CD2665

Research use only, not for human use.

CD2665 is an antagonist of RAR-beta/gamma (Ki: 110 nM and 306 nM for RARγ and RARβ).

CD2665 is an antagonist of RAR-beta/gamma (Ki: 110 nM and 306 nM for RARγ and RARβ).(In Vitro):In 3T3 cells, CD2665 (100 nM) abrogates the antiproliferative effects of ATRA, CD271 (adapalene, a RAR-β,γ agonist), and CD2043 (RAR-α,β,γ pan-agonist) returning cell numbers and percent LFCS to control level.(In Vivo):In mice submitted to 10 months of ethanol consumption, CD2665 (0.6 mg/kg; s.c.) decreases brain RARβ mRNA levels (50% relative to control), without any change in RXR β/γ mRNA levels.

CD2665 (100 nM; 9 days; 3T3 cells) has significant effects on cell growth and differentiation. Cell Proliferation Assay Cell Line:3T3 cells Concentration:100 nM Incubation Time:9 days Result:Abrogated the antiprolferative effects of ATRA , CD271 (adapalene, an RAR-β,γ agonist), and CD2043 (RAR-α,β,γ pan-agonist) returning cell numbers and percent LFCS to control level.

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. CD2665 is a selective retinoid antagonist and elicits the expected maturation delay and growth plate expansion. Animal Model:Mice submitted to 10 months of ethanol consumption.Dosage:0.6 mg/kg Administration:Subcutaneous injection; daily, for 22 days.Result:Decreased brain RARβ mRNA levels (50% relative to control), without any change in RXR β/γ mRNA levels.Animal Model:Male and female mice (3 weeks).Dosage:1.6 mg/kg Administration:Oral gavage/intragastric; daily, for 31 days.Result:Growth plate closure had largely been prevented in LDE225/antagonist co-treated mice compared with those receiving LDE225 only.

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Metabolic Enzyme/Protease

Retinoid Receptor

DNA/RNA Synthesis

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170355-78-9

486.608

C31H34O5

>98% (HPLC)

In Vitro:?DMSO : 62.5 mg/mL (128.44 mM)

COCCOCOc1cc2ccc(cc2cc1C12C[C@H]3C[C@H](C[C@H](C3)C1)C2)-c1ccc(cc1)C(O)=O

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(-20℃)

With Ice Pack

≥ 2 years