Opthea Ltd — Investor Presentation 2017

Jan 8, 2017

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OPT-302: A novel therapy for Wet AMD Corporate Presentation, January 2017 Megan Baldwin PhD, CEO & Managing Director

Disclaimer

Investment in Opthea Limited (‘Opthea’) is subject to investment risk, including possible loss of income and capital invested. Neither Opthea nor any other member company of the Opthea Group guarantees any particular rate of return or performance, nor do they guarantee the repayment of capital.

This presentation is not an offer or invitation for subscription or purchase of or a recommendation of securities. It does not take into account the investment objectives, financial situation and particular needs of the investor. Before making any investment in Opthea, the investor or prospective investor should consider whether such an investment is appropriate to their particular investment needs, objectives and financial circumstances and consult an investment advisor if necessary.

This presentation may contain forward-looking statements regarding the potential of the Company’s projects and interests and the development and therapeutic potential of the company’s research and development. Any statement describing a goal, expectation, intention or belief of the company is a forward-looking statement and should be considered an at-risk statement. Such statements are subject to certain risks and uncertainties, particularly those inherent in the process of discovering, developing and commercialising drugs that are safe and effective for use as human therapeutics and the financing of such activities. There is no guarantee that the Company’s research and development projects and interests (where applicable) will receive regulatory approvals or prove to be commercially successful in the future. Actual results of further research could differ from those projected or detailed in this presentation. As a result, you are cautioned not to rely on forward-looking statements. Consideration should be given to these and other risks concerning research and development programs referred to in this presentation.

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Corporate Summary

• OPT-302 blocks VEGF-C and VEGF-D

• In development for treatment of wet AMD

• Potential in a range of eye diseases

• Combination therapy with approved a-VEGF-A therapies to more completely shut-down VEGF pathway

• Targets mechanism of resistance and sub-optimal clinical response to existing therapies targeting VEGF-A

• Combination therapy for wet AMD is a multi-billion dollar market opportunity

• Phase 1/2A clinical trial ongoing under FDA approved IND at US clinical sites

• Management team with substantial experience in developing drugs targeting the VEGF pathway

• Near-term clinical milestones

OPT-302 Wet AMD Program: Milestones

 Initiated Phase 1/2A clinical trial: 30 June 2015 Ph 1 Primary Safety Data Analysis:  April 16 Ph 1 Data Analysis (2[o] Objectives):  July 16 Ph 2A Primary Data Analysis: 1Q17 Initiate Phase 2B clinical trial: 2017

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Financial Position (Unaudited)

Key Financial Details	ASX: OPT	ASX: OPT
Ticker Symbol	ASX:OPT
Share Price (Jan 5 2017)	~A$0.875
Total Ordinary Shares on Issue	150,237,078
Options on Issue	49,675,922
Market Capitalisation (Jan 5 2017)	~A$131m (~USD95m)
Trading Range (last 12 months)	A$0.30 – 0.915
Cash Balance (Dec 31 2016)	~A$13.1m
Forecast Net Operating Cash Burn (CY 2017)	~$7.8m
Top 10 Shareholders Own	69%
Institutional Holders	79%
Substantial Shareholders		% Holding
Biotechnology Value Fund (BVF)		18%
Baker Bros (NY, USA)		9%
Packer & Co.		8.5%

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Share Price Performance (Jan 2015 - Jan 2017)
1.00
0.90
0.80
0.70
0.60
0.50
0.40
0.30
0.20
0.10
-
Shareholders by Region
Retail
21% US Funds
30%
AUD
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0.10
-
Shareholders by Region
Retail
21% US Funds
30%
EU/Other Funds Australian Funds 30%
19%
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Board of Directors & Executive Management

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Megan Baldwin, PhD, MAICD

CEO and Managing Director

Appointed CEO Feb ’14, joined company in 2008. Over 20 years experience in research and drug development of therapies targeting angiogenesis. Previously held roles at Genentech (now Roche) in US, in R&D and commercial divisions. PhD in Medicine on VEGF-D biology from University of Melbourne & Ludwig Institute for Cancer research

Geoffrey Kempler, B.Sc Grad. Dip. App.Soc. Psych

Non-Executive Chairman

Appointed Chairman Dec ’15. Extensive experience in the global biopharmaceutical industry. Founded and currently CEO Prana Biotechnology. Listed Prana on both ASX and NASDAQ. Strong investment markets experience and networks of domestic and international sophisticated investors. Qualified psychologist, BSc (Monash University) and Grad. Dip. App.Soc.Psych (Swinburne)

