Peptide with both antimicrobial and neurotoxin activities. Inhibits voltage-dependent potassium channels. Potently blocks Kv1.1/KCNA1 (IC(50)=6.7-87 pM) and Kv1.3/KCNA3 (IC(50)=10-250 pM) (PubMed:8567178, PubMed:15665253, PubMed:9830012, PubMed:10545177, PubMed:23919482, PubMed:26288216, PubMed:28194851). Less potently blocks Kv1.4/KCNA4 (IC(50)=0.31 nM), and Kv1.6/KCNA6 (IC(50)=0.16 nM) (PubMed:9830012). Shows moderate activity on Kv1.2/KCNA2 (IC(50)=9 nM), Kv1.7/KCNA7 (IC(50)=11.5 nM), and KCa3.1/KCNN4 (Kd=0.03-30 nM) (PubMed:10419508, PubMed:9830012). Blocks Kv channels by binding to a shallow vestibule at the outer entrance to the ion conduction pathway and occluding the entrance to the pore (PubMed:10419508, PubMed:9830012). Shows antibacterial activity against all tested bacteria (the Gram-positive bacteria B.subtilis and S.aureus, and the Gram-negative bacteria S.typhimurium and P.aeruginosa) (PubMed:28796463). Synthetic analog ShK-186 is under clinical trial by 'Kv1.3 Therapeutics, Inc.' under the name dalazatide. Dalazatide has been validated in multiple models of autoimmune disease and has demonstrated proof of concept in a Phase 1b study in psoriasis. Dalazatide is ready to begin Phase 2 clinical studies for inclusion body myositis (IBM) a rare disease with no approved treatment options and generally poor prognosis for the patients. The dalazatide development program is focused on providing a breakthrough treatment first for IBM and then followed by other rare and autoimmune diseases. ShK-186 contains an L-phosphotyrosine attached via an aeea (mini-PEG) hydrophilic linker to Arg-1 and is amidated. Does not show or very weak activity on Kv1.5/KCNA5, Kv3.1/KCNC1, and Kv3.4/KCNC4 (IC(50)>100 nM). The synthetic analog ShK-192 has a paraphosphono-Phe (Ppa) at position 0, a Norleucine at position 21, and is amidated. It is stable at acidic pH values and high temperatures. The circulating half-life of the synthetic mutant is estimated to be about 30 minutes in rats. However, low concentrations of functionally active peptide are detected in the blood 72 hours after the injection. The synthetic mutant effectively inhibits the proliferation of T lymphocytes (T(EM)) cells in rats and suppresses delayed type hypersensitivity when administered at 10 or 100 ug/kg by subcutaneous injection once daily. The synthetic analog ShK-145 has a 20 kDa polyethylene glycol (PEG), and a Lys at position 16. In vivo, its injection into rat model of multiple sclerosis inhibits the progression of the disease. In addition, weekly administration of ShK-145 suppress interleukin-17 (IL-17) cytokine secretion from T cells in cynomolgus monkeys and does not show adverse side effects. The synthetic analog ShK-L5 contains a L-phosphotyrosine linked via a hydrophilic linker to the N-terminus of the ShK peptide. It is a highly specific Kv1.3/KCNA3 blocker that exhibits 100-fold selectivity for Kv1.3/KCNA3 over Kv1.1/KCNA1 and greater than 250-fold selectivity over all other channels tested. In vivo, it does not cause cardiac toxicity and does not alter clinical chemistry and hematological parameters after 2-week therapy. It also prevents and treats experimental autoimmune encephalomyelitis and suppresses delayed type hypersensitivity in rats. Belongs to the sea anemone type 1 potassium channel toxin family. Type 1a subfamily.