Acts as a gating modifier on both Kv and Nav ion channels, and also acts on blood pressure. Voltage-dependently inhibits voltage-gated potassium channels Kv3 (Kv3.1/KCNC1, Kv3.2/KCNC2 and Kv3.4/KCNC4) and slows inactivation of the voltage-gated sodium channel Nav1.7/SCN9A (PubMed:16177043, PubMed:22442564, PubMed:9506974). Inhibits all Kv3.1, Kv3.2 and Kv3.4 by about 50% when tested at a voltage of +40 mV (45%, 48% and 56%, respectively). May act by binding residues in voltage-sensing domains S3b and S4 of Kv3 (PubMed:16177043). On sodium channel, tests have been done on human Nav1.7/SCN9A (expressed in HEK293 cells) (EC(50)=3 nM) and rat SCG neurons that mostly carry Nav1.7 channels (EC(50)=300 nM) (PubMed:22442564). This toxin also reduces blood pressure (Ref.1). This toxin does not have effect on Nav1.1/SCN1A and Nav1.6/SCN8A sodium channels (PubMed:22442564). It has little or no functional effect on cardiac muscle, as well as on skeletal muscle myotubes, suggesting lack of functional interaction with Nav1.4/SCN4A or Nav1.5/SCN5A (PubMed:9506974). This protein sequence is identical to BDS-1 from A.viridis (AC P0DMX6). Belongs to the sea anemone type 3 (BDS) potassium channel toxin family. Opinions are divided on whether Anemonia viridis (Forsskal, 1775) and Anemonia sulcata (Pennant, 1777) are separate species.