36626-24-1

Basic information

• Product Name: 1,4-Naphthalenedione, 2,3-diphenoxy-
• CAS NO: 36626-24-1
• Molecular Formula: C22H14O4
• Molecular Weight: 342.351
• Mol File: 36626-24-1.mol
• Article Data: 8

Chemical Properties

• CAS DataBase Reference: 1,4-Naphthalenedione, 2,3-diphenoxy-(CAS DataBase Reference)
• NIST Chemistry Reference: 1,4-Naphthalenedione, 2,3-diphenoxy-(36626-24-1)
• EPA Substance Registry System: 1,4-Naphthalenedione, 2,3-diphenoxy-(36626-24-1)

Safety Data

• Hazardous Substances Data: 36626-24-1(Hazardous Substances Data)

Upstream product

• 117-80-6 2,3-Dichloro-1,4-naphthoquinone 
• 139-02-6 sodium phenoxide 
• 130-15-4 [1,4]naphthoquinone 
• 83809-76-1 1-(4-hydroxyphenyl)-5-methyldihydrouracil 
• 1310679-87-8 1-[4-(3-chloro-1,4-dihydro-1,4-dioxonaphthalen-2-yloxy)-phenyl]-5,6-dihydro-5-methylpyrimidine-2,4(1H,3H)-dione 
• 108-95-2 phenol 
• 90-15-3 α-naphthol 
• 100-67-4 potassium phenolate 

Downstream Products

• 1301627-07-5 N-(3-phenoxy-1,4-dioxo-1,4-dihydronaphthalen-2-yl)benzenesulfonamide 
• 102632-13-3 C₃₆H₂₄O₆ 
• 102632-12-2 2,2-Dimethyl-propionic acid 4-(2,2-dimethyl-propionyloxy)-2,3-diphenoxy-naphthalen-1-yl ester 
• 102632-11-1 Propionic acid 2,3-diphenoxy-4-propionyloxy-naphthalen-1-yl ester 
• 102632-10-0 2,3-diphenoxy-1,4-di(methylcarbonyloxy)naphthalene 
• 101605-36-1 2-aziridin-1-yl-3-phenoxy-[1,4]naphthoquinone 

Relevant articles and documents

Structure-activity relationships and colorimetric properties of specific probes for the putative cancer biomarker human arylamine N-acetyltransferase 1

A naphthoquinone inhibitor of human arylamine N-acetyltransferase 1 (hNAT1), a potential cancer biomarker and therapeutic target, has been reported which undergoes a distinctive concomitant color change from red to blue upon binding to the enzyme. Here we describe the use of in silico modeling alongside structure-activity relationship studies to advance the hit compound towards a potential probe to quantify hNAT1 levels in tissues. Derivatives with both a fifty-fold higher potency against hNAT1 and a two-fold greater absorption coefficient compared to the initial hit have been synthesized; these compounds retain specificity for hNAT1 and its murine homologue mNat2 over the isoenzyme hNAT2. A relationship between pKa, inhibitor potency and colorimetric properties has also been uncovered. The high potency of representative examples against hNAT1 in ZR-75-1 cell extracts also paves the way for the development of inhibitors with improved intrinsic sensitivity which could enable detection of hNAT1 in tissue samples and potentially act as tools for elucidating the unknown role hNAT1 plays in ER+ breast cancer; this could in turn lead to a therapeutic use for such inhibitors.

1,4-QUINONES AND THEIR SULFUR ANALOGUES USEFUL AS LIGANDS OF N-ACETYLTRANSFERASES

The invention provides 1,4-quinones, 1,4-naphthoquinones and their sulphur analogues as inhibitors of hNAT1, an enzyme which is both a diagnostic marker and drug target for breast cancer. Some of the compounds of the invention are also chromogenic in the

METHOD FOR TREATING DISEASE STATES IN MAMMALS WITH NAPHTHALENE LIPOXYGENASE-INHIBITTNG AGENTS

Psoriasis in mammals is relieved by topically administering naphthalenes of the formula: wherein: R1 is lower alkoxy or optionally substituted phenoxy, R2 is the same as R1, or R2 is hydrogen, lower alkyl, optionally substituted phenyl or optionally substituted phenylalkyl, R3 is hydrogen, lower alkyl, lower alkoxy, halo, optionally substituted phenyl, optionally substituted phenyl-lower-alkyl or optionally substituted phenyl-lower-alkoxy, and m is 1 or 2; both X groups are the same and X is either -C(O)OR4 or -C(O)NR5R6 , wherein R4 is alkyl, phenyl or benzyl optionally substituted with one or two lower alkyl groups, lower alkoxy groups or halo; and R5 and R6 are independently hydrogen, lower alkyl, cycloalkyl or phenyl optionally substituted with one or two lower alkyl groups, lower alkoxy groups or halo. The compounds of this invention are also useful for the treatment of disease-states caused by lipoxygenase activity in mammals, particularly 5-lipoxygenase activity, when administered systemically.