G-1

G-1 is a nonsteroidal, high-affinity and selective agonist of GPR30 with a K_i of 11 nM. IC50 & Target:Ki: 11 nM (GPR30)^[1] In Vitro: G-1 is a nonsteroidal, high-affinity and selective agonist of GPR30 with a K_i of 11 nM^[1].
Treatment with G-1 (10 μM and 100 μM) for 48 and 72 h significantly decreases cell proliferation (P<0.001). At 72 h, the IC₅₀ value for G-1 is calculated to be 20 μM. Treatment of A549 cells with G-1 at a concentration of 20 μM reveals a significant increase in apoptosis, consistent with its antiproliferative effect (P<0.001)^[2].
Cell cycle analysis of H295R cells after 24 h of G-1 treatment demonstrates a cell cycle arrest in the G₂ phase. The presence of G-1 increases Bax expression while decreases Bcl-2^[3]. In Vivo: The results at 14 days post-injury show that the Basso mouse scale (BMS) scores are significantly higher in the G-1 group compared with the other groups (P<0.05). The number of caspase-3-positive cells in the cross sections is counted, and G-1 group has fewer positive cells compare with the other groups (P<0.05), and there is no difference between the two groups (P>0.05)^[1].
G-1 administration produces a statistically significant decrease in tumor volume from day 14 post treatment. Grafted tumors harvested after three-week treatment with G-1 show a significant decrease in tumor weight compare to vehicle treated animals^[3].