G protein-coupled estrogen receptor (GPER), or GPR30, specifically binds natural and man-made estrogens.[1] It is thought to be involved in estrogen-sensitive cancers.[1],[2] GPER knockout mice are fertile, although they exhibit thymic atrophy, impaired glucose tolerance, and altered bone growth.[1] G-36 is a cell-permeable non-steroidal antagonist of GPER, inhibiting activation by either 17β-estradiol or the GPER-selective agonist G-1 (IC50 = 112 and 165 nM, respectively).[3] It has no detectable binding activity to either ERα or ERβ.3 G-36 blocks the activation of PI3K or calcium mobilization triggered by estrogen through GPER and it suppresses ERK activation by estrogen or G-1 but not by EGF.[3] G-36 can be used in combination with GPER-selective agonists, like G-1, to distinguish the roles of GPER from those of ERα and ERβ in complex biological systems.[3],[4]

Reference:
[1]. Filardo, E.J., and Thomas, P. Minireview: G protein-coupled estrogen receptor-1, GPER-1: Its mechanism of action and role in female reproductive cancer, renal and vascular physiology. Endocrinology 153(7), 2953-2962 (2012).
[2]. Chevalier, N., Vega, A., Bouskine, A., et al. GPR30, the non-classical membrane G protein related estrogen receptor, is overexpressed in human seminoma and promotes seminoma cell proliferation. PLoS One 7(4), 34672 (2012).
[3]. Dennis, M.K., Field, A.S., Burai, R., et al. Identification of a GPER/GPR30 antagonist with improved estrogen receptor counterselectivity. Journal of Steroid Biochemistry and Molecular Biology 127(3-5), 358-366 (2011).
[4]. Brailoiu, G.C., Arterburn, J.B., Oprea, T.I., et al. Bradycardic effects mediated by activation of G protein-coupled estrogen receptor in rat nucleus ambiguus. Experimental Physiology 98(3), 679-691 (2013).