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Best Peptides for Macular Degeneration: Compound Comparison
The peptides under investigation for retinal neuroprotection differ fundamentally in mechanism, administration route, and the stage of disease where intervention might theoretically work. Thymalin Immune modulation. Reduces T-cell-mediated inflammation in reti
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- The peptides under investigation for retinal neuroprotection differ fundamentally in mechanism, administration route, and the stage of disease where intervention might theoretically work.
- Thymalin
- Immune modulation. Reduces T-cell-mediated inflammation in retinal tissue
- Poor (systemically active, does not cross BRB)
- 10–100 mcg subcutaneous 2–3×/week
- Early dry AMD with drusen accumulation
- Addresses upstream inflammation but lacks direct retinal cell protection. Best combined with antioxidants
- Cerebrolysin
- Neurotrophic factor delivery. Mimics BDNF and NGF to support photoreceptor survival
- Moderate (small peptide fragments cross during inflammation)
- 0.5–2.5 mL/kg intramuscular or intraperitoneal
- Intermediate dry AMD or wet AMD with neovascularization
- Most data from CNS models, not retina-specific. Mechanism is sound but clinical translation unproven
- Dihexa
- Synaptic plasticity enhancement. Activates HGF receptors to increase dendritic density
- Excellent (lipophilic, crosses BRB passively)
- 1–5 mg/kg subcutaneous or oral
- Late dry AMD where synaptic loss compounds photoreceptor death
- Crosses BRB efficiently but no direct photoreceptor protection. Addresses downstream connectivity, not cell death
- P21 (research reference)
- Neuroplasticity modulator. Derived from CNTF, supports retinal ganglion cell survival
- Moderate (requires active transport)
- 1–10 mg/kg subcutaneous
- Wet AMD, diabetic retinopathy
- Emerging data in optic nerve injury models. Retinal application is early-stage