MARKET ANNOUNCEMENT

Invion Limited ABN 76 094 730 417

Unit 2, 120 Bluestone Circuit, Seventeen Mile Rocks, QLD 4073 P +61 7 3295 0500 F +61 7 3295 0599 www.invion.com.au

MARKET ANNOUNCEMENT

Dr Greg Collier presents Invion at AsiaBiotech

BRISBANE, 3 JUNE 2013: Australian drug development company Invion Limited (ASX: IVX) is

pleased to release a copy of the presentation that Managing Director and CEO, Dr Greg Collier will

deliver this week during investor meetings in Singapore and Hong Kong, and to the

AsiaBiotech Invest conference.

The conference presentation will occur on Wednesday 5 June at 12:05pm, local time at the

Sheraton Hotel and Towers, Hong Kong.

Dr Collier will provide an overview of the Company's current activities, including:

• phase II clinical trials of INV102 (nadolol) in asthma and chronic bronchitis;

• the phase II development of INV103 (ala-Cpn10) as a potential therapy for lupus; and,

• Invion's expected value drivers over the next 12 - 36 months

Information about the AsiaBiotech Invest 2013 conference can be found at

http://asiabiotechinvest.com.

About Invion Limited

Invion Limited (ASX:IVX) is a life sciences company with two drug assets in three FDA-regulated, phase II clinical

programs. With operations in the US and Australia, the strategic focus of IVX is the development of treatments for

major market opportunities in inflammatory diseases, including asthma and COPD ($34B) and lupus (to $4B).

The company’s corporate focus is the cost-effective advancement of its assets to late phase II before negotiating

commercial partnerships.

INV102 (nadolol) is a beta blocker that has been used in more than 10 million people for the treatment of high

blood pressure, migraine and chest pain. Invion is repurposing INV102 to treat lung indications and to date the

company has completed two phase II clinical trials which demonstrated acceptable safety as well as dose-related

reduction of airway hyper-responsiveness. A further phase II trial in asthma - funded by the US National

Institutes of Health in excess of $4 million - is now underway, and a trial in chronic bronchitis patients is due to

commence. INV103 (ala-Cpn10) is a modified naturally occurring human protein that has shown to reduce IL-6,

a key marker in the inflammatory disease, lupus. A phase II trial in lupus is anticipated to commence in Q2 2013,

under a US IND submitted 24 April 2013.

FOR MORE INFORMATION CONTACT:

Investor Relations: Rebecca Wilson, Buchan Consulting P: 03 9866 4722 rwilson@buchanwe.com.au

Media Relations: Jane Lowe, Buchan Consulting P: 02 9237 2807 jlowe@buchanwe.com.au

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Invion Limited (ASX:IVX)

Clinical-stage life sciences company targeting chronic inflammation

Corporate Presentation June | 2013

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Disclaimer This presentation has been prepared by Invion Limited (Invion or the Company) solely for its use at presentations to

be made by the Company. The information contained in this presentation is an overview and does not contain all

information necessary to make investment decisions. Although reasonable care has been taken to ensure that facts

stated in this presentation are accurate and that the opinions expressed are fair and reasonable, no representation,

expressed or implied, is made as to the fairness, accuracy, completeness or correctness of the information and

opinions contained in this presentation and no reliance should be placed on such information or opinions. This

presentation does not constitute an offer, invitation, solicitation or recommendation with respect to the purchase or

sale of any security in the Company nor does it constitute financial advice nor take into consideration your investment

objectives. This presentation contains or may contain forward-looking statements that are based on management’s

belief, assumptions and expectations and on information currently available to management. All statements that are

not historical, including those statements that address future operating performance and events of developments that

we expect or anticipate will occur in the future, are forward looking statements. Although management believes these

forward looking statements are fair and reasonable you should not place undue reliance on these statements.

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Invion proposition

> Two phase II proprietary therapeutic candidates that target chronic

inflammation

> INV102 (nadolol) (chronic bronchitis, asthma, cystic fibrosis)

> INV103 (ala-Cpn10) (lupus)

> Advancing clinical-stage company with reduced clinical risk

> Experienced and well credentialed Board and international KOL

networks

> Experienced management team with significant FDA experience

> Existing NIH linkage grants with scope for additional non-dilutive

capital

> Significant valuation drivers: from 12 months - 3 year horizon

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Experienced management team

Greg Collier, PhD., MD and CEO

> 20 year career in pharma research, development and commercialisation.

