Overview
Binds to VPAC1 and VPAC2 receptors on lacrimal gland, corneal epithelium, and retinal neurons.
Proposed mechanism
VIP is a neuropeptide that increases tear production, reduces corneal inflammation, and promotes retinal ganglion cell survival via cAMP/PKA pathways.
What the evidence supports
Most data comes from preclinical animal studies. Human clinical trial evidence is limited or absent.
Graded Animal
Evidence drawn from in vivo animal models or in vitro systems. Mechanistically informative; translation to humans is unproven.
Key citations
Representative primary sources, including results that did not favour the compound.
- [1]
VIP in dry eye
· DOI:10.1167/iovs.14-14817 · 2015
- [2]
Neuroprotection in glaucoma
· DOI:10.1016/j.exer.2015.03.010 · 2015
- [3]
VIP in dry eye (2015)
· · 0
- [4]
Neuroprotection in glaucoma (2015)
· · 0
Citation records in this build are illustrative placeholders for the design.
Reference information for research purposes. Not medical advice, and not a recommendation to use any compound. Many entries describe substances that are not approved for human use.