R,4 S)-(+)-ketoconazole (top) (2 S,4 R)-(-)-ketoconazole (bottom) Pronunciation   Trade names Nizoral, others Other names R-41400; KW-1414 AHFS/ Drugs.com Monograph MedlinePlus a682816 License data
Pregnancy category Routes of administration By mouth ( tablets), topical ( cream, shampoo, solution) ATC code Legal status
UK: POM (Prescription only)  
US: ?-only In general (Prescription only) Bioavailability By mouth: 37-97%  Protein binding 84 to 99% Metabolism Extensive liver (predominantly oxidation, O-dealkylation) Metabolites N-deacetyl ketoconazole Elimination Biphasic Excretion Biliary (major) and kidney 
CAS Number PubChem CID IUPHAR/BPS DrugBank ChemSpider UNII KEGG ChEBI ChEMBL PDB ligand CompTox Dashboard ( EPA) ECHA InfoCard 100.059.680 Formula C 26 H 28 Cl 2 N 4 O 4 Molar mass g·mol -1 3D model ( JSmol) Chirality Racemic mixture  
(what is this?) (verify) Ketoconazole, sold under the brand name Nizoral among others, is an antifungal medication used to treat a number of fungal infections. Applied to the skin it is used for  fungal skin infections such as tinea, cutaneous candidiasis, pityriasis versicolor, dandruff, and seborrheic dermatitis. Taken  by mouth it is a less preferred option and only recommended for severe infections when other agents cannot be used. Other uses include treatment of  excessive hair growth and Cushing's syndrome.
side effects when applied to the skin include redness. Common side effects when taken by mouth include  nausea, headache, and liver problems. Liver problems may result in death or the need for a  liver transplantation.  Other severe side effects when taken by mouth include  QT prolongation, adrenocortical insufficiency, and anaphylaxis.  It is an  imidazole and works by affecting the production of ergosterol required for the fungal cell membrane thereby slowing growth.
Ketoconazole was patented in 1977 and came into medical use in 1981.
It is available as a  generic medication and formulations that are applied to the skin are over the counter in the United Kingdom. In 2018, it was the 186th most commonly prescribed medication in the United States, with more than 3million prescriptions.   The formulation that is taken by mouth was  withdrawn in the European Union and in Australia in 2013  and in China in 2015.  In addition, its use was restricted in the United States and Canada in 2013. 
Topically administered ketoconazole is usually prescribed for fungal infections of the skin and mucous membranes, such as
athlete's foot, ringworm, candidiasis (yeast infection or thrush), jock itch, and tinea versicolor. Topical ketoconazole is also used as a treatment for  dandruff (seborrheic dermatitis of the scalp) and for seborrheic dermatitis on other areas of the body, perhaps acting in these conditions by suppressing levels of the fungus on the skin. Malassezia furfur  
Ketoconazole has activity against many kinds of fungi that may cause human disease, such as
, Candida , Histoplasma , and Coccidioides (although it is not active against Blastomyces ), Aspergillus chromomycosis and paracoccidioidomycosis.  First made in 1977,  ketoconazole was the first orally-active  azole antifungal medication. However, ketoconazole has largely been replaced as a first-line systemic antifungal medication by other azole antifungal agents, such as  itraconazole, because of ketoconazole's greater toxicity, poorer absorption, and more limited spectrum of activity. 
Ketoconazole is used orally in dosages of 200 to 400 mg per day in the treatment of superficial and deep fungal infections.
Ketoconazole shampoo in conjunction with an oral
5?-reductase inhibitor such as finasteride or dutasteride has been used off label to treat androgenic alopecia. It was speculated that antifungal properties of ketoconazole reduce scalp microflora and consequently may reduce follicular inflammation that contributes to alopecia.
Limited clinical studies suggest ketoconazole shampoo used either alone
 or in combination with other treatments  may be useful in reducing hair loss in some cases. 
The side effects of ketoconazole are sometimes harnessed in the treatment of non-fungal conditions. While ketoconazole blocks the synthesis of the sterol
ergosterol in fungi, in humans, at high dosages (>800 mg/day), it potently inhibits the activity of several enzymes necessary for the conversion of cholesterol to steroid hormones such as testosterone and cortisol.  Specifically, ketoconazole has been shown to inhibit  cholesterol side-chain cleavage enzyme, which converts cholesterol to pregnenolone, 17?-hydroxylase and 17,20-lyase, which convert  pregnenolone into androgens, and 11?-hydoxylase, which converts 11-deoxycortisol to cortisol. All of these enzymes are mitochondrial  cytochrome p450 enzymes. Based on these  antiandrogen and antiglucocorticoid effects, ketoconazole has been used with some success as a second-line treatment for certain forms of advanced prostate cancer  and for the suppression of  glucocorticoid synthesis in the treatment of Cushing's syndrome. However, in the treatment of prostate cancer, concomitant glucocorticoid administration is needed to prevent  adrenal insufficiency. Ketoconazole has additionally been used, in lower dosages, to treat  hirsutism and, in combination with a GnRH analogue, male-limited precocious puberty. In any case, the risk of  hepatotoxicity with ketoconazole limits its use in all of these indications, especially in those that are benign such as hirsutism.