CEO ChemGenex Pharmaceuticals (sold to Cephalon $230M). 150 peer reviewed

publications, 33 patents, Roche Award for Excellence.

Mitchell Glass, M.D., EVP R&D and CMO

> 25 year veteran of Pharma (AZ, GSK) and Biotech (AGIX). Managed more than 40

drug developments including “first in class” and beta blocker carvedilol (Coreg). 5

FDA approved drugs.

James Campbell, PhD., Executive Director

> 20 years international research, management and venture capital experience.

COO and CFO ChemGenex Pharmaceuticals. Member of two VC investment

committees and commercialization advisor to several universities.

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Pipeline: three phase II trials underway in 2013

Preclinical Phase I Phase II

INV102 (nadolol)

INV103 (ala-Cpn10)

New chemical entity

Asthma

Chronic Bronchitis

Lupus (SLE)

INV102 (nadolol)

Chronic bronchitis

Cystic fibrosis

NIH funded, US$4m+ non-dilutive funding (oral delivery)

In patients undergoing smoking cessation (oral delivery)

Large unmet medical need

Inhaled program

Inhaled program

Academic alliance Beta-2 adrenergic

inverse agonist

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INV102 (nadolol) • existing drug being repurposed for a new target

• aim to develop an inhaled drug for the treatment of respiratory

diseases including asthma and COPD

• short term path to commercialisation with oral treatment of COPD

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INV102 (nadolol)

> An inverse -agonist

> block agonist stimulation of the receptor; AND,

> inactivate intracellular inflammatory events that are stimulated spontaneously

or by agonists

> Current indications: high blood pressure, chest pain, migraine

> Being repurposed to treat: inflammatory lung conditions

> Suite of patents granted and in prosecution

Data to date

> Preclinical data confirms nadolol:

> As adrenergic inverse agonist providing unique anti-inflammatory activity

> Possesses unique activity to protect airway or reverse mucus metaplasia

> Two phase II clinical trials completed

> 80% positive response against objective endpoint

> acceptable safety

> dose-related reduction of airway hyper-responsiveness

References: Bond et al. ‘Complementary anti-inflammatory effects of a -blocker and a corticosteroid in asthma’ Arch

Pharmacol 2011

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Significant market opportunity

References: Respiratory and Inflammation, AstraZeneca Annual Report, 2011; Smoking Cessation Drugs: World Market

Prospects 2012-2022, Visiongain Reports 2012 ; Healthcare Finance, Bloomberg Brief, 13 August 2012; Full-Year and

Fourth-Quarter 2011 Financial Results, Merck & Co. * Company estimates

Respiratory world market $

21.6B

12.9B 8.4B

21.7B

> Prescription respiratory world market $64.6B

> Asthma and COPD prescription drugs $34B

> Advair Diskus ® (asthma and COPD) $8.1B

> Singulair ® (asthma) $5.5B

> Symbicort ® (asthma and COPD) $3.1B

> FDA Black box warning on all Long

Acting Beta Agonists (LABAs) and

LABA/Steroid combinations:

increased risk of death

> Smoking cessation drug market $2.4B

> Nicotine replacement therapy (NRT) is

bulk of existing market - does not address

lung healing

> 10-15% of early failures due to cough

associated with excess mucus*

> Opportunity to expand existing market

Asthma COPD

Rhinitis Other

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INV102: Mechanism of action

> Healthy lung tissue consists of

mostly ciliated epithelial cells with

smaller numbers of (secretory)

goblet cells

> In disease states the proportion of

goblet cells increases, lining the

lung with a “mucous plug” that

impairs gas transfer

> Further, smooth muscle cells

spasm causing bronchoconstriction

Ciliated epithelia Goblet cell

Airspace

Airway surface liquid

Smoking Asthma

Mucous plug

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Mechanism of action targets multiple pathways

> Reduction of goblet cell metaplasia

> Reduced mucous hypersecretion

> Restoration of ciliated epithelium

> Reduced levels of pro-inflammatory

cytokines: IL-5, IL-10, IL-13

> Down-regulation of bronchoconstriction:

> 2x Phospholipase Cb

> 6x Phosphodiesterase 4d

> 50% reduction in eosinophils

> Restoration of lung function

Ciliated epithelia Goblet cell

Airspace

Airway surface liquid

Mucous plug

Healing INV102

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Preclinical studies demonstrate airway healing

Proof of concept has been achieved in pre-clinical studies with inhaled INV102

Chronic Exposure to Beta-Blockers Attenuates Inflammation and Mucin Content in a Murine Asthma Model. Nguyen et al. Am J

Respir Cell Mol Biol. 2008 Mar;38(3):256-62. See also. β-Adrenoceptor signaling is required for the development of an asthma

phenotype in a murine model. Nguyen et al. Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2435-40.

