All SK channels can be pharmacologically blocked by quaternary ammonium salts of a plant-derived neurotoxin bicuculline. In addition, SK channels (SK1-SK3) but not SK4 (IK) are sensitive to blockade by the bee toxin apamin, and the scorpion venoms tamapin and charybdotoxin (ChTx), all via competitive antagonism for access to the mouth of the pore formation. All known blockers compete for roughly the same binding site, the pore, in all subtypes.  This provides a physical blockage to the channel pore.  Since all blockers are universal to all three types of SK channels, there is an incredibly narrow therapeutic window that does not allow for blocking of a specific SK channel subtype.  Quaternary ammonium salts like bicuculline and tetraethylammonium (TEA) enter the pore via the selectivity filter by acting as a potassium mimic in the dehydration step of pore permeation.
The following molecules are other toxins and organic compounds that also inhibit all three small SK channel subtypes to any (even minimal) degree:
*Dequalinium
*d-Tubocurarine
*UCL-1684
*UCL-1848
*Cyproheptadine
*Fluoxetine, the active ingredient in Prozac
*NS8593
*Scyllatoxin (Leiurotoxin-I)
*Lei-Dab7
*N-methyl-laudanosine
*N-Me-bicuculline
*Pancuronium
*Atracurium
*1-ethyl-1H-benzo[d]imidazol-2(3H)-on
*6,7-dichloro-3-(hydroxyimino)indolin-2-one
*N-cyclohexyl-2-(3,5-dimethyl-1H-pyrazol-1-yl)-6-methylpyrimidin-4-amine
*(R)-N-(1,2,3,4-tetrahydronaphthalen-1-yl)-1H-benzo[d]imidazol-2-amine