GW-1100 is a selective antagonist of GPR40 (pIC50: 6.9). GW1100 also plays the role of a GPR40 inverse agonist.

GW-1100 (1 μM) produces a significant rightward shift in the concentration-response curve to GW9508 (pEC50=7.17±0.08 in the absence and pEC50=6.79±0.09 in the presence of 1 μM GW-1100; P<0.05; n=3). At concentrations of GW-1100 (3 μM and higher) shows a significant decrease in the maximal response is observed with a continuing rightward shift in the pEC50 response[2]. CHO-K1/bFFAR1 cells are incubated for 15 min with 10 μM GW1100 or vehicle (0.1% DMSO) and then stimulated with vehicle, oleic acid, linoleic acid or GW9508. GW-1100 significantly reduces the increase in intracellular calcium induced by 300 μM oleic acid (AUC(60-150 s), p<0.05), 100 μM linoleic acid (AUC(60-150 s), p<0.05) and 10 μM GW9508 (AUC(60-150 s), p<0.05)[3]. GW-1100 dose dependently suppresses GPR40-mediated Ca2+ elevations stimulated by GW9508 and linoleic acid (pIC50: 5.99±0.03 and 5.99±0.06, respectively). GW-1100 causes FFAR1 ligand-induced intracellular calcium in CHO-K1/bFFAR1 cells and neutrophils.

These effects are inhibited by intracerebroventricular pretreatment with GW-1100 (10 μg), a GPR40 antagonist. The intracerebroventricular injection of DHA (50 μg) and GW9508 (1.0 μg) are a GPR40-selective agonist. This obviously decreases mechanical allodynia and thermal hyperalgesia on day 7, but not on day 1, after CFA injection[4].

306974-70-9

C27H25FN4O4S

520.58

DMSO:50 mg/mL (96.05 mM),Need ultrasonic
Powder: -20°C for 3 years
In solvent: -80°C for 2 years