ESSA PharmaNASDAQ: EPIX

Evercore ISI HealthCONxDecember 1 - 3, 2020

Forward Looking StatementThis presentation may contain forward-looking statements. Forward-looking statements and information are subject tovarious known and unknown risks and uncertainties, many of which are beyond the ability of ESSA to control or predict,and which may cause ESSA’s actual results, performance or achievements to be materially different from those expressedor implied thereby. Such statements reflect ESSA’s current views with respect to future events, are subject to risks anduncertainties and are necessarily based upon a number of estimates and assumptions that, while considered reasonableby ESSA as of the date of such statements, are inherently subject to significant medical, scientific, business, economic,competitive, political and social uncertainties and contingencies. In making forward-looking statements, ESSA may makevarious material assumptions, including but not limited to the market and demand for the securities of ESSA, generalbusiness, market and economic conditions, obtaining positive results of clinical trials, and obtaining regulatory approvals.

Forward-looking information is developed based on assumptions about such risks, uncertainties and other factors set outherein and in ESSA’s Annual Report on Form 20-F dated December 20, 2019 under the heading “Risk Factors”, a copy ofwhich is available on ESSA’s profile on the SEDAR website at www.sedar.com, ESSA’s profile on EDGAR at www.sec.gov,and as otherwise disclosed from time to time on ESSA’s SEDAR profile. Forward-looking statements are made based onmanagement's beliefs, estimates and opinions on the date that statements are made and ESSA undertakes no obligationto update forward-looking statements if these beliefs, estimates and opinions or other circumstances should change,except as may be required by applicable Canadian and United States securities laws. Readers are cautioned againstattributing undue certainty to forward-looking statements.

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ESSA Corporate OverviewFocused on the development of novel therapies for the treatment of prostate and other hormone-driven cancers

Founded with technology licensed from The University of British Columbia and the BC Cancer Agency

Sites in Houston, South San Francisco and Vancouver

First-in-class N-terminal domain (NTD) inhibitors of the androgen receptor (“Anitens”)

EPI-7386 phase 1 study began 2Q2020

Clinical development initially focused on resistant mCRPC as a single agent with future development in combination with anti-androgens in CRPC and CSPC

Potential in triple-negative androgen receptor-positive breast cancer

Listed on NASDAQ (EPIX)

Completed raise of $45M in 2020

Cash balance of ~$80M(June 30, 2020)

Company Technology & Products Financial Details

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Experienced Management Team

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David R. Parkinson, MDPresident & Chief Executive Officer

Peter Virsik, MS, MBAEVP & Chief Operating Officer

David S. Wood, MBA, CPA, CMAChief Financial Officer

Alessandra Cesano, MDChief Medical Officer

PUBLIC HEALTH PROBLEM

LARGE MARKET

VALIDATED THERAPEUTIC TARGET

NEED FOR NEW THERAPEUTIC STRATEGIES

Prostate Cancer Disease Landscape

51. Surveillance Research, American Cancer Society. 2019.2. Robinson D, et al. Cell. 2015.3. Katsogiannou M, et al. Cancer Treat Rev. 2015.

• Prostate cancer is the 2ndmost common cause of male cancer deaths

• Each year in the US, ~175,000 men are diagnosed with and ~33,000 die due to prostate cancer1

• Over $7.5B in global sales generated in 2019 by leading anti-androgens, Zytiga® (abiraterone acetate), Xtandi®(enzalutamide) and Erleada (apalutamide).

• Prostate cancer disease progression is associated with androgen receptor (AR) signaling. 2,3,4

• An estimated ~60% of mCRPC tumors post-Xtandi or Zytiga failure may still be AR-driven 5

• Despite new therapies, mCRPC anti-androgen resistance is inevitable 6,7

4. Azad AA, et al. Clin Cancer Res. 2015.5. Wyatt. JAMA. 2016. 6. Watson PA, et al. Nat Rev Cancer. 2015.

7. Attard G, et al. ASCO Annual Meeting. 2017.

Current Anti-Androgen Therapies Only Target the Androgen Receptor Ligand Binding Domain

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• All current anti-androgens function through the ligand-binding domain of the androgen receptor

• Known anti-androgen resistance mechanisms develop at the ligand binding domain

N-terminal domain DNA-binding domain Ligand-binding domain

AR Amplification1

Splice variants3,4,5

Promiscuous activation (i.e., glucocorticoids, progesterone) 6,7

Gain-of-function mutations1,2

ANDROGEN

Zytiga® (abiraterone acetate)Eligardä, Lupron® (leuprolide)Zoladex® (goserelin)Firmagon® (degarelix)

