PanOph

Anti-VEGF agents in ophthalmology

Retina & Vitreous

Key Points

  • •Five anti-VEGF agents: bevacizumab (off-label, cheapest), ranibizumab (Fab fragment), aflibercept (VEGF trap — binds VEGF-A/B + PlGF), brolucizumab (scFv — vasculitis risk), faricimab (bispecific anti-VEGF-A + anti-Ang-2)
  • •CATT/IVAN: bevacizumab equivalent to ranibizumab for nAMD at 1/40th the cost; Protocol T: aflibercept superior for DME with VA ≤20/50
  • •Treat-and-extend is the standard regimen — monthly loading × 3, then extend by 2 weeks if stable, shorten if recurrence; maximum interval 12–16 weeks
  • •Endophthalmitis risk ~0.02–0.05% per injection; povidone-iodine 5% is the most important preventive measure; brolucizumab carries ~3–4% retinal vasculitis risk
  • •Faricimab (TENAYA/LUCERNE) and aflibercept 8 mg (PULSAR) extend dosing to up to 16 weeks — reducing treatment burden while maintaining efficacy
1. Definition

Anti-vascular endothelial growth factor (anti-VEGF) agents are intravitreal biologics that inhibit VEGF-mediated angiogenesis, vascular permeability, and inflammation — the cornerstone of treatment for neovascular age-related macular degeneration (nAMD), diabetic macular oedema (DME), retinal vein occlusion (RVO) oedema, and myopic choroidal neovascularisation. Five agents are currently in widespread clinical use: bevacizumab (Avastin), ranibizumab (Lucentis), aflibercept (Eylea), brolucizumab (Beovu), and faricimab (Vabysmo). These drugs have revolutionised the management of retinal vascular diseases and are among the most frequently administered intravitreal injections worldwide.

2. Epidemiology

Anti-VEGF intravitreal injections are the most commonly performed ophthalmic procedure worldwide — an estimated >20 million injections administered annually globally (2024 data). nAMD is the most common indication (~50% of all anti-VEGF injections), followed by DME (~25%) and RVO (~15%). The mean number of injections per eye per year is ~7–9 for nAMD (treat-and-extend) and ~6–8 for DME. The global anti-VEGF market exceeds $15 billion annually. Bevacizumab accounts for the majority of injections in lower- and middle-income countries due to its lower cost (~$50 per dose vs ~$1,200–2,000 for branded agents).

3. Aetiology and causes

VEGF biology — the rationale for anti-VEGF therapy:

  1. VEGF-A (the primary target): a potent angiogenic cytokine with 6 isoforms (VEGF-A121, VEGF-A145, VEGF-A165 [most pathogenic], VEGF-A183, VEGF-A189, VEGF-A206)
  2. VEGF-A actions: promotes angiogenesis (new vessel formation), increases vascular permeability (oedema), recruits inflammatory cells, promotes endothelial cell survival
  3. VEGF receptors: VEGFR-1 (Flt-1), VEGFR-2 (KDR — primary signalling receptor for pathological angiogenesis), VEGFR-3
  4. Placental growth factor (PlGF): binds VEGFR-1; promotes inflammation and pathological angiogenesis — targeted by aflibercept and conbercept
  5. Angiopoietin-2 (Ang-2): destabilises blood vessels and promotes vascular leakage — targeted by faricimab (dual mechanism)

Diseases driven by VEGF overproduction:

  • nAMD: choroidal neovascularisation (CNV) driven by VEGF from RPE
  • DME: retinal ischaemia → VEGF → macular oedema
  • RVO: venous occlusion → retinal ischaemia → VEGF → macular oedema ± neovascularisation
  • ROP: retinal ischaemia in premature infants → VEGF → abnormal neovascularisation
  • NVG: ischaemia → VEGF → iris/angle neovascularisation → neovascular glaucoma
4. Pathogenesis

Mechanism of action — by agent:

