Absorption, Distribution and Excretion
Catechol is readily absorbed by the gastrointestinal tract and intact skin of mice, and may also be absorbed through the lungs… Some catechol binds to glucuronic acid, sulfuric acid, and other acids in the body and is excreted in the urine, along with a small amount of “free” catechol. These conjugates are readily hydrolyzed in the urine, releasing “free” catechol, which is oxidized by air to form a dark substance, giving the urine a “smoky” appearance. When mice are exposed to cigarette smoke containing radioactively labeled catechol, the catechol readily distributes into the blood and tissues; 90% of the radioactivity is excreted in the urine within 24 hours. Catechol… is absorbed in the respiratory tract. …Very small amounts are excreted in the urine as free catechol.
In the American Association of Industrial Hygiene Scientists (ACGIH) list, the "S" skin marker refers to "exposure to the substance via the skin (including mucous membranes and eyes) that is likely to have a significant impact on overall exposure, whether through exposure to vapors or (potentially more importantly) direct skin contact with the substance."
Metabolisms/Metabolites

Some catechols are oxidized to benzoquinone by polyphenol oxidase. Another portion binds to glucuronic acid, sulfuric acid, and other acids in the body… These conjugates are readily hydrolyzed in urine, releasing free catechols…
Catechols are converted to guaiacol in rats. In rabbits, catechols are metabolized to o-hydroxyphenyl-β-D-glucuronide, o-hydroxyphenyl sulfate, and hydroxyquinoline.
Structure-reactivity studies in rats indicate that the ortho-hydroxy group is a necessary condition for methylation, providing evidence for the mechanism of action of catechol O-methyltransferase.
In rabbits given oral catechol, 18% is excreted as sulfate, 70% as monoglucuronide, and 2% as free catechol.
For more complete data on the metabolism/metabolites of catechols (9 metabolites in total), please visit the HSDB record page.
Known human metabolites of catechols include diphenylglucuronide, o-methoxyphenyl sulfate, and catechol sulfate.
Catechols are known human metabolites. Metabolites of phenol.

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Biological half-life
The calculated biological half-life of catechol in humans is 3-7 hours.

According to the International Agency for Research on Cancer (IARC) of the World Health Organization, catechols are potentially carcinogenic.
Solid; white; odorless. Sinks to the bottom and dissolves in water. (USCG, 1999)
Catechol is a hydroquinone composed of a benzene ring and two ortho-hydroxyl substituents. It is a genotoxin, allelochemical, and plant metabolite. It is the conjugate acid of catechol(1-).
Catechol is a metabolite found in or produced by Escherichia coli (K12 strain, MG1655 strain).
Exposure to catechol may occur during its production and use. Skin contact with catechol can cause eczematous dermatitis in humans. In humans, skin absorption can cause illness similar to that caused by phenol, but with more pronounced seizures. High doses of catechol can cause central nervous system depression and sustained hypertension in animals. Due to the lack of information regarding the duration of exposure in the above studies, it is unclear whether these health effects are due to acute (short-term) exposure or chronic (long-term) exposure. Proventricular tumors have been observed in rats with oral exposure. The International Agency for Research on Cancer (IARC) has classified catechols as Group 2B carcinogens, meaning they are possibly carcinogenic to humans. The U.S. Environmental Protection Agency (EPA) has not yet classified the potential carcinogenicity of catechols. Catechols have been reported to be found in red pine (Pinus densiflora), star anise (Illicium simonsii), and other organisms with relevant data. Catechol, commonly known as catechol or benzene-1,2-diol, is a hydroquinone with the molecular formula C6H4(OH)2. It was first prepared by H. Reinsch in 1839 through distillation of catechins (the juice of the mimosa plant). This colorless compound exists naturally, but approximately 20,000 tons are artificially produced annually, primarily as precursors for pesticides, fragrances, and flavorings. Its sulfonic acid content is commonly found in the urine of many mammals. Fruits and vegetables naturally contain small amounts of catechols, as well as polyphenol oxidase. When an enzyme is mixed with its substrate and exposed to oxygen (e.g., when a potato or apple is cut), colorless catechols oxidize to reddish-brown benzoquinone derivatives. Adding acid (e.g., lemon juice) or refrigeration inactivates the enzyme. Isolation from oxygen also prevents the browning reaction. Catechols have a melting point of 28°C and a boiling point of 250°C. They are used medically as expectorants. Dimethyl ether or resveratrol is also used in pharmaceuticals. Many other catechin derivatives have been proposed for therapeutic applications.

