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2-HYDROXYESTRADIOL, also known as a metabolite of Estradiol, is a 2-hydroxy steroid that consists of 17beta-estradiol with an additional hydroxy group at position 2. It is characterized by its pale yellow solid appearance and plays a significant role in various biological processes.

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  • 362-05-0 Structure
  • Basic information

    1. Product Name: 2-HYDROXYESTRADIOL
    2. Synonyms: estra-1,3,5(10)-triene-2,3,17-beta-triol;2-HYDROXY 17-BETA-ESTRADIOL;2-HYDROXYESTRADIOL;2,3,17BETA-TRIHYDROXY-1,3,5[10]-ESTRATRIENE;1,3,5(10)-ESTRATRIEN-2,3,17-BETA-TRIOL;1,3,5[10]-ESTRATRIENE-2,3-17BETA-TRIOL;(17b)-Estra-1,3,5(10)-triene-2,3,17-triol;2,3,17b-Trihydroxyestra-1,3,5(10)-triene
    3. CAS NO:362-05-0
    4. Molecular Formula: C18H24O3
    5. Molecular Weight: 288.38
    6. EINECS: N/A
    7. Product Categories: Metabolites & Impurities;Steroids
    8. Mol File: 362-05-0.mol
  • Chemical Properties

    1. Melting Point: 96-104°C
    2. Boiling Point: 370.61°C (rough estimate)
    3. Flash Point: 227.6°C
    4. Appearance: /
    5. Density: 1.1285 (rough estimate)
    6. Vapor Pressure: 4.4E-10mmHg at 25°C
    7. Refractive Index: 1.5000 (estimate)
    8. Storage Temp.: −20°C
    9. Solubility: ≤20mg/ml in ethanol;20mg/ml in DMSO;20mg/ml in dimethyl formamide
    10. CAS DataBase Reference: 2-HYDROXYESTRADIOL(CAS DataBase Reference)
    11. NIST Chemistry Reference: 2-HYDROXYESTRADIOL(362-05-0)
    12. EPA Substance Registry System: 2-HYDROXYESTRADIOL(362-05-0)
  • Safety Data

    1. Hazard Codes: Xn
    2. Statements: 40
    3. Safety Statements: 22-36
    4. WGK Germany: 3
    5. RTECS: KG7675000
    6. HazardClass: N/A
    7. PackingGroup: N/A
    8. Hazardous Substances Data: 362-05-0(Hazardous Substances Data)

362-05-0 Usage

Uses

Used in Pharmaceutical Industry:
2-HYDROXYESTRADIOL is used as a pharmaceutical compound for its potential therapeutic applications. As a metabolite of Estradiol, it may have implications in hormone regulation and could be utilized in the development of treatments for hormone-related conditions.
Used in Research and Development:
In the field of research and development, 2-HYDROXYESTRADIOL serves as an essential compound for studying the effects of Estradiol and its metabolites on various biological systems. This can lead to a better understanding of hormone function and the development of new drugs targeting hormone-related disorders.
Used in Analytical Chemistry:
2-HYDROXYESTRADIOL can be used as a reference compound in analytical chemistry for the development and validation of methods to detect and quantify steroid hormones and their metabolites. This is crucial for monitoring hormone levels in various clinical and environmental samples.
Used in Endocrinology:
In the field of endocrinology, 2-HYDROXYESTRADIOL is used as a research tool to study the role of Estradiol and its metabolites in hormone regulation, reproductive health, and other endocrine functions. This can contribute to the development of targeted therapies for endocrine disorders.
Used in Toxicology:
2-HYDROXYESTRADIOL may also be used in toxicology studies to investigate the potential toxic effects of Estradiol and its metabolites on various organs and systems. This can help in understanding the risks associated with exposure to these compounds and inform safety guidelines.