  1. Bevacizumab (Avastin):
  • Full-length humanised monoclonal antibody (IgG1, 149 kDa) against all isoforms of VEGF-A
  • Originally developed for metastatic colorectal cancer — used off-label in ophthalmology
  • Binds VEGF-A only (not PlGF)
  • Half-life in vitreous: ~6–10 days
  • Requires compounding pharmacy (not FDA-approved for intraocular use)
  1. Ranibizumab (Lucentis):
  • Humanised monoclonal antibody Fab fragment (48 kDa) against all isoforms of VEGF-A
  • Specifically designed for intraocular use — smaller molecule for better retinal penetration
  • Binds VEGF-A only (not PlGF)
  • Half-life in vitreous: ~7–9 days
  • FDA-approved for nAMD, DME, RVO, myopic CNV
  1. Aflibercept (Eylea):
  • Recombinant fusion protein (115 kDa) — 'VEGF trap' composed of VEGFR-1 and VEGFR-2 extracellular domains fused to IgG1 Fc
  • Binds VEGF-A (all isoforms), VEGF-B, and PlGF — broader spectrum than ranibizumab/bevacizumab
  • Higher binding affinity for VEGF-A than ranibizumab (Kd ~0.5 pM)
  • Half-life in vitreous: ~7–9 days; intravitreal duration of action ~4–6 weeks
  • FDA-approved: nAMD, DME, RVO, diabetic retinopathy, myopic CNV
  • Aflibercept 8 mg (Eylea HD): higher dose formulation for extended dosing intervals (up to every 16 weeks for nAMD; PULSAR trial)
  1. Brolucizumab (Beovu):
  • Humanised single-chain variable fragment (scFv, 26 kDa) — smallest anti-VEGF molecule
  • Binds all VEGF-A isoforms
  • Small size allows higher molar concentration in a 0.05 mL injection (6 mg dose = 120 mg/mL)
  • Longer duration of action: up to every 12 weeks for nAMD
  • Safety concern: associated with retinal vasculitis and retinal vascular occlusion in ~3–4% of patients (HAWK/HARRIER post-marketing data) — limits adoption
  1. Faricimab (Vabysmo):
  • Bispecific antibody (150 kDa) — simultaneously binds VEGF-A and angiopoietin-2 (Ang-2)
  • First bispecific antibody approved for intraocular use
  • Dual mechanism: anti-VEGF (reduces oedema/neovascularisation) + anti-Ang-2 (stabilises blood vessels, reduces inflammation)
  • Dosing interval: up to every 16 weeks for nAMD and DME
  • FDA-approved: nAMD, DME
5. Classification

By molecular structure:

  • Full-length monoclonal antibody: bevacizumab (149 kDa)
  • Fab fragment: ranibizumab (48 kDa)
  • Fusion protein (VEGF trap): aflibercept (115 kDa)
  • Single-chain variable fragment (scFv): brolucizumab (26 kDa)
  • Bispecific antibody: faricimab (150 kDa)

By VEGF targets:

  • VEGF-A only: bevacizumab, ranibizumab, brolucizumab
  • VEGF-A + VEGF-B + PlGF: aflibercept (broadest VEGF spectrum)
  • VEGF-A + Ang-2: faricimab (dual pathway)

By regulatory status (ophthalmic):

  • FDA-approved for intraocular use: ranibizumab, aflibercept, brolucizumab, faricimab
  • Off-label: bevacizumab (approved only for systemic cancer therapy)
  • Biosimilars available: ranibizumab (Byooviz, Cimerli); bevacizumab (Mvasi, Zirabev for systemic use)

By dosing regimen:

  • Fixed monthly: traditional protocol (used in pivotal trials)
  • PRN (pro re nata / as needed): inject only when disease activity recurs
  • Treat-and-extend (T&E): most commonly used in practice — extend injection intervals progressively if stable; treat at every visit
6. Risk factors and associations

Factors affecting anti-VEGF response:

  • Baseline visual acuity: lower baseline VA → greater absolute VA gain (ceiling effect)
  • Lesion type (nAMD): occult/type 1 CNV responds slightly less than classic/type 2
  • Duration of disease: longer duration → more scarring → poorer response
  • Genetic factors: CFH, ARMS2/HTRA1 polymorphisms — limited clinical utility for predicting response
  • Age: older patients may have less robust responses
  • Diabetic control (DME): poor glycaemic control → reduced treatment response
  • Macular ischaemia: extensive capillary dropout predicts poor visual outcome regardless of anti-VEGF
  • Subretinal fibrosis: indicates end-stage disease — poor response

