Opthea Limited · ASX:OPT
Opthea — Investor Presentation (September 2020)
72 slides from Opthea's investor presentation, September 2020
Slide 1: Developing OPT-302 to improve outcomes for patients with retinal eye diseases
Developing OPT-302 to improve outcomes for patients with retinal eye diseases Corporate Presentation, September 2020 Megan Baldwin PhD, CEO & Managing Director
Slide 2: Disclaimer
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 ca
Slide 3: Opthea Limited
Opthea Limited Opthea Limited • Public co listed on ASX (ASX:OPT) developing OPT-302 for wet AMD and DME • OPT-302 (sVEGFR-3) is the first ‘Trap’ inhibitor of VEGF-C and VEGF-D designed specifically for the eye OPT-302 has a novel • In combination with anti-VEGF-A therapies, completely shuts-down VE
Slide 4: Financial Position (Unaudited)
Financial Position (Unaudited) Key Financial Details ASX: OPT Share Price Performance (2018 - 2020) Ticker Symbol ASX:OPT 3.50 Share Price (Aug 3 2020) ~A$2.40 3.00 Total Ordinary Shares on Issue 269,157,769 2.50 AUD Market Capitalisation ~A646m 2.00 (Aug 3 2020) (~USD460m) 1.50 Trading Range (last
Slide 5: Wet AMD & DME are distinct diseases with Unmet Medical Need
Wet AMD & DME are distinct diseases with Unmet Medical Need VEGF-A VEGF-C/D Wet Age-Related Macular Degeneration Central-involved Diabetic Macular Edema Steroids# Driver: • Ageing • Sustained hyperglycaemia Prevalence: • Increasing prevalence due to ageing population • Increasing due to diabetes epi
Slide 6: Wet AMD & DME are the leading causes of vision loss in the elderly & diabetics
Wet AMD & DME are the leading causes of vision loss in the elderly & diabetics Increasing prevalence; large unmet medical need Wet Age-Related Macular Degeneration Diabetic Macular Edema (DME) U.S. & EU Edema caused by abnormal vasculature growth which Epidemiology A complication of diabetes that ma
Slide 7: Existing Therapies Primarily Target VEGF-A
Existing Therapies Primarily Target VEGF-A OPT-302 has potential to improve clinical EFFICACY by targeting VEGF-C/D OPT-302 inhibits VEGF-C/D VEGF-C OPT-302: Rationale VEGF-D Ranibizumab • Long-term therapy with selective VEGF-A (Lucentis®) inhibitors is associated with sub-optimal responses Broluci
Slide 8: VEGF-A Inhibition Upregulates VEGF-C/D
VEGF-A Inhibition Upregulates VEGF-C/D Clinical data suggest VEGF-C/D may mediate resistance & sub-optimal response to anti-VEGF-A therapy Metastatic Colorectal Cancer 1 Neovascular AMD 2 2,500 10.00 8.91 66% Aqueous Humor VEGF-C (pg/ml) * 2,000 8.00 6.91 * VEGF-C (pg/ml) 1,500 6.00 5.37 1,000 4.00
Slide 9: A Currently Unmet Medical Need for wet AMD and DME
A Currently Unmet Medical Need for wet AMD and DME With >$10bn market opportunity Despite receiving a VEGF-A inhibitor Large and Growing Market Opportunity (ranibizumab, aflibercept or bevacizumab)*: • Wet AMD and DME are the leading causes of blindness in the >50% Do not achieve significant vision
Slide 10: OPT-302: A 'trap' inhibitor of VEGF-C and VEGF-D
OPT-302: A ‘trap’ inhibitor of VEGF-C and VEGF-D VEGF-C OPT-302: A soluble form of VEGFR-3 Strategy VEGF-D • Comprises the extracellular domains 1-3 of VEGFR-3 and the Fc • To develop OPT-302 for use in combination with inhibitors of VEGF-A fragment of human IgG1 to address the unmet medical need in
Slide 11: Ocular Biodistribution and Systemic PK following IVT
