HuagongsheHuagongshe Chemie-Druckbericht · Nur für Forschungszwecke
9,10-Phenanthrenchinon
Phenanthrene-9,10-dione · 9,10-PHENANTHRENEQUINONE · PHENANTHRENE-9,10-QUINONE · 9,10-PHENANTHRAQUINONE · 9,10-PHENANTHRENEDIONE · PHENANTHRAQUINONE · Phenanthroquinone · 9,10-phenanthroquinone
Identifikatoren & physikalische Daten
| CAS No. | 84-11-7 |
|---|---|
| Summenformel | C14H8O2 |
| Durchschnittliche Molmasse | 208,21 g/mol |
| Monoisotopische Masse | 208,05242949 g/mol |
| SMILES | O=C1C(=O)c2ccccc2-c2ccccc21 |
| InChIKey | YYVYAPXYZVYDHN-UHFFFAOYSA-N |
| PubChem CID | 6763 |
| ChEMBL | CHEMBL51931 |
| ChEBI | CHEBI:37454 |
| EC No. | 201-515-5 |
| DTXSID | DTXSID3058901 |
| Lokaler Name | 9,10-Phenanthrenchinon |
Chemische & physikalische Eigenschaften
| XLogP | 2,5 |
|---|---|
| Polarare Oberfläche (TPSA) | 34,1 |
| H-Brücken-Donoren | 0 |
| H-Brücken-Akzeptoren | 2 |
| Frei drehbare Bindungen | 0 |
| Schwere Atome | 16 |
| Formalladung | 0 |
| Komplexität | 289 |
| LogP (Verteilungskoeffizient) | log Kow = 2.52 |
| Dichte | 1.405 g/cu cm at 22 °C |
| Color/Form | Orange-red crystalsOrange needles, orange-red plates |
| Löslichkeit | Solubility in water: 0.4 mg/mLSolubility in ethanol: 1 mg/mLsolubility in ethylene glycol methyl ether: 7 mg/mLSoluble in benzene, ether, glacial acetic acid, hot alcoholSoluble in sulfuric acid7.5mg/lInsoluble in water. |
| Siedepunkt | About 360 °C |
| Schmelzpunkt | 206-207 °C209-212 °C(lit.) |
| Dampfdruck | 0.00000002 [mmHg] |
| Physical Description | Orange-red solid[Merck Index] Powder[Alfa Aesar MSDS] |
| Kovats Retention Index | 1935362.04360.3362.7 |
| Other Experimental Properties | Sublimes above 360 °CWith concentrated sulfuric acid gives a dark green colorCyclohexane/water partition coefficient: 1.39 (log) |
| Brechungsindex | 1.5681 (estimate) |
| Flammpunkt | 245 °C |
| Lagerbedingungen | Store below +30°C. |
| Aggregatzustand | Powder |
| Farbe | Orange-brownish |
| Merck | 14,7213 |
| BRN | 608838 |
| Henry-Konstante | 3.7×103 mol/(m3Pa) at 25℃, HSDB (2015) |
| Stabilität | Stable. Incompatible with strong oxidizing agents. |
| InChI | 1S/C14H8O2/c15-13-11-7-3-1-5-9(11)10-6-2-4-8-12(10)14(13)16/h1-8H |
| InChIKey | YYVYAPXYZVYDHN-UHFFFAOYSA-N |
| SMILES | O=C1C(=O)c2ccccc2-c3ccccc13 |
| CAS Datenbank | 84-11-7(CAS DataBase Reference) |
| NIST chemische Informationen | 9,10-Phenanthroquinone(84-11-7) |
| EPA chemische Informationen | 9,10-Phenanthrenedione (84-11-7) |
Sicherheit & Vorschriften
| GHS-Einstufung | WarningH315 (96.7%): Causes skin irritation [Warning Skin corrosion/irritation]H319 (100%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]H335 (27%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposureRespiratory tract irritation]P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 152 reports by companies from 8 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website. |
|---|---|
| Regulatorische Informationen | Chemical: 9,10-Phenanthrenedione9,10-Phenanthrenequinone: Does not have an individual approval but may be used under an appropriate group standard |
| Gefahrenübersicht | Emergency treatment: Polynuclear aromatic hydrocarbonsAcute toxicity of PAHs is lowPAHs may cause photosensitivity and may cause cancer after chronic exposure[HSDB] No evidence of teratogenicity in miceNo information available on effects to human reproduction or lactation[REPROTOX] Causes other changes in respiration and effect on inflammation in acute intratracheal study of mice[RTECS] An irritant[Alfa Aesar MSDS] See POLYCYCLIC AROMATIC HYDROCARBONS. |
| Toxic Combustion Products | When heated to decomposition, emits acrid smoke and fumes. |
| Hazard Classes and Categories | Skin Irrit. 2 (96.7%)Eye Irrit. 2A (100%)STOT SE 3 (27%) |
| Entsorgungsverfahren | SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air qualitypotential migration in soil or watereffects on animal and plant lifeand conformance with environmental and public health regulations. |