Biological Activity

2-hydroxyestradiol is an angiogenesis inhibitor via the hif-1a pathway.hif-1a, a basic helix-loop-helix pas domain containing protein, is reported as the master transcriptional regulator of cellular and developmental response to hypoxia.

in vitro

in vitro evidences suggested that most of the cellular effects of 2-hydroxyestradiol were mediated by 2-methoxyestradiol, a metabolite of 2-hydroxyestradiol as an anti-cancer agent acting as an angiogenesis inhibitor via the hif-1a pathway. inhibition of catechol-o-methyltransferase (comt), the enzyme methylating 2-hydroxyestradiol to 2-methoxyestradiol, blocked the ability of 2-hydroxyestradiol to inhibit growth of vascular smooth muscle cells, cardiac fibroblasts, as well as renal mesangial cells. moreover, 2-hydroxyestradiol could inhibit vascular smooth muscle cell growth in cells obtained from wild-type mice but not in cells cultured from comt knockout mice. in contrast to 2ohe, treatment of vascular smooth muscle cells with 2-methoxyestradiol inhibited serum-induced growth of cells from both wild-type and comtknockout mice [1].

in vivo

animal study showed that after administration of 2-hydroxyestradiol, plasma levels of 2-hydroxyestradiol declined extremely rapidly. concomitant with the disappearance of 2-hydroxyestradiol, 2-methoxyestradiol occurred and then declined. after administration of 2-methoxyestradiol, plasma levels of 2meoe declined with a plasma cl of 50 ml min(-1) kg(-1). we could not detect 2-hydroxyestradiol in plasma from rats receiving 2-methoxyestradiol. thus, the authors conclude that the conversion of 2-hydroxyestradiol to 2-methoxyestradiol was so efficient, and the administration of 2-hydroxyestradiol is bioequivalent to administration of 2-methoxyestradiol itself [1].

references

[1] zacharia, l. c.,piché, c.a.,fielding, r.m., et al. 2-hydroxyestradiol is a prodrug of 2-methoxyestradiol. journal of pharmacology and experimental therapeutics 309(3), 1093-1097 (2004).

Check Digit Verification of cas no

The CAS Registry Mumber 362-05-0 includes 6 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 3 digits, 3,6 and 2 respectively; the second part has 2 digits, 0 and 5 respectively.
Calculate Digit Verification of CAS Registry Number 362-05:
(5*3)+(4*6)+(3*2)+(2*0)+(1*5)=50
50 % 10 = 0
So 362-05-0 is a valid CAS Registry Number.
InChI:InChI=1/C18H24O3/c1-18-7-6-11-12(14(18)4-5-17(18)21)3-2-10-8-15(19)16(20)9-13(10)11/h8-9,11-12,14,17,19-21H,2-7H2,1H3/t11-,12+,14-,17-,18-/m0/s1

362-05-0SDS

SAFETY DATA SHEETS

According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 13, 2017

Revision Date: Aug 13, 2017

1.Identification

1.1 GHS Product identifier

Product name 2-hydroxy-17β-estradiol

1.2 Other means of identification

Product number -
Other names 2-Oh-estradiol

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:362-05-0 SDS

362-05-0Relevant articles and documents

Short synthesis of 2-methoxyestradiol and 2-hydroxyestradiol

Kiuru, Paula S.,Waehaelae, Kristiina

, p. 373 - 375 (2003)

The estrogen metabolite 2-methoxyestradiol was synthesized from estradiol bis-THP-ether which was 2-hydroxylated using the superbase LIDAKOR, trimethyl borate, and H2O2, then methylated and deprotected to obtain 2-methoxyestradiol in three steps and 61% yield. 2-Hydroxyestradiol was obtained by deprotecting the 2-hydroxyestradiol bis-THP-ether from the first step.

CYCLODEXTRIN-FACILITATED BIOCONVERSION OF 17β-ESTRADIOL BY A PHENOLOXIDASE FROM MUCUNA PRURIENS CELL CULTURES

Woerdenbag, Herman J.,Pras, Niesko,Frijlink, Henderik W.,Lerk, Coenraad F.,Malingre, Theo M.

, p. 1551 - 1554 (1990)

After complexation with β-cyclodextrin, the phenolic steroid 17β-estradiol could be ortho-hydroxylated into a catechol, mainly 4-hydroxyestradiol, by a phenoloxidase from in vitro grown cells of Mucuna pruriens.By complexation with β-cyclodextrin the solubility of the steroid increased from almost insoluble to 660μM.The bioconversion efficiency after 72 hr increased in the following order: freely suspended cells (0percent), immobilized cells (1percent), cell homogenate (6percent), phenoloxidase preparation (40percent).Mushroom tyrosinase converted 17β-estradiol, as a complex with β-cyclodextrin, solely into 2-hydroxyestradiol, with a maximal yield of 30percentafter 6-8 hr.Uncomplexed 17β-estradiol was not converted at all in any of these systems.

