM+EHP-101 is shown (original magnification x 25). (C) Quantification of CD31 vessel staining (average vessel perimeter), and expression of TNC and a-SMA. Values are expressed as mean ± SEM. **p<0.01, *p<0.05 versus control group, ##p<0.01 versus BLM group.

WWW.EMERALDPHARMA.LIFE 33 EHP-101: Efficacy Demonstrated in SSc

Efficacy in validated bleomycin (BLM) scleroderma model

• Prevents dermal thickening

• Prevents collagen accumulation and macrophage accumulation CD31 CD34 • Prevents lung fibrosis

• Prevents blood vessel fibrosis

• Increases skin vascular markers

Effect of EHP-101 on vascular markers in skin. Double immunofluorescence labelling of skin (CD31, red fluorescence) (CD34, green fluorescence) in control (BLM+vehicle) and BLM+EHP-101. CD31 labeling is marked by white arrows and CD34 labeling is marked by yellow arrows. Quantification of CD31+/CD34+ endothelial cells (average of blood vessel perimeter). Values are expressed as mean ± SEM. **p<0.01, *p<0.05 versus control group, ###p<0.001, #p<0.05 versus BLM group. P values are calculated by Kruskal-Wallis test.

WWW.EMERALDPHARMA.LIFE 34 EHP-101: Our Path to the Clinic

2017 2018 2019 2020

Completed non-clinical Formed MS and SSc KOL SSc IND clearance proof-of-concept for MS Clinical Advisory Boards Received DEA determination that our HD EMA Orphan and SSc Designation Completed a Pre-IND NCE is not a Controlled H1 meeting with Substance First patient in - AUS Developed an oral US FDA (for MS) formulation and initiated Completed a Pre-IND First patient in - US manufacturing for Phase I Completed final clinical- meeting with enabling studies US FDA (for SSc) Completion of 6- & 9-mth Designed Phase I Initiated 6- and 9-month Initiated GLP toxicity rat and dog tox studies studies protocol based on FDA rat and dog tox studies feedback to be applicable for Phase II in MS US IND submission H2 Applied and got US FDA both MS and SSc Completed Phase I study MS IND clearance and EMA grant of Orphan MS Phase II initiation Drug Designation for Initiated Phase I human SSc IND submission Canada SSc CTA systemic scleroderma study in Australia submission SSc Phase IIa initiation Initial SSc Phase IIa data

WWW.EMERALDPHARMA.LIFE 35 EHP-101: Phase I Completed

A Phase 1, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Safety, Tolerability, Pharmacodynamics, Pharmacokinetics, and Food Effect of Single Ascending Doses and Multiple Ascending Doses* of EHP-101 in Healthy Subjects.

• 104 healthy volunteers

• Doses tested: 0.91mg to 185mg (anticipated therapeutic dose = 25mg-50mg/day)

• No clinically relevant laboratory, cardiac, or other abnormalities

• PK data support intended dosage and administration regimen for Phase II

• Biomarker analysis underway for support of mechanism of action

• All doses tested were well tolerated with only mild to moderate adverse events - No maximum tolerated dose reached - Adverse reactions included mild to moderate paresthesia, headache, blurred vision

* The Multiple Ascending Dose part of the study was 7 days of dosing, in increasing doses once daily and twice daily

WWW.EMERALDPHARMA.LIFE 36 EHP-101: Phase I Pharmacokinetics Summary

Phase I: PK supports dosage and administration Blue: 185 mg Pink: 100 mg • Maximum VCE-004.8 plasma levels (Cmax) occurred Green: 50 mg within 4 hours of dosing in all cohorts Brown line: 20 mg Purple line: 9 mg Dark Green line: 3 mg • A proportional increase in Cmax and drug exposure (area Red line: 0.91 mg under the curve, AUC) observed with increasing dose

• No drug accumulation observed after repeated dosing

• Anticipated therapeutic dose between 25 and 50 mg per day based on Cmax and AUC

