Selected from data included with permission and copyrighted by First Databank, Inc. This copyrighted material has been downloaded from a licensed data provider and is not for distribution, except as may be authorized by the applicable terms of use.
CONDITIONS OF USE: The information in this database is intended to supplement, not substitute for, the expertise and judgment of healthcare professionals. The information is not intended to cover all possible uses, directions, precautions, drug interactions or adverse effects, nor should it be construed to indicate that use of a particular drug is safe, appropriate or effective for you or anyone else. A healthcare professional should be consulted before taking any drug, changing any diet or commencing or discontinuing any course of treatment.
Fluconazole, commonly known as Diflucan, is an antifungal drug used for the treatment of both systemic and superficial fungal infections in a variety of tissues. It was initially approved by the FDA in 1990. This drug is an azole antifungal, in the same drug family as ketoconazole and itraconazole. Fluconazole has many advantages over the other antifungal drugs including the option of oral administration. The side effect profile of this drug is minimal. It has been demonstrated as an efficacious treatment for vaginal yeast infections in one single dose.2
TypeSmall MoleculeGroupsApproved, InvestigationalStructureMonoisotopic: 306.104065446Chemical FormulaC13H12F2N6OSynonyms
- Diflucan
- Difluconazole
- Fluconazol
- Fluconazole
- Fluconazolum
- Triflucan
Fluconazole can be administered in the treatment of the following fungal infections27:
1) Vaginal yeast infections caused by Candida 2) Systemic Candida infections 3) Both esophageal and oropharyngeal candidiasis 4) Cryptococcal meningitis 5) UTI (urinary tract infection) by Candida 6) Peritonitis (inflammation of the peritoneum) caused by Candida
A note on fungal infection prophylaxis
Patients receiving bone marrow transplantation who are treated with cytotoxic chemotherapy and/or radiation therapy may be predisposed to candida infections, and may receive fluconazole as prophylactic therapy.27
A note on laboratory testing
Obtaining specimens for fungal culture and other important laboratory studies such as serology or pathology is advised before starting fluconazole therapy in order to isolate the organisms to be eliminated through treatment. It is permissible to start therapy before the results are available, however, adjusting the therapy once laboratory results confirm the causative organism may be necessary.27
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PharmacodynamicsFluconazole has been demonstrated to show fungistatic activity against the majority of strains of the following microorganisms, curing fungal infections27:
Candida albicans, Candida glabrata (Many strains are intermediately susceptible), Candida parapsilosis, Candida tropicalis, Cryptococcus neoformans
This is achieved through steroidal inhibition in fungal cells, interfering with cell wall synthesis and growth as well as cell adhesion, thereby treating fungal infections and their symptoms.27,2,5
The fungistatic activity of fluconazole has also been shown in normal and immunocompromised animal models with both systemic and intracranial fungal infections caused by Cryptococcus neoformans and for systemic infections caused by Candida albicans.27 It is important to note that resistant organisms have been found against various strains of organisms treated with fluconazole.11,12,13 This further substantiates the need to perform susceptibility testing when fluconazole is considered as an antifungal therapy.14,20
A note on steroidal effects of fluconazole
There has been some concern that fluconazole may interfere with and inactivate human steroids/hormones due to the inhibition of hepatic cytochrome enzymes.26 Fluconazole has demonstrated to be more selective for fungal cytochrome P-450 enzymes than for a variety of mammalian cytochrome P-450 enzymes. Fluconazole 50 mg administered daily for up to 28 days in individuals of reproductive age has been show to have no effect on testosterone plasma concentrations of males and plasma concentrations of steroids in females. A 200-400 mg dose of fluconazole showed no clinically relevant effect on steroid levels or on ACTH-stimulated steroid response in healthy males, in one clinical study mentioned on the European Medicines Agency label.26 Other studies have shown no significant effects of fluconazole on steroid levels, further confirming these data.10,18
