Nomenclature	ClC‐Ka	ClC‐Kb	ClC‐3	ClC‐4
HGNC, UniProt	CLCNKA, P51800	CLCNKB, P51801	CLCN3, P51790	CLCN4, P51793
Activators	niflumic acid (pEC50 3–5)	niflumic acid (pEC50 3–5)	–	–
Channel blockers	3‐phenyl‐CPP, DIDS, niflumic acid	3‐phenyl‐CPP, DIDS	phloretin (pIC50 4.5)	Zn2+ (pIC50 4.3) [68], Cd2+ (pIC50 4.2) [68]
Functional Characteristics	γ = 26 pS; linear current‐voltage relationship except at very negative potentials; no time dependence; inhibited by extracellular protons (pK = 7.1); potentiated by extracellular Ca2+	Bidirectional rectification; no time dependence; inhibited by extracellular protons; potentiated by extracellular Ca2+	Cl‐/H+ antiporter [58]; pronounced outward rectification; slow activation, fast deactivation; activity enhanced by CaM kinase II; inhibited by intracellular Ins(3,4,5,6)P4 and extracellular acidosis	Cl‐/H+ antiporter (2Cl‐:1H+) [3, 73, 87]; extreme outward rectification; voltage‐dependent gating with midpoint of activation at +73 mV [67]; rapid activation and deactivation; inhibited by extracellular acidosis; non‐hydrolytic nucleotide binding required for full activity
Comments	CIC‐Ka is constitutively active (when co‐expressed with barttin), and can be blocked by benzofuran derivatives	CIC‐Kb is constitutively active (when co‐expressed with barttin), and can be blocked by benzofuran derivatives	insensitive to the channel blockers DIDS, NPPB and tamoxifen (10 μM)	–