18717-72-1

Basic information

• Product Name: NORCOCAINE
• Synonyms: NORCOCAINE;(-)-norcocain;5-alpha-h-nortropane-2-beta-carboxylicacid,3-beta-hydroxy-1-alpha-methyl;ester,benzoate(ester);norcocaine--dea schedule ii item;NORCOCAINE HYDROCHLORIDE COCAINE METABOL ITE, P;(1R,2R,3S,5S)-3-(Benzoyloxy)-8-azabicyclo[3.2.1]octane-2-carboxylic Acid Methyl Ester;N-Demethylcocain
• CAS NO: 18717-72-1
• Molecular Formula: C₁₆H₁₉NO₄
• Molecular Weight: 289.33
• Product Categories: Intermediates & Fine Chemicals;Metabolites & Impurities;Pharmaceuticals
• Mol File: 18717-72-1.mol
• Article Data: 15

Chemical Properties

• Melting Point: 77-82°C
• Boiling Point: 402.2 °C at 760 mmHg
• Flash Point: 197.1 °C
• Appearance: /
• Density: 1.24 g/cm³
• Vapor Pressure: 1.11E-06mmHg at 25°C
• Storage Temp.: Controlled Substance, -20?C Freezer, Under Inert Atmosphere
• CAS DataBase Reference: NORCOCAINE(CAS DataBase Reference)
• NIST Chemistry Reference: NORCOCAINE(18717-72-1)
• EPA Substance Registry System: NORCOCAINE(18717-72-1)

Safety Data

• Hazard Codes: T+
• Statements: 60-26/27/28-43
• Safety Statements: 22-36/37/39-45
• Hazardous Substances Data: 18717-72-1(Hazardous Substances Data)

Usage

Description

Norcocaine, a minor metabolite of Cocaine, is a controlled substance with chemical properties of a white to off-white solid. It is derived from the parent compound, Cocaine, through metabolic processes in the body.

Uses

Used in Pharmaceutical Industry:
Norcocaine is used as an active pharmaceutical ingredient for its potential therapeutic applications. As a metabolite of Cocaine, it may possess properties that can be harnessed for specific medical uses, although its exact applications are not explicitly detailed in the provided materials.
Used in Research and Development:
Norcocaine is used as a research compound for understanding the metabolic pathways of Cocaine and its potential effects on the human body. This knowledge can contribute to the development of new drugs or therapies that target these pathways.
Used in Forensic Analysis:
Norcocaine is used as a forensic marker in the detection and analysis of Cocaine use. Its presence in biological samples can help confirm the consumption of Cocaine and provide insights into the individual's exposure to the drug.
Used in Regulatory Compliance:
Norcocaine is used as a controlled substance in regulatory compliance, ensuring that its production, distribution, and use are monitored and controlled to prevent misuse and maintain public health and safety.
Please note that the provided materials do not specify the exact applications of Norcocaine in different industries. The uses listed above are inferred based on the information given and general knowledge about metabolites and controlled substances.

InChI:InChI=1/C16H19NO4.ClH/c1-20-16(19)14-12-8-7-11(17-12)9-13(14)21-15(18)10-5-3-2-4-6-10;/h2-6,11-14,17H,7-9H2,1H3;1H/t11-,12+,13-,14+;/m0./s1

Upstream product

• 50-36-2 Cocaine 
• 69610-28-2 (1R,2R,3S,5S)-3-Benzoyloxy-8-aza-bicyclo[3.2.1]octane-2,8-dicarboxylic acid 2-methyl ester 8-(2,2,2-trichloro-ethyl) ester 
• 67-56-1 methanol 
• 53-21-4 (-)-cocaine hydrochloride 

Downstream Products

• 138704-14-0 l-cocain- 
• 72904-33-7 N-Benzylnorcocaine 
• 137668-43-0 N-acetyl-N-norcocaine 
• 172954-47-1 3-<(benzoyl)oxy>-<1R-(exo,exo)>-8-bromoethyl-8-azabicyclo<3.2.1>octane-2-carboxylic acid methyl ester 
• 178929-46-9 (1R,2R,3S,5S)-8-(4-Azido-butyl)-3-benzoyloxy-8-aza-bicyclo[3.2.1]octane-2-carboxylic acid methyl ester 
• 204514-80-7 Norcocaine carbobenzoxy-β-alanine 
• 41889-45-6 benzoylnorecgonine 
• 275355-66-3 methyl (1R,2R,3S,5S)-3-(benzoyloxy)-8-(prop-2-yn-1-yl)-8-azabicyclo[3.2.1]octane-2-carboxylate 
• 150283-68-4 anhydronorecgonine 
• 183793-33-1 succinyl norcocaine 

Related news

Hemodynamic effects of centrally administered NORCOCAINE (cas 18717-72-1) in the rat09/30/2019

Norcocaine is the N-demethylated metabolite of cocaine. It is present in the CNS and is reported to be pharmacologically active. The present study was designed to evaluate the cardiovascular actions of norcocaine following central administration. Wistar Kyoto (WKY) rats were anesthetized with pe...detailed

NORCOCAINE (cas 18717-72-1) is a potent modulator of haemodynamic responses, plasma catecholamines and cardiac hormone release in conscious rats09/29/2019

We examined the effects of intravenously administered cocaine and norcocaine on the haemodynamics, the plasma immunoreactive atrial natriuretic peptide (ANP), the N-terminal peptide of proANP (NT-ANP) and the plasma catecholamine levels in conscious, chronically cannulated Sprague-Dawley rats. C...detailed

Synthesis of 8-oxa analogues of NORCOCAINE (cas 18717-72-1) endowed with interesting cocaine-like activity09/28/2019

