ESSA Pharma(NASDAQ: EPIX; TSX-V: EPI)

Non-Confidential Slide Deck dated Jun 1, 2018

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.

ESSA Corporate Overview

• Founded in 2009 with technology licensed from The University of British Columbia and the BC Cancer agency

• Sites in South San Francisco, Vancouver and Houston

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Focused on the development of novel therapies for the treatment of metastatic castrateresistant 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 Aniten compounds advancing to IND

Technology & Products

Financial Details

• Listed on NASDAQ & TSXV

• Completed $26M financing Jan 2018

Experienced Management Team

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

Cancer Institute

Peter Virsik, MS, MBA• EVP & Chief Operating Officer• XenoPort, Gilead Sciences, J.P. Morgan,

Genentech

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

Pharmaceuticals, TerraGen Discovery

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ESSA’s Goal

• The Challenge: o The need for new, complementary approaches to inhibition of androgen receptor

(AR)-driven biology in prostate cancer

• ESSA’s Approach:o Development of unique inhibitors of the N-terminal domain (NTD) of AR, overcoming

resistance to anti-androgens, creating the opportunity for the treatment of both patients progressing on anti-androgens as well as in combination therapy

• Progress to Date:o Phase I clinical trial has confirmed both the safety and the proof-of-concept in

patients of this approach, while revealing the need for a more potent agento These next generation agents are being screened in preparation for clinical

development

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Metastatic Castrate-Resistant Prostate Cancer (mCRPC): An Unmet Medical Need

• Public Health Problem: Prostate cancer is 2nd most common cause of death in men 1o Yearly, there are ~160,000 new prostate cancer cases and ~26,000 US deaths due to the disease

• Large Market: In 2017, leading anti-androgens, Zytiga® (abiraterone acetate, approved 2011) and Xtandi® (enzalutamide, approved 2012), generated global sales of over $5B

• Validated Therapeutic Target: 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

• Need for New Therapeutic Strategies: Despite new therapies, development of resistance limits treatment options and survival 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, 20154. Azad AA, et al. Clin Cancer Res, 2015

5. Wyatt, JAMA, 2016 6. Watson PA, et al. Nat Rev Cancer, 20157. Attard, G, et al. ASCO Annual Meeting, 2017

Current Anti-androgen 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)

Androgen

Inhibit synthesis

Block ligand binding

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

Xtandi® (enzalutamide)Erleada® (apalutamide)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

5. Sun S, et al. J Clin Invest, 20106. Chen EJ, et al. Clin Cancer Res, 20157. Culig Z, et al. Cancer Res, 1994

Androgen Receptor

1. Azad AA, et al. Clin Cancer Res, 20152. Joseph JD, et al. Cancer Discov, 20133. Antonarakis ES, et al. NEJM, 20144. Mostaghel EA, et. Al. Clin Cancer Res, 2011

Gain-of-function mutations 1,2

Tau-5

EPI362

C404

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

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

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

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

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

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

Progress Towards a Novel Mechanism of AR Inhibition

• Validated target pathway relevant in patients progressing on anti-androgens

• Mechanisms of resistance to anti-androgens understood

• NTD inhibition overcomes these mechanisms & can be administered safely

• More potent NTD inhibitors are being prepared for IND study

• Strong IP protection (2037+ for next gen compounds)

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First Generation NTD Inhibition:Summary of the EPI-506 Experience

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)

• Apparent specificity in binding (imaging, protein-binding studies)

• Toxicology quite unremarkable (minor weight loss & reversible)

• Combination with anti-androgens reveals activity greater than either NTD inhibitor or

anti-androgen alone

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EPI-506 (tri-acetate prodrug) EPI-002 (active drug)

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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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 docetaxelchemotherapy

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

• Minimal time with drug concentrations >IC50

CONFIDENTIAL

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

• Significant first-pass metabolism seen

• Short effective T1/2

First-Generation EPI-506 Phase 1 Pharmacokinetic Data

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-30

-20

-10

0

10

20

30

40

50

02-00

02

04-00

01

03-00

04

05-00

01

04-00

12

05-00

05

04-00

09

02-00

03

01-00

01

04-00

02

03-00

08

03-00

01

03-00

03

03-00

11

03-00

05

05-00

03

04-00

06

02-00

01

03-00

06

03-00

09

04-00

04

02-00

05

04-00

07

04-00

13

04-00

05

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

%P

SA

Cha

nge

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

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

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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.

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

Lessons from the Phase 1 Experience with EPI-506

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

• The experience outlined the specifications for a next-generation Anitencompound:o Higher potencyo Less metabolismo Longer half-lifeo Commercial formulationo Ease of manufacturing / shelf-life stability

• New technology enables patient biological characterization and more informative, efficient trial conduct:o ctDNA to assess tumor AR status and verify continued reliance on AR pathwayo CTC mRNA gene expression to monitor PK/PD

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Next-Generation Aniten Compounds

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ESSA Next-Generation Aniten Program Status

TPP Criteria Status Specifics

Increase potency ✓ In vitro potency goal achieved (10X more potent than EPI-506/002)

Oral activity in vivo ✓ Orally active at lower doses than EPI-506 in LNCaP xenograft studies

Clean off-target profile ✓ CEREP screening indicates that the lead compounds have minimal off-target binding

Improved ADME profile ✓ Significant in vitro ADME screening undertaken

• Block metabolism ✓ New chemical structures block major metabolic pathways

• Simple synthesis ✓ Simple synthetic route established

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

Strong IP ✓ IP filings made; 2037 anticipated patent expiration

ESSA Next-Generation Lead Compounds Are More Potent than First-Generation EPI-002 in In Vitro Studies

• All three lead compounds show significant improvements in potency over EPI-002.

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0

2

4

6

8

10

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Fold-Increase in Potency over EPI-002

Lead 1 Lead 2 Lead 3

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)

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

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

2018 $26M raise included Clarus, BVF, Eventide, Omega

Cash reported March 31 2018: $21.7M

Common Shares 8.0M

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 ADME properties compared to EPI-506

• mCRPC represents a significant market opportunity – 160,000 new cases of prostate cancer each year in the US and annual global sales of over $5B

• Highly experienced management team with significant oncology experience

• IND filing of next-generation Aniten compound anticipated by 1H2019

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