Vandria SA is a Swiss biotechnology company developing novel therapeutics that target mitochondrial function and cellular energetics in age-related neurodegenerative diseases, including both Alzheimer's disease and Parkinson's disease. Founded in 2018 and headquartered in Geneva, Switzerland, Vandria focuses on modulating mitochondrial quality control mechanisms to protect neurons from degeneration[1].
The company's lead program, VNA-318, targets mitochondrial dysfunction—a fundamental contributor to neuronal death in Alzheimer's disease. A second program, VNA-100, is specifically directed at Parkinson's disease and targets mitophagy defects that are central to dopaminergic neuron degeneration[2].
| Program | Mechanism | Indication | Phase | Status |
|---|---|---|---|---|
| VNA-318 | Mitochondrial modulator | Alzheimer's Disease | Phase 1 | Active |
| VNA-100 | Mitophagy inducer | Parkinson's Disease | Preclinical | IND-enabling |
VNA-100 represents Vandria's entry into Parkinson's disease, leveraging the company's expertise in mitochondrial quality control to address PD-specific pathology[3].
PD is uniquely tied to mitochondrial dysfunction through both genetic and environmental evidence:
VNA-100 targets the PINK1-PARKIN mitophagy pathway, which is directly impaired in familial PD:
VNA-100 is in IND-enabling studies, with the program focused on:
Vandria is also exploring targeted protein degradation approaches including monobody-based PROTAC technologies for Parkinson's disease. This first-in-class approach aims to selectively degrade pathological proteins using monobody scaffolds linked to E3 ligase recruiters.
Parkinson's disease is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta. These neurons have exceptionally high energy demands due to their pacemaking activity and extensive axonal arborizations, making them particularly vulnerable to mitochondrial dysfunction[3:1].
Key mitochondrial mechanisms in PD include:
VNA-100 is Vandria's preclinical program targeting Parkinson's disease. Unlike VNA-318, which has a broader mitochondrial mechanism, VNA-100 is specifically designed to enhance mitophagy—the cellular process responsible for removing damaged mitochondria.
Mechanism of Action:
Rationale:
The rationale for mitophagy enhancement in PD is supported by genetic evidence. PINK1 and Parkin mutations cause early-onset autosomal recessive PD, demonstrating that impaired mitophagy is sufficient to cause dopaminergic neuron degeneration[5:1]. Similarly, mutations in GBA (glucocerebrosidase) which increase the risk of PD, are associated with impaired mitochondrial function and autophagy[8].
VNA-100 is currently in preclinical development with IND-enabling studies underway. The program builds on Vandria's platform capabilities:
VNA-318 is a first-in-class small molecule targeting mitochondrial function:
VNA-318 entered Phase 1 clinical trials in 2024, with first-in-human studies in healthy volunteers[2:1]. The trial program includes:
Mitochondrial dysfunction is an early and central event in Alzheimer's disease:
VNA-318 addresses these issues through:
Vandria's platform is built on understanding mitochondrial biology:
| Platform | Application |
|---|---|
| Mitochondrial assays | OCR, ATP, membrane potential |
| Cellular models | iPSC-derived neurons |
| In vivo models | Mitochondrial dysfunction models |
Vandria maintains collaborations with leading Swiss academic institutions including the University of Geneva and EPFL[1:1].
Vandria SA is a privately held company based in Geneva, Switzerland, with funding from Swiss and international venture capital investors[1:2].