ESSA PharmaNASDAQ: EPIX; TSX-V: EPI

March 20, 2019

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 13, 2018 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 OverviewFocus on the development of novel therapies for the treatment of metastatic castrate resistant prostate cancer

Founded in 2009 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) transcription inhibitors of the androgen receptor (“Anitens”) overcome resistance to current anti-androgens; first generation EPI-506 clinical trial established clinical proof-of-concept

Next-generation Aniten compounds being prepared for IND; initial indication in anti-androgen progression but potential combination Rx with anti-androgens

Listed on NASDAQ & TSXV

Cash balance of $12.2 M(Dec 31, 2018)

Company Technology & Products Financial Details

David R. Parkinson, MDPresident & Chief Executive Officer, Director

Peter Virsik, MS, MBAEVP & Chief Operating Officer

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

Experienced Management Team

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PUBLIC HEALTH PROBLEM

LARGE MARKET

VALIDATED THERAPEUTIC TARGET

NEED FOR NEW THERAPEUTIC STRATEGIES

Metastatic Castration-Resistant Prostate Cancer (mCRPC)

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An Unmet Medical Need

1. Surveillance Research, American Cancer Society. 2018.2. Robinson D, et al. Cell. 2015.3. Katsogiannou M, et al. Cancer Treat Rev. 2015.

• Prostate cancer is the 2nd

most common cause of male cancer deaths1

• Each year in the US, 165,000 men are diagnosed and 29,000 die due to prostate cancer

• Over $5B in global sales generated in 2017 by leading anti-androgens, Zytiga® (abirateroneacetate) and Xtandi®(enzalutamide)

• 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 Target the AR Ligand Binding Domain

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• The AR is comprised of 3 distinct, independently acting domains

• Current therapies target the ligand-binding domain (LBD) of the AR

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

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

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

Inhibit synthesis

Block ligand binding

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

ANDROGEN RECEPTOR

Mechanisms of AR Resistance Occur in the Ligand Binding Domain

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AR Amplification1

Splice variants3,4,5

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

5. Sun S, et al. J Clin Invest. 2010.6. Chen EJ, et al. Clin Cancer Res. 2015

1. Azad AA, et al. Clin Cancer Res. 2015.2. Joseph JD, et al. Cancer Discov. 2013.

Gain-of-function mutations1,2

3. Antonarakis ES, et al. NEJM. 2014.4. Mostaghel EA, et al. Clin Cancer Res. 2011.

7. Culig Z, et al. Cancer Res. 1994.

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

• Proposed binding of Anitens to Tau-5 region of AF11

• Anitens inhibit wild-type, LBD mutant, and splice-variant AR activity2,3,4

• Anitens inhibit AR transcriptional activity by blocking interaction with key transcriptional proteins (RAP74 & CBP)5,6

81. 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

5. Myung JK, et al. J Clin Invest. 2013.6. Andersen RJ, et al. Cancer Cell. 2010.

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

EPI-506: First Generation NTD Inhibitor

• In vitro & in vivo inhibited AR-driven gene expression in both wild-type AR (LNCaP, VCaP) and androgen-resistant AR settings (LNCaP95)

• Specific binding (imaging, protein-binding studies) w/ moderate potency (>10µM IC50)

• Toxicology unremarkable (minor weight loss & reversible)

• Combination with anti-androgens revealed activity greater than either NTD inhibitor or anti-androgen alone

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EPI-002 (active drug)

EPI-506 (tri-acetate prodrug)

OO

(S)(S)

O(S)(S)

O

Cl

O

EPI-506O

O O

EPI-002

First-Generation EPI-506 Phase 1 Study in Patients w/mCRPC

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DESIGN An adaptive Phase 1 first-in-man dose escalation / dose expansion study

DOSE EPI-506 (EPI-002 active) oral once-daily or twice-daily dosed as a soft-gel capsule

POPULATION mCRPC patients progressing after abiraterone, enzalutamide, or both; allowed to have also failed one regimen of docetaxel chemotherapy