Control lung tissue Lung tissue of ‘asthmatic’ mice treated

with INV102 (nadolol) for 28 days:

restored epithelium

Lung tissue of ‘asthmatic’ mice: epithelial

cells have been converted to mucus-

producing goblet cells. No effect on

alprenolol

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Successfully completed two phase II clinical trials

Objective: Proof-of-concept to evaluate safety and effects on airway with escalating doses

administered to 19 subjects with mild asthma

Primary endpoint: Objective measure of airway hyper- responsiveness (PC20 MeChFEV1),

the diagnostic hallmark of asthma

Key Findings: Led NIH to fund phase IIb study in asthma:

> Safety: well tolerated in doses up to 40mg

> Efficacy: airway hyper-responsiveness:

> dose response with ineffective dose at 10mg/day

> 9 -10 weeks of treatment produced a dose-dependent decrease in airway hyper-

responsiveness that achieved clinically significant improvement

> Lung function:

> attenuation of first dose decrease in FEV1 by titration

> same benefit and commercial strategy as Coreg in CHF

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INV102: Clinical strategy Oral programs support development of inhaled product

Preclinical Phase I Phase II

Oral program

Asthma

Chronic Bronchitis

Inhaled program

Chronic bronchitis

Cystic fibrosis

NIH funded, US$4m+ non-dilutive funding

In patients undergoing smoking cessation

Oral data supports strategy

Large unmet clinical need

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Medical, regulatory and commercial precedent Precedent: Chronic Heart Failure (CHF)

Invion target: Chronic Obstructive Pulmonary Disease (COPD)

CONTRAINDICATED

Warning against use of

beta blockers in CHF for > 25 years.

Carvedilol annual sales (1998) $40m

STANDARD OF CARE

After careful titration, beta blocker

Carvedilol reduced mortality in

all classes of CHF

First in class: Carvedilol peak annual

sales $1.5 BILLION (2010)

FROM TO

CONTRAINDICATED

Warning against use of

beta blockers in COPD for > 25 years.

Nadolol current sales: $ nominal

(generic)

STANDARD OF CARE

After careful titration, beta blocker

INV102 (nadolol) targeted to reduce

airflow obstruction due to damaged

airways.

Target: First in class

FROM TO

NOTE: Nadolol effect on airways cells is unique among β blockers

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Trial name INV102 (nadolol) in smoking cessation of patients with pre-existing COPD

Trial design Double-blinded, randomised, placebo-controlled

Patients 130 (65 per arm: 54 needed for analysis)

Timing Start Q2 2013 Initial data Q4 2013

Inclusion criteria Previously failed to quit, have COPD and chronic cough

Principal Investigator Dr Albert Rizzo, Chief of Pulmonary and Critical Care Medicine, Christiana Care;

Past Chair (2011-12) American Lung Association

Site Christiana Care (Wilmington, Delaware)

Doses 1.25mg, 2.5mg, 5mg, 10mg, 25mg, 50mg (dose titration)

Primary endpoints Abstinence from smoking in last 2 weeks of trial

Secondary endpoints Number of cigarette-free days; clinical COPD questionnaire; MMRC Dyspnea

Scale; markers of COPD; sputum markers of COPD

Safety endpoints Change in FEV1; requirement for rescue medication; COPD exacerbation rate

Comment Data will support broader oral and inhaled development program

Regulatory Status www.clinicaltrials.gov ID: NCT01825122

INV102: phase II trial design – smoking cessation F

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INV102: phase II trial design – mild asthma

Trial name INV102 (nadolol) in mild asthma (NIMA)

Trial design Double-blinded, randomised, placebo-controlled, multi-centre

Patients 60 subjects (30 subjects in each of two treatment arms)

Timing Start Q1 2013 Finish 2015

Inclusion criteria Mild asthma: only β agonists as needed

Principal Investigator Nicola A. Hanania, M.D., M.S., Baylor College of Medicine

Sites Baylor, Washington University, Duke University

Doses 1.25mg, 2.5mg, 5mg, 10mg, 25mg, 50mg (dose titration)

