AZ1729

AZ1729 is an allosteric FFAR2 modulator in human neutrophils that initiates NADPH-oxidase activation and, together with Cmp58, potently activates superoxide generation without inducing Ca²⁺ transients^[2].
AZ1729 (pre-incubation for 15 minutes; incubation at 25 °C for 1 hour) can stimulate Gi-mediated [³⁵S]GTPγS binding in Flp-In T-REx 293 membranes expressing hFFA2-eYFP, with a pEC₅₀ of 7.23^[4].
AZ1729 (treatment at 25 °C for 2 hours) only weakly modulated [³H]GLPG0974 binding to hFFA2 in Flp-In T-REx 293 membranes, maximally reducing specific binding by 16.7%, with an apparent pK_i of 6.77^[4].
AZ1729 (30 min) is a potent Gi-biased full agonist and PAM of hFFA2 in Flp-In T-REx 293 cells, inhibiting Forskolin (HY-15371)-stimulated cAMP with a pEC₅₀ of 6.90 and enhancing C3 potency, αβ = 85.22^[4].
AZ1729 (up to 30 µM; treatment at 37 °C for 2 hours) lacks direct Gq/G11-mediated IP1 agonism at hFFA2 in Flp-In T-REx 293 cells up to 30 µM, and acts as an insurmountable allosteric antagonist of C3 in this pathway with an estimated affinity of 6.12^[4].
AZ1729 (37 °C treatment for 5 minutes) produced only weak, PTX-sensitive Gi-mediated partial agonism of phospho-ERK1/2 in Flp-In T-REx 293 cells, with a pEC₅₀ of 5.66, and acted as an agonist PAM when Gq/G11 was blocked^[4].
AZ1729 (30 min co-incubation) is a Gi-coupled agonist and PAM of mFFA2 in Flp-In T-REx 293 cells, inhibiting Forskolin-stimulated cAMP with a potency of 6.16 and enhancing C3 potency, αβ = 13.49^[4].
AZ1729 (treatment at 37 °C for 2 hours) inhibits isoproterenol-stimulated lipolysis in primary mouse adipocytes, with a pEC₅₀ of 5.03^[4].
AZ1729 (3-10 µM; treatment at 37 °C for 1.5 hours) induces human neutrophil migration^[4].

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