STUDY SIZE 26 patients

ENDPOINTS Safety, PK, maximum tolerated dose, recommended Phase 2 dose

STUDY STATUS Completed at 5 sites in US and Canada

First-Generation EPI-506 Phase 1 Pharmacokinetic Data:Minimal time with drug concentration >IC50

Significant first-pass metabolism seen

Insufficient exposures with minimal time above target IC50

0 6 12 18 241

10

100

1000

10000

100000

EPI-002 PK - day 8

Time (hr)

EPI-0

02 [p

lasm

a] in

ng/

mL

80 mg

160 mg

320 mg

640 mg

1280 mg

2400 mg

3600 mg

1800 mg bid

1800 mg bid simulatedEPI-002 cell IC50

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First-Generation EPI-506 Phase 1 PSA Response:Maximal PSA Change at Any Time from Start of Multi-dose Period (N=27)

-50

-25

0

25

5075

100M

ax %

Dec

line

in P

SA

1800

mg

(BID

)16

0 m

g32

0 m

g

640

mg

1800

mg

(BID

)36

00 m

g24

00 m

g12

80 m

g64

0 m

g80

mg

1280

mg

80 m

g36

00 m

g80

mg

2400

mg

320

mg

3600

mg

320

mg

640

mg

640

mg

160

mg

640

mg

160

mg

1280

mg

2400

mg

640

mg

640

mg

2400

mg

1280

mg

3600

mg

1280

mg

1800

mg

(BID

)

Patients receiving < 1280 mgPatients receiving > 1280 mg

320

mg

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EPI-506: Safe and Well-tolerated Until Very High Doses

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Most Commonly Reported Adverse Event > 10% All Grades, N (%)Diarrhea, nausea 13 (46%)

Fatigue 7 (25%)

Decreased appetite, pain in extremity 6 (21%), each

Vomiting 5 (18%)

Back Pain 4 (14%)

Abdominal distension, anemia, arthralgia, musculoskeletal pain, UTI 3 (11%), each

Adverse Events ≥ Grade 3 N (%) Relationship to Study DrugAnemia 3 (11%) Not related.

AST elevated 2 (7%) Probably related, Possibly related.

Neutropenia 2 (7%) Not related.

Abdominal pain, diarrhea 1 (4%), each Possibly related.

ALT elevated, amylase elevated, angina, hypertension, dizziness postural 1 (4%), each Probably related.

Arthralgia, gastrointestinal hemorrhage, pain in extremity, syncope, thrombocytopenia, urinary retention

1 (4%), each Not related.

Lessons From the Phase 1 Experience With EPI-506

Experience informed the specifications for a next-generation Aniten compound:• Higher potency

• Less metabolism with a longer half-life• Maintain on-target specificity

• Commercial formulation• Ease of manufacturing / shelf-life stability

New technology enables patient biological characterization and more informative, efficient trial conduct:• ctDNA to assess tumor AR status and verify continued reliance on AR pathway

• CTC mRNA gene expression to monitor PK/PD

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EPI-506 was well-tolerated with evidence of a successful POC, but was not potent enough and was metabolized rapidly with a short half-life

ESSA: Next-Generation Aniten Development: Goals and Process

• Goals: o To generate potent and specific NTD inhibitors with long half-lives and commercial

grade pharmaceutical properties

• Process:o Strengthened ESSA’s chemistry and preclinical team in early 2018

o Augmented external chemistry efforts to expand the synthesis of new molecules» >400 new compounds designed; >250 compounds screened in vitro for potency and ADME profile

o Preclinical ADME characterization of molecules» Comprehensive molecule profiling program

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TPP CRITERIA STATUS SPECIFICS

Increased potency In vitro potency goal achieved (>15X more potent than EPI-506 / 002)

ENZ-resistant activity In vitro cellular activity in ENZ-resistant cell lines

Xenograft in vivo activity Equal anti-tumor activity to ENZ at similar doses in ENZ-sensitive xenograft model

Clean off-target profile CEREP screening indicates minimal off-target binding

Reduced metabolism Major metabolic pathways blocked (> 5X less metabolized in vitro than EPI-506 / 002)

In vivo PK profile Mouse PK studies support once-daily dosing and predict significant human exposures

