Age-related macular degeneration (AMD)
Dry AMD (including geographic atrophy as the advanced form) and wet (neovascular) AMD — where AREDS2 supplementation (2013) is the Tier 1 risk-modification intervention for intermediate disease, intravitreal anti-VEGF therapy is the Tier 1 wet-AMD intervention with hard visual-acuity preservation evidence, the 2023 FDA approvals of pegcetacoplan (Syfovre, complement C3) and avacincaptad pegol (Izervay, complement C5) reshaped the geographic-atrophy conversation, and the editorial honest answer for this trigger is that no peptide in the Juno library has a defensible discovery-card case.
What changes during this transition
AMD is a defined clinical disease — progressive degeneration of the central retina (macula) driven by RPE and photoreceptor dysfunction, with three editorially distinct presentations that share a pathophysiologic family but carry different standard-of-care intervention sequences. Early AMD (Beckman classification: small drusen, mild RPE changes) typically carries no symptoms and routes through risk-factor modification and surveillance. Intermediate AMD (large drusen, pigmentary changes) is the AREDS2-supplementation window — the AREDS2 2013 trial established the formulation (vitamin C 500 mg, vitamin E 400 IU, zinc 80 mg or 25 mg in current dosing, copper 2 mg, lutein 10 mg, zeaxanthin 2 mg) with documented progression-rate reduction, and the AREDS2 formulation replaced the original AREDS beta-carotene component with lutein and zeaxanthin after the original AREDS trial showed beta-carotene increased lung-cancer risk in former smokers. Advanced AMD splits into geographic atrophy (the advanced dry form — well-demarcated areas of RPE and photoreceptor loss progressively expanding) and neovascular / wet AMD (choroidal neovascularization with subretinal and intraretinal fluid and hemorrhage destroying central vision). Roughly 20 million US adults have some form of AMD; geographic atrophy affects ~1 million; wet AMD ~1.5 million. AMD is the leading cause of severe central vision loss in adults over 50 in many high-income countries; East Asian and Japanese AMD epidemiology shows a higher prevalence of the polypoidal choroidal vasculopathy (PCV) subtype within the neovascular family. Standard-of-care is well-established. AREDS2 supplementation is Tier 1 for intermediate AMD risk-modification per the 2013 trial — use the zinc-only / beta-carotene-free formula if you're a current or former smoker. Smoking cessation is the single biggest modifiable risk factor (RR ~2-4 for progression). Mediterranean diet, omega-3, and dark leafy greens are AAO Preferred Practice Pattern lifestyle adjuncts. Wet AMD intervention is intravitreal anti-VEGF injection — Tier 1 with hard visual-acuity preservation evidence from MARINA, ANCHOR, CATT, IVAN, HAWK / HARRIER, and TENAYA / LUCERNE. Current agents: ranibizumab (Lucentis, FDA 2006), bevacizumab (Avastin, off-label intravitreal), aflibercept (Eylea 2011, Eylea HD 8 mg 2023), brolucizumab (Beovu 2019), faricimab (Vabysmo 2022, dual VEGF-A and Ang2). Port Delivery System (Susvimo) ranibizumab implant approved 2021, withdrawn 2022, re-approved 2024. Geographic atrophy intervention is the 2023 paradigm shift: pegcetacoplan (Syfovre, complement C3) FDA-approved February 2023 on OAKS / DERBY — slows GA lesion-growth rate by ~20-25% over 24 months; avacincaptad pegol (Izervay, complement C5) FDA-approved August 2023 on GATHER1 / GATHER2 — slows GA growth rate by ~14-18% over 12 months. Both slow progression — neither restores vision. Pegcetacoplan carries a documented ~7-12% rate of new wet-AMD conversion in treated eyes. Where Juno's library fits — narrowly and with deliberate non-elevation. No peptide in the library has a discovery-card-defensible AMD case. The five drafted substrate entries (SS-31, NMN, BPC-157, TB-500, GHK-Cu) exist for honest /ask answers when users probe specific compounds, not for browse elevation. SS-31 / elamipretide has the strongest mechanistic case (RPE mitochondrial / cardiolipin axis) and the library's only actual human-trial AMD signal — ReCLAIM-2 Phase 2b in geographic atrophy missed its primary endpoint December 2023, which is real data weighing against the case. The Barth syndrome FDA approval (March 2025) does not propagate to AMD per Rule 6. NMN sits adjacent to the nicotinamide-for-glaucoma trial program with two extrapolation steps (NMN-to-nicotinamide salvage substitution, plus glaucoma-to-AMD indication propagation) and no NMN AMD trials. BPC-157 and TB-500 both carry documented VEGF / angiogenic activity that is mechanistically opposed to the anti-VEGF intervention driving wet-AMD outcomes — this is the load-bearing safety thread for wet-AMD users and overlap-condition users (diabetic retinopathy, diabetic macular edema, retinal vein occlusion, myopic CNV). GHK-Cu's case is the most extrapolation-distant — copper-binding antioxidant cosmetic-dermatology peptide with no retinal model in any species, complicated by the AREDS2 copper-additive question. The honest editorial frame: retina-specialist coordination, AREDS2 supplementation, smoking cessation, anti-VEGF for wet AMD, and the 2023 complement-inhibitor interventions for geographic atrophy drive outcomes; no peptide in the library substitutes.