Ketoconazole has been used to prevent the
testosterone flare at the initiation of GnRH agonist therapy in men with prostate cancer.
Oral ketoconazole has various
contraindications, such as concomitant use with certain other drugs due to known drug interactions. Other contraindications of oral ketoconazole include  liver disease, adrenal insufficiency, and known hypersensitivity to oral ketoconazole.
Vomiting, diarrhea, nausea, constipation, abdominal pain, upper abdominal pain, dry mouth,
dysgeusia, dyspepsia, flatulence, tongue discoloration may occur.
The drug may cause
adrenal insufficiency so the level of the adrenocortical hormones should be monitored while taking it.  Oral ketoconazole at a dosage range of 400 to 2,000 mg/day has been found to result in a rate of  gynecomastia of 21%.
In July 2013, the
U.S. Food and Drug Administration (FDA) issued a warning that taking ketoconazole by mouth can cause severe liver injuries and adrenal gland problems: adrenal insufficiency and worsening of other related to the gland conditions. It recommends oral tablets should not be a first-line treatment for any fungal infection. It should be used for the treatment of certain fungal infections, known as endemic mycoses, only when alternative antifungal therapies are not available or tolerated.  As contraindication it should not be used in people with acute or chronic liver disease. 
Anaphylaxis after the first dose may occur. Other cases of hypersensitivity include urticaria. 
The topical formulations have not been associated with liver damage, adrenal problems, or drug interactions. These formulations include creams, shampoos, foams, and gels applied to the skin, unlike the ketoconazole tablets, which are taken by mouth.
Ketoconazole is categorized as
pregnancy category C in the US. Research in animals has shown it to cause  teratogenesis when administered in high doses. A subsequent trial in Europe failed to show a risk to infants of mothers receiving ketoconazole. 
In the event of an
overdose of oral ketoconazole, treatment should be supportive and based on symptoms.  Activated charcoal may be administered within the first hour following overdose of oral ketoconazole.
The concomitant use of the following medications is contraindicated with ketoconazole tablets:
methadone, disopyramide, dronedarone
irinotecan, lurasidone, colchicine
alprazolam, oral midazolam, oral triazolam
felodipine, ranolazine, tolvaptan, eplerenone
HMG-CoA reductase inhibitors: lovastatin, simvastatin
ergot alkaloids: ergotamine, dihydroergotamine, ergometrine, methylergometrine Others: cisapride, nisoldipine, dofetilide, pimozide
And is not recommended:
 Ritonavir is known for increasing activity of the ketoconazole so it is recommended to reduce dosage.
There is also list of drugs which significantly decrease systemic exposure to the ketoconazole and drugs whose systemic exposure is increased by the ketoconazole.
As an antifungal, ketoconazole is structurally similar to
imidazole, and interferes with the fungal synthesis of ergosterol, a constituent of fungal cell membranes, as well as certain enzymes. As with all azole antifungal agents, ketoconazole works principally by inhibiting the enzyme cytochrome P450 14?-demethylase (CYP51A1). This enzyme participates in the  sterol biosynthesis pathway that leads from lanosterol to ergosterol. Lower doses of fluconazole and itraconazole are required to kill fungi compared to ketoconazole, as they have been found to have a greater affinity for fungal cell membranes.
Resistance to ketoconazole has been observed in a number of clinical fungal isolates, including
Candida albicans. Experimentally, resistance usually arises as a result of mutations in the sterol biosynthesis pathway. Defects in the sterol 5-6 desaturase enzyme reduce the toxic effects of azole inhibition of the 14-alpha demethylation step. Multidrug-resistance (MDR) genes can also play a role in reducing cellular levels of the drug. As azole antifungals all act at the same point in the sterol pathway, resistant isolates are normally cross-resistant to all members of the azole family. 
antiandrogen, ketoconazole operates through at least two mechanisms of action. First, and most notably, high oral doses of ketoconazole (e.g. 40 mg three times per day) block both testicular and adrenal androgen biosynthesis, leading to a reduction in circulating testosterone levels.  It produces this effect through inhibition of  17?-hydroxylase and 17,20-lyase, which are involved in the synthesis and degradation of steroids, including the precursors of testosterone. Due to its efficacy at reducing systemic androgen levels, ketoconazole has been used with some success as a treatment for androgen-dependent prostate cancer.  Second, ketoconazole is an  androgen receptor antagonist, competing with androgens such as testosterone and dihydrotestosterone (DHT) for binding to the androgen receptor. This effect is thought to be quite weak however, even with high oral doses of ketoconazole.
Ketoconazole, along with
miconazole, has been found to act as an antagonist of the glucocorticoid receptor. 
