AGN 193109 是一种类视黄醇类似物，是一种有效的特异性 RAR 拮抗剂，可抑制RARα、RARβ和RARγ的活性，Kd值分别为 2 nM、2 nM 和 3 nM。

AGN 193109, a retinoid analog, is a potent and specific antagonist of RARs (Kds: 2 nM, 2 nM, and 3 nM for RARα, RARβ, and RARγ).

AGN 193109 is completely RAR specific because it does not bind to or transactivate through any of the RXRs [1]. AGN 193109 (100 nM) inhibits the TTNPB (a retinoic acid receptor agonist)-dependent morphological change in ECE16-1 cells. AGN193109 half-reverses retinoid-dependent growth suppression at 10 nM, and completely shows this effect at 100 nM in ECE16-1 cells. AGN193109 (100 nM) also eliminates TTNPB-induced decrease in levels of K5, K6, K14, K16, and K17 and increases in levels of K7, K8, and K19 [2].

AGN 193109 (0.30 or 1.20 μmol/kg) by topical treatment significantly reduces both weight loss and cutaneous toxicity caused by oral TTNPB cotreatment. AGN 193109 (1.15 μmol/kg) does not cause overt toxicity and has no effect on spleen weight on the mice, but it suppresses TTNPB-induced increase in spleen weight of the mice. AGN 193109 also significantly reduces the cutaneous toxicity induced by ATRA [3].

Cells (10,000/cm2) are seeded in complete medium and allowed to attach overnight. The cells are then shifted to defined medium (DM), allowed to equilibrate for 24 h, and treatment is initiated by the addition of fresh DM or DM containing epidermal growth factor (EGF) or retinoid. After 3 days of daily treatment with retinoid, the cells are harvested with 0.025% trypsin, 1 mM EDTA, fixed in isotonic buffer containing 4% formaldehyde, and counted using a counter [2].

Mice (n=6) are treated topically on the dorsal skin with vehicle (92.5% acetone/7.5% DMSO), 0.072 μmol/kg of TTNPB, 1.15 μmol/kg of AGN 193109, or 0.072 μmol/kg of TTNPB plus 0.072, 0.288, or 1.15 μmol/kg of AGN 193109 for 5 days. Mice are euthanized on Day 8 [3].

171746-21-7

C28H24O2

392.49

DMSO:10mM
Powder: -20°C for 3 years
In solvent: -80°C for 2 years