Ocular Biodistribution and Systemic PK following IVT OPT-302 has comparable ocular biodistribution & PK profile to aflibercept, with low systemic exposure Ocular Biodistribution OPT-302 vs Aflibercept in Rabbits Mean OPT-302 serum concentrations following IVT (Ph1/2a trial data) 100.0 OPT-302 Monoth
Slide 12: OPT-302 Clinical Program
OPT-302 Clinical Program Combination 1o Data Upcoming Agent Preclinical Phase 1 Phase 2a Phase 2b Phase 3 Status Analysis Future Milestones Wet AMD April 2017 OPT-302 Ranibizumab Complete Primary Endpoint Met Target: VEGF-C/D Target: VEGF-A Ph 1/2a (n=51) (Safety) August 2019 Primary Positive Endpoi
Slide 13: OPT-302 well-tolerated and active in Phase 1/2a study
OPT-302 well-tolerated and active in Phase 1/2a study Visual acuity benefit observed as monotherapy & in combination with ranibizumab Visual Acuity Gains (Baseline to Wk 12) following OPT-302 Phase 1/2a Key Take-Aways2 Monotherapy OPT-302 (q4w x3) 25 Treatment-Naive 25 Prior Treated • OPT-302 met th
Slide 14: Phase 2b
Phase 2b A multicenter, randomized, double-masked, sham controlled study of intravitreal OPT-302 in combination with ranibizumab, in participants with neovascular (wet) AMD Conducted at 113 sites across 10 countries: US, EU, Israel OPT-302-1002; NCT ClinicalTrials.gov Identifier: NCT03345082 14
Slide 15: OPT-302 Phase 2b wet AMD
OPT-302 Phase 2b wet AMD Patients randomised 1:1:1 to treatment arms with intravitreal dosing every 4 weeks (x 6) OPT-302 (2.0 mg) + ranibizumab (0.5 mg) Week 24 Follow-up Wet AMD OPT-302 (0.5 mg) + ranibizumab (0.5 mg) Naïve Pts Sham + ranibizumab (0.5 mg) Primary Outcome: ClinicalTrials.gov Identi
Slide 16: Study Overview
Study Overview Treatment naïve patients Key Inclusion Criteria with neovascular AMD Key Exclusion Criteria Screening • Active CNV >50% lesion, classic / • Subfoveal fibrosis or >25% of total lesion minimally classic / occult • Haemorrhage >50% total lesion • BCVA ≥ 25 and ≤ 60 letters • Other clinic
Slide 17: Study Demographics and Baseline Characteristics
Study Demographics and Baseline Characteristics Demographic / Baseline Disease Characteristic Sham + 0.5 mg OPT-302 + 2.0 mg OPT-302 + ranibizumab ranibizumab ranibizumab N=121 N=122 N=123 Mean Age – years ± SD 76.1 ± 9.48 78.8 ± 8.16 77.8 ± 8.82 Sex – n (%) Male 48 (39.7%) 49 (40.2%) 45 (36.6%) Fem
Slide 18: OPT-302 Combination Therapy Demonstrated Superiority in Visual Acuity over Ranibizumab
OPT-302 (2.0 mg) Combination Therapy Demonstrated Superiority in Visual Acuity over Ranibizumab Primary Endpoint Achieved: Mean Change in Best Corrected Visual Acuity Baseline to Week 24 20 Δ = +3.4 (p=0.0107) 20 Mean change in BCVA (SEM) Mean change in BCVA (SEM) 15 15 14.22 (letters) (letters) 10
Slide 19: Vision Gain & Vision Loss - Baseline to Week 24
Vision Gain & Vision Loss - Baseline to Week 24 More patients gain, and fewer patients lose, ≥15, ≥10 and ≥5 letters of vision in OPT-302 combination group 100 100 100 80 80 80 85.0 % Participants 75.9 % Participants % Participants 70.0 60 60 60 57.8 40 45.0 40 40 40.5 20 20 20 0 0 0 % Gaining 15
Slide 20: Central Subfield Thickness
Central Subfield Thickness Reduction in CST in OPT-302 combination group compared to sham + ranibizumab Mean Change in CST – Mean CST at Week 24 Baseline to Week 24 300 -100 277.84 265.57 Mean change in CST (SEM) 250 Mean CST (SEM) -120 (m) (m) -133.80 200 -140 -146.70 150 -160 100 Sham + 0.5 mg r
Slide 21: Sub-retinal Fluid and Intra-retinal Cysts at Week 24