In order to further explore the importance of cocaine's bridge nitrogen atom in binding to the dopamine transporter (DAT), we have synthesized the previously known racemic 8-oxa-norcocaines 3–6 in which the nitrogen atom has been replaced by oxygen. Additionally, to avoid incorrect interpr...detailed

Determination of cocaine, benzoylecgonine, cocaethylene and NORCOCAINE (cas 18717-72-1) in human hair using solid-phase extraction and liquid chromatography with tandem mass spectrometric detection10/01/2019

A quantitative analytical procedure for the determination of cocaine, benzoylecgonine and cocaethylene and norcocaine in hair has been developed and validated. The hair samples were washed, incubated, and any drugs present were quantified using mixed mode solid-phase extraction and liquid chroma...detailed

Development of a method for the determination of cocaine, cocaethylene and NORCOCAINE (cas 18717-72-1) in human breast milk using liquid phase microextraction and gas chromatography-mass spectrometry09/27/2019

Most licit and illicit substances consumed by the nursing mother might be excreted in breast milk, which may cause potential short and long term harmful effects for the breastfed infant. The extraction of substances from this matrix represents an analytical challenge due to its high protein and ...detailed

NORCOCAINE (cas 18717-72-1) in human hair as a biomarker of heavy cocaine use in a high risk population09/24/2019

In hair analysis, cocaine (COC) and its metabolites have been studied relatively extensively with a consistent focus of distinguishing active drug use and excluding external contamination. Although quantitative cut-offs using major metabolite, benzolecgonine (BE), in hair have been proposed to d...detailed

Relevant articles and documents

Catalyzation of cocaine N-demethylation by cytochromes P4502B, P4503A, and P4502D in fish liver

Cocaine N-demethylation by microsomal cytochrome P450s is the principal pathway in cocaine bioactivation and hepatotoxicity. P450 isozymes involved in N-demethylation of cocaine have not been elucidated yet and they differ from species to species. In humans and mice, P4503A contributes to cocaine N-demethylase activity, whereas in rats, both P4503A and P4502B participate. In the present study, contribution of different P450 isozymes to cocaine N-demethylase activity was studied in vitro with fish liver microsomes. The specific cocaine N-demethylase activity was found to be 0.672 ± 0.22 nmol formaldehyde formed/min/mg protein (mean ± SD, n = 6). Cocaine N-demethylase exhibited biphasic kinetics, and from the Lineweaver-Burk plot, two Km values were calculated as 0.085 and 0.205 mM for the high- and low-affinity enzyme. These results indicate that N-demethylation of cocaine in mullet liver microsomes is catalyzed by at least two cytochrome P450 isozymes. Inhibitory effects of cytochrome P450 isozyme-selective chemical inhibitors, ketoconazole, cimetidine, SKF-525A, and quinidine, on cocaine N-demethylase activity were studied at 50, 100, and 500 μM concentrations of these inhibitors. At 100 μM final concentrations, ketoconazole (P4503A inhibitor), SKF-525A (inhibitor of both P4502B and P4503A), and cimetidine (P4503A inhibitor) inhibited N-demethylation activity by 73, 69, and 63%, respectively. Quinidine, P4502D-specific inhibitor, at 100 μM final concentration, reduced N-demethylation activity down to 64%. Aniline, a model substrate for P4502E1, did not alter N-demethylase activity in the final concentration of 100 μM. IC50 values were calculated to be 20 μM for ketoconazole, 48 μM for cimetidine (both specific P4503A inhibitors), 164 μM for quinidine (P4502D inhibitor), and 59 μM for SKF-525A (inhibitor of both P4503A and P4502B). The contribution of P4502B to cocaine N-demethylase activity in mullet liver microsomes was further explored by the use of purified mullet cytochrome P4502B in the reconstituted system containing purified mullet P450 reductase and lipid. The turnover number was calculated as 4.2 nmol HCOH/(min nmol P450). Overall, these results show that P4503A and P4502B are the major P450s responsible for N-demethylation of cocaine, whereas contribution of P4502D is a minor one, and P4502E1 is not involved in the N-demethylation of cocaine in mullet liver microsomes.

NOVEL COCAINE HAPTENS AND NANOFIBER-BASED COCAINE VACCINES

Certain embodiments are directed to chemically defined self-adjuvanting cocaine vaccines composed of novel cocaine haptens and self-assembling peptide domains.

Induction of protective and specific antibodies against cocaine by intranasal immunisation using a glyceride adjuvant

The goal of this study was to investigate an intranasal cocaine vaccine containing the mucosal adjuvant macrogol-6-glycerol capylocaprate (RhinoVax). Cocaine-KLH conjugate was prepared and administered in two formulations. Ten mice were immunised intranasally using RhinoVax as adjuvant and ten subcutaneously using aluminium hydroxide as an adjuvant. A negative control group (n=10) received unconjugated KLH with RhinoVax intranasally. Specific cocaine antibodies in serum were measured following primary and booster immunisation. Relative antibody responses in serum indicated that the immunisation was successful. Animals were then challenged with cocaine either intranasally or intraperitoneally with subsequent measurement of drug distribution into the serum, brain and olfactory bulb. The cocaine-immunised groups revealed significantly lower cocaine levels in the brain compared to the negative control group. The inhibition of cocaine distribution to the brain in the intranasal immunised group was comparable to that of the subcutaneous immunised group. This was unexpected because the cocaine specific antibody levels in serum were fivefold lower in the intranasal immunised group. However, the presence of mucosal cocaine specific antibodies after intranasal immunisation could play an important role in hindering direct access of cocaine into the brain via the olfactory bulb.