Primary endpoints Improved airway hyper-responsiveness via change in methacholine PC20 (based

on FEV1)

Safety endpoints Safety of titration and 6 months’ dosing

Exploratory endpoints Reduced airway inflammation and mucous metaplasia; increased β2AR density,

affinity and signaling in airway epithelial cells; change in exhaled (eNO)

Comment Clinical program under US IND (submitted Feb ’07)

Regulatory Status www.clinicaltrials.gov ID: NCT01804218

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INV102: phase II milestones

Asthma

> An NIH funded phase II study ($4.4 million non-dilutive funds) was initiated Q1

2013

> Initial data obtained Q1 2014 on airway histology and sputum biomarkers

> Completed phase II data anticipated 2015

> Target outcomes: improve airway hyper-responsiveness, reduce airway

inflammation and mucus metaplasia

Chronic bronchitis (smoking cessation)

> Phase II initiation anticipated Q2 2013

> Target outcomes: increase smoking cessation, reduce airway inflammation,

decrease peri-operative complications

> Initial data obtained Q4 2013 – sputum and smoking cessation

> Data will support broader oral and inhaled development program

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INV103 (ala-Cpn10) • modified natural human protein targeting inflammatory disease

• demonstrated anti-inflammatory and immunoregulatory activity

in multiple indications

• strong safety profile

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INV103 (ala-Cpn10)

> Modified version of human Chaperonin 10

> Cpn10 has demonstrated anti-inflammatory and immuno-regulatory activity in a variety of

contexts

> Activity ideally suited to the treatment of inflammation associated with autoimmune

disease

> Data to date

> Dose response reduction in biomarkers of inflammation including serum IL-6, MCP1,

TNF and IL-1

> Strong safety profile >250 patients

> Subcutaneous and intravenous dosing data

> Intellectual Property position

> Composition of matter protection in all the major markets

> US protection to 2026

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Significant market opportunity

> March 2011 FDA approved the first new drug for lupus in more than 50 years

> Reflection of the complexity of the disease

> Clear indication of a major unmet clinical need

> Forecast: sales of over $4B in the US and five major EU markets by 2020

References: Datamonitor: Systemic Lupus Erythematosus Market Forecast, 22 August 2011; Decision Resources:

Systemic Lupus Erythematosus, 2012

0

1000

2000

3000

4000

2007 2011 2020

Lupus market size ($millions)

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INV103: Mechanism of action

> Chaperonins play roles unrelated to protein folding, incl. interplay with

cells involved in the innate and adaptive immune responses

> Expression of Cpn10 is up-regulated in response to inflammation and

can be measured extra-cellularly

> Cpn10 has demonstrated anti-inflammatory and immunoregulatory

activity in a variety of contexts

> Cpn10 is proposed as a ‘resolution-associated molecular patterns’

(RAMPs) molecule

> RAMPs exist in a healthy system to regulate the inflammatory response

> RAMPs activity generates signals which restore immune homeostasis

by deactivating cells with inflammatory phenotypes and expanding

regulatory cells

References: Resolution-associated molecular patterns (RAMPs) in the acute inflammatory response. Inflammation initiates the

over-expression and release of RAMPs, such as Cpn10 (Hsp10). These help limit and resolve the inflammatory responses via

a variety of direct and indirect mechanisms. (Shields A.M., et. al., 2011, Clin and Exp. Immunology, 165, 292-300)

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INV103: Pre-clinical results in lupus models

> Strong pre-clinical data in lupus animal model

(3 studies)

> significantly reduced kidney pathology

> improved survival

> prevented cutaneous lupus

> reduced renal and circulating levels of key

pro-inflammatory mediators (TNF-α, IL-6

and MCP-1) reduced CD4+ T cells and

auto-reactive T cells and increased the

number of activated DC (critical in the

establishment of self tolerance)

> Cpn10 also binds nucleic acid-based ligands

(e.g. DNA, RNA) implicated in SLE

> may be a mechanism for removing altered

self-molecules that activate and perpetuate

the inflammatory response in these patients

Untreated Cpn10 treated

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Systemic lupus erythematosus (SLE or lupus)

