Glaucoma
Primary open-angle, normal-tension, and angle-closure glaucoma — IOP-lowering through the prostaglandin / SLT (LiGHT 2019) / iDose TR (FDA December 2023) ladder is the only intervention with hard visual-field preservation evidence, 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
Glaucoma is a defined clinical disease — characteristic optic nerve head damage and visual-field defects with intraocular pressure (IOP) as the primary modifiable risk factor — diagnosed and managed by ophthalmology with a tightly defined standard-of-care ladder. Primary open-angle glaucoma (POAG) is the dominant subtype; normal-tension glaucoma (NTG) sits within the open-angle family with IOP at or below the population mean and is the subtype where non-IOP mechanisms (vascular dysregulation, mitochondrial dysfunction, glymphatic-system contributions) get the most editorial traction; angle-closure glaucoma is a separate anatomic emergency category requiring laser iridotomy or lens extraction. Pseudoexfoliation and pigmentary glaucoma are open-angle subtypes with their own management nuances. Roughly 3 million US adults are diagnosed with glaucoma; meaningfully more are undiagnosed in early disease. It is the second leading cause of irreversible blindness globally after cataract. Standard-of-care is well-evidenced and procedurally rich. Tier 1 first-line pharmacotherapy: prostaglandin analogs (latanoprost, bimatoprost, travoprost, tafluprost) are the dominant first-line agents — once-daily dosing, ~25-35% IOP reduction, well-tolerated systemic profile. Second-line and adjunct: beta-blockers (timolol with cardiopulmonary contraindications), alpha-2 agonists (brimonidine), carbonic anhydrase inhibitors (dorzolamide, brinzolamide topical; acetazolamide systemic), rho-kinase inhibitors (netarsudil — Rhopressa; latanoprostene bunod — Vyzulta as combination product). Selective laser trabeculoplasty (SLT) was elevated to first-line status by the LiGHT 2019 Lancet trial, which showed SLT achieved target IOP without drops in 74% of patients at 3 years and was cost-effective compared to prostaglandin first-line. The iDose TR (travoprost intracameral implant) FDA-approved December 2023 represents the newer sustained-release drug-delivery paradigm — 3+ years of continuous travoprost from a single intracameral procedure, sidestepping the adherence problem that plagues drop therapy. Bimatoprost SR (Durysta) FDA-approved 2020 covers a shorter intracameral-implant interval. MIGS (minimally invasive glaucoma surgery — iStent, Hydrus microstent, Xen gel stent, Kahook Dual Blade) sits between drops and incisional surgery for mild-to-moderate disease, often combined with cataract surgery. Trabeculectomy and tube shunts (Ahmed, Baerveldt) remain the incisional options for advanced or refractory disease. The neuroprotection conversation has been the white whale of glaucoma research for thirty years. Memantine failed in glaucoma Phase 3 (Allergan 2008). Brimonidine has neuroprotection claims supported by the Low-Pressure Glaucoma Treatment Study (LoGTS) showing reduced visual-field progression at 4 years versus timolol — a real signal but indirect (LoGTS was IOP-controlled comparison, mechanism inference). Citicoline holds the closest-to-actual-neuroprotection registered status — registered in Italy and adjacent jurisdictions as a nutraceutical adjunct (OLBA, NEUROBA, and other branded preparations) for glaucoma neuroprotection, with Parisi 1999 / 2008 / 2018 visual-evoked potential improvement evidence, the Lanza 2019 retinal ganglion cell function evidence, and ongoing open-label cohort studies — the multi-jurisdictional Italian clinical use here is real evidence that US FDA non-approval doesn't erase. Citicoline is not currently a Juno library entry — that gap is editorially honest to note when users ask about peptide-class neuroprotection for glaucoma, because the strongest registered case for the broad question is a compound the library doesn't yet cover. The published human nicotinamide-in-glaucoma trial program (De Moraes 2022 JAMA Ophthalmology and successors, 1.5-3 g/day for 12 weeks improving inner-retinal ERG function) is the other active neuroprotection conversation worth honoring — also not currently a Juno library entry as a glaucoma-axis peptide. Where Juno's library fits — narrowly and with deliberate non-elevation. No peptide in the library has a discovery-card-defensible glaucoma case. The five peptides drafted on this substrate axis (NMN, Cerebrolysin, Semax, SS-31, BPC-157) exist for honest /ask answers when users probe specific compounds, not for browse elevation. NMN sits adjacent to the nicotinamide trial program but with the salvage-pathway substitution untested in human glaucoma. Cerebrolysin's 50+ country registration covers stroke, vascular dementia, and TBI; Rule 6 blocks indication propagation to glaucoma. Semax's Russian registration includes optic-nerve atrophy and small Russian-language glaucoma exploration exists, but cross-jurisdictional independent replication is absent and the indication doesn't extend to glaucoma in any jurisdiction. SS-31 has the most mechanistically defensible RGC-survival case via its cardiolipin-stabilizing mechanism, but no published human glaucoma trial — the closest neighboring evidence is LHON and dry AMD (ReCLAIM-2 Phase 2b primary endpoint missed), neither of which propagates. BPC-157 is community-extrapolated from systemic anti-inflammatory framing with no ophthalmic trial bridge and a VEGF-mechanism concern for the anti-VEGF-treatment overlap subsets common in glaucoma cohorts. The honest editorial frame: ophthalmology coordination, the IOP-lowering ladder, and the active neuroprotection conversation with your ophthalmologist (nicotinamide for the broad program, citicoline for the Italian registered tier, brimonidine for the LoGTS signal) drive outcomes; no peptide in the library substitutes.