• Daily doses in Phase II study not expected to exceed 100 mg per day

WWW.EMERALDPHARMA.LIFE 37 NCAM1 EHP-101: Phase I Biomarker Analysis

p = 0.009 Drug-related biomarkers being evaluated to possibly support mechanism of action (MoA)

• Exploratory: potential to show changes related to the HIF pathway (vascular endothelial cell function; angiogenesis) and PPARγ

and CB2 receptor activity (inflammation & immunomodulation)

• Preliminary analysis supports EHP-101 MoA: APOA4

- 19 proteins up-regulated* 6 hours post administration (Tmax 2-4h) p = 0.0009 o 7 related to vascular endothelial cell function (HIF pathway activation), such as VCAM1, NCAM1 and ECM1

o 4 related to lipid metabolism and control of inflammation (PPARγ activation), such as APO1, APOA4, APOE and APOM - 39 proteins down-regulated** at 6 hours post administration

o Several related to CB2 and PPARγ activation (e.g., FGB, LDHB, PCOLCE) (inflammation and immunomodulation)

* Up regulation is increased expression of a gene or protein that increases a target action (e.g., activation of HIF, leading to vasculogenesis and others positive physiologic processes)

** Down regulation is reduced expression of a gene or protein associated with a process (e.g., reduction of markers mediated by PPARg/CB2 activation – anti-inflammatory/immunomodulatory) WWW.EMERALDPHARMA.LIFE 38 EHP-101: Phase II Plan (Based on Pre-IND Discussions with FDA)

SSc: Phase II, Double-Blind, Placebo-Controlled Study to Evaluate the Safety, Tolerability, and Preliminary Efficacy in Patients with Diffuse Cutaneous Systemic Sclerosis (36 patients) Primary Objective: Safety and tolerability of various doses over 12 weeks Secondary Objective: Treatment effect by Composite Response Index in dcSSc (CRISS) over 12 weeks Exploratory Objectives: Treatment effect on patient-reported outcomes; treatment effect based on potential biomarkers related to the mechanism of action; molecular skin score

MS: Phase II Study in Patients with Relapsing Forms of Multiple Sclerosis (RMS) to Evaluate Safety, Tolerability, and Preliminary Efficacy (60-120 patients) Co-Primary Objectives: Safety and tolerability and treatment effect based on MRI at 6 months Secondary Objectives: Disease progression and disability status; MS Functional Composite and Expanded Disability Status Scale; time to first study relapse; annual relapse rate Exploratory Objectives: Treatment effect based on changes from baseline for: serum neurofilament light chain, diffusivity by Diffusion Tensor Imaging, patient reported outcome by multiple sclerosis impact scale-29, biomarkers

WWW.EMERALDPHARMA.LIFE 39 EHP-101: Planned Phase II Biomarker Analysis

In addition to clinical efficacy endpoints, biomarkers will be assessed in Phase II to possibly provide further evidence of efficacy

• Examples: - Neurofilament light chain in MS patients and gene expression in skin biopsies of SSc patients

• Preclinical evidence supports the relevant biomarkers and endpoints:

Ø MS: Neurofilament expression in spinal cord shows EHP-101 prevents axonal damage and preserves myelination

Ø SSc: EHP-101 reduces the expression of genes associated with fibrosis and inflammation

• As in Phase I, drug-related biomarkers will also be tested in the diseased populations (higher probability of effect with longer treatment in Phase II)

WWW.EMERALDPHARMA.LIFE 40 EHP-102: Second Product Candidate

CBG A patented CBG derivative (NCE)

• Being developed for oral delivery

• Preclinical proof-of-concept established

• Designed to target receptors and pathways involved EHP-102 in neurodegenerative diseases O O H Air • Clinical-enabling studies initiated N EtNH2 HO EtOH HO t.a., 1.2 h O 71% O

VCE-003 VCE-003.2

WWW.EMERALDPHARMA.LIFE 41 EHP-102: Why Parkinson’s Disease?