Sub-retinal Fluid and Intra-retinal Cysts at Week 24 Fewer participants with retinal fluid present in OPT-302 combination group compared to sham + ranibizumab % Participants % Participants with with SRF present IR Cysts present 30 30 29.3 25 25 21.6 20 20 % Participants % Participants 18.5 16.8 15 1
Slide 22: Total Lesion Area and CNV Area - Baseline to Week 24
Total Lesion Area and CNV Area – Baseline to Week 24 Greater reduction in Total Lesion and CNV Area in OPT-302 combination group compared to sham + ranibizumab Mean Change in Mean Change in Total Lesion Area CNV Area 0 0 Mean change in Total Lesion Area (SEM) Mean change in CNV Area (SEM) -2 -2 (mm2
Slide 23: Phase 2b Pre-Specified Subgroup Analyses
Phase 2b A multicenter, randomized, double-masked, sham controlled study of intravitreal OPT-302 in combination with ranibizumab, in participants with neovascular (wet) AMD Pre-Specified Subgroup Analyses OPT-302-1002; NCT ClinicalTrials.gov Identifier: NCT03345082 23
Slide 24: 60% of the World's Population is Asian
60% of the World’s Population is Asian Polypoidal Choroidal Vasculopathy (PCV) • Most common sub-type of neovascular (wet) AMD in Asian populations • Estimated to be the most prevalent form of wet AMD world-wide • PCV lesions typically less responsive to anti-VEGF-A therapy 24
Slide 25: Polypoidal Choroidal Vasculopathy
Polypoidal Choroidal Vasculopathy Mean change in BCVA to Week 24 in participants with and without PCV at baseline 20 Δ = 2.71 Δ = 6.70 (*p = 0.0491) (*p = 0.0253) Mean change in BCVA (SEM) 15 14.2 13.5 (letters) 11.5 10 6.9 5 98 99 20 22 0 Absent Present PCV Detected at Baseline Sham + 0.5 mg ranibi
Slide 26: Neovascular (wet) AMD Lesion Types
Neovascular (wet) AMD Lesion Types Differ in vessel location, leakiness and responsiveness to VEGF-A inhibitors PREDOMINANTLY CLASSIC MINIMALLY CLASSIC OCCULT . . . . ≥50% vessels above RPE Highly responsive to VEGF-A inhibition . <50% vessels above RPE Moderately responsive to VEGF-A inhibition . 1
Slide 27: Mean Change in BCVA Over Time by Lesion Type
Mean Change in BCVA Over Time by Lesion Type Small number of predominantly classic patients Predominantly Classic Minimally Classic Occult 20 20 20 Mean change in BCVA (SEM) Mean change in BCVA (SEM) Mean change in BCVA (SEM) 15 15 15 (letters) (letters) (letters) 10 10 10 5 5 5 0 0 0 0 4 8 12 16 20
Slide 28: Mean Change in BCVA at Week 24 by Lesion Type
Mean Change in BCVA at week 24 by Lesion Type Greater vision gains at Week 24 in OPT-302 2.0 mg group in minimally classic and occult lesions Minimally Classic Occult 20 20 Δ = 6.0 (*p = 0.0008) Δ = 2.7 Mean change in BCVA (SEM) Mean change in BCVA (SEM) 16.2 15 15 13.7 (letters) (letters) 11.1 10 1
Slide 29: 2-Line and 3-Line Vision Gain at Week 24 by Lesion Type
2-Line and 3-Line Vision Gain at Week 24 by Lesion Type >20% increase in 3-line gainers in participants with occult lesions treated with OPT-302 combination therapy Minimally Classic Occult Minimally Classic Occult 80 80 60 60 76.9 55.8 66.0 60 60 58.0 % Participants % Participants % Participants %
Slide 30: 2-Line and 3-Line Vision Loss at Week 24 by Lesion Type
2-Line and 3-Line Vision Loss at Week 24 by Lesion Type Fewer patients with minimally classic and occult lesions lose ≥10 and ≥15 letters following OPT-302 combination therapy Minimally Classic Occult Minimally Classic Occult 10 10 6 6 9.6 5.8 8 8 % Participants % Participants % Participants % Parti
Slide 31: Central Subfield Thickness by Lesion Type