Mechanism of actionFluconazole is a very selective inhibitor of fungal cytochrome P450 dependent enzyme lanosterol 14-α-demethylase. This enzyme normally works to convert lanosterol to ergosterol, which is necessary for fungal cell wall synthesis. The free nitrogen atom located on the azole ring of fluconazole binds with a single iron atom located in the heme group of lanosterol 14-α-demethylase.16 This prevents oxygen activation and, as a result, inhibits the demethylation of lanosterol, halting the process of ergosterol biosynthesis.17 Methylated sterols are then found to accumulate in the fungal cellular membrane, leading to an arrest of fungal growth.16 These accumulated sterols negatively affect the structure and function of the fungal cell plasma membrane.8
Fluconazole resistance may arise from an alteration in the amount or function of the target enzyme (lanosterol 14-α-demethylase), altered access to this enzyme, or a combination of the above.8 Other mechanisms may also be implicated, and studies are ongoing.19
AbsorptionThe pharmacokinetic properties of fluconazole are comparable after administration by the intravenous (IV) and oral (PO) routes. In healthy volunteers, the bioavailability of orally administered fluconazole is measured to be above 90%.27 It is extensively absorbed in the gastrointestinal tract when an oral dose is taken.23 Oral absorption is not affected by food intake with fluconazole but may increase the time until the maximum concentration is reached.26,21
Tmax (or the time taken to achieve the maximum concentration) in one clinical study of healthy patients receiving 50 mg/kg of fluconazole was 3 hours.21
Peak plasma concentrations (Cmax) in fasting and healthy volunteers occur between 1-2 hours post-dose.27 Steady-state concentrations are achieved within 5 to 10 days after oral doses of 50-400 mg administered once daily. Administration of a loading dose on the first day of fluconazole treatment, or twice the usual daily dose, leads to plasma concentrations close to steady-state by the second day.27 Mean AUC (area under the curve) was 20.3 in healthy volunteers receiving 25 mg of fluconazole.21
A note on the capsule and powder form and malabsorption syndromes
The capsule forms of fluconazole often contain lactose and should not be administered with hereditary galactose intolerance, Lapp lactase enzyme deficiency, or malabsorption of glucose/galactose.27 The powder form, used for the oral suspension, lists sucrose as an ingredient and should not be used in patients who have been diagnosed with fructose, glucose/galactose malabsorption, and sucrase-isomaltase enzyme deficiency.27
Volume of distributionThe apparent volume of distribution is said to be similar to the volume of distribution of total body water.27 One clinical study of healthy volunteers administered 50 mg/kg of fluconazole was 39L, based on a body weight of 60kg.21
Fluconazole shows substantial penetration in many body fluids, which is a property that renders it an ideal treatment for systemic fungal infections, especially when administered over a longer time.21,27 Fluconazole is found in high concentrations in the stratum corneum and dermis-epidermis of skin, in addition to eccrine sweat. Fluconazole is found to accumulate especially well in the stratum corneum, which is beneficial in superficial fungal infections.26 Saliva and sputum concentrations of fluconazole are found to be similar to the plasma concentrations.25 In patients diagnosed with fungal meningitis, fluconazole CSF (cerebrospinal fluid) levels are measured to be about 80% of the corresponding plasma levels. Therefore, fluconazole crosses the blood-brain barrier.26 The meninges are increasingly permeable to fluconazole in states of inflammation, facilitating treatment in meningitis.22
Protein bindingThe protein binding of fluconazole is low and estimated to be 11 to 12%.27,21
MetabolismFluconazole is metabolized minimally in the liver. Fluconazole is an inhibitor of CYP2C9, CYP3A4 and CYP2C19.26,27 Two metabolites were detected in the urine of healthy volunteers taking a 50 mg radiolabeled dose of fluconazole; a glucuronidated metabolite on the hydroxyl moiety (6.5%) and a fluconazole N-oxide metabolite (2%).23 The same study indicated that no signs of metabolic cleavage of fluconazole were observed, suggesting a difference in metabolism when compared to other agents in the same drug class, which are heavily metabolized in the liver.23,24
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Route of eliminationIn normal volunteers, fluconazole is cleared primarily by renal excretion, with approximately 80% of the administered dose measured in the urine as unchanged drug.27 About 11% of the dose is excreted in the urine as metabolites.27. A study of a 50mg radiolabeled dose of fluconazole revealed that 93.3% of the dose was found excreted in the urine.23
