ATC161 exposure and alpha-synuclein aggregate degradation
Reference paper ↗A reduced AUTOTAC PK/PD model linking ATC161 exposure to concentration-dependent degradation and recovery of alpha-synuclein aggregates.
- Therapeutic
- ATC161
- Modality
- Targeted protein degrader
- Target
- alpha-synuclein aggregates, SNCA aggregates, p62, SQSTM1
- Disease
- Preclinical Parkinson disease and synucleinopathy models
- Model type
- PKPD
Complete model workspace
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- Parameters
- 6
- States
- 3
- Equations
- 3
- Derived outputs
- 8
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Choose a starting point to view its result. Adjust key model inputs when you want to explore a different outcome.
Starting configuration
PO 20 mg/kg first-order PK/degradation
PO 20 mg/kg first-order PK/degradation
How does ATC161 exposure control the time course and recovery of alpha-synuclein aggregate reduction? Explore this biological starting configuration through Plasma ATC161, ATC161 molar concentration, Aggregate degradation effect, Alpha-synuclein aggregate fraction.
Starting result
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Starting configuration
Time: 0–24 h; step 0.1
| Input | Default | Available range |
|---|---|---|
| Oral ATC161 half-life | 3.7 h | 1.85–5.55 h |
| Half-maximal degradation concentration | 100 nM | 50–150 nM |
| Aggregate degradation rate | 0.04 1/h | 0.02–0.06 1/h |
| Aggregate recovery rate | 0.001 1/h | 5.00e-4–0.0015 1/h |
| Baseline aggregate fraction | 1 dimensionless | 0.5–1.5 dimensionless |
Expected readouts
Plasma ATC161 concentration (ng/mL) · ATC161 molar concentration · Aggregate degradation effect · Alpha synuclein aggregate fraction (dimensionless)
Adjustable model parameters
This public explorer exposes 5 curated parameters. Sign in to edit all 6 declared model parameters.
More key parameters (1)
How the model represents the biology
A reduced AUTOTAC PK/PD model linking ATC161 exposure to concentration-dependent degradation and recovery of alpha-synuclein aggregates.
Solid arrows show modeled movement or change; two-headed arrows show reversible exchange; dashed arrows show modulation without material transfer.
Model scope: Oral absorption, brain distribution, p62 recruitment, autophagosome or lysosome states, ternary-complex binding, aggregate species, and neuronal outcomes are not represented.
Modeled relationships (6)
- Plasma ATC161 → ATC161 loss: first-order (loss)
- Plasma ATC161 → Degradation drive: saturable effect (modulation)
- Degradation drive → Aggregate fraction: aggregate loss (loss)
- Aggregate fraction → Baseline recovery: baseline deficit (modulation)
- Baseline recovery → Aggregate fraction: restoration (production)
- Plasma ATC161 → Cumulative exposure: integrates C (production)
Modeled relationships: Plasma ATC161 to ATC161 loss: first-order (loss); Plasma ATC161 to Degradation drive: saturable effect (modulation); Degradation drive to Aggregate fraction: aggregate loss (loss); Aggregate fraction to Baseline recovery: baseline deficit (modulation); Baseline recovery to Aggregate fraction: restoration (production); Plasma ATC161 to Cumulative exposure: integrates C (production).
Primary readouts: Plasma ATC161; ATC161 concentration; Degradation effect; Aggregate fraction.
Related models
Research use only — not for patient-specific prediction or dosing advice.
