6985-27-9

Basic information

• Product Name: beta-apo-14'-carotenal
• Synonyms: beta-apo-14'-carotenal;14'-apo-beta-carotenal
• CAS NO: 6985-27-9
• Molecular Formula: C₂₂H₃₀O
• Molecular Weight: 310.473
• Mol File: 6985-27-9.mol
• Article Data: 9

Chemical Properties

• Boiling Point: 457.6°C at 760 mmHg
• Flash Point: 224.5°C
• Appearance: /
• Density: 0.95g/cm³
• Vapor Pressure: 1.47E-08mmHg at 25°C
• Refractive Index: 1.546
• CAS DataBase Reference: beta-apo-14'-carotenal(CAS DataBase Reference)
• NIST Chemistry Reference: beta-apo-14'-carotenal(6985-27-9)
• EPA Substance Registry System: beta-apo-14'-carotenal(6985-27-9)

Safety Data

• Hazardous Substances Data: 6985-27-9(Hazardous Substances Data)

Usage

InChI:InChI=1/C22H30O/c1-18(10-6-7-17-23)11-8-12-19(2)14-15-21-20(3)13-9-16-22(21,4)5/h6-8,10-12,14-15,17H,9,13,16H2,1-5H3/b7-6+,11-8+,15-14+,18-10+,19-12+

Upstream product

• 90819-76-4 11-cis-retinylideneacetaldehyde 
• 1856-68-4 Retinyliden-malonsaeure-mononitril 
• 20638-88-4 9-trans-13-trans-dimethyl-7-(1,1,5-trimethyl-5-cyclohexen-6-yl)-7,9,11,13-nonatetraene-15-nitrile 
• 1856-64-0 2-Cyan-Vitamin-A-saeure 
• 3917-41-7 (2E,4E)-3-methyl-5-(2,6,6-trimethyl-1-cyclohexen-1-yl)-2,4-pentadienal 
• 5299-98-9 (2E,4E)-3-methyl-5-(2,6,6-trimethyl-cyclohex-1-enyl)-penta-2,4-dienenitrile 
• 79-77-6 (E)-β-ionone 
• 7235-40-7 beta-carotene 
• 13979-19-6 ethyl (2E,4E,6E,8E,10E)-5,9-dimethyl-11-(2,6,6-trimethylcyclohexen-1-yl)-2,4,6,8,10-undecapentaenoate 
• 116-31-4 all-trans-Retinal 
• 6980-77-4 Bishomoretinoic acid methyl ester 
• 6985-27-9 13-cis-retinylideneacetaldehyde 
• 1107-26-2 trans-β-apo-8'-carotenal 
• 6985-26-8 (2E,4E,6E,8E,10E)-5,9-dimethyl-11-(2,6,6-trimethylcyclohex-1-en-1-yl)undeca-2,4,6,8,10-pentaene-1-ol 

Downstream Products

• 107655-23-2 9-cis-retinylideneacetaldehyde 
• 6985-27-9 13-cis-retinylideneacetaldehyde 
• 5263-43-4 (E)-2,5-Bis-[(2E,4E,6E,8E,10E)-5,9-dimethyl-11-(2,6,6-trimethyl-cyclohex-1-enyl)-undeca-2,4,6,8,10-pentaen-(Z)-ylidene]-hex-3-enedinitrile 
• 145987-18-4 Butyl-[(2E,4E,6E,8E,10E)-5,9-dimethyl-11-(2,6,6-trimethyl-cyclohex-1-enyl)-undeca-2,4,6,8,10-pentaen-(E)-ylidene]-amine 

Relevant articles and documents

Synthesis of one double bond-inserted retinal analogs and their binding experiments with opsins: Preparation of novel red-shifted channelrhodopsin variants

In optogenetics, red-shifted channelrhodopsins (ChRs) are eagerly sought. We prepared six kinds of new chromophores with one double bond inserted into the polyene side chain of retinal (A1) or 3,4-didehy-droretinal (A2), and examined their binding efficie

Expansion of first-in-class drug candidates that sequester toxic all-trans-retinal and prevent light-induced retinal degeneration

All-trans-retinal, a retinoid metabolite naturally produced upon photoreceptor light activation, is cytotoxic when present at elevated levels in the retina. To lower its toxicity, two experimentally validated methods have been developed involving inhibition of the retinoid cycle and sequestration of excess of all-trans-retinal by drugs containing a primary amine group. We identified the first-in-class drug candidates that transiently sequester this metabolite or slow down its production by inhibiting regeneration of the visual chromophore, 11-cis-retinal. Two enzymes are critical for retinoid recycling in the eye. Lecithin:retinol acyltransferase (LRAT) is the enzyme that traps vitamin A (all-trans-retinol) from the circulation and photoreceptor cells to produce the esterified substrate for retinoid isomerase (RPE65), which converts all-trans-retinyl ester into 11-cis-retinol. Here we investigated retinylamine and its derivatives to assess their inhibitor/substrate specificities for RPE65 and LRAT, mechanisms of action, potency, retention in the eye, and protection against acute light-induced retinal degeneration in mice. We correlated levels of visual cycle inhibition with retinal protective effects and outlined chemical boundaries for LRAT substrates and RPE65 inhibitors to obtain critical insights into therapeutic properties needed for retinal preservation.

Reactions of beta-carotene with cigarette smoke oxidants. Identification of carotenoid oxidation products and evaluation of the prooxidant/antioxidant effect.

Recent intervention trials reported that smokers given dietary beta-carotene supplementation exhibited an increased risk of lung cancer and overall mortality. beta-Carotene has been hypothesized to promote lung carcinogenesis by acting as a prooxidant in the smoke-exposed lung. We have examined the interactions of cigarette smoke with beta-carotene in model systems. Both whole smoke and gas-phase smoke oxidized beta-carotene in toluene to several products, including carbonyl-containing polyene chain cleavage products and beta-carotene epoxides. A major product of the reaction was identified as 4-nitro-beta-carotene, which was formed by nitrogen oxides in smoke. Both cis and all-trans isomers of 4-nitro-beta-carotene were detected. The hypothesis that smoke-driven beta-carotene autoxidation exerts prooxidant effects was tested in a liposome system. Lipid peroxidation in dilinoleoylphosphatidylcholine liposomes exposed to gas-phase smoke was modestly inhibited by the incorporation of 0.1 mol % beta-carotene. Both the lipid soluble antioxidant alpha-tocopherol and the water soluble antioxidant ascorbate were oxidized more slowly by gas-phase smoke exposure in liposomes containing beta-carotene. These data indicate that beta-carotene exerts weak antioxidant effects against smoke-induced oxidative damage in vitro. It is unlikely that a prooxidant effect of beta-carotene occurs under biologically relevant conditions or is responsible for an increased incidence of lung cancer observed in smokers who consume beta-carotene supplements.