A note on renal failure
The pharmacokinetics of fluconazole are significantly affected by renal dysfunction. The dose of fluconazole may need to be reduced in patients with decreased renal function. A 3-hour hemodialysis treatment lowers plasma fluconazole concentrations by about 50%.27
Half-lifeThe terminal elimination half-life in the plasma is approximately 30 hours (range: 20-50 hours) after oral administration.27 The long plasma elimination half-life supports a single-dose therapy for vaginal candidiasis, once daily and once weekly dosing for other indications.26 Patients with renal failure may require dosage adjustment, and half-life can be significantly increased in these patients.21
ClearanceThis drug is mainly eliminated by the kidneys and the mean body clearance in adults is reported to be 0.23 mL/min/kg.27 One clinical study of healthy subjects showed total clearance of 19.5 ± 4.7 mL/min and renal clearance of 14.7 ± 3.7 mL/min (1.17 ± 0.28 and 0.88 ± 0.22 L/h).21
Clearance in the pediatric population varies according to age, as does clearance in patients with renal failure.27
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ToxicityAcute oral toxicity (LD50): 1271 mg/kg (rat) MSDS
Overdose information
Fluconazole overdoses have been associated with hallucination and paranoia, sometimes in combination.27 In cases of overdose, employ supportive treatment. Gastric lavage may be necessary.27 Other modalities such as forced diuresis or hemodialysis may also be used.27
A note on liver toxicity
The FDA label warns that this drug carries a risk of hepatotoxicity. Rare but serious cases of serious hepatic toxicity have been reported, especially in patients with serious underlying medical conditions using fluconazole. This group of patients has an increased risk of fatality when using fluconazole.27 In patients with existing liver dysfunction, use caution during fluconazole therapy. Those who are found to have abnormal liver function tests during therapy should be carefully monitored for the development of increasingly severe injury to the liver. Fluconazole should be stopped if its use is likely to be the underlying cause of liver injury, and medical attention should be sought.27,25 Fluconazole induced hepatotoxicity is usually reversible.27
Carcinogenesis, mutagenesis, and impairment of fertility
Fluconazole demonstrated no evidence of carcinogenic risk in mice and rats treated orally for 24 months at doses equivalent to approximately 2-7 time the recommended human dose). Male rats given fluconazole at doses equivalent to supratherapeutic human doses showed an increased incidence of hepatocellular adenomas. Cytogenetic studies in vivo and in vitro demonstrated no sign of chromosomal mutation. The significance of these findings for humans is unknown.27
Use in pregnancy
There are no sufficient and well-controlled studies of fluconazole use in pregnant women. Available human data do not show an increased risk of congenital anomalies after pregnant women were treated with standard doses (<200 mg/day) of fluconazole, either in a single dose or multiple doses in the first trimester did not appear to impact the fetus negatively.27 Several case reports describe rare but striking congenital anomalies observed in infants who were exposed to fluconazole at high doses reaching 400-800 mg/day, primarily in the first trimester of pregnancy. Similar findings were observed in animal studies. If this drug is administered during pregnancy, or if the patient becomes pregnant while taking fluconazole, the risk should be discussed thoroughly.27
Use in nursing
Fluconazole is secreted in breastmilk at high concentrations. Exercise caution if this drug is used during nursing.27
PathwaysNot AvailablePharmacogenomic Effects/ADRsNot AvailableDrug Interactions
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- Take with or without food. The absorption is unaffected by food.
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Product ImagesInternational/Other BrandsElazor / Flucazol / Flucostat / Flunizol / Pritenzol / Trican / TriflucanBrand Name Prescription ProductsNameDosageStrengthRouteLabellerMarketing StartMarketing EndRegionImageAct FluconazoleTablet100 mgOralTEVA Canada Limited2007-12-03Not applicableCanadaAct FluconazoleTablet50 mgOralTEVA Canada Limited2007-12-03Not applicableCanadaDiflucanSolution2 mg/1mLIntravenousRoerig2006-06-082006-06-08USDiflucanTablet150 mg/1OralA-S Medication Solutions1990-01-29Not applicableUSDiflucanTablet200 mg/1OralPD-Rx Pharmaceuticals, Inc.1990-01-29Not applicableUSDiflucanTablet100 mgOralPfizer Canada Ulc1990-12-31Not applicableCanadaDiflucanTablet100 