Michael Sistenich, MSc

Non-Executive Director

Appointed Dec ‘15. Over 18 years of experience as a healthcare specialist in international investment management and investment banking. He is currently Chief Executive Officer at Nohla Therapeutics Inc and his previous roles include Director of Corporate Finance at Bell Potter Securities and Director of International Equities and Head of Global Healthcare Investments at DWS Investments, Deutsche Bank, Frankfurt

Mike Tonroe, ACA, MAICD

Chief Financial Officer and Company Secretary

Appointed May ‘14. Over 20 yrs experience in finance and company secretarial roles. Previously CFO of the Australian Synchrotron Company Limited. Holds Graduate Degree in Business Studies from Buckingham University and is a Chartered Accountant.

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The Disease Process of Wet AMD

Normal Retina

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Choroid
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‘Wet’ AMD

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Figure: The Angiogenesis Foundation

Monitoring Patients & Endpoints in Wet AMD Trials

SD-OCT

Visual Acuity

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Change in Visual Acuity

(# letters) from Baseline

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Change in Retinal Subfield Thickness (CST) from Baseline – Indicator of fluid

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Large and Growing Market Opportunity

• Wet AMD is the leading cause of blindness in the western world in people >55 yrs

• Increasing prevalence due to ageing population

• Estimated 1.8m in US have wet AMD*

• Prevalence expected to double by 2020

• Existing therapies targeting VEGF-A are sub-optimally clinically effective in the majority of patients – major unmet medical need

• Approved therapies for wet AMD target VEGF-A, but not VEGF-C or VEGF-D

• VEGF-C and VEGF-D activate the same, as well as independent pathways, to VEGF-A

• VEGF-C and VEGF-D may mediate resistance to VEGF-A inhibitors, such as the blockbuster drugs Lucentis®, Eylea® and Avastin®

Our approach is novel and differentiated from the existing therapies, yet targets a validated pathway in wet AMD disease progression

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8
2015: >$7BN
40% Market Share
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:
Market Opportunity []
>$10BN
Worldwide
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60% Market Share

• *Cowen Analyst Report: Ophthotech July 7 2015

Lucentis[®] Phase 3 Registrational Studies

In MARINA trial (Phase 3 registrational): ~6 letters gain in vision compared to baseline at Week 12 in patients with minimally classic/occult wet AMD lesions treated with Lucentis® (ranibizumab)

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Wk12
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MARINA Ph3 Trial

Rosenfeld et al., NEJM, 355;14, pp 1419-1431, 2006

Naïve patients with minimally classic or occult lesions Monthly Lucentis® (ranibizumab) or Sham

•

•

At 3 mos, 5.9 letter gain At 2yrs, 33% ≥ 15 letter gain

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An Unmet Medical Need for Wet AMD

Despite receiving a VEGF-A inhibitor (Lucentis®, Eylea® or Avastin®):

50%

do not achieve significant vision gain

2/3

will continue to have fluid at the back of the eye

25%

will have further vision loss at 12 mos

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OPT-302 for Wet AMD

• Lead molecule:

• OPT-302 (soluble VEGFR-3, VEGF-C/-D ‘Trap’)

• Mechanism:

• Blocks VEGF-C and VEGF-D:

• Inhibits blood vessel growth

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VEGF-C/D VEGF-C/D
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Extra-Cellular Domains 1-3 hVEGFR-3

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hIgG1 Fc
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  - Inhibits vessel leak

• Strategy:

• To develop OPT-302 for use in combination with existing VEGF-A inhibitors for the treatment of wet AMD

• Achieve complete blockade of the VEGF pathway

• Blocks a mechanism of ‘escape’ from existing therapies

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Resistance to anti-VEGF-A Monotherapy

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Eylea [TM] Lucentis [TM] OPT-302
VEGF-B VEGF-C
PIGF VEGF-A VEGF-D
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• Long-term single-agent therapy with VEGF-A inhibitors is associated with sub-optimal response

• Sub-optimal improvements in visual acuity (<15-letter gain)

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• Persistent retinal fluid

• Resistance to VEGF-A monotherapy may be related to other VEGF family members

• OPT-302 combination therapy achieves more complete suppression of the VEGF/VEGFR pathway

• Targets incomplete response to VEGF-A inhibition

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VEGF-A inhibition upregulates VEGF-C/-D in Cancer

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“The association of alternate VEGF ligands with resistance to anti-VEGF therapy in metastatic colorectal cancer” - Lieu et al., 2013.