Functional and conformational modulation of human cytochrome P450 1B1 by anionic phospholipids

Jang, Hyun-Hee,Kim, Dong-Hyun,Ahn, Taeho,Yun, Chul-Ho

, p. 143 - 150 (2010)

We investigated the interaction of human P450 1B1 (CYP1B1) with various phospholipid bilayers using the N-terminally deleted (Δ2-4)CYP1B1 and (Δ2-26)CYP1B1 enzymes. Among anionic phospholipids, phosphatidic acid (PA) and cardiolipin specifically increased the catalytic activities, membrane binding affinities, and thermal stabilities of both CYP1B1 proteins when phosphatidylcholine matrix was gradually replaced with these anionic phospholipids. PA- or cardiolipin-dependent changes of CYP1B1 conformation were revealed by altered Trp fluorescence and CD spectra. However, both PA and cardiolipin exerted more significant effects with the (Δ2-4)CYP1B1 than the (Δ2-26)CYP1B1 implying the functional importance of N-terminal region for the interaction with the phospholipid membranes. In contrast, other anionic phospholipids such as phosphatidylserine and the neutral phospholipid phosphatidylethanolamine had no apparent effects on the catalytic activity or conformation of CYP1B1. These data suggest that the chemical and physical properties of membranes influenced by PA or cardiolipin composition are critical for the functional roles of CYP1B1.

Nitidine chloride-induced CYP1 enzyme inhibition and alteration of estradiol metabolism

Mao, Xu,Wang, Jian,Wang, Qian,Yang, Lan,Li, Yilin,Lin, Hao,Peng, Ying,Zheng, Jiang

, p. 919 - 927 (2019)

The cytochrome P450 (P450) 1 family is an important phase I enzyme involved in carcinogen activation. Nitidine chloride (NC) is a pharmacologically active alkaloid with polyaromatic hydrocarbon found in the roots of Zanthoxylum nitidum (Roxb.) DC, a traditional medicinal herb widely used in China. We examined the inhibitory effects of NC on CYP1A1, 1B1, and 1A2. NC significantly inhibited CYP1A1- and 1B1-catalyzed ethoxyresorufin O-deethylation activity (IC50 5 0.28±0.06 and 0.32±0.02 mM, respectively) in a concentration- dependent manner, but only showed slight inhibition of CYP1A2 activity (IC50 > 50 mM). Kinetic analysis revealed that NC competitively inhibited CYP1B1 with a Ki value of 0.47±0.05 mM, whereas NC caused a mixed type of inhibition on CYP1A1 with Ki and KI values of 0.14±0.04 and 0.19±0.09 mM, respectively. The observed enzyme inhibition neither required NADPH nor revealed time dependency. Molecular docking manifested the generation of strong hydrogen-bonding interactions of Ser116 in CYP1A1 and Ser127 in CYP1B1 with methoxy moiety of NC. Additionally, NC-induced alteration of estradiol (E2) metabolism was also investigated in the present study. Hydroxyestradiols, including 2-hydroxyestradiol [(2-OHE2) nontoxic] and 4-hydroxyestradiol [(4-OHE2) genotoxic] generated in recombinant enzyme incubation systems and cultured MCF-7 cells were analyzed, and NC was found to preferentially inhibit the nontoxic 2-hydroxylation activity of E2 mediated by CYP1A1. In conclusion, NCwas a mixed type inhibitor of CYP1A1 and a competitive inhibitor of CYP1B1. The remarkable inhibition on E2 2-hydroxylation might increase the risk of 4- OHE2-induced genotoxicity.

