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VIP for Neuroprotection: Research Model Comparison
The table below compares VIP's neuroprotective efficacy across common preclinical models, highlighting delivery routes, dose ranges, and therapeutic windows that define successful outcomes. MPTP Parkinson's Model Intranasal 50–200 μg/dose, daily × 7 days Withi
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- The table below compares VIP's neuroprotective efficacy across common preclinical models, highlighting delivery routes, dose ranges, and therapeutic windows that define successful outcomes.
- MPTP Parkinson's Model
- Intranasal
- 50–200 μg/dose, daily × 7 days
- Within 24h post-toxin
- 40–50% reduction in dopaminergic cell loss
- Strongest evidence for VIP neuroprotection; consistent across multiple studies
- Stroke (MCAO Model)
- 100–300 μg single dose
- Within 1–3h post-occlusion
- 30–40% reduction in infarct volume
- Narrow therapeutic window limits translational potential
- Traumatic Brain Injury (CCI)
- Intranasal or IV
- 50–150 μg within 1h post-injury
- Within 1–6h post-injury
- 35% lesion volume reduction, 50% neurological score improvement
- Acute intervention only; no chronic benefit demonstrated
- Alzheimer's (APP/PS1 Transgenic)
- Intranasal, chronic
- 100 μg 3×/week × 12 weeks
- Preventive dosing before plaque burden
- 25% reduction in hippocampal plaque load
- Modest effect; requires chronic dosing with unclear human translation
- Amyotrophic Lateral Sclerosis (SOD1 Model)
- Intranasal or subcutaneous
- 100–200 μg 3×/week
- Pre-symptomatic or early symptomatic
- 延ed disease onset by 10–15 days, no survival extension
- Limited efficacy in rapidly progressive models