| Umweltverhalten | TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 28(SRC), determined from a structure estimation method(2), indicates that 9,10-phenanthrenedione is expected to have very high mobility in soil(SRC). Volatilization of 9,10-phenanthrenedione from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.7X10-9 atm-cu m/mole(SRC), using a fragment constant estimation method(2). 9,10-Phenanthrenedione is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 8.5X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). One biodegradation study found 9,10-phenanthrenedione resistant to biodegradation(3).AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 28(SRC), determined from a structure estimation method(2), indicates that 9,10-phenanthrenedione is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 2.7X10-9 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). According to a classification scheme(4), an estimated BCF of 21(SRC), from its log Kow of 2.52(5), suggests the potential for bioconcentration in aquatic organisms is low(SRC). 9,10-Phenanthrenedione is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). 9,10-Phenanthrenedione absorbs UV light strongly at wavelengths >290 nm(6) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). One biodegradation study found 9,10-phenanthrenedione resistant to biodegradation(7).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 9,10-phenanthrenedione, which has an estimated vapor pressure of 8.5X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(2),will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase 9,10-phenanthrenedione is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC)the half-life for this reaction in air is estimated to be 2.6 days(SRC), calculated from its rate constant of 6.2X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Particulate-phase 9,10-phenanthrenedione may be removed from the air by wet and dry deposition(SRC). 9,10-Phenanthrenedione absorbs UV light strongly at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). |
| Soil Adsorption/Mobility | Using a structure estimation method based on molecular connectivity indices(1), the Koc of 9,10-phenanthrenedione can be estimated to be 28(SRC). According to a classification scheme(2), this estimated Koc value suggests that 9,10-phenanthrenedione is expected to have very high mobility in soil. |
| Natural Pollution Sources | 9,10-Phenanthrenedione has been identified as a biodegradation metabolite of phenanthrene in soil(1). |
| Atmospheric Concentrations | URBAN/SUBURBAN: 9,10-Phenanthrenedione was detected particulate matter of air samples collected from Kenmore Station, Boston MA in the summer of 1994 at a concentration of 0.427 ng/cu m(1). Mean 9,10-phenanthrenedione concentrations of 1.1 and 0.31 ng/cu m were detected in ambient air samples collected in Fresno CA in the winter (2004-2005) and summer (2005), respectively(2). |
| Human Toxicity Excerpts | /ALTERNATIVE and IN VITRO TESTS/ The trophoblast cell line, JEG-3, was used to study the cytotoxicity of phenanthrene, 9,10-phenanthrenequinone (PHEQ), anthracene, and 9,10-anthracenedione alone and with copper. The endpoints were the capacity of cultures to reduce alamar Blue (AB), a measure of energy metabolism, and to convert carboxyfluorescein diacetate acetoxymethyl ester (CFDA AM) to carboxyfluorescein, an indication of membrane integrity. Only PHEQ elicited a cytotoxic response. PHEQ caused a concentration-dependent decline in AB but not in CFDA AM readings, suggesting an impairment to energy metabolism. In the presence of copper, PHEQ concentration-response curves were shifted to the left for AB and were obtained with CFDA AM. The Cu/PHEQ synergy is attributed to an increase in redox cycling and production of reactive oxygen species (ROS), which overwhelm antioxidant defenses, damaging energy metabolism first and then membrane integrity. The impermeable copper chelator, bathocuproine, reduced the PHEQ/copper interaction, but the permeable chelator, neocuproine, and copper together were cytotoxic./ALTERNATIVE and IN VITRO TESTS/ A typical antioxidant, N-acetyl-L-cysteine (NAC) generally protects cells from oxidative damage induced by reactive oxygen species (ROS). 9,10-Phenanthrenequinone (9,10-PQ), a major quinone in diesel exhaust particles, produces ROS in redox cycling following two-electron reduction by NAD(P)H:quinone oxidoreductase 1 (NQO1), which has been considered as a cause of its cyto- and genotoxicity. In this study, we show that NAC unexpectedly augments the toxicity of 9,10-PQ in cells with low NQO1 activity. In four human skin cell lines, the expression and the activity of NQO1 were lower than in human adenocarcinoma cell lines, A549 and MCF7. In the skin cells, the cytotoxicity of 9,10-PQ was significantly enhanced by addition of NAC. The formation of DNA double strand breaks accompanying phosphorylation