In MRC-5 cells, 8-hydroxyquinoline (8HQ) (Compd 1) exhibits cytotoxicity with an IC50 of 6.27 μM[1]. When combined with CuCl2, 10.0 μM, for one hour, 8-hydroxyquinoline (8-OHQ) (Compd 1) creates a complex with copper that facilitates copper transport into human breast cancer DCIS cells [2]. When 8-hydroxyquinoline is combined with CuCl2, 0–20.0 μM, it binds to copper and produces a complex that has tyrosine kinase inhibitor-like activity (1–5 μM, 2–12 hours)[2]. causes time- and dose-dependent cell death in DCIS cells [2]. In Raw 264.7 cells, hydroxyquinoline (0-100 μM, 30 minutes) suppresses regulatory factors by blocking NO generation and iNOS expression through the activation of NF-κB and decreasing C/EBPb DNA-binding activity [3].

In CD1 mice, a single intraperitoneal injection of 8-hydroxyquinoline (HOQ) at a dose of 25–100 mg/kg significantly increases the quantity of micronucleated polychromatic erythrocytes (MPCE) [4]. Hair growth and loss are caused by 8-Hydroxyquinoline (8-HQ) (0.3%, Skin Appearance, 4 times weekly), with growth patterns altering over time [5].

Cell Viability Assay[2]
Cell Types: DCIS Cell
Tested Concentrations: 1, 2.5, 5, 10, 20 μM
Incubation Duration: 1 or 8 hrs (hours)
Experimental Results: Binds to copper and forms a complex, causing cells to agglomerate and separate, at a certain concentration and Induces cell death in a time-dependent manner. 8-OHQ- and CQ-Cu, but not their analogs and mixtures of Cu, can induce cancer cell death in a concentration- and time-dependent manner.

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Western Blot Analysis[2]
Cell Types: DCIS Cell
Tested Concentrations: 1, 2.5, 5 μM
Incubation Duration: 0, 2, 4, 8, 12 hrs (hours)
Experimental Results: CuCl2 mixture inhibited CT-like activity in a concentration and time dependent manner. Mixtures of CuCl2 diminished proteasome activity and increased accumulation of ubiquitinated proteins and Bax in a time-dependent manner.

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RT-PCR[3]
Cell Types: Lipopolysaccharide-stimulated original 264.7 cells
Tested Concentrations: 25, 50, 75, 100 μM
Incubation Duration: 30 minutes
Experimental Results: Inhibited of LPS-induced NO and iNOS expression.br/> Inhibits transcription of iNOS. Had not affect phosphorylation of MAPKs. Inhibited NF-jB-binding activity and C/EBPb-binding activity.

Animal/Disease Models: CD1 mice[4]
Doses: 25,50,100 mg/kg
Route of Administration: intraperitoneal (ip) injection
Experimental Results: All doses tested resulted in micronucleated polychromatic erythrocytes (MPCE) numbers over a 24-hour sampling period Significant dose-related increase.

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Animal/Disease Models: C57BL mice [5]
Doses: 0.3% Administration 4 times a week: Dermal administration
Experimental Results: Causes depigmented hair to grow in a time-varying manner. Frequent enough use results in nearly complete depigmentation in young adult C57BL female mice, whereas a single application results in isolated bands of depigmented hair.

Absorption, Distribution and Excretion
Oxyquinoline is excreted in both the primarily in the urine with some in the bile.
IN RATS /MALE, DONRYU STRAIN, IV INJECTION/ 8-HYDROXYQUINOLINE WAS METABOLIZED TO GLUCURONIDE & SULFATE CONJUGATES. MORE 8-HYDROXYQUINOLINE GLUCURONIDE WAS EXCRETED IN URINE THAN 8-HYDROXYQUINOLINE SULFATE CONJUGATE. ONLY THE GLUCURONIDE CONJUGATE WAS EXCRETED IN BILE.
8-HYDROXYQUINOLINE WAS METABOLIZED TO GLUCURONIDE & SULFATE CONJUGATES AFTER IV ADMIN IN RATS /MALE, DONRYU STRAIN/. THE GLUCURONIDES WERE EXCRETED IN BILE & URINE, BUT THE SULFATES WERE EXCRETED EXCLUSIVELY IN THE URINE. UNMETABOLIZED FORMS WERE ONLY SLIGHTLY EXCRETED.

