🔬 2D Microvascular & Blood-Brain Barrier Kinetic Visualizer
Plasma Molecule
CNS Molecule
Active P-gp Pump
Blood-Brain Barrier (BBB) Mechanism
In mammals, endothelial cells lining capillary walls express high levels of P-glycoprotein (MDR1 efflux pumps). Even though ivermectin is lipophilic, P-glycoprotein actively transports drug molecules back into systemic circulation, preventing CNS penetration at standard dose levels (0.15–0.20 mg/kg).
📈 Pharmacokinetic Plasma & CNS Profiles
NORMAL THERAPEUTIC
Plasma Cmax
48.2 ng/mL
CNS Conc.
1.4 ng/mL
AUC (0-72h)
1184 ng·h/mL
GluCl Occupancy
94.5%
GABA_A Occupancy
2.1%
🎛️ Dosing Regimen & Physiological Parameters
🧬 Target Receptor Binding Matrix & Clinical Evidence
Ivermectin Pharmacokinetics & Receptor Mechanism Simulator
Receptor Selectivity Comparison
| Receptor Type | Host Organism | Affinity (Kd) | Primary Function | Clinical Effect |
|---|---|---|---|---|
| GluCl (Glutamate Chloride) | Nematodes / Arthropods | ~0.25–1.0 nM | Pharyngeal muscle & motoneuron gates | Hyperpolarization & Paralysis |
| GABA_A (γ-Aminobutyric) | Mammals (Central Nervous System) | ~100–300 nM | Inhibitory CNS neurotransmission | Protected by BBB efflux |
FDA / WHO Approved Indications vs. Toxicity Mechanisms
- Nobel Prize 2015: Awarded to William C. Campbell and Satoshi Ōmura for discovering Avermectins, revolutionizing treatment for Onchocerciasis (River Blindness) and Lymphatic Filariasis.
- Anti-Parasitic Safety Margin: GluCl channels in parasites possess ~100x higher affinity for ivermectin than mammalian GABA_A receptors.
- Neurotoxicity Risk: At high non-indicated doses (>1.0 mg/kg) or in MDR1-deficient individuals, drug concentrations breach the BBB, binding CNS GABA_A receptors and causing ataxia, lethargy, coma, or seizure.