GL64

GL64 (10 μM) stimulates CRE-luciferase activity by more than 1.5-fold in ADGRD1-overexpressing HEK293T cells^[1].
GL64 (10 μM) increases CRE-luciferase and endogenous adenosine cAMP levels in wt MEFs but has no effect on Adgrd1^−/− cells^[1].
GL64 (0-100 μM) does not increase CRE-luciferase in HEK293T cells overexpressing adhesion GPCRs, such as ADGRD2, ADGRG5, ADGRG6, CELSR1, CELSR2, CELSR3, and ADGRG4, and does not activate nonadhesion GPCRs, including GPR68, NPFFR1, GPR183, and GPRC5B^[1].
GL64 has weak agonist activity against ADGRD1 (EC₅₀ = 16.89 μM) in stachel peptide-treated in ADGRD1-overexpressing HEK293T cells^[1].
GL64 (10 μM, 6 days) inhibits the differentiation of male WT bone marrow-derived macrophages (BMMs) into mature osteoclasts but has no effect on Adgrd1^−/− BMMs^[1].
GL64 (10 μM, 6 days) down-regulates the mRNA expression levels of Dc-stamp, Acp5, and Nfatc1, during male mouse osteoclast maturation in BMMs^[1].
GL64 (30 μM) increases endogenous cAMP levels in male BMMs^[1].
GL64 (10 μM, 2 days) reduces NFATC1 nuclear localization in BMMs^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.