Table 2.

Bicyclic amides with N‐ethoxycarbonyl or N‐butoxycarbonyl sulfonamide moieties synthesized according to Scheme 2–4.

Cmpd	Structure	K i hAT2R [nM][a]	%‐Inhibition of hAT1R at 10 μM[b]	Cmpd	Structure	K i hAT2R [nM][a]	%‐Inhibition of hAT1R at 10 μM[b]
C93		110 (29[c])	22 %	88		870	7.7 %
C97		110 (83[c])	23 %	89		1300	26 %
C102		420 (2.2[c])	30 %	90		120	NDI[g]
83		>1500[d]	15 %	91		120	28 %
84		700	22 %	92		290	15 %
85		360	7.5 %	93		760	19 %
86		56 IC50=818 nM[e]	34 % IC50 >10 000 nM[f]	94		1300	1.5 %
87		270	45 %	95		850	11 %
–	–	–	–	96		1100	15 %

[a] Radioligand displacement from hAT₂R in membranes from HEK‐293 cells overexpressing hAT₂R (assay 1). N=2. [b] Inhibition of radioligand binding from hAT₁R expressed in HEK‐293 cells (assay 1). [c] Radioligand displacement from AT₂R in pig uterus membrane.29 [d] K _i estimated to more than 1500 nM, IC₅₀ was determined to be >3 000 nM. [e] Radioligand displacement from hAT₂R expressed in HEK‐293 cells (assay 2). [f] Radioligand displacement from hAT₁R expressed in HEK‐293 cells, ligands were not active on hAT₁R at the concentrations tested (assay 2). N=9 [g] NDI=no detectable inhibition.