Important caveat
AMD is retina-specialist-managed standard-of-care disease — dilated comprehensive eye exam with macular OCT, fundus autofluorescence (for geographic-atrophy area tracking), fluorescein angiography (for active wet-AMD assessment), low-luminance visual acuity, and Amsler grid home monitoring are the workup and surveillance tools, and the AREDS2 + anti-VEGF + complement-inhibitor ladder is the load-bearing therapeutic intervention sequence. No peptide substitutes for that ladder. AREDS2 supplementation is Tier 1 for intermediate AMD risk-modification per the 2013 trial — current and former smokers should use the zinc-only / beta-carotene-free variant due to the original AREDS beta-carotene lung-cancer-incidence signal. The 'more antioxidants is better' assumption is NOT what the AREDS / AREDS2 data show — formulation specifics matter, and unsupervised supplement-stacking on top of AREDS2 is not an evidence-supported step. Smoking cessation is the single biggest modifiable risk factor (RR ~2-4 for progression) and outranks any peptide adjunct conversation. Wet-AMD conversion is an urgent retina-specialist event — new metamorphopsia (straight lines wavy on Amsler grid), new central scotoma, or sudden vision change requires same-day or next-day retina-specialist evaluation for anti-VEGF initiation; the cost of treating wet-AMD onset as 'try a peptide first' is permanent central vision loss. Wet-AMD users on anti-VEGF (Lucentis, Eylea, Eylea HD, Vabysmo, Beovu, off-label Avastin) face a specific peptide-side concern: BPC-157 and TB-500 both carry documented angiogenic / VEGF-pathway activity that is mechanistically OPPOSED to anti-VEGF intravitreal therapy, and the same concern extends to overlap conditions in AMD cohorts (diabetic retinopathy, diabetic macular edema, retinal vein occlusion, myopic CNV) — those peptides without explicit retina-specialist sign-off are layering mechanistically opposed compounds. Geographic-atrophy users on pegcetacoplan (Syfovre, FDA February 2023) or avacincaptad pegol (Izervay, FDA August 2023) face the procedural risks of intravitreal injection (endophthalmitis, retinal detachment, IOP elevation) and the documented ~7-12% new-wet-AMD-conversion rate with pegcetacoplan. No Juno library peptide is surfaced as an AMD discovery card — SS-31, NMN, BPC-157, TB-500, and GHK-Cu are substrate-only with editorially deliberate non-elevation because no published human AMD trial defensibly supports any of them (the SS-31 ReCLAIM-2 Phase 2b primary-endpoint miss December 2023 is the closest the library comes to engaged AMD trial evidence, and that signal points against rather than toward enthusiastic adjunct use). Rule 6 non-propagation is editorially load-bearing on this trigger: SS-31's Barth syndrome FDA approval (March 2025) does NOT propagate to AMD; SS-31 / elamipretide LHON exploration does NOT propagate; TB-500 / RGN-259 ARISE Phase 3 corneal-surface evidence does NOT propagate from corneal epithelium to retina; BPC-157's Sikiric foundational corpus is gastric and tendon and does NOT propagate to any ophthalmic indication. Cancer-history users: any peptide layered on AMD management deserves oncology coordination; the angiogenic mechanism of BPC-157 and TB-500 and the copper-redox mechanism of GHK-Cu interact with several oncology mechanisms. Choroidal melanoma history is a specific contraindication for angiogenic-mechanism peptides. WADA athletes: BPC-157 (S0) is prohibited at all times; TB-500 (S2 peptide hormones and growth factors) is prohibited at all times; the federation anti-doping liaison is the resource for confirmation, not a peptide clinician. Vision loss from AMD wet-conversion or geographic-atrophy expansion is largely irreversible — central vision lost to untreated CNV does not return, and that is the editorial reason the library does not elevate any peptide to the discovery surface for this trigger.
Want this list to grow? The library is editorial — if there’s a peptide you think belongs on this page with documented or mechanistically-clear evidence, send us a note with the citation and we’ll review it under the same evidence-tier discipline as every other entry.