Central Subfield Thickness by Lesion Type Reduction in CST in participants with occult lesions treated with OPT-302 combination compared to sham + ranibizumab Minimally Classic Occult -80 -80 -100 -100 -103.5 Mean change in CST (SEM) Mean change in CST (SEM) -120 -120 ( m) ( m) -134.6 -140 -140 -1
Slide 32: Sub-Retinal Fluid & Intra-Retinal Fluid at Week 24 by Lesion Type
Sub-Retinal Fluid & Intra-Retinal at Week 24 by Lesion Type Fewer participants with minimally classic and occult lesions have retinal fluid at week 24 following OPT-302 combination therapy % Patients with Sub-Retinal Fluid Present % Patients with Intra-Retinal Fluid Present Minimally Classic Occult
Slide 33: Total Lesion Area at Week 24 in Minimally Classic and Occult Lesions
Total Lesion Area at Week 24 in Minimally Classic and Occult Lesions Greater reductions in Total Lesion Area following OPT-302 combination therapy Minimally Classic Occult 0 0 Mean change in Total Lesion Area (SEM) Mean change in Total Lesion Area (SEM) -2 -2 (mm2) (mm2) -3.3 -3.9 -4 -4 -4.4 -4.9 -6
Slide 34: CNV Area at Week 24 in Minimally Classic and Occult Lesions
CNV Area at Week 24 in Minimally Classic and Occult Lesions Greater reductions in CNV Area following OPT-302 combination therapy Minimally Classic Occult 0 0 Mean change in CNV Area (SEM) Mean change in CNV Area (SEM) -2 -2 (mm2) (mm2) -3.4 -4 -4 -4.4 -4.6 (p = 0.0555) -5.6 -6 -6 Sham + 0.5 mg ranib
Slide 35: Lesion classification at Baseline and at Week 24
Lesion classification at Baseline and at Week 24 Lesions shift to an occult, quiescent biology or no CNV following treatment Lesion Classification Lesion Classification at Baseline at Week 24 50 50 45 44 44 45 40 43 40 41 % Participants % Participants 35 30 30 31 20 20 17 14 10 13 12 10 0 0 Predomin
Slide 36: Retinal Angiomatous Proliferation (RAP) Lesions
Retinal Angiomatous Proliferation (RAP) Lesions Have a distinct biology and vessel proliferation occurs within the retina (not the choroid) • No consensus of which treatment is optimal for RAP lesions* • Favorable short-term results with anti-VEGF-A treatments but long-term results are conflicting 3
Slide 37: Improved Visual Acuity in OPT-302 + ranibizumab treated patients
Improved Visual Acuity in OPT-302 + ranibizumab treated patients Mean change in BCVA to Week 24 in participants without RAP at baseline (>86% study participants) 20 Δ = 4.4 *p = 0.0025 Mean change in BCVA (SEM) 15 15.0 (letters) 10 10.6 5 102 103 0 Sham + 0.5 mg ranibizumab 2.0 mg OPT-302 + 0.5 mg r
Slide 38: Mean Change in BCVA Over Time by Lesion Type (RAP Absent)
Mean Change in BCVA Over Time by Lesion Type (RAP Absent) In participants without RAP at baseline, +4.7 letter gain in minimally classic and +6.5 letter gain in occult participants treated with OPT-302 combination therapy compared to sham + ranibizumab Minimally Classic Occult 20 20 Mean change in B
Slide 39: Mean Change in BCVA at Week 24 by Lesion Type (RAP Absent)
Mean Change in BCVA at Week 24 by Lesion Type (RAP Absent) Minimally Classic Occult 20 20 Δ = 6.5 Δ = 4.7 *p = 0.0005 Mean change in BCVA (SEM) *p = 0.0415 Mean change in BCVA (SEM) 16.7 15 15.4 15 (letters) (letters) 10 10.7 10 10.1 5 5 40 39 47 49 0 0 Sham + 0.5 mg ranibizumab 2.0 mg OPT-302 + 0.5
Slide 40: Improved Visual Acuity in patients with Occult-containing lesions (RAP Absent)
Improved Visual Acuity in patients with Occult-containing lesions (RAP Absent) 71% study participants had occult-containing lesions with RAP absent at baseline Minimally Classic & Occult Minimally Classic & Occult 20 Δ = 5.74 *p = 0.0002 20 Mean change in BCVA (SEM) Mean change in BCVA (SEM) 16.1 +1