of histone H2AX, was also remarkably augmented. On the other hand, the cyto- and genotoxicity were suppressed by addition of NAC in the adenocarcinoma cells. Two contrasting experiments: overexpression of NQO1 in CHO-K1 cells which originally expressed low NQO1 levels, and knock-down of NQO1 in the adenocarcinoma cell line A549 by transfection of RNAi, also showed that NAC suppressed 9,10-PQ-induced toxicity in cell lines expressing high NQO1 activity and enhanced it in cell lines with low NQO1 activity. The results suggested that dual effects of NAC on the cyto- and genotoxicity of 9,10-PQ were dependent on tissue-specific NQO1 activity./ALTERNATIVE and IN VITRO TESTS/ Persistent inhalation of diesel exhaust particles results in damaged lung cells through formation of reactive oxygen species (ROS), but the details of the toxicity mechanism against monocytes are poorly understood. In this study, we used human promyelomonocytic U937 cells as surrogates of monocytes and investigated the toxicity mechanism initiated by exposure to 9,10-phenanthrenequinone (9,10-PQ), a major quinone component in diesel exhaust particles. A 24-hr incubation with 9,10-PQ provoked apoptotic cell death, which was due to signaling through the enhanced ROS generation and concomitant caspase activation. Flow cytometric analyses of U937 cells after long-term exposure to 9,10-PQ revealed induction of differentiation that was evidenced by increasing expression of CD11b/CD18, a cell-surface marker for monocytic differentiation into macrophages. The 9,10-PQ-induced differentiation was significantly abolished by ROS inhibitors, suggesting that ROS generation contributes to cell differentiation. The 9,10-PQ treatment increased the expression of aldo-keto reductase (AKR) 1C3, which reached a peak at 1 to 2 day post-treatment and then declined. The bell-shaped curve of the AKR1C3 expression by 9,10-PQ resembled that caused by phorbol 12-myristate 13-acetate, a differentiation inducer. Additionally, the concomitant treatment with tolfenamic acid, a selective AKR1C3 inhibitor, sensitized the differentiation induced by 9,10-PQ. These results suggest that ROS formation during 9,10-PQ treatment acutely leads to apoptosis of U937 cells and the initiation of monocytic differentiation, which proceeds after the provisional overexpression of AKR1C3./ALTERNATIVE and IN VITRO TESTS/ 9,10-Phenanthrenequinone (9,10-PQ), a major component in diesel exhaust particles, is suggested to generate reactive oxygen species (ROS) through its redox cycling, leading to cell toxicity. l-Xylulose reductase (XR), a NADPH-dependent enzyme in the uronate pathway, strongly reduces alpha-dicarbonyl compounds and was thought to act as a detoxification enzyme against reactive carbonyl compounds. Here, we have investigated the role of intracellular ROS generation in apoptotic signaling in human acute T-lymphoblastic leukemia MOLT-4 cells treated with 9,10-PQ and the role of XR in the generation of ROS. Treatment with 9,10-PQ elicited not only apoptotic signaling, including mitochondrial membrane dysfunction and activation of caspases and poly(ADP-ribose) polymerase, but also intracellular ROS generation and consequent glutathione depletion. The apoptotic effects of 9,10-PQ were drastically mitigated by pretreatment with intracellular ROS scavengers, such as N-acetyl-l-cysteine, glutathione monoethyl ester, and polyethylene glycol-conjugated catalase, indicating that intracellular ROS generation is responsible for the 9,10-PQ-evoked apoptosis. Surprisingly, the ROS generation and cytotoxicity by 9,10-PQ were augmented in an XR-transformed cell line. XR indeed reduced 9,10-PQ and produced superoxide anion through redox cycling. In addition, the expression levels of XR and its mRNA in the T lymphoma cells were markedly enhanced after the exposure to 9,10-PQ, and the induction was completely abolished by the ROS scavengers. Moreover, the 9,10-PQ-induced apoptosis was partially inhibited by the pretreatment with XR-specific inhibitors. These results suggest that initially produced ROS induce XR, which accelerates the generation of ROS. |
