ESSA Pharmaceuticals(NASDAQ: EPIX; TSX: EPI)

J.P. Morgan 36th Annual Healthcare Conference

Forward Looking Statement

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This 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 thoseexpressed or implied thereby. Such statements reflect ESSA’s current views with respect to future events, are subject torisks and uncertainties and are necessarily based upon a number of estimates and assumptions that, while consideredreasonable by 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, ESSAmay make various material assumptions, including but not limited to the market and demand for the securities of ESSA,general business, market and economic conditions, obtaining positive results of clinical trials, and obtaining regulatoryapprovals.

Forward-looking information is developed based on assumptions about such risks, uncertainties and other factors set outherein and in ESSA’s prospectus dated January 5, 2018 under the heading “Risk Factors”, a copy of which is available onESSA’s profile at the SEDAR website at www.sedar.com, and as otherwise disclosed from time to time on ESSA’sSEDAR profile. Forward-looking statements are made based on management's beliefs, estimates and opinions on thedate that statements are made and ESSA undertakes no obligation to update forward-looking statements if these beliefs,estimates and opinions or other circumstances should change, except as may be required by applicable Canadiansecurities laws. Readers are cautioned against attributing undue certainty to forward-looking statements.

Corporate Overview

• Founded with technology licensed from the labs of Dr. Andersen (UBC) & Dr. Sadar (BCCA)

• Headquartered in Vancouver, Canada with CA & TX sites

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Focused on the development of novel therapies for the treatment of metastatic castrate resistant prostate cancer

Company

• First-in-class N-terminal domain (NTD) transcription inhibitors of the androgen receptor (AR)

• First generation EPI-506 established clinical proof-of-concept• Promising next-generation compounds advancing to IND

Technology & Products

Financial Details

• Listed on TSXV & NASDAQ• $4.0M as of Sept 2017

Investment Highlights

• Through first-generation compound EPI-506, the clinical safety and proof-of-mechanism established for NTD inhibition of the androgen receptor in mCRPC

• Promising next-generation Aniten compounds have increased potency and improved pharmaceutical properties compared to EPI-506

• mCRPC represents a significant market opportunity – 160,000 new cases of prostate cancer annually

• Highly experienced management team with significant oncology experience

• IND filing of next-generation Aniten compound anticipated by 1Q2019

Experienced Management Team

David R. Parkinson, MD• President & Chief Executive Officer, Director• Nodality, Novartis, Amgen, Biogen Idec, National

Cancer Institute

Peter Virsik, MS, MBA• Executive Vice President and Chief Operating Officer• XenoPort, Gilead Sciences, J.P. Morgan, Genentech

Frank Perabo, MD, PhD, FEBU• Chief Medical Officer & Executive Vice President of

Clinical Development• Astellas Global, Oncology World GmbH, P & S Partner

Consulting, Bonn University

David S. Wood, MBA, CPA, CMA• Chief Financial Officer• Celator Pharmaceuticals, Cubist Pharmaceuticals,

TerraGen Discovery

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Management

2017-09-25, 3:51 PM

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Prostate Cancer: Unmet Medical Need

• Prostate cancer is 2nd most common cause of death in men 1

o Yearly, there are ~160,000 new prostate cancer cases and ~26,000 US deaths due to the disease

• In 2015, Zytiga® (abiraterone, approved 2011) and Xtandi® (enzalutamide,approved 2012) generated global sales of over $4B

• Disease progression strongly driven by androgen receptor (AR) signaling 2,3,4

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

• Despite new therapies, development of resistance limits treatment options andsurvival 6,7

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1. Surveillance Research, American Cancer Society, 20162. Robinson D, et al. Cell, 20153. Katsogiannou M, et al. Cancer Treat Rev, 2015

4. Azad AA, et al. Clin Cancer Res, 20155. Wyatt, JAMA, 2016 6. Watson PA, et al. Nat Rev Cancer, 20157. Attard, G, et al. ASCO Annual Meeting, 2017

Current Therapies Target the AR Ligand Binding Domain

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• AR is comprised of 3 distinct,independently acting domains

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

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

AndrogenInhibit synthesis

Block ligand binding

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

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

Mechanisms of AR Resistance Occur in the Ligand Binding Domain

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N-terminal domain(NTD)

DNA-binding domain Ligand-binding domain(LBD)