Ketoconazole is a
racemic mixture consisting of cis-(2 S,4 R)-(-) and cis-(2 R,4 S)-(+) enantiomers. The  cis-(2 S,4 R) isomer was more potent in inhibiting progesterone 17?,20-lyase than its enantiomer ( IC values of 0.05 and 2.38 50 ?M, respectively) and in inhibiting 11?-hydroxylase (IC 50 values of 0.152 and 0.608 ?M, respectively). Both isomers were relatively weak inhibitors of human placental aromatase.
Oral ketoconazole has been used clinically as a steroidogenesis inhibitor in men, women, and children at dosages of 200 to 1,200 mg/day.
  Numerous small studies have investigated the effects of oral ketoconazole on hormone levels in humans.  It has been found in men to significantly decrease testosterone and estradiol levels and to significantly increase  luteinizing hormone, progesterone, and 17?-hydroxyprogesterone levels, whereas levels of androstenedione, follicle-stimulating hormone, and prolactin were unaffected.   The ratio of testosterone to estradiol is also decreased during oral ketoconazole therapy in men.  Suppression of testosterone levels by ketoconazole is generally partial and has often been found to be transient.  Better effects on suppression of testosterone levels have been observed in men when ketoconazole is combined with a  GnRH agonist to suppress the hypothalamic-pituitary-gonadal axis, which prevents compensatory upregulation of luteinizing hormone secretion and consequent activation of gonadal testosterone production. In  premenopausal women with polycystic ovary syndrome, ketoconazole has been found to significantly decrease levels of androstenedione and testosterone and significantly increase levels of 17?-hydroxyprogesterone and estradiol.  Studies in  postmenopausal women with breast cancer have found that ketoconazole significantly decreases androstenedione levels, slightly decreases estradiol levels, and does not affect estrone levels. This indicates minimal inhibition of aromatase by ketoconazole  in humans. in vivo Ketoconazole has also been found to decrease levels of  endogenous corticosteroids, such as cortisol, corticosterone, and aldosterone, as well as vitamin D. 
Ketoconazole has been found to displace
dihydrotestosterone and estradiol from sex hormone-binding globulin , but this was not found to be relevant in vitro . in vivo
Ketoconazole has been found to inhibit the activity of the cation channel
TRPM5. Too much of Ketoconazole can cause Brain damage .
When administered orally, ketoconazole is best absorbed at highly
acidic levels, so antacids or other causes of decreased stomach acid levels will lower the drug's absorption. Absorption can be increased by taking it with an acidic beverage, such as cola. Ketoconazole is very  lipophilic and tends to accumulate in fatty tissues.
Ketoconazole is a
synthetic imidazole.  It is a  nonsteroidal compound.  It is a  racemic mixture of two enantiomers, levoketoconazole ((2 S,4 R)-(-)-ketoconazole) and dextroketoconazole ((2 R,4 S)-(+)-ketoconazole).  Levoketoconazole is under development for potential clinical use as a steroidogenesis inhibitor with better  tolerability and less toxicity than ketoconazole. Other steroidogenesis inhibitors besides ketoconazole and levoketoconazole include the nonsteroidal compound aminoglutethimide and the steroidal compound abiraterone acetate.
Ketoconazole was discovered in 1976 at
Janssen Pharmaceutica. It was  patented in 1977, followed by introduction in the  United States in July 1981.    Following its introduction, ketoconazole was the only systemic antifungal available for almost a decade.  Ketoconazole was introduced as the prototypical medication of the imidazole group of antifungals.  Oral ketoconazole has been replaced with oral  itraconazole for many mycoses.
Due to incidence of serious
liver toxicity, the use of oral ketoconazole was suspended in France in July 2011 following review. This event triggered an evaluation of oral ketoconazole throughout the rest of the  European Union as well. In 2013, oral ketoconazole was withdrawn in  Europe and Australia, and strict restrictions were placed on the use of oral ketoconazole in the United States and Canada. Oral ketoconazole is now only indicated for use in these countries when the indication is a severe or life-threatening systemic infection and alternatives are unavailable.  However, topical ketoconazole, which does not distribute systemically, is safe and widely used still. 
Ketoconazole HRA was approved for use in the European Union for treatment of Cushing's syndrome in November 2013.
As of March 2019, oral
levoketoconazole (developmental code name COR-003, tentative brand name Recorlev) is phase III clinical trials for the treatment of Cushing's syndrome. Oral levoketoconazole may have a lower risk of liver toxicity than oral ketoconazole. 
Society and culture
Ketoconazole is the generic name of the drug and its , INN , USAN , and BAN . JAN   
Ketoconazole has been marketed under a large number of brand names.
  
Ketoconazole is available widely throughout the world.
In 2013, the
European Medicines Agency's Committee on Medicinal Products for Human Use (CHMP) recommended that a ban be imposed on the use of oral ketoconazole for systemic use in humans throughout the European Union, after concluding that the risk of serious liver injury from systemic ketoconazole outweighs its benefits.
Ketoconazole is sometimes prescribed as an antifungal by
veterinarians for use in pets, often as unflavored tablets that may need to be cut to smaller size for correct dosage.
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