Structure via PubChem · Public domain (PubChem)
vesamicol
Sign in to saveVesamicol is an experimental drug, acting presynaptically by inhibiting acetylcholine (ACh) uptake into synaptic vesicles and reducing its release. Vesamicol may have applications for the treatment of adenocarcinoma in situ of the lung.
Chemical data
- Formula
- C17H25NO
- Molecular weight
- 259.4 g/mol
- IUPAC name
- 2-(4-phenylpiperidin-1-yl)cyclohexan-1-ol
via PubChem
Drug data · ChEMBL
- Molecule type
- Small molecule
via ChEMBL · EBI
Research
345 papers- In Vivo and In Vitro Characteristics of Radiolabeled Vesamicol Analogs as the Vesicular Acetylcholine Transporter Imaging Agents.Contrast media & molecular imaging · 2018
- Astatine-211-labeled aza-vesamicol derivatives as sigma receptor ligands for targeted alpha therapy.Nuclear medicine and biology · 2023
- Acetylcholine transporter--vesamicol receptor pharmacology and structure.Progress in brain research · 1993
- The pharmacology of vesamicol: an inhibitor of the vesicular acetylcholine transporter.General pharmacology · 1992
- (+)-p-[(11)C]Methylvesamicolphenoxy).2004
via PubMed
Wikidata facts
- Mass
- 259.19361442
Show 3 more facts
- chemical formula
- C₁₇H₂₅NO
- canonical SMILES
- C1CCC(C(C1)N2CCC(CC2)C3=CC=CC=C3)O
- Commons category
- Vesamicol
Sources (2)
via Wikidata · CC0
~1 min read
Article
2 sectionsContents
- Mechanism of action
- References
Vesamicol is an experimental drug, acting presynaptically by inhibiting acetylcholine (ACh) uptake into synaptic vesicles and reducing its release. Vesamicol may have applications for the treatment of adenocarcinoma in situ of the lung.
== Mechanism of action == Vesamicol can be broadly categorized as a cholinergic physiological antagonist, because it reduces the apparent activity of cholinergic neurons, but does not act at the postsynaptic ACh receptor. Vesamicol causes a non-competitive and reversible block of the intracellular transporter VAChT responsible for carrying newly synthesized ACh into secretory vesicles in the presynaptic nerve terminal. This transport process is driven by a proton gradient between cell organelles and the cytoplasm. Blocking of acetylcholine loading leads to empty vesicles fusing with neuron membranes, decreasing ACh release.