| Artificial Pollution Sources | 9,10-Phenanthrenedione's production and use as an intermediate in the production of dyes, herbicides, plant growth regulators, fungicides and pharmaceuticals and in UV-curable coatings and adhesives(1,2) may result in its release to the environment through various waste streams(SRC). The atmospheric gas-phase reaction of phenanthrene with OH and NO3 radicals may be a major source of 9,10-phenanthrenedione found in the ambient atmosphere(3). 9,10-Phenanthrenedione has been identified as a biodegradation metabolite of phenanthrene in soil(4). 9,10-Phenanthrenedione is emitted in the particulate emissions from diesel exhaust(4). |
| Environmental Biodegradation | AEROBIC: 9,10-Phenanthrenedione was detected as a metabolite from the biodegradation of phenanthrene in soil(1). In biodegradation tests using either non-polluted garden soil or activated sludge as inoculum, and 15-60 day incubation periods, 9,10-phenanthrenedione was resistant to degradation with a 0% CO2 evolution and virtually no theoretical BOD(2). |
| Sediment/Soil Concentrations | SOIL: 9,10-Phenanthrenedione was detected at a concentration of 17.0 ug/g soil in contaminated soil samples collected from a former gas work site in Stockholm, Sweden(1). |
| Environmental Bioconcentration | An estimated BCF of 21 was calculated in fish for 9,10-phenanthrenedione(SRC), using a log Kow of 2.52(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC). |
| Volatilization from Water/Soil | The Henry's Law constant for 9,10-phenanthrenedione is estimated as 2.7X10-9 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that 9,10-phenanthrenedione is expected to be essentially nonvolatile from water surfaces(2). 9,10-Phenanthrenedione's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). 9,10-Phenanthrenedione is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 8.5X10-7 mm Hg(SRC), determined from a fragment constant method(1). |
| Non-Human Toxicity Excerpts | /LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A series of naphthalene diols, quinones, and related compounds were examined for their ability to inhibit mixed-function oxidase in liver microsomes obtained from rats which had been pretreated with 3-methylcholanthrene (3-Mc) or phenobarbital (PB). Using benzo(a)pyrene monooxygenase as a measure of mixed-function oxidase activity, it was found that phenanthrene-9, 10-quinone was the most active compound tested with a K1 = 0.79 uM. Phenanthrene-9, 10-quinone did not affect cytochrome c reductase but did inhibit aminopyrine N-demethylase and p-nitroanisole-O-demethylase in both 3-MC and PB-induced microsome with almost identical inhibition constants. 1,2-Naphthoquinone exerted similar effects as phenanthrene-9,10-quinone on cytochrome c reductase, aminopyrine N-demethylase and p-nitroanisole-O-demethylase. Both quinones stimulated NADPH oxidase activity but the extent of this stimulation did not explain their inhibition of microsomal oxidation. Kinetic studies using benzo(a)-pyrene monooxygenase with phenanthrene-9, 10-quinone and 1,2-naphthoquinone indicated that they were noncompetitive with benzo(a)pyrene and mixed noncompetitive with NADPH. Both of these quinones inhibited benzo(a)pyrene induced oncogenic transformation in C3H10T1/2CL8 cells in culture in a dose response manner, presumably by inhibition of the cellular microsomal enzyme which activate benzo(a)pyrene. Phenanthrene-9, 10-quinone and 1,2-naphthoquinone seem to inhibit microsomal oxidative processes by interaction at the level of cytochrome P-450 possibly with a cytochrome P-450-substrate-oxygen complex./GENOTOXICITY/ The estimated cancer risk from diesel exhaust particles (DEP) in the air is approximately 70% of the cancer risk from all air pollutants. DEP is comprised of a complex mixture of chemicals whose carcinogenic potential has not been adequately assessed. The polycyclic aromatic hydrocarbon quinone 9,10-phenanthrenequinone (9,10 PQ) is a major component of DEP and a suspect genotoxic agent for DEP induced DNA damage. 9,10 PQ undergoes redox cycling to produce reactive oxygen species that can lead to oxidative DNA damage. /The authors/ used two systems in the yeast Saccharomyces cerevisiae to examine possible differential genotoxicity of 9,10 PQ. The DEL assay measures intra-chromosomal homologous recombination leading to DNA deletions and the CAN assay measures forward mutations leading to canavanine resistance. Cells were exposed to 9,10 PQ aerobically and anaerobically followed by DNA damage assessment. The results indicate that 9,10 PQ induces DNA deletions and point mutations in the presence of oxygen while exhibiting negligible effects anaerobically. In contrast to the cytotoxicity observed aerobically, the