Risk factors for complications:

  • Endophthalmitis risk: ~0.02–0.05% per injection (reduced with povidone-iodine, lid speculum, no talking)
  • Thromboembolic events: ~1–2% annual risk (similar to age-matched controls per CATT/IVAN meta-analysis)
  • RPE tears: ~1–3% in nAMD — more common with large PEDs
  • Sustained IOP elevation: ~5–10% with repeated injections — may require glaucoma treatment
7. Clinical features

Indications and clinical settings:

1. Neovascular AMD (nAMD):

  • Active CNV with subretinal/intraretinal fluid, haemorrhage, or lipid
  • All anti-VEGF agents effective; choice based on cost, dosing interval, and patient factors
  • Treatment typically lifelong — most patients require ongoing injections

2. Diabetic macular oedema (DME):

  • Centre-involving DME with visual impairment (VA ≤6/9 or worse)
  • Protocol T (DRCR.net): aflibercept superior to bevacizumab for eyes with baseline VA 20/50 or worse; all agents equivalent if VA 20/32 to 20/40
  • May combine with focal/grid laser for persistent DME

3. Retinal vein occlusion (RVO):

  • Macular oedema secondary to CRVO or BRVO
  • Anti-VEGF reduces oedema and improves VA — monthly injections initially, then PRN or T&E

4. Myopic choroidal neovascularisation:

  • CNV secondary to pathological myopia
  • Ranibizumab (RADIANCE/MYRROR) or aflibercept — fewer injections needed than nAMD

5. Retinopathy of prematurity (ROP):

  • Intravitreal bevacizumab (BEAT-ROP) or ranibizumab for zone I/posterior zone II disease
  • Allows vascularisation of avascular retina (advantage over laser which destroys it)

6. Neovascular glaucoma (NVG):

  • Adjunctive anti-VEGF to regress iris/angle neovascularisation before definitive surgery

7. PCV (polypoidal choroidal vasculopathy):

  • Anti-VEGF ± PDT (EVEREST II: combination superior for polyp closure)
8. Investigations

Pre-treatment assessment:

  1. OCT macula: mandatory before every injection — assess central macular thickness (CMT), subretinal fluid, intraretinal fluid, PED height, outer retinal integrity
  2. FFA: baseline assessment of CNV type, extent, perfusion status; not needed before every injection
  3. OCTA: non-invasive assessment of CNV morphology, activity; increasingly replaces FFA for monitoring
  4. ICGA: for PCV diagnosis (polyps, branching vascular network); guides PDT planning
  5. Widefield imaging: peripheral retinal assessment for diabetic retinopathy severity, ischaemia, neovascularisation
  6. Visual acuity (BCVA): assessed at every visit — primary treatment outcome measure
  7. IOP measurement: pre- and post-injection; monitor for sustained IOP elevation with repeated injections

Treatment monitoring (at each visit):

  • BCVA
  • OCT: fluid status (SRF, IRF), CMT, PED
  • Fundus examination: haemorrhage, exudation, injection site
  • IOP

Retreatment criteria (treat-and-extend):

  • Extend interval by 2 weeks if: no SRF, no IRF, stable PED, stable VA
  • Shorten interval by 2–4 weeks if: new/increased SRF or IRF, decreased VA, new haemorrhage
  • Maximum extension: typically every 12–16 weeks (depending on agent and protocol)
9. Differential diagnosis

Conditions that may mimic anti-VEGF-responsive diseases (and would NOT respond to anti-VEGF):

