75659-91-5

Basic information

• Product Name: 14-O-Acetyl Noroxycodone
• Synonyms: 14-O-Acetyl Noroxycodone
• CAS NO: 75659-91-5
• Molecular Formula: C₁₉H₂₁NO₅
• Molecular Weight: 343.37
• Mol File: 75659-91-5.mol
• Article Data: 2

Chemical Properties

• Appearance: /
• CAS DataBase Reference: 14-O-Acetyl Noroxycodone(CAS DataBase Reference)
• NIST Chemistry Reference: 14-O-Acetyl Noroxycodone(75659-91-5)
• EPA Substance Registry System: 14-O-Acetyl Noroxycodone(75659-91-5)

Safety Data

• Hazardous Substances Data: 75659-91-5(Hazardous Substances Data)

Upstream product

• 108-24-7 acetic anhydride 
• 76-42-6 Oxycodone 

Downstream Products

• 99307-36-5 14-Hydroxy-N-propylnorcodeinon 
• 57664-96-7 noroxycodone 

Relevant articles and documents

Activation of G-Proteins by Morphine and Codeine Congeners: Insights to the Relevance of O- and N-Demethylated Metabolites at μ- and δ-Opioid Receptors

Phenotypic differences in analgesic sensitivity to codeine (3-methoxymorphine) results from polymorphisms in cytochrome P450-2D6, which catalyzes O-demethylation of codeine to morphine. However, O-demethylation reportedly is not required for analgesic activity of the 7,8-saturated codeine congeners dihydrocodeine, hydrocodone, and oxycodone. This study determined the potency and efficacy of these compounds and their demethylated derivatives to stimulate μ- and δ-opioid receptor-mediated G-protein activation using agonist-stimulated guanosine 5′-O-(3-[35S]thio)triphosphate ([35S]GTPγS) binding. Results showed that 7,8-saturated codeine congeners were more efficacious than codeine in activating μ-receptors, but only dihydrocodeine was more efficacious at δ-receptors. Hydrocodone and oxycodone were ～10-fold more potent than codeine and dihydrocodeine at either receptor. Morphine-like compounds with a 3-hydroxy group were ～30- to 100-fold more potent than their 3-methoxy analogs at the μ-receptor, and these compounds generally exhibited greater efficacy (e.g., morphine produced 2-fold greater maximal stimulation than codeine). Removal of the N-methyl group did not affect efficacy or potency of codeine congeners to activate μ-receptors, whereas this modification generally increased efficacy but decreased potency of morphine congeners. At the δ receptor, morphine congeners showed greater potency and structure-dependent differences in efficacy compared with codeine congeners, whereas removal of the N-methyl group had effects similar to those observed at the μ-receptor. These results demonstrate that 7,8-saturated codeine congeners are more efficacious than codeine, which may explain their lack of requirement for 3-O-demethylation in vivo. Nonetheless, because all 7,8-saturated codeine congeners were significantly less potent than their morphine derivatives, further research is needed to understand the relationship between metabolism and in vivo activity of these compounds.