Catalytic activities of tumor-specific human cytochrome P450 CYP2W1 toward endogenous substrates

Zhao, Yan,Wan, Debin,Yang, Jun,Hammock, Bruce D.,De Montellano, Paul R. Ortiz

, p. 771 - 780 (2017/02/10)

CYP2W1 is a recently discovered human cytochrome P450 enzyme with a distinctive tumor-specific expression pattern. We show here that CYP2W1 exhibits tight binding affinities for retinoids, which have lownanomolar binding constants, andmuch poorer binding constants in the micromolar range for four other ligands. CYP2W1 converts alltrans retinoic acid (atRA) to 4-hydroxy atRA and all-Trans retinol to 4-OH all-Trans retinol, and it also oxidizes retinal. The enzyme much less efficiently oxidizes 17b-estradiol to 2-hydroxy-(17b)-estradiol and farnesol to a monohydroxylated product; arachidonic acid is, at best, a negligible substrate. These findings indicate that CYP2W1 probably plays an important role in localized retinoid metabolism that may be intimately linked to its involvement in tumor development.

A methoxyflavonoid, chrysoeriol, selectively inhibits the formation of a carcinogenic estrogen metabolite in MCF-7 breast cancer cells

Takemura, Hitomi,Uchiyama, Harue,Ohura, Takeshi,Sakakibara, Hiroyuki,Kuruto, Ryoko,Amagai, Takashi,Shimoi, Kayoko

experimental part, p. 70 - 76 (2011/02/22)

A 17β-estradiol (E2) is hydrolyzed to 2-hydroxy-E2 (2-OHE2) and 4-hydroxy-E2 (4-OHE2) via cytochrome P450 (CYP) 1A1 and 1B1, respectively. In estrogen target tissues including the mammary gland, ovaries, and uterus, CYP1B1 is highly expressed, and 4-OHE2 is predominantly formed in cancerous tissues. In this study, we investigated the inhibitory effects of chrysoeriol (luteorin-3′-methoxy ether), which is a natural methoxyflavonoid, against activity of CYP1A1 and 1B1 using in vitro and cultured cell techniques. Chrysoeriol selectively inhibited human recombinant CYP1B1-mediated 7-ethoxyresorufin-O-deethylation (EROD) activity 5-fold more than that of CYP1A1-mediated activity in a competitive manner. Additionally, chrysoeriol inhibited E2 hydroxylation was catalyzed by CYP1B1, but not by CYP1A1. Methylation of 4-OHE2, which is thought to be a detoxification process, was not affected by the presence of chrysoeriol. In human breast cancer MCF-7 cells, chrysoeriol did not affect the gene expression of CYP1A1 and 1B1, but significantly inhibited the formation of 4-methoxy E2 without any effects on the formation of 2-methoxy E2. In conclusion, we present the first report to show that chrysoeriol is a chemopreventive natural ingredient that can selectively inhibit CYP1B1 activity and prevent the formation of carcinogenic 4-OHE2 from E2..

An expedient one-pot entry to catecholestrogens and other catechol compounds via IBX-mediated phenolic oxygenation

Pezzella, Alessandro,Lista, Liliana,Napolitano, Alessandra,D'Ischia, Marco

, p. 3541 - 3544 (2007/10/03)

A one-pot procedure for the preparation of catecholestrogens in over 90% yield is reported, involving oxygenation of 17β-estradiol or estrone with o-iodoxybenzoic acid (IBX) followed by reduction with methanolic NaBH 4. The procedure, which was extended to the o-hydroxylation of a number of representative phenols in good-to-high yields, expands significantly the scope of phenolic oxidation mediated by IBX.

Synthesis of the catechols of natural and synthetic estrogens by using 2-iodoxybenzoic acid (IBX) as the oxidizing agent

Saeed, Muhammad,Zahid, Muhammad,Rogan, Eleanor,Cavalieri, Ercole

, p. 173 - 178 (2007/10/03)

