| Compound Code | KAT-NEU-09 |
| Pharmacological Tag | MAO-B Inhibitor / Dopaminergic Modulator / Neuroenergetic Probe |
| Structural Class | Propargylated Phenylethylamine |
| Mechanism (Putative) | Irreversible inhibition of MAO-B → ↑ Dopamine in striatum ↓ H2O2 production → Neuroprotection (oxidative hypothesis) Propargyl moiety → Mitochondrial anti-apoptotic signaling Metabolized to D-amphetamine → Central stimulation |
| Functional Role | Cognitive preservation in Parkinson's Delay of L-DOPA dependence Stimulant adjunct in depressive states Mitochondrial resilience enhancer Experimental anti-aging vector |
| Structural Analogues | Rasagiline Desmethylselegiline (L)-Deprenyl Methamphetamine Pargyline |
| Predicted Onset | Slow (irreversible enzyme binding requires cumulative dosing) |
| Predicted Duration | Long (>24h due to MAO-B regeneration kinetics) |
| Affinity Profile | MAO-B: high (irreversible covalent binding) DAT/NET/SERT: Robust (via metabolites) Mitochondrial apoptotic cascade: indirect interference Sigma receptors: speculative binding |
| Computational Predictions | CNS Activity: high BBB Penetration: confirmed Neuroplasticity: potential via BDNF upregulation Mitochondrial Bioenergetics: preserved under stress Risk of Stimulation: high (via amphetamine metabolites) Neurotoxicity: Neglectible Longevity Pathways: candidate for caloric-mimetic synergy |
| Interpretation | An amphetamine in disguise — dressed in neuroprotective garb. (D)-Deprenyl occupies a unique biochemical duality: stimulant & safeguard. While pharmacologically "clean", its metabolic afterlife is dirtied by amphetamine. Used in Parkinson's but peeking into anti-aging labs. It doesn’t merely delay death — it modulates hypothamalic neuronal-aging center. Perfect neuropharmacologically. |