Important caveat
Glaucoma is ophthalmology-managed standard-of-care disease — comprehensive eye exam with dilated optic-nerve assessment, OCT RNFL/GCL imaging, standard automated perimetry (visual fields), gonioscopy for angle assessment, and IOP measurement (Goldmann applanation tonometry with corneal-thickness correction) are the diagnostic workup, and the IOP-lowering ladder is the load-bearing therapeutic intervention. No peptide substitutes for that ladder. Prostaglandin analogs (latanoprost, bimatoprost, travoprost, tafluprost) are Tier 1 first-line pharmacotherapy; SLT was elevated to alternative first-line by the LiGHT 2019 Lancet trial; the iDose TR (travoprost intracameral implant, FDA-approved December 2023) represents the newer sustained-release paradigm; Bimatoprost SR (Durysta, FDA-approved 2020) covers shorter intracameral intervals. MIGS sits between drops and incisional surgery for mild-to-moderate disease; trabeculectomy and tube shunts remain the options for advanced or refractory disease. Acute angle closure is an ophthalmic emergency — sudden severe eye pain, nausea, halos around lights, red eye, decreased vision — requires immediate ED or ophthalmology presentation for IOP-lowering and laser iridotomy; do NOT treat suspected acute angle closure as a peptide-protocol decision. Normal-tension glaucoma is the subset where the non-IOP mechanism conversation has the most editorial traction (vascular dysregulation, mitochondrial dysfunction, glymphatic-system contributions are active research directions), and even there the standard-of-care intervention is IOP-lowering AND aggressive cardiovascular risk-factor management AND screening for sleep apnea (an established NTG association). The neuroprotection conversation that exists outside the IOP-lowering ladder is dominated by citicoline (registered in Italy as a nutraceutical adjunct, not currently a Juno library entry — Parisi 1999/2008/2018 and Lanza 2019 are the published anchors) and the nicotinamide trial program (De Moraes 2022 JAMA Ophthalmology, 1.5-3 g/day for 12 weeks improving inner-retinal ERG function); both are honest editorial referrals when users ask about peptide-class neuroprotection, and the library's gap on those compounds is editorially honest to acknowledge. Brimonidine has the LoGTS visual-field-progression signal versus timolol at 4 years — a real but indirect neuroprotection inference that lives within the IOP-lowering toolkit. No Juno library peptide is surfaced as a glaucoma discovery card — NMN, Cerebrolysin, Semax, SS-31, and BPC-157 are substrate-only with editorially deliberate non-elevation because no published human glaucoma trial supports any of them and the standard-of-care ladder dominates. Cancer-history users: any peptide layered on glaucoma management deserves oncology coordination, and the anti-VEGF overlap (diabetic retinopathy, neovascular AMD, macular edema) is a specific concern for BPC-157's VEGF-upregulation mechanism. WADA athletes: BPC-157 (S0) is prohibited at all times; CJC-1295 and other GH-secretagogues (S2) are prohibited; the federation anti-doping liaison is the resource for confirmation, not a peptide clinician. Vision loss from glaucoma is irreversible — the cost of substituting peptides for the IOP-lowering ladder is permanent visual-field damage, 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.