Nubeqa ® (darolutamide)Erleada® (apalutamide)Xtandi® (enzalutamide)Nilandron® (nilutamide)Casodex® (bicalutamide)Eulexin® (flutamide)

Inhibit androgen synthesis

Block androgen binding

Anti-androgen Resistance Mechanisms

6. Chen EJ, et al. Clin Cancer Res, 20157. Culig Z, et al. Cancer Res, 1994

4. Mostaghel EA, et. Al. Clin Cancer Res, 20115. Sun S, et al. J Clin Invest, 2010

1. Azad AA, et al. Clin Cancer Res, 20152. Joseph JD, et al. Cancer Discov, 20133. Antonarakis ES, et al. NEJM, 2014

Targeting the AR NTD: Novel Transcription Factor Inhibition of Androgen-Driven Prostate Cancer Biology

• Novel method of inhibiting the AR

• Binding formally demonstrated for EPI-001, the racemic form of EPI-002

o Proposed binding of Anitens to the Tau-5 region of AF1 1

• Anitens active against multiple forms of AR:o Wild-type AR, LBD mutant AR, and splice-

variant AR2,3,4

71. De Mol E, et al. ACS Chem Biol. 2016.2. Andersen RJ, et al. Cancer Cell. 2010.

N-terminal domain DNA-binding domain Ligand-binding domain

Granted unique USAN drug stem of “Aniten” as an N-terminal inhibitor of AR

3.De Mol E, et al. ACS Chem Biol. 2016.4.Yang YC, et al. Clin Cancer Res. 2016.

EPI362

C404

438

Tau-5

Aniten

Prostate Cancer Clinical Treatment Model

AR-V7 Nuclear Positive2 à 0% 75%+ à

1. Adopted from Scher, HI et al. J Clin Oncol 2016.2. Sharp, A et al. J Clin Invest 2019.

Clinically Localized Disease

Rising PSA Noncastrate

mCSPC

nmCRPC

mCRPC3rd Line

mCRPC2nd Line

mCRPC1st Line

Prostate Cancer1

Local Systemic

Currently Approved Treatments

Surgery Radiation +/- ADT

ADT+/-lutamides

Abiraterone / -lutamides Docetaxel/Cabazitaxel/Radium

/ Olaparib

Abiraterone Enzalutamide Apalutamide Darolutamide

Potential EPI-7386 Treatments EPI-7386

ComboEPI-7386Combo

EPI-7386Combo

EPI-7386 Monotherapy

EPI-7386Combo

Rucaparib / Experimental

Agents

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The Development of N-Terminal Domain Inhibitors of the Androgen Receptor

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Early 2000’s: Basic scientific work on AR NTD conducted; identified first Aniten POC molecules

2009: ESSA Pharma formed

2015-2017: Phase 1 clinical study conducted with the first-generation Aniten, EPI-506. Demonstrated signs of antitumor activity but also highlighted the need for improved potency and ADME properties.

2017-2019: Preclinical development of a second-generation Aniten conducted

2019: EPI-7386, selected as the next IND candidate

20202000

2020: EPI-7386 phase 1 mCRPC study begins

EPI-7386 EPI-506(EPI-002)Target Criteria Description

Potency In vitro potency similar to second generation ‘lutamide anti-androgens

Activity In vivo xenograft activity in both anti-androgen-sensitive & resistant models

ADME Low in vitro metabolism, good animal ADME & long predicted human T1/2

Selectivity Specific NTD on-target activity with minimal off-target binding

DDI Appropriate properties to combine with other drugs (e.g. drug-drug interactions (DDI), etc.)

