. Author manuscript; available in PMC: 2006 Feb 1.

Published in final edited form as: Bioorg Med Chem Lett. 2005 Nov 10;16(3):596–601. doi: 10.1016/j.bmcl.2005.10.054

Table 1.

Potency of a series of adenosine derivatives for four subtypes of human ARs and the efficacy at the A₃AR.

	Potency (K_i or EC₅₀, nM)				Efficacy^c
Compound	A₁^d	A_2A^d	A_2B^e	A₃^d	A₃
1^a	310^e	700^e	24,000	290^e	100
2^b	7.4 ± 1.7	132 ± 22	~10,000	5.8 ± 0.4	46 ± 8
3^b	16.8 ± 2.2	197 ± 34	>10,000	1.8 ± 0.1	0
4^b	222 ± 22	5360 ± 2470	>10,000	1.4 ± 0.3	100
5^f	193 ± 46	223 ± 36	ND	0.38± 0.07	114 ± 9
6^g	5870 ± 930	>10,000	>10,000	29.0 ± 4.9	0
7^g	6220 ± 640	>10,000	>10,000	15.5 ± 3.1	0
8	>10,000	>10,000	>10,000	315 ± 19	0

All experiments were done on CHO cells stably expressing one of four subtypes of human ARs. The binding affinity for A₁, A_2A and A₃ARs was expressed as K_i values and was determined by using agonist radioligands ([³H]R-PIA), ([³H]CGS21680), [¹²⁵I]I-AB-MECA, respectively. The potency at the A_2BAR was expressed as EC₅₀ values and was determined by stimulation of cAMP production in AR-transfected CHO cells. The efficacy at A₃ARs was determined by inhibition of forskolin-stimulated cAMP production in AR-transfected CHO cells, as described in the text. Data are expressed as mean ± standard error.

Values from reference ²¹.

Values from references 9, 21.

At a concentration of 10 μM, in comparison to the maximal effect of a full agonist NECA at 10 μM.

K_i in binding, unless noted.

cAMP assay.

K_i values from reference ¹³.

6, MRS3771; 7, LJ-1256.

ND not determined.