| Bioactivity | CD2665 is an orally active and selective RAR-β,γ antagonist, with Kd values of 306 nM, 110 nM for RAR-β and RAR-γ, repectively[1][3]. | |||||||||
| Target | Ki: 110 nM (RARγ), 306 nM (RARβ) | |||||||||
| Invitro | CD2665 (100 nM; 9 days; 3T3 cells) has significant effects on cell growth and differentiation[1]. Cell Proliferation Assay[1] Cell Line: | |||||||||
| In Vivo | CD2665 (0.6 mg/kg; Subcutaneous injection; daily, for 22 days) completely inhibits the overexpression of RARβ mRNA in the brain of alcohol treated mice[2]. CD2665 is a selective retinoid antagonist and elicits the expected maturation delay and growth plate expansion[3]. Animal Model: | |||||||||
| Name | CD2665 | |||||||||
| CAS | 170355-78-9 | |||||||||
| Formula | C31H34O5 | |||||||||
| Molar Mass | 486.60 | |||||||||
| Appearance | Solid | |||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | |||||||||
| Storage |
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| Reference | [1]. Kim MJ, et al. The role of specific retinoid receptors in sebocyte growth and differentiation in culture. J Invest Dermatol. 2000 Feb;114(2):349-53. [2]. Alfos S, Boucheron C, et al. A retinoic acid receptor antagonist suppresses brain retinoic acid receptor overexpression and reverses a working memory deficit induced by chronic ethanol consumption in mice. Alcohol Clin Exp Res. 2001 Oct;25(10):1506-14. [3]. Koyama E, et al.Premature Growth Plate Closure Caused by a Hedgehog Cancer Drug Is Preventable by Co-Administration of a Retinoid Antagonist in Mice. J Bone Miner Res. 2021 Jul;36(7):1387-1402. |