CMC Simple synthesis of drug substance and favorable pharmaceutical properties for the drug product

EPI-7386 Next Generation NTD Inhibitor of the AR:Comparison to First Generation EPI-506

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X

X

X

X

X

X

X

X

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EPI-7386+ENZA combination provides broader and deeper inhibition of the AR

pathway

Potency: EPI-7386 Displays Potent in vitro Activity in a Variety of Androgen-Receptor Driven Cellular Models

0.01 0.1 1 10 1000

25

50

75

100

125

Concentration (uM)

LNC

aP P

SA-L

uc %

act

ivity

± SD

EPI-002

EPI-7386

Enzalutamide

Darolutamide

Apalutamide

Bicalutamide

R1881 EPI-73867.5 uM

Vehicle Enza7.5 uM

Enza + EPI-73865 / 5uM

Full-Length Androgen Receptor Models Splice-Variant Androgen Receptor Models

LNCaP LNCaP95 PC-3

EPI-002 9.0 > 20 > 10

EPI-7386 0.56 3.7 > 10

Enzalutamide .35 > 10 > 10

Tumor Biology AR-FL AR-V7 & AR-FL Non-AR

Cellular Proliferation IC50 (uM)

(PSA)

Activity: EPI-7386 Works in a Spectrum of AR-Driven Xenograft Models Unlike Current anti-androgen Therapies

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Prostate Model

Biology Tumor Growth

MOA

ENZ Activity

EPI-7386 Activity

LNCaP anti-androgen sensitive model AR-FL ++ ++VCaP Initially anti-androgen sensitive; over time develops resistance to anti-androgens

AR-FL / AR-V7 + ++

LNCaP95 Resistant to anti-androgens AR-V7 - +22Rv1 Resistant to anti-androgens AR-V7 - +HID28 PDX model resistant to anti-androgens AR - +PC3 Not driven by the androgen receptor Non-AR - -“++” = Worked well “+” = Worked “-” = Did not work

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Activity: EPI-7386 Exhibits Excellent Anti-Tumor Response as a Monotherapy or in ENZ Combination in the VCaP Xenograft Model

Serum PSA at the End of Treatment

Individual Tumor Plot on Day 41 Dosing

Rationale for the Combination of EPI-7386 with Anti-Androgens

• Decades of clinical research link improved clinical results from better suppression of the AR axis

• Combining an NTD-inhibitor such as EPI-7386 with an LBD-inhibitor such as enzalutamide, provides two complementary ways of inhibiting AR biology

• Preclinical studies support deeper and broader suppression of AR-driven biology by combining EPI-7386 and anti-androgens (e.g. enzalutamide)o In vitro quantitative studieso Gene expression studieso In vivo preclinical androgen-responsive animal models

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ADME: EPI-7386 is Predicted to Achieve High Human Exposures and a Long Half-life

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Hepatocyte T1/2 (min)

Compound HumanEPI-7386 >360

Enzalutamide >360

0 4 8 12 16 20 24100

1,000

10,000

100,000

Mean plasma conc of EPI-7386 across species

Time (hr)

[pla

sma]

in n

g/m

L

RAT - EPI-7386 Susp50 mg/kgDOG - EPI-7386 Susp50 mg/kg

MOUSE - EPI-7386 Susp30 mg/kg

In Vitro Hepatocyte Stability

Estimated Human Pharmacokinetic Parameters

Selectivity and Drug-Drug Interactions: EPI-7386 is Selective for the AR with Minimal Off-Target Binding

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Compound AR ER aplha ER beta PR GREPI-002 >10 >10 >10 >10 >10EPI-7386 >10 >10 >10 5.61 >10

Enzalutamide 0.54 >10 >10 4.49 >10

Steroid Receptor LBD inhibition IC50 (uM)

CompoundEPI-002 17.6 21 uM IC50

EPI-7386 0.5 23% at 10 uMEnzalutamide Potential inducer 2.6 uM IC50

PXR % activation at 10 uM

GABA Cl-channel (TBOB site) inhibition

• Minimal off-targeting bindingo Nuclear receptor panelo CEREP SafetyScreenTM 87 & 44 panels

• No off-target activity against targets relevant to combination partners o No GABA-Cl channel; associated with seizure

risk with enzalutamide and apalutamide

• Favorable CYP inhibition profile

Favorable IND-enabling Toxicology Studies Allow a Relatively High Starting Dose of EPI-7386 in the Clinic

Dose (mg) Cmax (ng/mL) AUC0-24 (ng*hr/mL)50 1,729 34,320100 3,458 68,639200 6,915 137,278400 13,830 274,556800 27,659 549,113

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• The 200 mg EPI-7386 human starting dose is projected to deliver a similar drug exposure as biologically relevant exposures in the VCaP xenograft model

• Patient target EPI-7386 exposures are >300,000 AUC0-24

Projected EPI-7386 Human Exposures

0 5 10 15 20 250

200

400

600

800VCaP Castrated

Avg

Dosing Days

Tum

or V

olum

e (m

m3 )±

SEM

Vehicle (NMP/Capmul/TPGS/PEG400)

