| Compound Code | KAT-MCI-02 |
| Pharmacological Tag | Antidiabetic (withdrawn) / Mitochondrial disruptor |
| Structural Class | Biguanide |
| Mechanism (Putative) | Mitochondrial Complex I inhibition → ↓ ATP AMP accumulation → AMPK activation Suppression of hepatic gluconeogenesis ROS production in metabolically stressed cells |
| Functional Role | Insulin sensitization Glucose control (historic) Potential anti-neoplastic vector Metabolic deranger in tumor models |
| Structural Analogues | Metformin Buformin Cycloguanil Proguanil |
| Predicted Onset | Moderate (oral bioavailability ~50%) |
| Predicted Duration | 12–24 hours (extended hepatic retention) |
| Affinity Profile | Non-receptor based Targets cellular metabolism and redox states Minimal direct enzyme inhibition |
| Computational Predictions | CNS Activity: negligible BBB Penetration: low Mitochondrial Accumulation: high Lactic Acidosis Risk: elevated in hypoxic states Tumor Selectivity (hypoxia): plausible Mutagenicity: low Metabolism: CYP2D6 / hepatic deamination |
| Interpretation |
A post-mortem drug — pharmaceutically discontinued but pharmacologically resurrected
Exploited toxicity repurposed as a precision weapon in cellular energetics
Promising in oncological bioenergetics, yet clinically outlawed
Operates in a grey zone: metabolic sabotage as medicine. It enters cells more readily than metformin and is reported to be 10 times more potent, the binding affinity affinity for mitochondria membranes was reported as x 50 higher. Phenformin may increase DNA repair and switches metabolic energy to glycosis. |