“Mechanisms of evasion to antiangiogenic therapy in glioblastoma” Rose et al., 2010.

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Elevated VEGF-C in Wet AMD Patients

• VEGF-C levels in the retina increase with disease severity

• Aqueous levels of VEGF-C are significantly increased at 1 and 2 months following IVT injection of Avastin® (a-VEGF-A mAb) to wet AMD pts*

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(pg/ml)
66%
pg/ml
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* ARVO (Association for Research in Vision & Ophthalmology) Annual Meeting 2016, Cabral et al., Program 3341, Poster D0144

OPT-302

• OPT-302: a soluble form of VEGFR-3

• Comprises the extracellular domains 1-3 of VEGFR-3 and the Fc Fragment of human IgG1

• Potent inhibitor of VEGF-C (~5pM) and VEGF-D (~0.5 nM)

• A ‘trap’ that binds and neutralises the activity of VEGF-C and VEGF-D, blocking binding to the receptors VEGFR-2 and VEGFR-3

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ELISA VEGFR-2 bioassay VEGFR-3 bioassay
a ) V E G F -AV E G F -C b ) V E G F -C
1 2 5 V E G F -D 1 2 5 V E G F -D
1 0 0 1 0 0
7 5 7 5
5 0 5 0
2 5 2 5
0 0
O P T -3 0 2 (  g /m L )
O P T -3 0 2 (  g /m L )
0 .0 0 1 0 .0 1 0 .1 1 .0 1 0 0 .0 0 1 0 .0 1 0 .1 1 .0 1 0
L ig a n d A v tiv ity P e rc e n ta g e L ig a n d A v tiv ity P e rc e n ta g e
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The Ocular Biodistribution & PK of OPT-302 is Comparable to EYLEA[® ] in Rabbits

OPT-302 has comparable ocular biodistribution and PK profile in rabbits to EYLEA®.

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Retina
250,000
200,000
150,000
OPT-302
Retina VGX-300 OPT-302
100,000 Retina Eylea Aflibercept (EYLEA®)
50,000
0
1hr 12hr 24hr 72hr 168hr 336hr 504 hr 672 hr
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Vitreous Humor
400,000
350,000
300,000
250,000
200,000 Vitreous VGX-300 OPT-302
Vitreous Eylea Aflibercept (EYLEA®)
150,000
100,000
50,000
0
1hr 12hr 24hr 72hr 168hr 336hr 504 hr 672 hr
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Concentration ngEq/mL

OPT-302 Activity in Mouse Wet AMD Model

Combined inhibition of VEGF-A (Eylea®), VEGF-C and VEGF-D (OPT-302) is more effective than inhibition of VEGF-A alone

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Control OPT-302
EYLEA™ OPT-302 + EYLEA [®]
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70%
78%
91%

Pairwise comparison: OPT-302 vs Eylea + OPT-302 (p<0.02)
Eylea vs Eylea + OPT-302 (p<0.05)
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Tammela et al. Nature., 2008

The Opportunity for OPT-302

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• To increase the number of patients who experience a significant gain in vision

• To increase the magnitude of the vision gain

• To prolong response to therapy and prevent visual decline

• Potential to reduce dosing frequency

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OPT-302 Phase 1/2A

ClinTrials.gov ID#: NCT02543229

Dose-escalation & dose-expansion of repeated IVT injections

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Phase 1: Dose-escalation Phase 2A: Dose-expansion
(Open-label) (Randomised)
OPT-302 (2.0 mg) OPT-302 (2.0 mg)
Monotherapy Monotherapy
IVT Q4W x 3, n=5 IVT Q4W x 3, n=23 pts
Cohort 4
OPT-302 (2.0 mg) OPT-302 (2.0 mg)
+ Lucentis® (0.5 mg) + Lucentis® (0.5 mg)
IVT Q4W x 3, n=5 IVT Q4W x 3, n=8 pts
Cohort 3
OPT-302 (1.0 mg)
+ Lucentis® (0.5 mg)
IVT Q4W x 3, n=5
Cohort 2
OPT-302 (0.3 mg)
+ Lucentis® (0.5 mg)
IVT Q4W x 3, n=5
Cohort 1 Access to rescue anti-VEGF-A Tx
28 Day DLT window Follow-up to week 12
Primary Analysis after all
subjects complete 12 weeks
Long term follow-up at Week 24
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OPT-302 Phase 1/2A Study Objectives

