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. Author manuscript; available in PMC: 2016 Jun 10.
Published in final edited form as: J Control Release. 2015 Apr 14;207:120–130. doi: 10.1016/j.jconrel.2015.04.015

Table 1.

Mechanism of action and optimal concentration of drug inhibitors used in this study.

Drug Effect Optimal Concentration
Amiloride (AMD) Inhibition of Na+/H+ exchange[26,27] (MP) 50 μg/ml
Amantadine (AMN) Stabilization of clathrin-coated vesicles[28], increases endosomal pH [29] (CME) 100 μg/ml
Chlorpromazine (CPZ) Disrupts assembly and disassembly of clathrin from coated pits[30] (CME) 20 μM
Genistein (GST) Inhibits tyrosine phosphorylation preventing caveolae formation[31] (CavME) 20 μg/ml
Bafilomycin A1 (BFN) Prevents re-acidification of synaptic vesicles inhibiting release of endosomal cargo[32,33] (CME) 5 nM
Cytochalasin D (CCN) Inhibits actin polymerization and caveolae formation [34,35] (CavMe, Fusion) 10 μM
Azidothymidine (AZT) Inhibits reverse transcription[36] 20 μM