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The chemopreventive efficacy of Targretin was evaluated in various rodentcancer models. In the rat model of 4-hydroxybutyl(butyl)nitrosamine (OH-BBN)-inducedurinary bladder cancer, it was found that Targretin administered in the diet (beginningone week after the last OH-BBN treatment) for 5.5 months increased the numberand size of urinary bladder cancers. In the azoxymethane (AOM)-induced model ofcolon carcinogenesis (in which rats develop minimally invasive colonic cancers),Targretin was ineffective as a chemopreventive agent, decreasing neither tumorincidence nor multiplicity. Treatment of Min mice with Targretin for 45 days similarlyfailed to decrease the multiplicity of small intestinal tumors. Similarly, nopreventive efficacy was noted for Targretin when the incidence of tumors in thehead and neck model (squamous cell tongue tumors) induced by 4-nitroquinoline1-oxide (4-NQO) were examined. In contrast, use of even a suboptimal dose of Targretin(40 ppm) in a sensitive breast cancer model [methylnitrosourea (MNU)-induced ER+mammary cancers] reduced cancer multiplicity by 60%. Finally, based on the hypothesisthat Targretin may decrease the expression of COX‑2, the effects of Targretinand COX inhibitors were compared in these models. There was minimal overlap ofefficacy. That is, models which were relatively susceptible to NSAIDs or COX-2inhibitors tended not to be sensitive to Targretin and vice versa.

Chemopreventive efficacy of Targretin in rodent models of urinary bladder, colon/intestine, head and neck and mammary cancers