• Primary Objectives:

• To evaluate the safety and establish the dose of OPT-302 administered by intravitreal (IVT) injection in combination with IVT Lucentis® in subjects with wet AMD

• Secondary Objectives:

• Mean change in BCVA (visual acuity) (ETDRS) from baseline

• Mean change in central retinal thickness from baseline (SD-OCT)

• Mean change in CNV lesion area from baseline (FA)

• Mean time to, and number of, retreatment injections of anti-VEGF-A therapy during long term follow-up (week 12 to 24)

• Need for ‘rescue therapy’ with ranibizumab in subjects receiving OPT-302 monotherapy

• Pharmacokinetics (PK) of OPT-302

• Incidence of anti-OPT-302 antibody formation

• Exploratory Objective(s):

• To evaluate changes in systemic levels of angiogenesis-related biomarkers

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OPT-302 Phase 1: Patient Demographics

• Run under FDA IND at 14 clinical sites in the US

• 20 pts (mean age 74.8)

• 14/20 females, 6/20 males

• 17/20 occult, 2/20 min classic, 1/20 predominantly classic

• Each patient received 3 intravitreal injections of Lucentis® of OPT-302 either alone or in combination with Lucentis ® every 4 weeks, with a week 12 follow-up one month after the third dose.

• 70% difficult to treat patients sub-responsive to anti-VEGF-A therapy

• 30% treatment-naïve

Cohort	Treatment	# Naïve Pts	# Prior Treated Pts
1	OPT-302(0.3 mg)+ Lucentis®(0.5 mg)	2	3
2	OPT-302(1.0 mg)+ Lucentis® (0.5 mg)	0	5
3	OPT-302(2.0 mg)+ Lucentis® (0.5 mg)	2	3*
4	OPT-302(2.0 mg)	2	3

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*One pt with metastatic ovarian cancer died prior to the week 12 (day 78) visit due to intercurrent illness unrelated to study drugs.

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OPT-302 Safe & Well Tolerated in Phase 1 Study

• OPT-302 successfully met primary safety objective in Phase 1 dose escalation study

• No dose limiting toxicities (and MTD not reached) through week 12 in:

• OPT-302 monotherapy (2.0 mg), and

• Cohorts of OPT-302 (0.3, 1, 2 mg) in combination with Lucentis® (0.5 mg)

• No signs of infection (endophthalmitis)

• No clinically significant changes in:

• Intraocular pressure

• ECGs

• Blood pressure

• Blood chemistry or other vital signs

• No evidence of drug-related immunogenicity

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Phase 1 Secondary Endpoints

• Overall, 16/19 evaluable pts maintained or gained vision from baseline to week 12

• No patient lost more than 3 letters. All of the patients that lost VA from baseline received combination OPT-302 + Lucentis® therapy.

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Treatment-Naïve Patients: Visual Acuity

Mean Change in Visual Acuity at Week 12 from Baseline

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18 16.5
16
14
12
9.5
10
8.7 Letters [Fovista® + Lucentis® W12 (Ophthotech Ph2b)]
8
6 5.9 Letters Lucentis® W12 (MARINA Ph3)
5.1 Letters Lucentis® W12 (Ophthotech Ph2b)
4
2
0
OPT-302 + OPT-302 (2mg) +
Lucentis® Lucentis®
(n=4) (n=2)
Baseline at Wk 12 (# letters)
Mean change in Visual Acuity from
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Treatment-Naïve Patients: Retinal Thickness

Mean Central Subfield Thickness (CST)

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M)

Central Subfield Thickness (
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600
500
400
214 uM (42.7%)
300
200
100
0
Baseline Week 12
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OPT-302 + Lucentis® (n=4)

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Prior-Treated Patients: Visual Acuity

• Majority of vision gain in Lucentis® treated patients occurs within 3 months

• Plateau “ceiling effect”of response with no other treatment options

• Difficult to treat patient population, very large market opportunity

• Mean number of Prior anti-VEGF-A therapies: 10.5 (Mean 3 – 55)

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MARINA Phase 3 in wet AMD. Rosenfeld et al., NEJM, 355;14, pp 1419-1431, 2006

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Prior-Treated Patients: Visual Acuity & Retinal Thickness