anaerobic effects of 9,10 PQ seem to be cytostatic in nature, reducing growth without affecting cell viability. Thus, 9,10 PQ requires oxygen for genotoxicity while different toxicities exhibited aerobically and anaerobically suggest multiple mechanisms of action./GENOTOXICITY/ Phenanthrene and 9 K-region derivatives, most of them potential metabolites of phenanthrene, were tested for mutagenicity by the reversion of histidine-dependent Salmonella typhimurium TA1535, TA1537, TA1538, TA98 and TA100 and the rec assay with Bacillus subtilis H17 and M45. The strongest mutagenic effects in the reversion assay were observed with phenanthrene 9,10-oxide, 9-hydroxyphenanthrene and N-benzyl-phenanthrene-9,10-imine. Interestingly, the mutagenic potency of the arene imine was similar to that of the corresponding arene oxide. This is the first report on the mutagenicity of arene imine. The mutagenic effects of all these phenanthrene derivatives were much weaker than that of the positive control benzo[a]pyrene 4,5-oxide. Even weaker mutagenicity was found with cis-9,10-dihydroxy-9,10-dihydrophenanthrene and with trans-9,10-dihydroxy-9-10-dihydrophenanthrene. The other derivatives were inactive in this test. However, 9-10-dihydroxyphenanthrene and 9,10-phenanthrenequinone were more toxic to the rec- B. subtilis M45 strain than to the rec+ H17 strain. This was also true for phenanthrene 9,10-oxide and 9-hydroxyphenanthrene, but not with the other test compounds that reverted (9,10-dihydroxy-9,10-dihydrophenanthrenesN-benzyl-phenanthrene 9,10-iminebenzo[a]pyrene 4,5-oxide) or did not revert (phenanthrene, 9,10-bis-(p-chlorophenyl)-phenanthrene 9,10-oxide, 9-10-diacetoxyphenanthrene) the Salmonella tester strains. Although the K region is a main site of metabolism and although all potential K-region metabolites were mutagenic, phenanthrene did not show a mutagenic effect in the presence of mouse-liver microsomes and an NADPH-generating system under standard conditions. However, when epoxide hydratase was inhibited, phenanthrene was activated to a mutagen that reverted his- S. typhimurium. This shows that demonstration of the mutagenic activity of metabolites together with the knowledge that a major metabolic route proceeds via these meta/GENOTOXICITY/ The metabolic pathway by which 9,10-phenanthrenequinone caused mutagenicity was investigated in Salmonella typhimurium TA104 tester strain as were the detoxification pathways. The two electron reduction of the quinone by NAD(P)H-quinone oxidoreductase was not mutagenic, whereas the 1 electron reduction, catalyzed by NADPH cytochrome p450 reductase was mutagenic. Mutagenicity via this pathway was attributable to the generation of oxygen radicals. Cytochrome p450 monooxygenase also played a significant role in the detoxification of this quinone. Phenanthrenequinone was converted to a nonmutagenic metabolite in a cytochrome p450 dependent reaction.For more Non-Human Toxicity Excerpts (Complete) data for 9,10-PHENANTHRENEDIONE (6 total), please visit the HSDB record page. |
| Environmental Abiotic Degradation | The rate constant for the vapor-phase reaction of 9,10-phenanthrenedione with photochemically-produced hydroxyl radicals has been estimated as 6.2X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 2.6 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). 9,10-Phenanthrenedione absorbs UV light strongly at wavelengths >290 nm(2) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). 9,10-Phenanthrenedione is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). |
| Wassergefährdungsklasse (WGK) | 3 |
| TSCA-Inventar-Status | TSCA listed |
| UN-Transportnummer | UN3077 |
| Zollcode | 29146990 |
| RTECS-Nr. | SF7875000 |
| R-Sätze (R) | 36/37/38 |
| Toxizität | LD50 orally in Rabbit: > 16000 mg/kg |
| Gefahrensymbole | Xi |
| Sicherheitshinweise (S) | 26-36-24/25-22 |
| Gefahrenklasse | 9Aquatic Acute 1Eye Irrit. 2 |
| Verpackungsgruppe | III |
| Lagerklasse | 11 - Combustible Solids |
| Gefahrstoffdaten | 84-11-7(Hazardous Substances Data) |
| Selbstentzündungstemperatur | 630 °C DIN 51794 |
Anwendungen & Verwendung
Beschreibung
Das 9,10-Phenanthrenchinon bildet orangefarbene, wasserunlösliche, leicht oxidable Kristalle. Die Verbindung besitzt nur wissenschaftliches Interesse.
Verwenden
9,10-Phenanthrenequinone is used in the formation of spirophosphoranes containing acyclic 5-methyl-2-phenyl-2H-1,2,3-diazaphosphol-4-yl substituent.