Crenezumab PK and amyloid-beta binding
Reference paper ↗A TMDD PK/PD model coupling intravenous crenezumab disposition to free and antibody-bound amyloid-beta 1-40 and 1-42 turnover.
- Therapeutic
- Crenezumab, MABT5102A, RG7412
- Modality
- Monoclonal antibody
- Target
- Amyloid beta / APP, beta-amyloid, Abeta(1-40), Abeta(1-42)
- Disease
- Alzheimer disease
- Model type
- PKPD, TMDD
Complete model workspace
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- Parameters
- 20
- States
- 9
- Equations
- 9
- Derived outputs
- 33
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style 15 mg/kg every 4 weeks IV
How does crenezumab dose change free and bound amyloid-beta 1-40 and 1-42 over time? Explore this intervention regimen through Crenezumab concentration, Free amyloid-beta 1-40, Free amyloid-beta 1-42, Crenezumab–amyloid-beta 1-40 complex, Crenezumab–amyloid-beta 1-42 complex.
Starting result
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Starting configuration
Time: 0–168 day; step 1
| Input | Default | Available range |
|---|---|---|
| Elimination clearance | 0.159 L/day | 0.0795–0.2385 L/day |
| Internalization clearance | 1.01 L/day | 0.505–1.515 L/day |
| Central distribution volume | 2.89 L | 1.445–4.335 L |
| Aβ40 dissociation constant | 12 nM | 6–18 nM |
| Aβ42 dissociation constant | 9.37 nM | 4.685–14.06 nM |
Expected readouts
Crenezumab concentration · Free amyloid beta 1 40 · Free amyloid beta 1 42 · Crenezumab amyloid beta 1 40 complex · Crenezumab amyloid beta 1 42 complex
Adjustable model parameters
This public explorer exposes 5 curated parameters. Sign in to edit all 20 declared model parameters.
More key parameters (1)
How the model represents the biology
A TMDD PK/PD model coupling intravenous crenezumab disposition to free and antibody-bound amyloid-beta 1-40 and 1-42 turnover.
Solid arrows show modeled movement or change; two-headed arrows show reversible exchange; dashed arrows show modulation without material transfer.
Model scope: All public regimens are intravenous, so the model's structural subcutaneous depot and absorption pathway are inactive and omitted from this overview. Brain or CSF compartments, plaque dynamics, cognition, disease progression, and explicit kinetic binding states are not represented; binding is algebraic QSS.
Modeled relationships (10)
- IV crenezumab → Systemic crenezumab: IV input (flow)
- Systemic crenezumab → System removal: linear drug CL (loss)
- Aβ production → Total Aβ40: Aβ40 synthesis (production)
- Aβ production → Total Aβ42: Aβ42 synthesis (production)
- Systemic crenezumab → Crenezumab–Aβ complexes: QSS drug allocation (modulation)
- Total Aβ40 → Crenezumab–Aβ complexes: Aβ40 QSS allocation (modulation)
- Total Aβ42 → Crenezumab–Aβ complexes: Aβ42 QSS allocation (modulation)
- Total Aβ40 → System removal: target turnover (loss)
- Total Aβ42 → System removal: target turnover (loss)
- Crenezumab–Aβ complexes → System removal: complex internalization (loss)
Modeled relationships: IV crenezumab to Systemic crenezumab: IV input (flow); Systemic crenezumab to System removal: linear drug CL (loss); Aβ production to Total Aβ40: Aβ40 synthesis (production); Aβ production to Total Aβ42: Aβ42 synthesis (production); Systemic crenezumab to Crenezumab–Aβ complexes: QSS drug allocation (modulation); Total Aβ40 to Crenezumab–Aβ complexes: Aβ40 QSS allocation (modulation); Total Aβ42 to Crenezumab–Aβ complexes: Aβ42 QSS allocation (modulation); Total Aβ40 to System removal: target turnover (loss); Total Aβ42 to System removal: target turnover (loss); Crenezumab–Aβ complexes to System removal: complex internalization (loss).
Primary readouts: Central crenezumab; Free and total Aβ40; Free and total Aβ42; Drug–Aβ complexes.
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Research use only — not for patient-specific prediction or dosing advice.