PD is a chronic, progressive neurodegenerative disorder with no current cure

• More than 10 million people worldwide have Parkinson's disease

• A disease where damaged neurons do not produce sufficient dopamine (dopamine helps transmit impulses from the brain to the muscles)

• EHP-102 provides neuroprotection, partially through PPARγ activity and reduction in proinflammatory mediators

WWW.EMERALDPHARMA.LIFE 42 Oral VCE-003.2 (20 mg/kg) in sesame oil EHP-102: Efficacy Demonstrated in PD Clinical Symptoms

Pole test Cylinder rearing test 40 1.0 SHAM ** SHAM Demonstrated efficacy in 2 models of PD * 6-OHDA + vehicle 6-OHDA + vehicle 30 6-OHDA + VCE-003.2 0.5 6-OHDA + VCE-003.2

(6-OHDA and LPS models) 20 #

## 0.0 Latency (s) 10 Score (preference for ipsilateral paw) for ipsilateral

0 -0.5 • Improves clinical symptoms and *p<0.05, **p<0.01 versus vehicle-treated control mice; #p<0.05, ##p<0.01 versus vehicle-treated 6-hydroxydopamine-lesioned mice recovers movement parameters OralOral VCE VCE-003.2-003.2 (20 (20 mg/kg) mg/kg) in in sesame sesame oil oil Dopaminergic Neurons

Lesioned side Non-lesioned side (motor coordination and activity) Inflammatory Markers Lesioned side Non-lesioned side THTH immunostaining immunostaining 150 150 SHAMSHAM • Reduces inflammatory marker 6-OHDA6-OHDA + +vehicle vehicle 6-OHDA + VCE-003.2 control 6-OHDA + VCE-003.2 control 100100 expression #### ****** 50 50 ****** + 6-OHDA + 6-OHDA

• Prevents dopaminergic Immunostaining density Immunostaining density 0 (%versus non lesioned side) lesioned non (%versus 0 (%versus non lesioned side) lesioned non (%versus neuronal loss *p<0.05, **p<0.01, ***p<0.001 versus vehicle-treated control mice + VCE-003.2 + VCE-003.2 WWW.EMERALDPHARMA.LIFE 43 EHP-102: Why Huntington’s Disease?

HD causes progressive breakdown of cells

• An orphan disease

• EHP-102 targets PPARγ with improved activity

• Also targets other pathways involved in neuronal survival

WWW.EMERALDPHARMA.LIFE 44 Figure 4 Click here to access/download;Figure;Figure 4.pptx Figure 4 Click here to access/download;Figure;Figure 4.pptx a DARPP32 Htt DAPI Merge a DARPP32 Htt DAPI Merge 250

2502

2 200 ## Veh 200/mm ## Veh /mm 150 **

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50 mtHtt

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2.0 Iba-1 Htt aDAPIVeh Merge DARPP32 Htt DAPI Merge 200 ## Demonstrated efficacy in 2.0 # 200 Iba-1 Htt## DAPIVeh 250 Merge 1.5 ** 2502 2

# 150 tHtt 2 Increase ## 1.5 ** 200 w Veh 2 ** tHtt

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Increase 1.0 /mm w Veh ** Veh /mm 150 3 models of HD Fold 100 **

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mtHtt 50 NeuN mtHtt 0.0 VCE 50 Latency NeuN 003.2 VCE 50 0.0 Veh VCE-003.2 Veh VCE-003.2 mtHtt 0 - DARRP32

003.2 0 Veh VCE-003.2 Veh VCE-003.2 0 003.2 - Veh VCE-003.2 Veh VCE-003.2 - wtHtt mtHtt DARRP32 0 Veh Veh VCE-003.2

003.2 VCE-003.2 Veh VCE-003.2 Veh VCE-003.2 - wtHtt mtHtt wtHtt mtHtt Veh VCE-003.2 Veh VCE-003.2 VCE

Motor function assessed by the VCE

wtHtt mtHtt VCE wtHtt mtHtt wtHtt mtHtt RotaRod test and mean latency to fold VCE Confocal microscopy characterization with selective antibodies • quantified (*p<0.05, **p<0.01 vs AAV- Improved motor b for the MSN marker DARPP32 andb Neurogenesishuntingtin. (**p<0.01 vs htt16Q Vehicle; #p<0.05, ##p<##0.01 vs AAV-htt16Q Vehicle; ##p<0.01 vsb its respective Vehicle). b Veh its respective2.0 Vehicle).** 200 ## Veh ## Fig. 4 Veh function & clinical scores ** 200 mtHtt ## 2.0 Fig.Veh 4 Neurogenesis b