A method for the synthesis of 2-hydroxyestrone/estradiol, 4-hydroxyestrone/estradiol, 3′-hydroxydiethylstilbestrol, 3′-hydroxyhexestrol, and 3′-hydroxydienestrol is reported, in which 2-iodoxybenzoic acid (IBX) and the corresponding phenolic estrogen are reacted. Treatment of the natural estrogens, estrone/estradiol, with stoichiometric amounts of IBX in dimethylformamide initially yielded a mixture of estrone/estradiol-2,3- and -3,4-quinones, which were reduced in situ to the corresponding catechols by treatment with a 1 M aqueous solution of ascorbic acid. Chromatographic separation of the reaction products afforded 2- and 4-hydroxyestrone/estradiol in good overall yields (79%). In the case of the synthetic estrogens containing two identical phenolic rings, protection of one ring is a prerequisite for the synthesis of the monocatechol. Thus, diethylstilbestrol and dienestrol were protected at one phenol ring as their methyl ethers. The resulting monophenols were treated with stoichiometric amounts of IBX for 1 h, followed by treatment with 1 M aqueous ascorbic acid to obtain the corresponding catechols in more than 70% yield. Furthermore, the catechol of diethylstilbestrol, protected at one ring, was reduced by catalytic hydrogenation at the C3-C4 double bond to obtain 3′-hydroxyhexestrol in 90% yield. Removal of the protected methoxy groups of the synthetic estrogen catechols was carried out by treatment with a 1 M solution of boron tribromide in dichloromethane. This method is highly efficient for the preparative scale synthesis of catechols of both natural and synthetic estrogens.

Roles of cytochromes P450 1A2 and 3A4 in the oxidation of estradiol and estrone in human liver microsomes

Yamazaki, Hiroshi,Shaw, Peter M.,Guengerich, F. Peter,Shimada, Tsutomu

, p. 659 - 665 (2007/10/03)

Of seven cDNA-expressed human cytochrome P450 (P450) enzymes (P450s 1A2, 2B6, 2C9, 2C19, 2D6, 2E1, and 3A4) examined, P450 1A2 was the most active in catalyzing 2- and 4-hydroxylations of estradiol and estrone. P450 3A4 and P450 2C9 also catalyzed these reactions although to lesser extents than P450 1A2. P450 1A2 also efficiently oxidized estradiol at the 16α-position but was less active in estrone 16α-hydroxylation; the latter reaction and also estradiol 16α-hydroxylation were catalyzed by P450 3A4 at significant levels. Anti-P450 1A2 antibodies inhibited 2- and 4-hydroxylations of these two estrogens catalyzed by liver microsomes of some of the human samples examined. Estradiol 16α-hydroxylation was inhibited by both anti-P450 1A2 and anti-P450 3A4, while estrone 16α-hydroxylation was significantly suppressed by anti-P450 3A4 in human liver microsomes. Fluvoxamine efficiently inhibited the estrogen hydroxylations in human liver samples that contained high levels of P450 1A2, while ketoconazole affected these activities in human samples in which P450 3A4 levels were high. α- Naphthoflavone either stimulated or had no effect on estradiol hydroxylation catalyzed by liver microsomes; the intensity of this effect depended on the human samples and their P450s. Interestingly, in the presence of anti-P450 3A4 antibodies, α-naphthoflavone was found to be able to inhibit estradiol and estrone 2-hydroxylations catalyzed by human liver microsomes. The results suggest that both P450s 1A2 and 3A4 have major roles in oxidations of estradiol and estrone in human liver and that the contents of these two P450 forms in liver microsomes determine which P450 enzymes are most important in hepatic estrogen hydroxylation by individual humans. P450 3A4 may be expected to play a more important role for some of the estrogen hydroxylation reactions than P450 1A2. Knowledge of roles of individual P450s in these estrogen hydroxylations has relevance to current controversies in hormonal carcinogenesis.

Glycosides of catechol estrogens

-

, (2008/06/13)

There are described novel glycosides of catechol estrogen, a method of preparing the same, and a medicament comprising one of the glycosides as an active ingredient. The glycosides are shown by the formula of STR1 wherein X is carbonyl group or STR2 R10 is hydroxyl group or glycosyloxy group, and R2 is a hydrogen atom or ethynyl group; R11 is a hydrogen atom, hydroxyl group, or glycosyloxy group; R12 is hydroxyl group or glycosyloxy group; and R13 is hydroxyl group or glycosyloxy group, in which glycosyloxy group is selected from the group consisting of glucosyloxy, galactosyloxy, mannosyloxy, arabinosyloxy, ribosyloxy, xylosyloxy, fructosyloxy, rhamnosyloxy, fucosyloxy, maltosyloxy, cellobiosyloxy, lactosyloxy, sucrosyloxy, maltotriosyloxy, maltotetraosyloxy, maltopentaosyloxy, maltohexaosyloxy, maltoheptaosyloxy, and sialosyloxy, and in this case, at least one of R10, R11, R12, and R13 is glycosyloxy group as defined above.

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