Slide 41: Safety
Safety OPT-302 well tolerated with very low incidence of ocular inflammation N Participants (%) Sham + 0.5 mg OPT-302 + 2.0 mg OPT-302 + ranibizumab ranibizumab ranibizumab N=121 N=120 N=124 Treatment emergent AEs (TEAEs) 84 (69.4%) 87 (72.5%) 93 (75.0%) Ocular AEs - Study Eye – related to study pro
Slide 42: Conclusions – OPT-302 Phase 2b wet AMD Trial
Conclusions – OPT-302 Phase 2b wet AMD Trial • Phase 2b trial met primary endpoint • OPT-302 (2.0 mg) combination therapy demonstrated superiority in visual acuity over ranibizumab + sham • Vision gain of 3.4 letters • Statistically significant (p=0.0107) • High ranibizumab control arm • Secondary o
Slide 43: Ongoing Clinical Trials
Ongoing Clinical Trials Phase 1b/2a DME Phase 1b/2a study of OPT-302 in combination with aflibercept for persistent central-involved diabetic macular edema 43
Slide 44: Diabetic Macular Edema
Diabetic Macular Edema Up to 10% diabetics develop DME which is responsible for most of the central vision loss in the diabetic population Standard of Care Treatments & An Unmet Medical Need • VEGF-A inhibitors are first-line standard of care therapy for DME • Aflibercept (Eylea) & ranibizumab (Luce
Slide 45: Patients With Persistent DME Are a Significant Unmet Need
Financial Patients With Persistent Disclosures DME Are a Significant Unmet Need There is a need for novel therapeutic approaches to improve clinical outcomes Many patients have limited gains despite regular anti-VEGF-A monotherapy* In Protocol I, patients with DME received ranibizumab + sham injecti
Slide 46: Phase 1b/2a Trial of OPT-302 Combination Therapy for Persistent DME
Phase 1b/2a Trial of OPT-302 Combination Therapy for Persistent DME All patients enrolled had persistent center-involved DME despite prior anti-VEGF-A treatment Phase 1b: • Patients received escalating doses of OPT-302 (0.3, 1 or 2 mg) + aflibercept (2 mg) across 3 cohorts (total of 9 patients) • Tr
Slide 47: OPT-302 DME Trial Design
OPT-302 DME Trial Design Previously anti-VEGF-A-treated patients with persistent DME, a difficult-to-treat population Phase 1b Dose Escalation (N=9) Phase 2a Dose Expansion: Randomized 2:1 (N=~108) OPT-302 (2.0 mg) OPT-302 (2.0 mg) + Aflibercept (2.0 mg) + Aflibercept (2.0 mg) Follow-up to week 12 1
Slide 48: OPT-302 Phase 1b/2a Study Disclosures
OPT-302 Phase 1b/2a Financial Disclosures Phase 1b dose escalation and Phase 2a randomised, controlled, double masked, proof-of-concept study • Heterogeneous all comer’s population for prior anti-VEGF-A history (aflibercept / ranibizumab / bevacizumab) in patients with persistent DME • Variable trea
Slide 49: Phase 1b Dose Escalation
Phase 1b Dose Escalation Dose-responsive gains in visual acuity following OPT-302 combination therapy and reductions in retinal thickness 49
Slide 50: Phase 1b: Baseline Ocular Characteristics
Phase 1b: Baseline Ocular Characteristics Generally well-balanced across treatment groups OPT-302 (0.3 mg) OPT-302 (1 mg) + OPT-302 (2 mg) + Aflibercept (2.0 Aflibercept (2.0 + Aflibercept (2.0 Total Number of Characteristic mg) mg) mg) Subjects (N=3) (N=3) (N=3) (N= 9) Vision Mean BCVA, ETDRS lette
Slide 51: OPT-302 + aflibercept in DME: Phase 1b Safety Results
OPT-302 + aflibercept in DME: Phase 1b Safety Results • OPT-302 (0.3, 1 or 2 mg) + aflibercept (2 mg) OPT-302 (0.3 mg) + OPT-302 (1 mg) + OPT-302 (2 mg) + Selected Adverse Events: Aflibercept (2.0 mg) Aflibercept (2.0 mg) Aflibercept (2.0 mg) Total Number of administered by IVT injection (Baseline,