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Veh EHP-102 Veh EHP-102NeuN Veh EHP-102 Veh EHP-102

Veh EHP-102 Veh EHP-102 Veh EHP003.2 -102 Veh EHP-102

0 003.2 0 - Striatal

Fig. 3 - NeuN wtHtt mtHtt VehwtHttEHP-102 Veh EHPmtHtt-102 wtHtt mtHtt Veh EHP-102 Veh EHP-102 wtHtt mtHtt 003.2

Fig. 3 - VCE Fig.VCE 4 Confocal microscopy characterizationwtHtt mtHtt of migrating wtHtt mtHtt

VCE Fig. 4 neuroblasts identified with doublecortin antibody and quantification in the striatum of the indicated mice groups WWW.EMERALDPHARMA.LIFE . 45 Publications NATURE

• Go to https://emeraldpharma.life/scientific-publications/ to get all our publications OPEN NATURE r a ***

γ γ γ γ in vivo +

Cannabinoids the main active compounds of marijuana (Cannabis sativa), and its endogenous counterparts anandamide and 2-arachidonoyl glycerol have attracted the interest of the scientifc community in the last decade owing to their prominent efects on neurodegenerative and neuroinfammatory conditions1 . Cannabinoids exert neuroprotective actions in various experimental models of neurodegenerative diseases, and most of their efects are mediated via the presynaptic CB1 receptor. CB1 receptor levels notably diminish at early stages of Huntington’s

Centro de VivaCell *

Scientific RepoRts 1

WWW.EMERALDPHARMA.LIFE 46 Experienced Pharma & Biotech Management

Giovanni Appendino, PhD Jim DeMesa, MD, MBA Eduardo Muñoz, MD, PhD Scientific Advisor, SAB Chief Executive Officer Chief Scientific Officer, SAB Chairman One of the world's thought leaders 30 years in pharma product >30 years in biomedical research, in cannabinoid research; Professor of development and management, Professor of Immunology, author Pharmaceutical Chemistry at the including preclinical and clinical trial of 200 articles, patents and book chapters University of Eastern Piedmont; Author management, and partnering with with nearly 5,000 citations of 250 articles and 10 book chapters. pharma companies. 15 years as CEO of public biotech companies. Rao Movva, PhD Scientific Advisor, SAB

Alain Rolland, PharmD, PhD Nancy Coulson, MBA 30 years in drug discovery and Chief Operating Officer SVP, Regulatory & Quality Affairs development; Novartis Distinguished Scientist; pioneered chemical biology >30 years in global pharma and biotech >30 years of leadership experience in efforts that led to the discovery and the regulatory mgmt with J&J, BMS, and others. biotech/pharma R&D, product, strategic understanding of TOR pathways and business development Clinical Advisory Boards: Lisa Sanford, CPA Joachim Schupp, MD, Dr. med MS: Emmanuelle Waubant, MD, PhD Chief Financial Officer Chief Medical Officer Juan Antonio Garcia-Merino, MD, PhD SSc: John Varga, MD >30 years of diversified finance and >30 years in clinical drug development, Janet Pope, MD accounting experience in life sciences, medical monitoring and clinical trial mgmt Patricia Carreira, MD pharmaceuticals and biotechnology. with Ciba-Geigy, Novartis, & others

WWW.EMERALDPHARMA.LIFE Thank you

TO LEARN MORE PLEASE CONTACT :

Jim DeMesa, MD Bernie Hertel

CHIEF EXECUTIVE OFFICER VP FINANCE & COMMUNICATIONS EMERALD HEALTH PHARMACEUTICALS EMERALD HEALTH SCIENCES

T. 1 858 352 0622 T. 1 604 727 0106

E. [email protected] E. [email protected]

48 Developing medicines based on cannabinoid science