Disease relevance of CD 3106

• We show here that RA, GGOH, GGPP and GGA stimulate osteoclastic bone resorption and that this action is reversed by the RAR antagonist AGN-193109 [1].
• TTNPB pretreatment caused precipitous weight loss and, in the absence of AGN 193109 intervention, 60% mortality [2].
• AGN 193109 treatment at all dose levels significantly accelerated recovery of body weight and prevented death in TTNPB-intoxicated mice [2].
• TTNPB caused skin flaking, skin abrasions, and splenomegaly, and these effects were blocked in a dose-dependent fashion by AGN 193109 cotreatment [2].
• The purpose of the present study was to determine if AGN 193109 functions as an RAR antagonist in vivo and thus could prevent and/or treat retinoid toxicity [2].

High impact information on CD 3106

• In contrast, the RAR antagonist AGN 193109 abrogates reconstituting ability, most likely by promoting the differentiation of the primitive stem cells [3].
• In marked contrast, lin- c-kit+ Sca-1+ cells cultured with AGN 193109 for 7 days had virtually no short- or long-term repopulating ability, but displayed an approximately 6-fold increase in the pre-CFU-S population [3].
• Furthermore, the ability of 13-cis RA to induce apoptosis cannot be recapitulated by 9-cis RA or ATRA, and it is not inhibited by the presence of a retinoid acid receptor (RAR) pan-antagonist AGN 193109 [4].
• Inhibition of RA signaling, with the selective inhibitor AGN 193109, blocked RA-mediated induction of the Smad proteins and chondrocyte differentiation [5].
• The activity of AGN 193109 on MRP-8 is cell type specific [6].

Anatomical context of CD 3106

• Cell type and gene-specific activity of the retinoid inverse agonist AGN 193109: divergent effects from agonist at retinoic acid receptor gamma in human keratinocytes [6].

Gene context of CD 3106

• This suggests that the AhR/ARNT pathway and not the RAR/RXR pathway is mediating the elevation of CYP1A1 mRNA levels by AGN 193109, at least in the Hepa-1c1c7 cells [7].
• The synthetic retinoid AGN 193109 is a potent pan retinoic acid receptor (RAR) antagonist [7].
• TTNPB-induced skin irritation was blocked in a dose-dependent fashion by co-treatment with the RAR pan-antagonist AGN 193109 but was not blocked by co-treatment with the RAR alpha-specific antagonist AGN 194301 [8].

References