Enzalutamide - 15 mg/kg- PO qd

EPI-7386 - 3 mg/kg- PO qd

EPI-7386 - 10 mg/kg- PO qd

EPI-7386 - 30 mg/kg- PO qd

VCaP Castrated Average

AUC0-24: ~300,000

AUC0-24: ~80,000

EPI-7386 Xenograft Exposures

CMC: EPI-7386 Has Favorable Pharmaceutical Properties

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Active Pharmaceutical Ingredient• EPI-7386 active pharmaceutical ingredient (API) simple to manufacture• Crystalline high-melting point API

Drug Product• Drug product able to be absorbed at high

concentrations• Multiple strength tablet formulations manufactured

o Tested in dogs and exhibit similar performance to GLP toxicology suspension formulation

EPI-7386: First Human Clinical Studies

Patient population:

-mCRPC patientsprogressing on standard of care (including the latest anti-androgens)

Study design:

-3+3 design-n= ~ 18 pts-n= ~10 dose expansion pts

Study endpoints:

-Recommended Phase 2 dose (RP2D)-Safety & PK-PSA response

Correlative studies:

-CTC conversion-CTC-ARV7 -ctDNA

Timeline:

-IND filed in 1Q 2020-FPI July 14, 2020Monotherapy

Study

Combination Study

-mCRPC patients -PK design-n= ~10pts

-Recommended Phase 2 dose (RP2D)-Safety & PK-PSA response

-CTC conversion-CTC-ARV7 -ctDNA

-FPI early 2021

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♦

EPI-7386: US Prostate Cancer Market Opportunity is Large*

* Sher, H. et al. .PLOS One, 2015.; 3L mCRPC patients are estimated as the yearly mortality incidence due to prostate cancer.

EPI-7386 in Combination w/ Anti-androgens

EPI-7386 as a Monotherapy

US Prostate Cancer Prevalence Estimated in 2020 by Stage of Disease* (in thousands)

33

500

4842

112

237

3L mCRPC nmCRPC2L mCRPC 1L mCRPC High Risk CSPC

mCSPC Total

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Anti-androgens Approved or in a Pivotal P3 Study

(►= Approved)(♦= In P3 Study)

►

►

►

►

►► ►

► ►

►♦♦

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Financial Position & Capitalization

Nasdaq: EPIXCash $36.5M at June 30th; plus $45M (net) raise July 31st ; (no debt O/S)

Share Price (11/12/2020) $6.47 (NASDAQ)

Shares ~41M – 33.6 I/O common shares and 7.4 prefunded warrants

Stock Options ~5.3M @ $3.19

Top Shareholders Pfizer Inc; Soleus Capital, BVF, RA Capital, Blackstone Group, Eventide Healthcare Fund; Omega Fund, OrbiMed; Vivo Capital

Covering Analysts Mark Breidenbach, Oppenheimer; David Martin, Bloom Burton; Joe Pantginis, HCW; Maury Raycroft, Jefferies

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• Current cash funds ESSA’s 2020 to 2023 program which includes completion of Phase 1 dose-escalation & expansion studies, Phase 1 combination studies with anti-androgens and Phase 2 prep.

• ESSA also planning additional preclinical studies w/ Anitens in breast & other cancer models.

STATUS SPECIFICS

Complete all preclinical studies needed for IND filing

IND filing of EPI-7386 by 1Q20

First patient dosed July 2020 in EPI-7386 Phase 1 study in mCRPC patients failing second generation anti-androgens

Establish the recommended phase 2 dose (RP2D)

Expand phase 1 cohort to enroll more patients at the RP2D

Begin combination study w/ one or more anti-androgens in first-line mCRPC patients

ESSA Upcoming Milestones

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X

X

X

Summary

• EPI-7386 is a unique inhibitor of the N-terminal domain of the AR, with single agent activity against both wild-type and mutated AR

• The agent is more potent, has a longer half-life, and has improved pharmaceutical properties over the first-generation NTD inhibitor, EPI-506

• Combining EPI-7386 with anti-androgens suppresses AR-driven biology more broadly and deeply than with either approach alone

• Initial clinical development will be single-agent treatment in men resistant to current anti-androgens, with recent FDA Fast Track designation

• Subsequent development will be in earlier lines of treatment in combination with anti-androgens

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For further information, please contact:

Peter Virsik, COOpvirsik@essapharma.com

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