  1. Geographic atrophy (dry AMD): RPE and photoreceptor atrophy without CNV — anti-VEGF not indicated; pegcetacoplan (complement C3 inhibitor) is the treatment
  2. Vitreomacular traction / epiretinal membrane: causes macular thickening on OCT that may mimic oedema — requires vitrectomy, not anti-VEGF
  3. Cystoid macular oedema (post-surgical / Irvine-Gass): responds to topical NSAIDs and steroids; anti-VEGF is second-line
  4. Central serous chorioretinopathy (CSC): serous macular detachment — treatment is PDT or observation; anti-VEGF only if secondary CNV develops
  5. Macular telangiectasia type 2: parafoveal telangiectasis — does not respond well to anti-VEGF (unlike DME)
  6. Adult-onset foveomacular vitelliform dystrophy: vitelliform material at fovea — mimics CNV on OCT; does not respond to anti-VEGF
  7. Subretinal fibrosis (end-stage nAMD): disciform scar — irreversible; anti-VEGF will not improve vision
10. Complications

Injection-related (per injection):

  • Endophthalmitis: ~0.02–0.05% per injection (~1 in 2,000–5,000) — most serious complication
  • Subconjunctival haemorrhage: ~10–20% — benign, self-resolving
  • Transient IOP spike: ~20–30% immediately post-injection — usually resolves within minutes
  • Vitreous floaters: from air bubbles or drug particulates
  • Corneal abrasion: from speculum or lid manipulation
  • Vitreous haemorrhage: ~0.1–0.5%
  • Lens damage (traumatic cataract): ~0.1% — from needle touching the lens

Drug-related (cumulative):

  • Sustained IOP elevation: ~5–10% with repeated injections (especially aflibercept) — may require IOP-lowering therapy
  • RPE tear: ~1–3% in nAMD (especially with large PED — sudden flattening during anti-VEGF reduces PED volume rapidly)
  • Retinal detachment: ~0.01–0.02% per injection (rhegmatogenous, from needle entry site)
  • Macular atrophy: ~10–20% over 5–7 years of monthly anti-VEGF for nAMD (CATT/IVAN 5-year data) — unclear if drug-related or disease progression
  • Subretinal haemorrhage (breakthrough): despite treatment — more common with PCV

Brolucizumab-specific:

  • Retinal vasculitis: ~3–4% (including occlusive vasculitis)
  • Retinal vascular occlusion: ~0.7–1%
  • These safety concerns have significantly limited brolucizumab adoption despite its longer dosing interval

Systemic (rare):

  • Thromboembolic events (stroke, MI): ~1–2% annual risk — similar to age-matched controls in most studies
  • Hypertension: theoretical risk from systemic VEGF inhibition — not clinically significant in most patients
11. Management

Intravitreal injection technique:

  1. Preparation: topical anaesthesia (proparacaine/tetracaine or subconjunctival lidocaine), povidone-iodine 5% to conjunctival sac (most important infection prevention step), sterile lid speculum
  2. Injection site: 3.5 mm posterior to limbus (pseudophakic) or 4.0 mm (phakic) — through pars plana
  3. Needle: 30-gauge × 0.5 inch
  4. Volume: 0.05 mL (standard for all agents)
  5. Post-injection: check for hand motion vision (confirms no central retinal artery occlusion from IOP spike), IOP check if indicated, no eye patch needed
  6. No talking during procedure (reduces oral flora exposure to injection site)

Dosing regimens:

Fixed monthly:

  • Every 4 weeks — as used in pivotal trials (MARINA, ANCHOR)
  • Maximum efficacy but highest treatment burden
  • Rarely used in practice

PRN (pro re nata / as needed):

  • Monthly loading × 3, then inject only when disease activity recurs (fluid on OCT, VA drop)
  • Risk of under-treatment — patients may lose vision between visits
  • Used in CATT/IVAN trials

Treat-and-extend (T&E):

  • Most widely used regimen in clinical practice
  • Monthly loading × 3, then extend interval by 2 weeks if stable — inject at every visit
  • If recurrence: shorten interval by 2–4 weeks
  • Maximum interval typically 12–16 weeks
  • Advantages: reduces clinic visits, maintains continuous treatment, individualised intervals

Key landmark trials by indication:

nAMD:

