S-Geranylgeranyl-L-glutathione

S-geranylgeranyl-L-glutathione (100-1000 nM) inhibits the migration of human CD4⁺ and CD8⁺ T cells expressing P2RY8 towards CXCL12, and this effect is abrogated in P2RY8-deficient cells^[1].
S-geranylgeranyl-L-glutathione can be exported from HEK293T cells via Abcc1, as inhibition of Abcc1 reduces the migration inhibitory activity of HEK293T cell supernatant toward WEHI-231 cells expressing P2RY8^[1].
S-Geranylgeranyl-L-glutathione (100 pM-1 μM; 3 h) potently and selectively inhibits chemokine-mediated migration of P2RY8-GFP-transduced WEHI-231 cells^[2].
S-Geranylgeranyl-L-glutathione (100 nM; 1.5 h) inhibits chemokine-mediated migration of human primary tonsil germinal center (GC) B cells, follicular helper T (Tfh) cells, and naive B cells, with the strongest efficacy observed in GC B cells^[2].
S-Geranylgeranyl-L-glutathione (45 min) selectively induces endocytosis of P2RY8 in M12 cells transduced with P2RY8-OX56-Thy1.1, with no effect on other tested GPCRs^[2].
S-Geranylgeranyl-L-glutathione (100 nM) acts via P2RY8 and Gα13 to antagonize chemokine-induced Akt activation in GCB DLBCL cell lines, P2RY8-transduced WEHI-231 cells, and primary human tonsillar GC B cells^[2].
S-Geranylgeranyl-L-glutathione (100 nM-10 μM; 7-18 h) is specifically metabolized into an inactive form (S-geranylgeranyl-L-Cys-Gly) by Ggt5, thereby losing its P2RY8 biological activity^[2].
S-Geranylgeranyl-L-glutathione exists endogenously in mouse lymphoid tissues and human tonsils at nanomolar concentrations, and in mouse bile at micromolar concentrations^[2].

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