> Lupus is a vascular inflammatory disease

> IL-6 is a marker of vascular inflammation

> INV103 has a significant effect on IL-6

> Pre-IND meeting with US FDA Dec 12

> FDA confirmed lupus as important unmet clinical need

> Also confirmed IL-6 as useful marker for dose-ranging

> IND submission April 13 and phase II trial commencement June 13

> Target outcomes: safety in lupus patients, reduction of IL-6 in lupus

patients, improvement in lupus activity, PK to support future increased

dosing

INV103: Phase II clinical strategy F

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Trial name INV103 (ala-Cpn10) in mildly active Systemic Lupus Erythematosus (SLE)

Trial design Double-blinded, randomized, placebo-controlled, intravenous dosing

Patients 32 subjects (8 subjects per dose cohort, 4 cohorts)

Timing Start Q2 1013 Initial data Q4 2013

Inclusion criteria Mild lupus without clinical kidney disease

Principal Investigator Alan Kivitz, M.D., Altoona Center for Clinical Research

Sites Altoona, Pennsylvania; Dallas, Texas

Doses 10 mg - 300mg twice weekly

Primary endpoint Reduction from baseline serum IL-6 levels

Safety endpoints Safety and toxicity; pharmacokinetics; assessment of anti-drug antibodies

Exploratory endpoints SELENA-SLEDAI score (disease activity index); pharmacodynamics; markers of

systemic inflammation and vascular damage

Comment Clinical program under US IND (submitted April 2013)

Regulatory Status www.clinicaltrials.gov ID: NCT01838694

INV103: Phase II trial design – SLE F

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INV103: Phase II milestones

Lupus

> Q4 2013 completion of 1 or 2 cohorts: biochemical evidence of efficacy; safety

of increased doses

> Driver for scale manufacture of ala-CPN10

> Driver for full scale dose ranging in Lupus

> Optional: proof of concept in psoriasis with higher doses from first study

> H1 2014

> INV103: Second study (SLE)

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Summary 2 drug assets

3 FDA-regulated phase II clinical trials

experienced management team

significant valuation drivers: 12-36 months

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Pipeline: three phase II trials underway in 2013

Preclinical Phase I Phase II

INV102 (nadolol)

INV103 (ala-Cpn10)

New chemical entity

Asthma

Chronic Bronchitis

Lupus (SLE)

INV102 (nadolol)

Chronic bronchitis

Cystic fibrosis

NIH funded, US$4m+ non-dilutive funding (oral delivery)

In patients undergoing smoking cessation (oral delivery)

Large unmet medical need, 1 FDA approved drug in 50 years

Inhaled program

Inhaled program

Academic alliance Beta-2 adrenergic

inverse agonist

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Milestones to watch

2013

Q1 Asthma - phase II study in asthma initiated, enrollments and patient dosing underway

Q2 Lupus - IND filed with FDA

> Lupus - initiation of clinical trial and first patients dosed

Q3 > Chronic bronchitis (smoking cessation) - initiation of phase II study

Q4

> Asthma - enrolments completed for phase II trial

> Asthma - early signal of activity expected with secondary endpoints from sputum samples and inflammatory markers

2014

Q1 > Asthma - clinical signals from asthma study in Q1 2014

Q2 > Inhaled program - development of inhaled INV102 (nadolol) complete

> Lupus - interim (cohort) phase II results For

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Summary

2 drug candidates targeting chronic inflammatory diseases

− INV102 (nadolol)

− INV103 (ala-Cpn10)

3 FDA-regulated phase II programs underway in 2013

− asthma

− chronic bronchitis (smoking cessation)

− lupus

Large and growing markets

Data to support strategy

− medical, regulatory, commercial precedent

− phase II clinical trials already completed

Experienced management team For

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Corporate snapshot

Sector Life Sciences (Biotechnology)

Principal activities Clinical-stage pharmaceutical drug development

Pipeline 2 drug candidates in 3 phase II clinical programs

Operations USA & Australia

ASX code IVX

Share price (31 May 2013) $0.041 (4.1 cents)

Shares on issue ~409.4M

Options on issue ~23M

Market cap (30-Apr-13) ~$16.7 million

Cash at bank (31-Mar-13) $2.07 million

Cash burn (9 months to 31-Mar-13) ~$4.4 million For

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Contact: investor@invion.com.au

Invion Limited

2/120 Bluestone Circuit

Seventeen Mile Rocks

QLD 4073 Australia

P: +61 7 3295 0500

F: +61 7 3295 0599

W: www.invion.com.au

Managing Director and CEO

Dr Greg Collier

investor@invion.com.au

Investor and Media Relations

Buchan Consulting

rwilson@buchanwe.com.au

jlowe@buchanwe.com.au

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