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Metabolism / Metabolites
In the urine, 60% of the dose is excreted as glucuronide conjugates and 23% of the dose as sulfate conjugates. In the bile, 9% of the total dose is found as glucuronide conjugates.
IN RATS /MALE, DONRYU STRAIN, IV INJECTION/ 8-HYDROXYQUINOLINE WAS METABOLIZED TO GLUCURONIDE & SULFATE CONJUGATES.
8-HYDROXYQUINOLINE WAS METABOLIZED TO GLUCURONIDE & SULFATE CONJUGATES AFTER IV ADMIN IN RATS /MALE, DONRYU STRAIN/. UNMETABOLIZED FORMS WERE ONLY SLIGHTLY EXCRETED.

Toxicity Data
LC50 (rat) > 1,210 mg/m3/6h

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Interactions
AFTER LETHAL IM DOSES IN MICE (30 MG/KG) INJECTED D-PENICILLAMINE (1 G/KG) PREVENTED /TOXIC/ SYMPTOMS & DEATH BUT NOT TRANSIENT HYPERGLYCEMIA.
THE INFLUENCE OF RADIOPROTECTORS, CYSTEAMINE & AMINOETHYLISOTHIOURONIUM AS WELL AS OF THE AMINO ACIDS L-ALANINE, L-CYSTEINE, L-ARGININE, L-ASPARAGINE, L-GLUTAMIC ACID, L-HISTIDINE, & L-METHIONINE, ON THE CYTOGENETIC ACTION OF 8-HYDROXYQUINOLINE SULFATE WAS TESTED IN HUMAN LYMPHOCYTE CULTURES IN VITRO. EXCESS L-CYSTEINE, CYSTEAMINE, & L-ASPARAGINE ADDED SIMULTANEOUSLY WITH 8-HYDROXYQUINOLINE SULFATE DISTINCTLY REDUCED THE CHROMOSOME. DAMAGING EFFECT OF 8-HYDROXYQUINOLINE. L-GLUTAMIC ACID & AMINOETHYLISOTHIOURONIUM EXERTED LESSER PROTECTIVE ACTIVITY. L-METHIONINE DISPLAYED SOME EFFECT ONLY IN REDUCING THE RELATIVELY RARE ISOCHROMATID ABERRATIONS INDUCED BY 8-HYDROXYQUINOLINE SULFATE. THE OTHER AMINO ACIDS HAD NO EFFECT.
The formation of DNA-strand breaks was studied in cultured human lung cells (A 549) subjected to iron, either in the form of iron(III) citrate or in combination with the metal chelators ethylene diamine tetra-acetic acid (EDTA), nitrilo triacetic acid (NTA), or 8-hydroxyquinoline (8HQ). After 15 min exposure to 5 uM iron(III) citrate or iron chelate, the cellular levels of iron were found to be three times higher in cells subjected to iron-8HQ than in cells subjected to iron(III) citrate, iron-EDTA or iron-NTA. Exposure to iron-8HQ caused extensive DNA-strand breakage, whereas no such breakage was found in cells exposed to iron-EDTA or iron-NTA. The DNA damage caused by iron-8HQ increased with time and dose, and DNA-strand breakage was clearly demonstrable in cells after 15 min exposure to as little as 0.1 uM iron-8HQ. Moreover, iron-8HQ was strongly toxic to the cells and inhibited their growth after exposure. Along with the formation of DNA-strand breaks, the concentration of cellular malondialdehyde increased four-fold after exposure to iron-8HQ and two-fold after exposure to iron-EDTA or iron-NTA, suggesting that reactive oxygen metabolites might be involved in the toxic action. Moreover, both iron-EDTA and iron-NTA caused a considerable hydroxylation of deoxyguanosine (dG) residues in DNA in vitro, whereas iron(III) citrate and iron-8HQ only caused a minor hydroxylation of dG. This points to the possibility that iron-8HQ-mediated DNA-strand breakage in cells might be due to the action of a metal-bound oxyl radical formed from the iron-8HQ complex rather than to the formation of hydroxyl radicals. Altogether, these findings indicate that iron bound to the lipophilic chelator, 8HQ, has strong toxic properties and that it may cause substantial DNA-strand breakage and lipid peroxidation in living cells.

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Non-Human Toxicity Values
LD50 Rat oral 1200 mg/kg
LD50 Mice ip 48 mg/kg
LD50 Rat ip 50 mg/kg
LD50 Mouse sc 83,600 ug/kg
For more Non-Human Toxicity Values (Complete) data for 8-HYDROXYQUINOLINE (6 total), please visit the HSDB record page.