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Mean Change Visual Mean Central Subfield Thickness
Acuity from Baseline 400
at Wk 12
4.5 4 letters 390
4
380
3.5
42 uM (10.8%)
3 370
2.5
360
2
1.5 350
1
340
0.5
0 330
Week 12 Baseline Week 12
OPT-302 + Lucentis® OPT-302 + Lucentis®
(n=10) (n=10)
M)

Central Subfield Thickness (
Baseline at Wk 12 (# letters)
Mean change in Visual Acuity from
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Prior-Treated Patient: OPT-302 + Lucentis[®] (0.3 mg) (0.5 mg)

• Male aged 64

• Occult lesion

• Prior treatment: Eylea®/REGN-910-3 x6

Baseline

Week 4

Week 12

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VA: 77 letters CST: 365 µM

VA: 83 letters CST: 281 µM

VA: 79 letters CST: 298 µM

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Prior-Treated Patient: OPT-302 + Lucentis[®] (1.0 mg) (0.5 mg)

• Female aged 71

• Occult lesion

• Prior treatment: Avastin® x10

Baseline

Week 4

Week 12

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VA: 74 letters CST: 270 µM

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VA: 74 letters CST: 258 µM

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VA: 84 letters CST: 255 µM

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OPT-302 Monotherapy

• OPT-302 monotherapy included to identify clinical activity without a background standard of care

• Natural history of wet AMD: without treatment, often chronic, rapid decline in visual acuity and increase in retinal fluid

• a-VEGF-A rescue therapy offered to patients at physician discretion or if patient met criteria of progression according to defined criteria

• 3/5 patients did not require ‘rescue’ therapy

• At week 12, in patients that did not require rescue therapy, mean VA gain of 3.3 letters from baseline (range 2 to 6 letters) and mean increase in CST of 18 uM

• 2 patients were rescued (at d25 and d29). At week 12, despite rescue with ranibizumab, both had lost vision compared to baseline

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MARINA Phase 3 in wet AMD. Rosenfeld et al., NEJM, 355;14, pp 1419-1431, 2006

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Phase 1 Secondary Endpoints: VA and OCT Data Summary

• Overall, 16/19 evaluable pts maintained or gained vision from baseline to week 12

Treatment	Mean VA gain at Wk12 from Baseline (# letters)	Mean Reduction in Central Subfield Thickness at Wk12 from Baseline
Combo OPT-302 + Lucentis® in both Naïve & Prior Tx pts (n=14)	+8	-91M
Combo OPT-302 + Lucentis® in Naïve pts (n=4)	+16.5	-214M
Combo OPT-302 (2 mg) + Lucentis® in Naïve pts (n=2)	+9.5	-262M
Combo OPT-302 + Lucentis® in Prior Tx pts (n=10)	+4	-42M
OPT-302 Monotherapy in Non-Rescue pts (n=3)	+3	+18M

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OPT-302 Proposed Phase 2B in Wet AMD

Combination OPT-302 + Lucentis® vs Lucentis®

Wet AMD Naïve Pts

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OPT-302 (Dose 1) + Lucentis® (0.5 mg)
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Primary
Endpoint:
Mean Change in
Visual Acuity from
Baseline at Week 24/36
Secondary
Endpoints:
Retinal Thickness
(SD-OCT, wk 12, 24/36)
Area of CNV leakage
(FA, wk 12 & 24/36)
% pts ≥3 line gain in VA
Ocular & Systemic AEs
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OPT-302 (Dose 2) + Lucentis® (0.5 mg)
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Lucentis® (0.5 mg)
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All treatment arms : IVT dosing at every 4 weeks (x 6 or x9)

• Phase 2b Prospective, randomized, controlled trial

• 3 arms (randomized 1:1:1)

• Primary Analysis at 6 months

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Wet AMD Landscape of Novel Targets (non-VEGF-A)

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Phase 1
Phase 2
REGN2176-3 VEGF-C/-D
Phase 3
Marketed (Regeneron) OPT-302 (Opthea)
PDGF/VEGF-A
DS-7080
REGN910-3
(Daiichi Sankyo)
(Regeneron)
ROBO-4
Ang2/VEGF-A
HI-con1 (Iconic)
RG7716 (Roche)
Tissue Factor
Ang2/VEGF-A
Fovista®
(Ophthotech) OHR-102 (Ohr)
Unknown MOA
PDGF
X-82 (Tyrogenex)
PDGF/VEGF-A
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Intravitreal Topical Oral

* Failed to meet primary endpoint in Phase 3 or Phase 2 wet AMD clinical trial/s

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OPT-302 Intellectual Property