  • MARINA (2006): ranibizumab monthly vs sham — ranibizumab +6.6 letters vs -10.4 letters sham at 24 months (landmark trial establishing anti-VEGF for nAMD)
  • ANCHOR (2006): ranibizumab vs PDT for classic CNV — ranibizumab +11.3 letters vs -9.5 letters PDT at 24 months
  • CATT (2011): bevacizumab vs ranibizumab — equivalent VA outcomes (non-inferior); bevacizumab at 1/40th the cost
  • IVAN (2013): confirmed CATT findings — bevacizumab non-inferior to ranibizumab; monthly slightly better than PRN
  • VIEW 1/2 (2012): aflibercept every 8 weeks non-inferior to ranibizumab monthly for nAMD
  • HAWK/HARRIER (2019): brolucizumab every 12 weeks non-inferior to aflibercept every 8 weeks — but retinal vasculitis safety signal
  • TENAYA/LUCERNE (2022): faricimab up to every 16 weeks non-inferior to aflibercept every 8 weeks — longer intervals
  • PULSAR (2023): aflibercept 8 mg up to every 16 weeks non-inferior to aflibercept 2 mg every 8 weeks

DME:

  • Protocol T (DRCR.net, 2015): landmark trial comparing all 3 first-generation anti-VEGF agents for DME
  • At 1 year: aflibercept +13.3 letters, ranibizumab +11.2, bevacizumab +9.7
  • For eyes with baseline VA 20/50 or worse: aflibercept superior to both others
  • For eyes with VA 20/32–20/40: all three agents equivalent
  • At 2 years: differences narrowed — all agents acceptable
  • YOSEMITE/RHINE (2022): faricimab up to every 16 weeks non-inferior to aflibercept every 8 weeks for DME

RVO:

  • BRAVO (BRVO) and CRUISE (CRVO): ranibizumab monthly — significant VA gains
  • COPERNICUS/GALILEO (CRVO): aflibercept monthly → bimonthly — effective for CRVO macular oedema

Switching agents:

  • If suboptimal response to one anti-VEGF, switching to a different agent (especially from bevacizumab/ranibizumab to aflibercept or faricimab) may provide additional benefit
  • Switch to faricimab for patients requiring frequent injections (dual Ang-2/VEGF mechanism may extend intervals)
  • Switch from brolucizumab if vasculitis concern
12. Prognosis

nAMD:

  • With anti-VEGF: mean VA improvement of +5 to +10 letters at 1–2 years (vs -10 to -15 letters natural history)
  • Long-term (5–10 years): VA gradually declines despite treatment in many patients due to macular atrophy and fibrosis — ~20–30% lose ≥15 letters by year 7 (CATT/IVAN extension)
  • Real-world outcomes are generally worse than clinical trials (under-treatment, loss to follow-up)

DME:

  • Mean VA improvement +8 to +13 letters at 1–2 years with anti-VEGF
  • ~40–50% of DME patients achieve driving vision (≥6/12) at 2 years
  • Some patients achieve long-term remission and can stop treatment; others require ongoing therapy

RVO:

  • CRVO macular oedema: +12 to +18 letters at 6 months with anti-VEGF
  • BRVO macular oedema: +15 to +20 letters at 6 months
  • Many RVO patients can eventually stop anti-VEGF (unlike nAMD)

Treatment burden:

  • Average 7–9 injections/year for nAMD (treat-and-extend)
  • Average 6–8 injections/year for DME
  • Newer agents (faricimab, aflibercept 8 mg) aim to reduce this to 4–6 injections/year
  • Significant impact on quality of life — frequent clinic visits, injection anxiety, caregiver burden

