Table 1.

List of compounds used in this paper with their targets and potencies

Compound	Mechanism	Potency	Cross reactivity
Apyrase	Degradation of ATP and ADP		None
MRS2500	Inhibitor of P2Y1 receptor (endogenous ligands ADP ≫ ATP)	IC50 = 8.4 ± 0.8 nM (Kim et al. 2003)	None
AR-C 118925XX	Inhibitor of P2Y2 receptor (endogenous ligands ATP, UTP)	IC50 = 72.1 ± 12.4 nM (Rafehi et al. 2017)	None
NF157	Inhibitor of P2Y11 receptor (endogenous ligand ATP)	IC50 = 463 ± 59 nM (Ullmann et al. 2005)	P2X1 IC50 = 63.1 nM
CGS15943	Adenosine receptor antagonist (endogenous ligand adenosine)	IC50 = 20 nM at A1, 3 nM at A2 (Williams et al. 1987)
Suramin	Non-selective antagonist for P2 purinergic receptors	IC50 =  ~ 1 µM (Dunn and Blakeley 1988)	Also blocks G protein coupling to GPCRs
Pertussis Toxin (PTX)	ADP-ribosylation on α subunits of Gi, Go, and Gt	IC50 = 158 ± 40 pg/ml for Gi and 35 ± 8 pg/ml for Go (Liang and Galper 1988)	None
YM-254890 (YM)	Inhibitor of GDP release from the α subunit of Gq	IC50 = 0.15 ± 0.04 nM (Nishimura et al. 2010)

Most are specific P2Y receptor inhibitors, while others are broad-spectrum purinergic receptor antagonists. Apyrase is an ATP-diphosphohydrolase that catalyzes sequential hydrolysis of ATP to ADP and ADP to AMP releasing inorganic phosphate. PTX and YM target G protein coupling to GPCRs. PTX catalyzes ADP-ribosylation on α subunits of G proteins Gi, Go, and Gt, thus preventing them from interacting with receptors. YM on the other hand, inhibits the release of GDP from the α subunit of Gq. The endogenous ligands that activate the purinergic receptors are outlined in parentheses