Slide 52: OPT-302 + aflibercept in DME: Gains in Visual Acuity at Week 12
OPT-302 + aflibercept in DME: Gains in Visual Acuity at Week 12 Dose response relationship & reductions in retinal swelling in Phase 1b Visual Acuity Retinal Thickness 52 Error Bars: SEM; Mean Baseline CST = 434 µm
Slide 53: Patients with Bilateral DME
Patients with Bilateral DME Gains in visual acuity and reductions in retinal thickness in OPT-302 + aflibercept treated eyes Mean Change in BCVA Baseline Mean Change in CST (uM) to Week 12 Baseline to Week 12 • 5/9 patients enrolled in the Phase 1b trial had bilateral DME (DME in both eyes) • Study
Slide 54: Phase 2a Trial of OPT-302 Combination Therapy for Persistent DME
Phase 2a Trial of OPT-302 Combination Therapy for Persistent DME Total “Per Protocol” patient population with variable prior anti-VEGF-A treatment history of aflibercept / ranibizumab / bevacizumab 54
Slide 55: Phase 2a OPT-302 + aflibercept in persistent DME
Phase 2a OPT-302 + aflibercept in persistent DME Fully enrolled, primary data analysis 2Q CY 2020 ClinicalTrials.gov Identifier: NCT03397264 Week 12 Follow-up PRN anti-VEGF-A OPT-302 (2.0 mg) + aflibercept (2.0 mg) (Primary Endpoint) Week 12 to 24 IVT Q4w x3, n=~72 pts subjects complete 12 weeks Pri
Slide 56: Baseline Demographics
Financial Disclosures Baseline Demographics Well balanced across treatment groups in Phase 2a Aflibercept (2mg) + Sham Aflibercept (2mg) + OPT-302 (2 mg) Characteristic (N = 48) (N = 96) Mean age, years (SD) 61.2 (9.40) 61.8 (10.07) Male, n (%) 30 (62.5%) 60 (62.5%) Race, n (%) American Indian or Al
Slide 57: Baseline Demographics
Financial Disclosures Baseline Demographics Well balanced across treatment groups in Phase 2a Characteristic 2.0 mg aflibercept + 2.0 mg aflibercept + Sham (N=48) 2.0 mg OPT-302 (N=96) Vision Mean best corrected visual acuity (BCVA) – letters (±SD) 63.9 (9.44) 63.3 (8.31) >55 letters vision - n (%)
Slide 58: Prior Treatment History Study Eye
Prior Treatment History Study Eye Approximately one third of patients received regular prior aflibercept therapy Characteristic 2.0 mg aflibercept + 2.0 mg aflibercept + Sham (N=40) 2.0 mg OPT-302 (N=75) Mean Duration of Diabetic Macular Edema – years (±SD) 1.6 (1.70) 1.3 (1.30) Mean Number of Prior
Slide 59: Safety
Safety Financial Disclosures Well tolerated & consistent with previous OPT-302 Phase 1 and Phase 2b clinical trials in wet AMD Aflibercept (2mg) + Sham Aflibercept (2mg) + OPT-302 (2 mg) Selected Adverse Events (N = 49) (N =95) Study Eye or Systemic, n (%) Intraocular inflammation 1 (2.0%) 1 (1.1%)
Slide 60: Primary Efficacy Endpoint: Response Rate of ≥5 letter gain to Week 12
Financial Primary Efficacy Endpoint: Disclosures Response Rate of ≥ 5 letter gain to Week 12 Previously anti-VEGF-A treated DME patients after switching to OPT-302 + aflibercept combination therapy 100 80 % Participants 60 52.8 40 Pre-specified response rate for clinical activity* 20 0 ≥ 5 letter BC
Slide 61: Measures of Visual Function
Financial Disclosures Measures of Visual Function Persistent DME patients: Prior anti-VEGF-A therapy of aflibercept /ranibizumab / bevacizumab Mean BCVA at Baseline ≥10 Letter Gain ≥15 Letter Gain ≥ 5 Letter Loss and change at Week 12 At Week 12 At Week 12 At Week 12 75 30 30 20 26.7 70 +6.1 15 +5.9
Slide 62: Mean Change in Retinal Thickness
