60072-40-4

Basic information

• Product Name: 2-acetylnaphthalen-1-yl pyridine-3-carboxylate
• Synonyms: 3-Pyridinecarboxylic acid, 2-acetyl-1-naphthalenyl ester
• CAS NO: 60072-40-4
• Molecular Formula: C₁₈H₁₃NO₃
• Molecular Weight: 291.3007
• Mol File: 60072-40-4.mol
• Article Data: 5

Chemical Properties

• Boiling Point: 533.4°C at 760 mmHg
• Flash Point: 276.4°C
• Density: 1.257g/cm³
• Vapor Pressure: 1.86E-11mmHg at 25°C
• Refractive Index: 1.643
• CAS DataBase Reference: 2-acetylnaphthalen-1-yl pyridine-3-carboxylate(CAS DataBase Reference)
• NIST Chemistry Reference: 2-acetylnaphthalen-1-yl pyridine-3-carboxylate(60072-40-4)
• EPA Substance Registry System: 2-acetylnaphthalen-1-yl pyridine-3-carboxylate(60072-40-4)

Safety Data

• Hazardous Substances Data: 60072-40-4(Hazardous Substances Data)

Usage

Properties

1. Synthetic cannabinoid
2. Acts on cannabinoid receptors in the brain and nervous system
3. Potent agonist of CB1 and CB2 receptors
4. Produces effects similar to THC
5. Commonly used as a recreational drug
6. Marketed as a legal alternative to marijuana
7. Classified as a controlled substance in many countries
8. Associated with addiction, dependence, and adverse health outcomes

Specific content

1. Name: 2-acetylnaphthalen-1-yl pyridine-3-carboxylate (JWH-018)
2. Action: Acts on cannabinoid receptors in the brain and nervous system
3. Effects: Euphoria, relaxation, altered perception, increased heart rate
4. Usage: Commonly used as a recreational drug
5. Marketed as: Legal alternative to marijuana
6. Classification: Controlled substance in many countries
7. Health effects: Long-term effects not well understood, associated with addiction, dependence, adverse mental and physical health outcomes

Upstream product

• 10400-19-8 3-pyridinecarbonyl chloride 
• 711-79-5 1-hydroxy-2-acetonaphthone 
• 90-15-3 α-naphthol 
• 59-67-6 nicotinic acid 
• 830-81-9 1-naphthyl acetate 
• 20260-53-1 pyridine-3-carbonyl chloride hydrochloride 

Downstream Products

• 1939-53-3 UCCF-279 

Relevant articles and documents

Synthesis and structure-activity relationship studies of α-naphthoflavone derivatives as CYP1B1 inhibitors

Cytochrome P450 1B1(CYP1B1) has been recognized as an important target for cancer prevention and drug resistance reversal. In order to obtain potent and selective CYP1B1 inhibitors, a series of forty-one α-naphthoflavone (ANF) derivatives were synthesized, characterized, and evaluated for CYP1B1, CYP1A1 and CYP1A2 inhibitory activities. A closure look into the structure-activity relationship for the inhibitory effects on CYP1B1 indicated that modification of the C ring of ANF would decrease the CYP1B1 inhibitory potency, while incorporation of substituent(s) into the different positions of the B ring yielded analogues with varying CYP1B1 inhibitory capacity. Among these derivatives, compounds 9e and 9j were identified as the most potent two selective CYP1B1 inhibitors with IC50 values of 0.49 and 0.52 nM, respectively, which were 10-fold more potent than the lead compound ANF. In addition, molecular docking and a reasonable 3D-QSAR (three-dimensional quantitative structure-activity relationship) study were performed to provide a better understanding of the key structural features influencing the CYP1B1 inhibitory activity. The results achieved in this study would lay a foundation for future development of selective, potent, low-toxic and water-soluble CYP1B1 inhibitors.

Benzoflavone activators of the cystic fibrosis transmembrane conductance regulator: Towards a pharmacophore model for the nucleotide-binding domain

Our previous screen of flavones and related heterocycles for the ability to activate the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel indicated that UCCF-029, a 7,8-benzoflavone, was a potent activator. In the present study, we describe the synthesis and evaluation, using cell-based assays, of a series of benzoflavone analogues to examine structure-activity relationships and to identify compounds having greater potency for activation of both wild type CFTR and a mutant CFTR (G551D-CFTR) that causes cystic fibrosis in some human subjects. Using UCCF-029 as a structural guide, a panel of 77 flavonoid analogues was prepared. Analysis of the panel in FRT cells indicated that benzannulation of the flavone A-ring at the 7,8-position greatly improved compound activity and potency for several flavonoids. Incorporation of a B-ring pyridyl nitrogen either at the 3- or 4-position also elevated CFTR activity, but the influence of this structural modification was not as uniform as the influence of benzannulation. The most potent new analogue, UCCF-339, activated wild-type CFTR with a Kd of 1.7 μM, which is more active than the previous most potent flavonoid activator of CFTR, apigenin. Several compounds in the benzoflavone panel also activated G551D-CFTR, but none were as active as apigenin. Pharmacophore modeling suggests a common binding mode for the flavones and other known CFTR activators at one of the nucleotide-binding sites, allowing for the rational development of more potent flavone analogues.

Synthesis of some 1,5 benzodiazepines. II

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