ABN 16 165 160 841

Suite 401, 35 Lime Street, Sydney 2000, Australia Phone: +61 2 8003 3650 Email: info@innateimmuno.com

www.innateimmuno.com

ASX RELEASE 9 May 2018

Investor Presentation and Conference Call

Innate Immunotherapeutics Limited (ASX Code: IIL), following completion of the recent acquisition of Amplia Therapeutics, has prepared an Investor Presentation which is annexed hereto and will host an Investor Conference Call at 9.00 am on Thursday 10 May 2018.

The Investor Conference Call will provide shareholders, analysts, investors and interested parties with the opportunity to receive an update from the Company in relation to Amplia’s Focal Adhesion Kinase (FAK) pipeline, its two small molecule FAK inhibitors and the drug development program for the coming 12 months.

Investor Conference Call:

Date and Time: Thursday May 10th and at 9am (AEST)

Conference Code: 794986

Dial In Numbers:

Australia 1800 908 299 or +61 2 9007 8048

US/Canada 1855 624 0077

UK 0800 051 1453

Singapore 800 101 2702

Hong Kong 800 968 273

New Zealand 0800 452 795

Japan 0066 3386 8000

Investors can click HERE to preregister for the call or go to the following page on the Company's website: http://www.innateimmunotherapeutics.com/irm/content/presentations.aspx?RID=322

- End For Further Information:

Mr Simon Wilkinson, CEO Email: simon@innateimmuno.com

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Investor Presentation

10th May 2018

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Notice

The information contained in the presentation is not intended to be an offer for subscription, invitation or recommendation with respect to

shares of Innate Immunotherapeutics Limited (“Innate”) in any jurisdiction. No representation or warranty, express or implied, is made in

relation to the accuracy or completeness of the information contained in this document or opinions expressed in the course of this

presentation. The information contained in this presentation is subject to change without notification.

This presentation contains forward-looking statements which can be identified by the use of words such as “may”, “should”, “will”,

“expect”, “anticipate”, “believe”, “estimate”, “intend”, “scheduled” or “continue” or similar expressions. Any forward-looking statements

contained in this presentation are subject to significant risks, uncertainties, assumptions, contingencies and other factors (many of which

are outside the control of, and unknown to Innate, and its officers, employees, agents or associates), which may cause the actual results

or performance to be materially different from any future result so performed, expressed or implied by such forward-looking statements.

There can be no assurance or guarantee that actual outcomes will not differ materially from these statements. The data and results

pertaining to clinical subjects used in this presentation are illustrative of medical conditions and outcomes associated with potential

applications of Innate’s acquired product pipeline. Actual results from clinical trials may vary from those shown.

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Executive Summary

The acquisition of Amplia’s Focal Adhesion Kinase (FAK) pipeline

represents a compelling opportunity for Innate Immunotherapeutics

to rebuild shareholder value

Multiple “shots on goal” – two molecules and multiple indications

Streamlined pathway to Phase II in both cancer and fibrosis with a

capital effective strategy that is rapid and low risk

Multiple significant value inflection points in the next 12-18 months

Experienced drug development team and strong academic partners,

backed by the Cancer CRC (Australia) and Cancer Research UK

(CRUK)

Amplia team members also bring relevant experience / networks to

review cancer development options for MIS416

Fibrosis

Fibrotic

Cancers

Cancer

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FAK

Inhibition

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Background: Amplia Therapeutics

• Founded in May 2016

• Experienced commercial/development team

• “Amplia” refers to the potent multiplication effect

of combo therapies with FAK-targeting drugs

• Scientific advisory board to be led by Prof.

Margaret Frame (Edinburgh U.) – KOL in FAK

• Focused on development of two small molecule

FAK inhibitors – AMP945 and AMP886

Discovered by Australian-based

Cooperative Research Centre for

Cancer Therapeutics (CTx).

www.cancercrc.com

In-licensed from Cancer Research

UK, CRC’s commercialisation partner

Christian Behrenbruch, D.Phil (Oxon) MBA JD

• Life sciences/medtech entrepreneur

• Director, Factor Therapeutics (ASX : FTT)

• CEO of Telix Pharmaceuticals (ASX : TLX)

Chris Burns, PhD, FRSC FRACI

• Over 20yrs experience in Pharma, biotech and academia.