AR Amplification 1

Splice variants 3,4,5

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

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

Androgen Receptor

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

Gain-of-function mutations 1,2

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

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• Proposed binding of EPI compounds to Tau-5 region of AF11

• EPI compounds inhibit wild-type, LBD mutant, and splice-variant AR activity 2,3,4

Tau-5

EPI362

C404

438

1. De Mol E, et al. ACS Chem Biol, 20162. Andersen RJ, et al. Cancer Cell, 20103. De Mol E, et al. ACS Chem Biol, 2016

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

4. Yang YC, et al. Clin Cancer Res, 20165. Myung JK, et al. J Clin Invest, 20136. Andersen RJ, et al. Cancer Cell, 2010

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

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

EPI-506 Summary

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

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Parameter Details

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 who have experienced disease progression after abiraterone, enzalutamide,or both; allowed to have also failed one regimen of docetaxel chemotherapy

Study Size Phase 1: 26 patients

Endpoints Phase 1: safety, PK, maximum tolerated dose, recommended Phase 2 dose, biomarkers(CTCs)

Study Status Phase 1 study completed at 5 sites in US and Canada

First-Generation EPI-506 Phase 1 Pharmacokinetic Data

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EPI-002Pharmacokinetics(Mean± S.D.)onDay8

PKParameter

Cohort 62,400 mg

QD(n=3)

Cohort 71,800 mg

BID(n=2)

Cohort 83,600 mg

QD(n=2)

Cmax (ng/mL) 2,372 ± 813

3,057 ± 159

8,397 ± 1396

**tmax (hr)4.00

(2.00 - 4.00)2.00

(2.00 - 2.00)2.50

(1.00 - 4.00)

Clast (ng/mL) 70 ± 25 208 ± 85 195 ± 185

AUC0-24h(ng*h/mL)

13,829 ±6,758

23,524 ±5,380

42,988 ±24,841

**tmax reportedasmedian(min– max)

Mean Steady-State EPI-002 Plasma Concentration-vs-Time Profiles

Mean Steady-State EPI-002 PlasmaPharmacokinetics

First-Generation EPI-506 Phase 1 Interim Exposure and Treatment Duration Data (N=28)

130 100 200 300 400 500

04-001404-001105-000405-000104-0012

01-0001 03-0004 05-000504-0013

03-0003 02-0002 03-0011

03-0001 04-0007

04-0002 02-000303-0008

04-0001 04-000904-000605-0003

03-0005 02-0005

02-0001 03-000904-0004

03-0006 04-0005

Exposure (in days)

Patie

nt #

160, 320, 640, 1280, 2400640, 1280640, 1280

80, 1602400

2400320640, 12806402400

32012801280

80128080

1601800 (BID)

160

1800 (BID)3600

Doses Received (mg)

320

3600

535416

219219

187172

128125

10589888787878381

7970

6058

5544

21

3130

129

640

6401800 (BID)3600

8 1800 (BID)

Continuing on study drug

Discontinued

Time of best PSA decline

Median # exposure days = 87

Data as of Aug 28, 2017

-30.00

-20.00

-10.00

0.00

10.00

20.00

30.00

40.00

50.00

First-Generation EPI-506 Interim PSA Response - Maximal PSA Change at Any Time from Start of Multi-dose Period (N=25*)

160

mg

320

mg

320

mg

640

mg

1280

mg

80 m

g

80 m

g

160

mg

640

mg

320

mg

640

mg

160

mg

2400

mg

640

mg

2400

mg

1280

mg

3600

mg

1280

mg

%PS

A C

hang

e

Pts receiving ≥ 1280 mg

Pts receiving < 1280 mg

3600

mg

1800

mg

(BID

)

2400

mg

1280

mg

1800

mg

(BID

)

1280

mg

640

mg

*Of 28 enrolled pts: 25 were evaluable (had at least a WK4 PSA reading), 1 has not reached WK4, 2 discontinued before reaching WK4

Data as of Aug 28, 2017

Example of Patient PSA Response: Patient 04-0013 (3600 mg)

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100

200

300

400

500

600

700

800

900

1000

Previous Therapies:Cabazitaxel Dec 2014 – Jun 2015Enzalutamide Sep 2015 – Nov 2016Radium-223 Nov 2016 – Mar 2017