Mean Change in Retinal Thickness Persistent DME patients: Prior anti-VEGF-A therapy of aflibercept /ranibizumab / bevacizumab Mean Change in CST Mean Change in CST Baseline to Week 12 At Week 12 Weeks 0 4 8 12 0 0 -10 Mean change in CST (SEM) Mean change in CST (SEM) -20 -20 -34.9 -30 (m) (m) -4
Slide 63: Exploratory subgroup analysis in patient population receiving prior aflibercept therapy
Phase 2a Trial of OPT-302 Combination Therapy for Persistent DME Exploratory subgroup analysis in patient population receiving prior aflibercept therapy 63
Slide 64: OPT-302 Phase 2a DME Study: Prior Aflibercept Subgroup
Financial OPT-302 Phase 2a DME Study Disclosures Exploratory subgroup analysis in patient population receiving previous aflibercept • More homogeneous population of anti-VEGF-A prior treatment history of previous aflibercept in patients with persistent DME • Less variable prior treatment history & g
Slide 65: Visual Acuity Gain following OPT-302 combination therapy
Visual Acuity Gain following OPT-302 combination therapy Financial Disclosures Exploratory Subgroup Analysis in patient population with a prior treatment history of aflibercept Mean Change in BCVA Mean Change in BCVA Baseline to Week 12 Baseline to Week 12 10 10 Δ = +3.2 8 8 Mean change in BCVA Mean
Slide 66: Gains in Visual Function, Reduced Vision Loss with OPT-302
Financial Gains in Visual Function, Disclosures Reduced Vision Loss with OPT-302 Exploratory Subgroup Analysis in patient population with a prior treatment history of aflibercept ≥10 Letter Gain ≥15 Letter Gain ≥ 1 Letter Loss At Week 12 At Week 12 At Week 12 30 30 30 27.3 23.1 20 20 20 % Patients %
Slide 67: Reduction of Retinal Thickness
Reduction of RetinalFinancial Thickness Disclosures Exploratory Subgroup Analysis in patient population with a prior treatment history of aflibercept Mean Change in CST Mean Change in CST % Patients ≤300 µm CST Baseline to Week 12 At Week 12 At Week 12 Weeks 40 0 25 4 8 12 22.7 20 -15.5 % Patients w
Slide 68: Conclusions
Conclusions Financial Disclosures OPT-302 Combination therapy in Previously Treated Patients with Persistent DME • Primary safety endpoint met: • The safety profile of OPT-302 combination therapy is favorable and consistent across two eye indications where a total of >1850 intravitreal injections ha
Slide 69: OPT-302 Phase 3 Pivotal Program
OPT-302 Phase 3 Pivotal Program Trial initiations early 2021 ShORe Study of OPT-302 in combination with Ranibizumab COAST Combination OPT-302 with Aflibercept STudy • Design: Multi-centre, double-masked, randomised (1:1:1), sham control • Sample size: 330 patients per arm, 990 per study 69 • Regulat
Slide 70: Opthea – Developing OPT-302 for Eye Diseases
Opthea – Developing OPT-302 for Eye Diseases • OPT-302 has broad development potential in a range of eye diseases, including wet AMD and DME • Targets validated VEGF/VEGFR pathway and mechanism of escape from existing therapies that is differentiated to VEGF-A inhibitors and other agents in developm
Slide 71: OPT-302 Intellectual Property
OPT-302 Intellectual Property Summary covering sVEGFR-3 for Eye Disease COMPOSITION OF MATTER TERM Covering OPT-302 molecule • Granted patents in the USA, Japan, Russia, Australia, South Africa & Singapore 2034* • Patents accepted for grant in Europe, Malaysia & Mexico • Applications pending in a fu
Slide 72: Megan Baldwin, CEO & Managing Director
Megan Baldwin CEO & Managing Director T +61 (3) 9826 0399 E megan.baldwin@opthea.com Suite 0403, Level 4, 650 Chapel Street, South Yarra 3141 Victoria Australia www.opthea.com