• Discovered clinically trialled drugs momelotiniband lexibulin

• 50+ scientific publications, 30+ patents

Mark Devlin, PhD

• Experienced drug discovery biologist

• Head of the CRC for Cancer Therapeutics (CTx) Translational Research

Mark Sullivan

• Experienced drug development professional (ex GSK, Gilead)

• Founder and Managing Director, Medicines Development for Global Health

Warwick Tong, MB ChB MPP GAICD

• Ex-GSK, experienced drug developer

• Former CEO and Director, Cancer CRC

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• Focal Adhesion Kinase is frequently up-

regulated in many cancer types

• Signals functions that are important for cancer

development and metastases

– Adhesion / Migration / Invasion /

Proliferation / Survival

• Co-opted by cancer to assist spread and to

develop resistance to therapy

• FAK-dependent signalling drives elevated levels

of regulatory T-Cells which in turn suppress the

all important anti-tumour T-cell response

• Role in fibrosis has impact in both “fibrotic

cancers” (e.g. pancreatic/ovarian), as well as

non-cancer fibrosis (e.g. lung/liver fibrosis)

FAKMigration

InvasionImmune

Suppression

Proliferation

& Survival

1) FAK has a fundamental role in cancer. Blocking FAK

opens the door for new combination therapies using

existing approved chemotherapeutics

2) FAK plays a major role suppressing the immune

attack on tumours. Blocking FAK allows immuno-

oncology drugs (e.g. checkpoint inhibitors) to work in

tough cancers like pancreatic cancer

3) The planned clinical development pathway creates

the opportunity for multiple indications in both cancer

and non-cancer applications

Key Messages:

FAK “101”

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FAK expression contributes to tumour immunity in fibrotic cancers

FAK Expression

Chemokines /

Cytokines

Regulatory

T-cells

(Tregs)

Tregs block Killer

T-cells from

attacking tumours(Checkpoint blockade)

Diagram adapted from Symeonides et. al. J Immunother Cancer. 2017; 5: 17.

Drugs that target FAK are

novel because they target

the tumour micro-

environment, the supportive

infrastructure that enables

cancer cells to “hide” from

the immune system

Inhibiting FAK appears to

unlock the potency of

checkpoint inhibitor drugs

(i.e.PD-1/PD-L1, CTLA-4),

particularly in fibrotic

cancers like pancreatic

cancer.

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Cytotoxic

Killer T-cells

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Fibrotic cancers

Fibrotic cancers have a

very different immunologic

profile. Fibrotic cancers

use the tumour micro-

environment as part of

their defence against the

immune system.

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TriC

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The biggest unmet need in cancer therapy is pancreatic cancer.

Pancreatic cancer is the epitome of a fibrotic tumour that can

potentially be attacked with a FAK inhibitor in combination with

other immuno-oncology therapies.

Pancreatic Cancer:

• worst survival outcome of the 21 most common cancers

• death rates are increasing while most other cancers declining

• predicted to overtake breast cancer as the 4th most common

cancer killer by 2030

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FAK is a proven important target in immuno-oncology

Inhibiting FAK decreases immunosuppressive cell

populations in tumours and may enable immunotherapy to

work in cancer populations that have a generally poor

response to checkpoint inhibitor drugs

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• Novel small molecule FAK inhibitors (FAKi)

AMP945 – Highly selective

AMP886 – Highly differentiated, multi-action

(FAK/FLT3/VEGFR3)

• Excellent potency and selectivity, very promising pharmacokinetics and physical-chemistry properties

• Expected superior safety profile in IO combo therapy compared to immuno-stimulatory modalities

• Scale-up (Kg scale) chemistry already developed in partnership with an international

commercial contract manufacturer

– Including methods that are suitable for GMP production of clinical trial material

– Highly cost effective common synthetic routes for both molecules

• Strong intellectual property position

– National phase filing in commercially important jurisdictions

– Clear strategy to expand scope of existing IP

The Amplia FAK assets

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AMP886 “Triple kinase FAKi” sensitizes tumours to chemotherapy*

Time after commencement of treatment (Days)

0 20 40 60 80 100 120 140 160

Me

an T

um

our

volu

me

(m

m3

)

0

200

400

600

800

1000

1200

1400

Time vs Irinotecan

Time vs FAK 886

Time vs Irino + 886 same day

Time vs Irino + 886 pretreat

Treatment Period

Inhibiting FAK with the multi-action AMP886 agent combined with

Irinotecan, has a significant impact on tumour growth and survival in

mouse models of pancreatic cancer (human PANC-1)