Clinical Pearls

1
CATT trial established that bevacizumab and ranibizumab are equivalent for nAMD — with bevacizumab at 1/40th the cost. This trial transformed global treatment patterns and made anti-VEGF therapy accessible in resource-limited settings.
2
Protocol T is the most important DME trial: for eyes with baseline VA 20/50 or worse, aflibercept is superior to both ranibizumab and bevacizumab at 1 year. For eyes with 20/32–20/40, all three agents are equivalent — bevacizumab is a cost-effective first choice.
3
Treat-and-extend is the dominant regimen in real-world practice — it reduces clinic visits while maintaining continuous treatment. The goal is to find each patient's maximum safe interval between injections.
4
Brolucizumab safety signal: retinal vasculitis and retinal vascular occlusion in ~3–4% of patients have significantly limited adoption despite its attractive 12-week dosing interval. Always counsel patients about this risk.
5
Faricimab is the first bispecific antibody (anti-VEGF-A + anti-Ang-2) — the dual mechanism targets both vascular leakage (VEGF) and vessel instability (Ang-2), potentially achieving longer dosing intervals (up to 16 weeks).
6
Exam trap — RPE tear complication: RPE tears are more likely with large PEDs during anti-VEGF treatment. The anti-VEGF contracts the CNV and reduces PED volume rapidly → the RPE, which is already stretched, tears. Sudden VA drop + altered PED morphology on OCT = RPE tear.
7
Exam trap — anti-VEGF does NOT treat geographic atrophy: dry AMD with RPE/photoreceptor atrophy has NO CNV — anti-VEGF is not indicated. The treatment for GA is complement inhibitors (pegcetacoplan). Incorrectly starting anti-VEGF for GA is a common exam pitfall.
8
Povidone-iodine 5% to the conjunctival sac before injection is the single most important step for preventing endophthalmitis — more important than antibiotics (which are NOT routinely recommended post-injection).

Oral-exam questions

  • What is the difference between bevacizumab and ranibizumab? — Bevacizumab is a full-length IgG antibody (149 kDa) developed for cancer, used off-label in ophthalmology. Ranibizumab is a Fab fragment (48 kDa) specifically designed for intraocular use. CATT/IVAN trials showed they are clinically equivalent for nAMD, but bevacizumab costs 1/40th as much.
  • What did Protocol T show? — Protocol T (DRCR.net, 2015) compared all three anti-VEGF agents for DME. For eyes with baseline VA 20/50 or worse, aflibercept was superior (+13.3 vs +11.2 vs +9.7 letters). For VA 20/32–20/40, all three were equivalent. This guides agent selection: aflibercept first-line for worse VA; bevacizumab acceptable for better VA.
  • Why is faricimab different from other anti-VEGF agents? — Faricimab is the first bispecific antibody — it simultaneously blocks VEGF-A (anti-angiogenic) and angiopoietin-2 (vessel stabiliser). This dual mechanism targets both vascular leakage and vessel instability, allowing intervals up to 16 weeks (TENAYA/LUCERNE).
  • What is the brolucizumab safety concern? — Brolucizumab is associated with retinal vasculitis in ~3–4% and retinal vascular occlusion in ~0.7–1% of patients — unique among anti-VEGF agents. This has significantly limited its adoption despite offering 12-week dosing intervals (HAWK/HARRIER).
  • What is the injection site and why? — 3.5 mm posterior to the limbus in pseudophakic eyes, 4.0 mm in phakic eyes — this enters the eye through the pars plana (avascular zone), avoiding the retina, lens, and ciliary body. Injection is given with a 30-gauge needle delivering 0.05 mL.

Mnemonics

BRAFT — Anti-VEGF agents (in order of approval)

B — Bevacizumab (off-label, full IgG, cheapest) R — Ranibizumab (Fab fragment, first approved) A — Aflibercept (fusion protein, VEGF trap, broadest spectrum) F — Faricimab (bispecific: VEGF-A + Ang-2) T — (Brolucizumab) — Tiny molecule (scFv, 26 kDa) but Trouble (vasculitis risk)

MAC-CATT — Key anti-VEGF trials for nAMD

M — MARINA (ranibizumab vs sham) A — ANCHOR (ranibizumab vs PDT) C — CATT (bev = ran, 1/40th cost) C — VIEW (aflibercept q8w = ran monthly) A — HAWK/HARRIER (brolucizumab q12w — vasculitis!) T — TENAYA/LUCERNE (faricimab q16w) T — PULSAR (aflibercept 8 mg q16w)

