Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume.

Four sequence-related potassium channel genes – shaker, shaw, shab, and shal – have been identified in Drosophila, and each has been shown to have human homolog(s).

[16] Kv1.3 is physically coupled through a series of adaptor proteins to the T-cell receptor signaling complex and it traffics to the immunological synapse during antigen presentation.

[20] The apoptotic protein Bax has been suggested to insert into the outer mitochondrial membrane and occlude the pore of Kv1.3 via a lysine residue.

In proof-of-concept studies, Kv1.3 blockers have prevented and treated disease in rat models of multiple sclerosis, type-1 diabetes mellitus, rheumatoid arthritis, contact dermatitis, and delayed-type hypersensitivity.

[31] Kv1.3 is also considered a therapeutic target for the treatment of obesity,[32][33] for enhancing peripheral insulin sensitivity in patients with type-2 diabetes mellitus,[34] and for preventing bone resorption in periodontal disease.

[38][39] Kv1.3 is blocked[35] by several peptides from venomous creatures including scorpions (ADWX1, OSK1,[41] margatoxin,[42] kaliotoxin, charybdotoxin, noxiustoxin, anuroctoxin, OdK2[43])[44][45] and sea anemone (ShK,[46][47][48][49][50] ShK-F6CA, ShK-186, ShK-192,[51] BgK[52]), and by small molecule compounds (e.g., PAP-1,[53] Psora-4,[54] correolide,[55] benzamides,[56] CP339818,[57] progesterone[58] and the anti-lepromatous drug clofazimine[59]).

The Kv1.3 blocker clofazimine has been reported to be effective in the treatment of chronic graft-versus-host disease,[60] cutaneous lupus,[61][62] and pustular psoriasis[63][64] in humans.