[1]. Lawung R, et.al. Repositioning of 8-hydroxyquinoline derivatives as a new promising candidate for combating multidrug resistant Neisseria gonorrhoeae. EXCLI J. 2018 Aug 23;17:840-846.
[2]. 8-hydroxyquinoline and clioquinol requires their capabilities to bind copper and transport copper into cells. J Biol Inorg Chem. 2010 Feb;15(2):259-69.
[3]. Zhai S, et.al. Tumor cellular proteasome inhibition and growth suppression by
[4]. Hamoud MA, et.al. Effects of quinoline and 8-hydroxyquinoline on mouse bone marrow erythrocytes as measured by the micronucleus assay. Teratog Carcinog Mutagen. 1989;9(2):111-8.
[5]. Searle CE. The selective depigmenting action of 8-hydroxyquinoline on hair growth in the mouse. Br J Dermatol. 1972 May;86(5):472-80.

8-hydroxyquinoline appears as white to off-white or faintly yellow crystalline powder. Phenolic odor. (NTP, 1992)
Quinolin-8-ol is a monohydroxyquinoline that is quinoline substituted by a hydroxy group at position 8. Its fungicidal properties are used for the control of grey mould on vines and tomatoes. It has a role as an antibacterial agent, an iron chelator, an antiseptic drug and an antifungal agrochemical. It derives from a hydride of a quinoline.
Oxyquinoline is a heterocyclic phenol and derivative of quinoline with antiseptic, disinfectant, and pesticide properties. It is used as a stabilizer for hydrogen peroxide, where it is sometimes added in cosmetic products.
8-Hydroxyquinoline has been reported in Cortinarius subtortus and Allium stipitatum with data available.
An antiseptic with mild fungistatic, bacteriostatic, anthelmintic, and amebicidal action. It is also used as a reagent and metal chelator, as a carrier for radio-indium for diagnostic purposes, and its halogenated derivatives are used in addition as topical anti-infective agents and oral antiamebics.
See also: Acetic acid; oxyquinoline (component of).

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Drug Indication
Oxyquinoline is used as a biocidal component of several over the counter products. These products are marketed for the purposes of inhibiting abnormal biological growth in the vagina and restoring natural pH.

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Mechanism of Action
The mechanism by which oxyquinoline exerts its biocidal effect is unknown.

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Therapeutic Uses
A BACTERIOSTATIC & FUNGISTATIC COMPOUND; USED PRINCIPALLY IN TREATMENT OF MINOR BURNS & OF HEMORRHOIDS.
OXYQUINOLINE SULFATE ... IS ... USED ... IN TREATMENT OF ATHLETE'S FOOT, VAGINITIS, & AS A GARGLE, EYEWASH, NASAL DOUCHE, & IN HEMORRHOIDAL PREPARATIONS ... /OXYQUINOLINE SULFATE/
/OVER THE COUNTER/ HYDROXYQUINOLINE IS 1 OF 4 ANTIFUNGAL AGENTS RECOMMENDED FOR ACTIVE TREATMENT OF FUNGUS ASSOCIATED WITH DIAPER RASH & PRICKLY HEAT IN BABIES. /HYDROXYQUINOLINE/
8-HYDROXYQUNIOLINE SULFATE INHIBITED FORMATION OF ARTIFICIAL CALCULUS IN VITRO & RAT CALCULUS IN VIVO. IN RATS, IT PREVENTED CALCULUS FORMATION WHEN APPLIED BY SWABBING OR BY INTRAORAL INSTILLATION. IN DOGS, FORMATION OF DENTAL PLAQUE WAS INHIBITED 33 TO 98% IN COMPARISON TO PLACEBO. ALSO, 25 TO 58% OF ESTABLISHED PLAQUE ACCUMULATIONS WERE REMOVED, WHEREAS PLACEBO REMOVED 2 TO 22%.
For more Therapeutic Uses (Complete) data for 8-HYDROXYQUINOLINE (7 total), please visit the HSDB record page.

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Pharmacodynamics
Oxyquinoline acts as a biocide to eliminate bacteria and fungi.

C9H7O

145.16

145.052

148-24-3

8-Hydroxyquinoline hemisulfate;134-31-6

1923

White crystals or white crystalline powder

1.3±0.1 g/cm3

267.0±0.0 °C at 760 mmHg

70-73 °C(lit.)

143.1±20.4 °C

0.0±0.5 mmHg at 25°C

1.691

1.87

1

2

0

11

138

0

O([H])C1=C([H])C([H])=C([H])C2C([H])=C([H])C([H])=NC=21

MCJGNVYPOGVAJF-UHFFFAOYSA-N

InChI=1S/C9H7NO/c11-8-5-1-3-7-4-2-6-10-9(7)8/h1-6,11H

quinolin-8-ol

NSC-2039; NSC 2039; Oxyquinoline

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)

DMSO : ~50 mg/mL (~344.45 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (17.22 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (17.22 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (17.22 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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