Comparison Tables

Anti-VEGF agents — molecular comparison
Bevacizumab
Molecule
Full IgG antibody
Size (kDa)
149
Targets
VEGF-A
Max interval
4–6 weeks
Key trial
CATT, IVAN
Ranibizumab
Molecule
Fab fragment
Size (kDa)
48
Targets
VEGF-A
Max interval
4–6 weeks
Key trial
MARINA, ANCHOR
Aflibercept 2 mg
Molecule
Fusion protein
Size (kDa)
115
Targets
VEGF-A/B, PlGF
Max interval
8 weeks
Key trial
VIEW, Protocol T
Aflibercept 8 mg
Molecule
Fusion protein
Size (kDa)
115
Targets
VEGF-A/B, PlGF
Max interval
16 weeks
Key trial
PULSAR
Brolucizumab
Molecule
scFv
Size (kDa)
26
Targets
VEGF-A
Max interval
12 weeks
Key trial
HAWK/HARRIER
Faricimab
Molecule
Bispecific Ab
Size (kDa)
150
Targets
VEGF-A, Ang-2
Max interval
16 weeks
Key trial
TENAYA/LUCERNE
Landmark anti-VEGF trials — key results
MARINA (2006)
Indication
nAMD
Key finding
Ranibizumab monthly: +7.2 vs -10.4 letters (sham) at 12 months; +6.6 vs -14.9 at 24 months
ANCHOR (2006)
Indication
nAMD
Key finding
Ranibizumab: +11.3 letters vs -9.5 PDT at 24 months
CATT (2011)
Indication
nAMD
Key finding
Bevacizumab equivalent to ranibizumab; 1/40th the cost
IVAN (2013)
Indication
nAMD
Key finding
Confirmed CATT: bevacizumab non-inferior to ranibizumab
VIEW 1/2 (2012)
Indication
nAMD
Key finding
Aflibercept q8 weeks non-inferior to ranibizumab monthly
HAWK/HARRIER (2019)
Indication
nAMD
Key finding
Brolucizumab q12 weeks non-inferior to aflibercept q8 weeks
TENAYA/LUCERNE (2022)
Indication
nAMD
Key finding
Faricimab up to q16 weeks non-inferior to aflibercept q8 weeks
PULSAR (2023)
Indication
nAMD
Key finding
Aflibercept 8 mg up to q16 weeks non-inferior to 2 mg q8 weeks
Protocol T (2015)
Indication
DME
Key finding
Aflibercept superior for VA ≤20/50; all equivalent for VA 20/32–20/40
YOSEMITE/RHINE (2022)
Indication
DME
Key finding
Faricimab up to q16 weeks non-inferior to aflibercept q8 weeks

Self-Assessment (5)

MCQ

A patient with diabetic macular oedema has a baseline visual acuity of 20/63. According to Protocol T (DRCR.net), which anti-VEGF agent demonstrated superior visual outcomes at 1 year for this level of visual acuity?

MCQ

Which anti-VEGF agent carries a unique risk of retinal vasculitis and retinal vascular occlusion?

MCQ

The CATT trial established that bevacizumab is non-inferior to ranibizumab for neovascular AMD. What is the approximate cost ratio between the two agents?

MCQ

Faricimab (Vabysmo) differs from other anti-VEGF agents because it:

MCQ

What is the single most important measure to prevent endophthalmitis after intravitreal injection?

References

  1. Rosenfeld PJ, Brown DM, Heier JS, et al. Ranibizumab for neovascular age-related macular degeneration (MARINA). N Engl J Med. 2006;355(14):1419-1431.
  2. CATT Research Group. Ranibizumab and bevacizumab for neovascular age-related macular degeneration (CATT). N Engl J Med. 2011;364(20):1897-1908.
  3. Diabetic Retinopathy Clinical Research Network. Aflibercept, bevacizumab, or ranibizumab for diabetic macular edema (Protocol T). N Engl J Med. 2015;372(13):1193-1203.
  4. Heier JS, Khanani AM, Quezada Ruiz C, et al. Efficacy, durability, and safety of intravitreal faricimab up to every 16 weeks for neovascular age-related macular degeneration (TENAYA and LUCERNE). Ophthalmology. 2022;129(7):790-801.
  5. AAO Basic and Clinical Science Course (BCSC), Section 12: Retina and Vitreous

Related Content

Age-Related Macular DegenerationDiabetic RetinopathyCentral Retinal Vein OcclusionPachychoroid Spectrum Disorders
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