Tertiapin was originally isolated from European honey bee Apis mellifera venom. Native and synthetic Tertiapin blocks a range of inward rectifier K+ channels (Kir), in particular ROMK1 (Kir1.1, IC50 = 2 nM) and GIRK (Kir3 family, IC50 for the Kir3.1/3.4 heteromer was 8.6 nM) but with no effect on Kir2 family members. In accordance, it was shown to inhibit acetylcholine induced K+ currents in mammalian cardiomyocytes.
Tertiapin-Q is a derivative of Tertiapin in which Met13 is substituted by Gln residue. However, unlike native Tertiapin, Tertiapin-Q is non-oxidizable and therefore is more stable.
Tertiapin-Q inhibits the above-mentioned channels with similar affinities and also inhibits Ca2+ activated large conductance BK-type K+ channels in a concentration, and voltage-dependent manner.
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