0 20 40 60 80 100 120 140 160

Time (Days)

Su

rviv

al

0.0

0.2

0.4

0.6

0.8

1.0

Irinotecan only

886 pre-treatment

before chemotherapy

*Unpublished data

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Non-cancer indications: FAK and fibrosis

• The Amplia FAK inhibitors have demonstrated excellent efficacy in standard fibrosis models*

• AMP945 has been extensively evaluated in both prevention models and treatment models, including on

a comparative basis with other FAK inhibitors under development

• Opens the potential both in fibrotic cancers, but also other chronic fibrotic diseases

Prevention Model

Bleomycin Lung Fibrosis Model

PBS (Control) Vehicle AMP-945 (40mg/kg) AMP-945 (80mg/kg) Comparator (15mg/kg)

Treatment Model

*Unpublished data

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Leads to a clinical development roadmap with multiple “shots on goal”

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Refractory/Progressive

Cancer (Ovarian Cancer)

Fibrosis(Idiopathic Pulmonary

Fibrosis - IPF)

Fibrotic

Cancers(Pancreatic Cancer)

FAK

+ Checkpoint Inhibitors

+ chemo (mTOR/BRAF, etc)

AMP945

AMP945

AMP886

Inhibition

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High-level development plan (18 months)

Initial clinical focus is to rapidly

obtain PK/PD, safety, and

tolerability data in CTN Phase 1

SAD & MAD healthy volunteer

study. This will provide IND Phase 2

enabling human data to potentially

underpin both oncology and fibrosis

patient trials.

GLP Tox

Fibrosis Indication (Partner)

Immuno-OncCombo Trial (IND)

AMP945Further Animal

Models (I/O Focus)

CTN Healthy Volunteer Study

(~50 pts)

AMP886 Further Animal Models

GLP Tox

Common Synthetic

RouteScale-Up/ GMP

Phase II – late Q3/early 4 ‘19

In progress

In progress

Oct ‘18 early ‘19

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Competitive landscape

Agent Company Status Notes

VS-4718 (PND-1186) Verastem PI First generation candidate

VS-6063 (PF-04554878) Verastem PI/PII Combo with Pfizer/Merck

GSK-2256098 GSK PI Paused

CT-707 Centaurus Pharma PI-Not yet recruiting Questions about selectivity

BI-853520 Boehringer-Ingelheim PI Two PI trials completed

ASN-006 Asana Discovery Early stage

• Established target but still relatively little commercial congestion around novel FAKi compounds

• Increased interest in the use of FAK inhibitors in the immuno-oncology setting as acombination therapy (Verastem-Pfizer partnership)

• Verastem (NASDAQ: VSTM, Market Cap USD $123m) is our nearest comparator

• Our differentiation is:

• AMP945 is extremely selective / “clean” for FAK inhibition compared with competitive products –important in immuno-oncology combo applications to maximise safety

• AMP866 has useful multi-target properties for chemotherapy combination use

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Capital requirements

• Current balance sheet sufficient to complete remaining Phase 1

enabling preclinical activities

• Running ‘virtually’ to minimise cashburn during preclinical and Phase 1

development with team build-up occurring pre Phase II

• Projected ~AUD $5m requirement to complete initial human studies and be

Phase II ready (Phase II planning assumes US IND)

• Completion of a capital raise targeted by end Q3/2018

• In parallel, several business development discussions with global

pharmaceutical companies

– Potential collaborations (pre-clinical and clinical)

– Cancer and Fibrosis

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Corporate Snapshot – 9 May 2018

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Key Statistics as at 9 May 2018

ASX Code IIL

Share price A$0.40 [post share consolidation]

Shares on issue 41,023,303

Market Cap A$16.4 million

Options 1,460,000 (A$4.00 or higher)

Cash A$2.2 million (Appendix 4C 31/03/18)

Substantial Holders ( => 5%)

CTxT Pty Ltd 11%

Christopher Collins 9.2%

Elk River Holdings (Chris Behrenbruch) 6.1%

34th Avenue Pty Ltd (Mark Devlin) 5.4%

Christopher Burns 5.4%

Citicorp Nominees Pty Ltd 5.3%

Register

Top 20 66.7%

Total shareholders 3,096

Voluntary Restricted Shares (May 2020) 18,460,308

NZ13%

Australia63%

USA17%

Other7%

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For further information please contact

Simon Wilkinson, CEO

simon@innateimmuno.com

+64 21 661 850

www.innateimmuno.com

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