PSA

(ng/

mL) Baseline

Pre 1

Pre 2WK4

WK1D1

Pt. is ongoing on study

WK8

22.2% decline

Safety / Tolerability Profile

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Most Commonly Reported Adverse Events > 10% All Grades, N (%)

Diarrhea, nausea FatigueDecreased appetite, pain in extremityVomitingBack painAbdominal distension, anemia, arthralgia, musculoskeletal pain, UTI

13 (46%) 7 (25%)6 (21%), each5 (18%)4 (14%)3 (11%), each

Adverse Events ≥ Grade 3 N (%) Relationship to study drugAnemia

AST elevated

Neutropenia

Abdominal pain, diarrhea

ALT elevated, amylase elevated, angina, hypertension, dizziness postural

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

3 (11%)

2 (7%)

2 (7%)

1 (4%), each

1 (4%), each

1 (4%), each

Not related

Probably related, Possibly related

Not related

Possibly related

Probably related

Not related

Lesson from the Phase 1 Experience with EPI-506

• NTD inhibition in mCRPC can be done safely; EPI-506 was well-tolerated with evidence of POC

• Specifications of next-generation Aniten compounds:o Higher potencyo Less metabolismo Longer half-lifeo Commercial formulationo Ease of manufacturing / shelf-life stability

• Opportunity to take advantage of new patient biological characterization:o ctDNA to assess tumor AR status and verify continued reliance on AR pathwayo CTC mRNA gene expression

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EPI Next-Generation Aniten Compounds

ESSA Next-Generation Aniten Program Goals

• Build on the strengths of the EPI-506 (EPI-002) chemical scaffold

• Increase potency

• Clean drug interaction profile

• Block anticipated metabolism/resistance

• Short, efficient, and scalable synthesis

• Commercially-acceptable formulation

• Strong & long-lasting IP – novel composition of matter

CONFIDENTIAL

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Next-Generation Aniten Program Status

TPP Criteria Status SpecificsHigh-potency scaffold ✓ New high-potency chemical scaffold discovered

• Additional SAR Additional SAR being conducted on additional chemical modifications

Increased potency ✓ AR luciferase screening shows ~10X higher potency for compounds

• In vitro activity ✓ LNCaP and LNCaP95 (splice-variant AR-driven) in vitro proliferation corroborate higher potency than EPI-002

• Oral activity in vivo ✓ One compound tested in xenograft LNCaP model to date; orally active at lower doses than EPI-002

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Next-Generation Aniten Program Status

TPP Criteria Status SpecificsClean off-target profile ✓ CEREP screening indicates that the lead compounds have minimal

off-target binding at 10µM

Improved ADME profile ✓ Key criteria screened

• Block metabolism ✓ New chemical structures designed specifically to minimize potential metabolism of EPI-002

• In vitro ADMEscreening

✓ Solubility, protein binding, Caco-2, S9 and hepatocyte intrinsic clearance all look favorable

• Chemical stability ✓ Initial stability appears greatly improved over EPI-506

Improved Pharmaceutical Properties

✓ Initial compound showed potential to be crystalized; may open path to solid dosage formulations

• Simple synthesis ✓ Simple 5-step process developed

Strong IP ✓ Worldwide IP filings made

Financial History and Highlights

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2010/12 $3.7M seed financings

2014/15 $12M Cancer Prevention Research Institute of Texas (CPRIT) Grant awarded

$16.3M IPO included Deerfield, Omega, Special Sits

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

2016 $20M financings including Clarus, Deerfield, Omega, Eventide

$10M SVB loan facility; $8M drawn

2018 $25M raise @ $0.20 per share including Clarus, BVF, Eventide, Omega

Cash reported Sept 30 2017: $4.0M

Shares outstanding post Jan 2018 financing: 155 M

Summary: ESSA Value Proposition and Near-term Milestones

• Initial clinical POC established for NTD inhibition

• New technologies enable patient selection and measurement of patient responses in a refractory mCPRC population

• Un-partnered Aniten franchise of high-potency compounds advancing to IND

• Sufficient cash resources to select IND candidate and conduct phase 1 study

• Near-term clinical and corporate milestones:

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Key Milestone Events Date• Designate a lead Aniten compound for IND-enabling studies 1H18• Advance discussions with strategic partners regarding a collaboration 2018• File and IND on the lead Aniten in mCRPC 1Q2019