Summary covering sVEGFR-3 for eye disease

COMPOSITION OF MATTER	TERM
Covering sVEGFR-3 (inc. OPT-302) • Granted Patents: Europe, Japan, Canada, Australia • Granted Patent: USA	2022 2026
Covering OPT-302 • Recently filed new specific composition of matter PCT international patent application	~2034
‘USE’ PATENT
• US Patent granted covering generic use of sVEGFR-3 capable of binding VEGF-C to inhibit blood vessels in mammal having disease characterised by expression of VEGFR-3 in blood vessels	2023
PATENT TERM EXTENSION/EXCLUSIVITY
+5 years under patent term extension OPT-302 entitled to data exclusivity (DE) and market exclusivity (ME) in many jurisdictions, eg. • US (12 years DE for biologics) • Europe (10 years made up of 8 years DE + 2 years ME) • Japan (up to 8 years de facto DE) • South Korea (5 years DE) • Canada (up to 8 years incl. up to 6 years DE + 2 years ME) • Australia (5 years DE)

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OPT-302 Program Highlights

• OPT-302 has broad development potential in a range of eye diseases

• Targets validated pathway involved in wet AMD progression and mechanism of escape from existing therapies that is differentiated to a-VEGF-A therapies

• Large unmet medical need for wet AMD, current treatments only target VEGF-A

• OPT-302 met primary objective of Phase 1 study (safe & well tolerated)

• Evidence of clinical activity:

• Naïve pts: promising results suggest OPT-302 + Lucentis® may lead to improved outcomes over Lucentis® alone

• Prior Tx pts: improved outcomes in difficult to treat, sub-responsive pts

• Monotherapy: evidence of clinical activity without background std of care

• A consistency of responses in pts:

• With different treatment histories

• Across various secondary outcome measures (VA, OCT)

• Data warrants further investigation of OPT-302 in Ph2B randomised, controlled trial

• Phase 2A fully recruited, primary data analysis 1Q’17

• Phase 2B wet AMD trial to initiate in 2017

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Snapshot

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OPT-302: OPT-302 + a-VEGF-A achieves more
- Soluble form VEGFR-3 complete blockade of VEGF pathway
Asset
- A ‘trap’ similar to Eylea™ with distinct MOA Strategy - Targets a mechanism of a-VEGF-A
resistance
-
Inhibits VEGF-C & VEGF-D Trial investigating monotherapy and
Mechanism - combination safety/activity
Anti-angiogenic
-
Inhibits vascular leakage As monotherapy, reduces wet AMD lesion
size and leakage to comparable extent as
Preclinical
Targets over-lapping & distinct pathways to VEGF-A inhibitors
Eylea®
Rationale - Validated VEGFR-2 pathway via VEGF-C/-D inhibition Data
Combination therapy significantly more
-
Also blocks VEGFR-3 pathway that is VEGF-A independent
effective than either agent alone
Wet AMD
Indication - Phase 1/2A trial ongoing in US under IND
Leading cause blindness in Western world in adults > 50 yrs -
- ~1.8M people in US have wet AMD Clinical Primary Objective: Safety (met for Ph 1
over 3 month assessment)
Trial
-
Market Opp. ~USD 10bn worldwide Early evidence of clinical activity in Ph1
-
Routine, non-invasive endpts to monitor
Unmet ~50% of people receiving Lucentis™/Eylea™ do not experience a clinical activity, clear reg path
Medical significant gain in vision
Near Term
Need Majority (50-70%) continue to have retinal fluid Clinical Phase 1/2A Primary Data Analysis 1Q’17
Initiation of Phase 2B wAMD trial in 2017
Existing Target VEGF-A, but not VEGF-C/-D Milestones
Therapies - Include blockbusters Lucentis®, Eylea®, off-label Avastin®
Potential to develop OPT-302 for other
Program
OPT-302 potentially complementary to existing and emerging agents, eye diseases, incl. DME
Landscape incl. PDGFR, Ang2 inhibitors, based on MOA. Limited number of novel
targeted therapies in development. Opthea raised funds (A$17.4m) for wet
AMD program from US/EU/AUS
Company
Intellectual Granted Composition of Matter patients (2022-2026) healthcare investors (Nov’14)
Composition of Matter patent pending (~2034) Significant value appreciation since
Property
Granted ‘Use’ Patent (2023, US). Additional patent term extensions. fundraising
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