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Mechanism of Action
This study used a single-absorption electrode clamp system, combined with internal perfusion and current or voltage clamping techniques (using electronic switching circuits), to investigate the effects of catechols on various ion channels in isolated bullfrog primary afferent neurons. The results showed that catechols, like 4-aminopyridine, specifically inhibited fast potassium ion channels. Calcium, sodium, and slow potassium ion channels were unaffected. Although both 4-aminopyridine and catechols are inhibitors of fast potassium ion channels, their sites of action are quite different. Catechols are effective on the outer surface of the cell membrane, while 4-aminopyridines primarily act intracellularly. We hypothesize that a single fast potassium channel has two distinct blocking agent binding sites: the catechol binding site is exposed to the external medium or located at the external opening of the channel, while the 4-aminopyridine binding site is located within the same channel but is more easily accessed from inside the nerve cell than from the outside. However, the 4-aminopyridine and catechol binding sites are not completely separate and independent, as we observed a synergistic effect between them. Catechols are an important naturally occurring industrial chemical that has been shown to have strong pro-cancer activity, inducing proventricular tumors in rodents. Furthermore, catechols are a major metabolite of the carcinogen benzene. To elucidate the carcinogenic mechanism of catechols, we investigated their damaging effects on DNA using human cultured cell lines and ³²P-tagged DNA fragments obtained from human p53 and p16 tumor suppressor genes and the c-Ha-ras-1 proto-oncogene. Catechols can increase the content of 8-oxodG (8-oxo-7,8-dihydro-2'-deoxyguanosine) in the human leukemia cell line HL-60, and 8-oxodG is known to be associated with cancer incidence. However, the content of 8-oxodG was not increased in its hydrogen peroxide (H₂O₂) resistant clone HP100. In the presence of Cu²⁺, catechols can increase the production of 8-oxodG in calf thymus DNA. In the presence of Cu²⁺, catechols can damage ³²P-tagged DNA fragments. DNA damage is significantly enhanced upon the addition of NADH, and can be observed at relatively low catechol concentrations (<1 μM). Piperidine treatment enhances DNA breakage, indicating that catechols and NADH not only cause deoxyribose phosphate backbone breakage but also base modification. Catechols and NADH frequently modify thymine residues. The specific Cu(+) chelator bartophenone and catalase inhibited DNA damage, indicating that Cu(+) and H₂O₂ are involved in DNA damage. Typical hydroxyl radical scavengers failed to inhibit catechol and Cu(2+)-induced DNA damage, while methylthion completely inhibited it. These results suggest that the reactive substance produced by the reaction of H₂O₂ with Cu(+) is involved in catechol-induced DNA damage. Therefore, the authors conclude that catechols play an important role in the carcinogenicity of catechols and benzene by generating H₂O₂-induced oxidative DNA damage. We investigated the relationship between the redox properties of “carcinogenic” catechols and “non-carcinogenic” hydroquinone and their different DNA damage activities and carcinogenicity using ³²P-tagged DNA fragments obtained from the human genome. In the presence of endogenous NADH and Cu²⁺, catechols induced stronger DNA damage than hydroquinone, but in the absence of NADH, the magnitudes of their DNA damage activities were opposite. In both cases, DNA damage was caused by base modifications of guanine and thymine residues, as well as Cu²⁺ and H₂O₂-induced chain breaks, which were generated during the oxidation of catechol and hydroquinone to 1,2-benzoquinone and 1,4-benzoquinone, respectively. EPR and ¹H NMR studies showed that 1,2-benzoquinone was directly converted to catechol via non-enzymatic two-electron reduction by NADH, while 1,4-benzoquinone was reduced to hydroquinone via two single-electron reduction cycles through a semiquinone radical intermediate. NADH reduced 1,2-benzoquinone at a faster rate than 1,4-benzoquinone. This study indicates that the rapid two-electron reduction of 1,2-benzoquinone accelerates the redox cycle between catechol and 1,2-benzoquinone, thereby enhancing DNA damage. These results suggest that the difference in the NADH-mediated redox properties of catechol and hydroquinone leads to their different carcinogenicities.
Catechol may be carcinogenic to humans (International Agency for Research on Cancer, IARC). The key mechanism likely involves the combined effects of its oxidative DNA-damaging action and the reducing-oxidizing effects of metals such as copper. We found that introducing an α-carbonyl group at the C4 position of catechol to form carbonylcatechol inhibits DNA damage. During oxidative DNA damage, catechol, but not carbonylcatechol, is oxidized to ortho-quinones; however, the coexisting Cu(II) is reduced to Cu(I). Carbonylcatechol may be stalled in the oxidation step of semiquinones in the presence of Cu(II). Based on changes in circular dichroism spectroscopy, Cu(I) binds to DNA more strongly than Cu(II). Carbonylcatechol did not induce this change, indicating that Cu(I) is chelated from DNA. Solid-phase extraction experiments and spectrophotometric analysis showed that Cu(I) forms a semiquinone chelate with catechol. Therefore, the formation of the chelate may explain the inhibitory mechanism of Cu-catechol-dependent DNA damage by terminating the redox cycle. Introducing structural modifications such as an α-carbonyl group at the C4 position of catechols helps reduce the risk of aromatic/phenolic compounds and enhances their application potential in industrial and medical fields…

110.036

120-80-9

26982-53-6;20244-21-7 (unspecified hydrochloride salt);115881-16-8;4918-96-1

289

Off-white to gray solid powder

1.3±0.1 g/cm3

245 ºC

103-106 ºC

131 ºC

0.0±0.5 mmHg at 25°C

1.612

0.88

2

2

0

8

62.9

0

C1=CC=C(C(=C1)O)O

YCIMNLLNPGFGHC-UHFFFAOYSA-N

InChI=1S/C6H6O2/c7-5-3-1-2-4-6(5)8/h1-4,7-8H

benzene-1,2-diol

NSC 1573; Katechol; Pyrocatechol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)