Strong IP coverage IP broadly filed on new Anitens; patent expirations anticipated 2037+

ESSA Next-Generation Aniten Program: Status

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In Vitro Potency and Stability of Next-Generation Anitens

17CONFIDENTIAL

Stability threshold

0

500

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4000

4500

0 20 40 60 80 100 120

In V

itro

Cel

lula

r IC

50 P

oten

cy (n

M)

In Vitro Half-Life Stability (min)

Potency threshold

Target compounds

• Significant gains made in in vitro potency and stability compared to EPI-002• Preclinical characterization limited to only the most potent and stable compounds

Enzalutamide

EPI-002 potency is >> 4500nM

Cellular Potency Increased > 15X Compared to EPI-002

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• Next-generation anitens exhibit cellular potency’s in a similar magnitude to the leading anti-androgens in a full-length androgen receptor cellular model

Compound IC50(nM) n

EPI-002 9,580 2EPI-7170 1,054 3EPI-7245 592 8EPI-7273 400 5EPI-7283 631 6EPI-7330 658 6EPI-7364 205 4EPI-7386 454 3

Bicalutamide 306 2Enzalutamide 189 8

In Vitro Activity in Three Separate ENZ-Resistant Cellular Models

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• ENZ shows no activity in three AR-V7-driven cellular models whereas next-generation anitens show potent activity in each

LNCaP95 Cell Proliferation AR-V7-Driven PSA Luciferase

AR-V7-Driven UBE2C Gene Expression

>85% Reduction

Significantly Improved In Vitro Metabolic Stability & Mouse PK

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• Next-generation anitens show significant improvements in hepatocyte in vitro stability and mouse pharmacokinetics compared to EPI-002

Compound Human Mouse RatEPI-002 38 N/A N/AEPI-7170 98 33 N/AEPI-7245 290 203 75EPI-7273 >360 86 31EPI-7283 >360 >360 56EPI-7330 >360 N/A >360EPI-7364 >360 >360 94EPI-7386 >360 >360 >360

Enzalutamide >360 N/A N/A

HepatocyteT1/2(min)

Next-Generation Molecules Exhibit Equal Anti-tumor Activity in Two Separate LNCaP Xenograft Models

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• Next-generation anitens show similar efficacy to ENZ at both clinically relevant (15 mg/kg ENZ) or supratherapeutic (30mg/kg) doses of ENZ

STATUS SPECIFICS

Select final Aniten molecules for selectivity and xenograft preclinical studies

Medical conference presentation(s) of the initial preclinical findings of Aniten molecules

IND candidate selection and initiation of IND-enabling studies

Medical conference presentation of the preclinical findings of Aniten molecules in antiandrogen-resistant prostate models and in combination with antiandrogens

IND filing of the next-generation Aniten

First patient dosed in phase 1 mCRPC study with next-generation Aniten

ESSA Upcoming Milestones

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FIRST-GENERATION

EPI-506 established clinical safety and proof-of-mechanism for NTD inhibition of the androgen receptor in mCRPC

POTENCY & ADME IMPROVED

Next-generation Aniten compounds have increased potency, longer half-lives and improved ADME properties compared to EPI-506

MARKET OPPORTUNITY

mCRPC represents a significant market opportunity - 165,000 new cases of prostate cancer each year in the US and annual global sales of over $5B

MANAGEMENT TEAM Highly experienced management team with significant oncology experience

IND FILING IND filing of next-generation Aniten compound anticipated 9-12 months following IND candidate selection in 1Q19

Investment Highlights

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Cash reported at Dec 31, 2018: $12.2MCommon Shares 8.0M (fully diluted)

Financial History and Highlights

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2010–12

• $3.7M seed financing

2014–15

• $12M Cancer Prevention Research Institute of Texas (CPRIT) grant awarded

• $16.3M IPO included Deerfield, Omega, Special Situations Fund

• Commenced trading on NASDAQ (EPIX) and TSX-V (EPI)

2018

• $26M raise included Clarus, BVF, Eventide, Omega

2016

• $20M financings included Clarus, Deerfield, Omega, Eventide

• $10M Silicon Valley Bank loan facility; $8M drawn