Nomenclature	ClC-1	ClC-2	ClC-Ka	ClC-Kb
HGNC, UniProt	CLCN1, P35523	CLCN2, P51788	CLCNKA, P51800	CLCNKB, P51801
Endogenous activators	–	arachidonic acid	–	–
Activators (EC50)	–	lubiprostone, omeprazole	niflumic acid (1x10-5 – 1x10-3 M)	niflumic acid (1x10-5 – 1x10-3 M)
Channel Blockers (IC50)	9-A-C, Cd2+, fenofibric acid, S-(-)CPB, S-(-)CPP, niflumic acid, Zn2+	Cd2+, DPC, NPPB, Zn2+, GaTx2 (Kd 1.5x10-11 M) [voltage dependent-100.0 mV]	3-phenyl-CPP, DIDS, niflumic acid (>1x10-3 M)	3-phenyl-CPP, DIDS
Functional characteristics	γ = 1–1.5 pS; voltage-activated (depolarization) (by fast gating of single protopores and a slower common gate allowing both pores to open simultaneously); inwardly rectifying; incomplete deactivation upon repolarization, ATP binding to cytoplasmic cystathionine β-synthetase related (CBS) domains inhibits ClC-1 (by closure of the common gate), depending on its redox status	γ = 2–3 pS; voltage-activated by membrane hyperpolarization by fast protopore and slow cooperative gating; channels only open negative to ECl resulting in steady-state inward rectification; voltage dependence modulated by permeant anions; activated by cell swelling, PKA, and weak extracellular acidosis; potentiated by SGK1; inhibited by phosphorylation by p34(cdc2)/cyclin B; cell surface expression and activity increased by association with Hsp90	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+
Comment	CIC-1 is constitutively active	CIC-2 is also activated by amidation	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