mg/1OralPhysicians Total Care, Inc.1990-01-292012-06-30USDiflucanTablet200 mg/1OralRoerig1990-01-29Not applicableUSDiflucanTablet50 mg/1OralRoerig1990-01-29Not applicableUSDiflucanPowder, for solution50 mg / 5 mLOralPfizer Canada Ulc1995-12-31Not applicableCanadaGeneric Prescription ProductsNameDosageStrengthRouteLabellerMarketing StartMarketing EndRegionImageApo-fluconazoleTablet100 mgOralApotex Corporation1998-10-13Not applicableCanadaApo-fluconazoleTablet50 mgOralApotex Corporation1998-10-13Not applicableCanadaApo-fluconazoleTablet200 mgOralApotex CorporationNot applicableNot applicableCanadaDirect RxTablet200 mg/1OralDirect Rx2015-01-012015-08-03USDom-fluconazoleTablet100 mgOralDominion Pharmacal2002-07-09Not applicableCanadaDom-fluconazoleTablet50 mgOralDominion Pharmacal2002-07-09Not applicableCanadaFluconazoleTablet200 mg/1OralDispensing Solutions, Inc.2006-01-25Not applicableUSFluconazoleTablet150 mg/1OralDispensing Solutions, Inc.2004-09-23Not applicableUSATC CodesJ01RA07 — Azithromycin, fluconazole and secnidazoleJ02AC01 — FluconazoleD01AC15 — FluconazoleChemical TaxonomyProvided by ClassyfireDescriptionThis compound belongs to the class of organic compounds known as fluorobenzenes. These are compounds containing one or more fluorine atoms attached to a benzene ring.KingdomOrganic compoundsSuper ClassBenzenoidsClassBenzene and substituted derivativesSub ClassHalobenzenesDirect ParentFluorobenzenesAlternative ParentsAryl fluorides / Triazoles / Tertiary alcohols / Heteroaromatic compounds / Azacyclic compounds / Organopnictogen compounds / Organonitrogen compounds / Organofluorides / Hydrocarbon derivatives / Aromatic alcoholsSubstituents1,2,4-triazole / Alcohol / Aromatic alcohol / Aromatic heteromonocyclic compound / Aryl fluoride / Aryl halide / Azacycle / Azole / Fluorobenzene / Heteroaromatic compoundMolecular FrameworkAromatic heteromonocyclic compoundsExternal Descriptorstertiary alcohol, triazole antifungal drug, conazole antifungal drug, difluorobenzene (CHEBI:46081)Affected organisms
UNII8VZV102JFYCAS number86386-73-4InChI KeyRFHAOTPXVQNOHP-UHFFFAOYSA-NInChI
InChI=1S/C13H12F2N6O/c14-10-1-2-11(12(15)3-10)13(22,4-20-8-16-6-18-20)5-21-9-17-7-19-21/h1-3,6-9,22H,4-5H2
IUPAC Name2-(2,4-difluorophenyl)-1,3-bis(1H-1,2,4-triazol-1-yl)propan-2-ol
SMILESOC(CN1C=NC=N1)(CN1C=NC=N1)C1=C(F)C=C(F)C=C1
Synthesis ReferenceUS4404216General References
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- Thamban Chandrika N, Shrestha SK, Ngo HX, Howard KC, Garneau-Tsodikova S: Novel fluconazole derivatives with promising antifungal activity. Bioorg Med Chem. 2018 Feb 1;26(3):573-580. doi: 10.1016/j.bmc.2017.12.018. Epub 2017 Dec 17. [Article]
- Berkow EL, Lockhart SR: Fluconazole resistance in Candida species: a current perspective. Infect Drug Resist. 2017 Jul 31;10:237-245. doi: 10.2147/IDR.S118892. eCollection 2017. [Article]
- Ghannoum MA, Rice LB: Antifungal agents: mode of action, mechanisms of resistance, and correlation of these mechanisms with bacterial resistance. Clin Microbiol Rev. 1999 Oct;12(4):501-17. [Article]
- Trosken ER, Adamska M, Arand M, Zarn JA, Patten C, Volkel W, Lutz WK: Comparison of lanosterol-14 alpha-demethylase (CYP51) of human and Candida albicans for inhibition by different antifungal azoles. Toxicology. 2006 Nov 10;228(1):24-32. doi: 10.1016/j.tox.2006.08.007. Epub 2006 Aug 12. [Article]
- Magill SS, Puthanakit T, Swoboda SM, Carson KA, Salvatori R, Lipsett PA, Hendrix CW: Impact of fluconazole prophylaxis on cortisol levels in critically ill surgical patients. Antimicrob Agents Chemother. 2004 Jul;48(7):2471-6. doi: 10.1128/AAC.48.7.2471-2476.2004. [Article]
- de Carvalho Santana R, Schiave LA, Dos Santos Quaglio AS, de Gaitani CM, Martinez R: Fluconazole Non-susceptible Cryptococcus neoformans, Relapsing/Refractory Cryptococcosis and Long-term Use of Liposomal Amphotericin B in an AIDS Patient. Mycopathologia. 2017 Oct;182(9-10):855-861. doi: 10.1007/s11046-017-0165-1. Epub 2017 Jun 27. [Article]
- Jessup CJ, Pfaller MA, Messer SA, Zhang J, Tumberland M, Mbidde EK, Ghannoum MA: Fluconazole susceptibility testing of Cryptococcus neoformans: comparison of two broth microdilution methods and clinical correlates among isolates from Ugandan AIDS patients. J Clin Microbiol. 1998 Oct;36(10):2874-6. [Article]
- Garnacho-Montero J, Diaz-Martin A, Garcia-Cabrera E, Ruiz Perez de Pipaon M, Hernandez-Caballero C, Aznar-Martin J, Cisneros JM, Ortiz-Leyba C: Risk factors for fluconazole-resistant candidemia. Antimicrob Agents Chemother. 2010 Aug;54(8):3149-54. doi: 10.1128/AAC.00479-10. Epub 2010 May 24. [Article]
- Alastruey-Izquierdo A, Melhem MS, Bonfietti LX, Rodriguez-Tudela JL: SUSCEPTIBILITY TEST FOR FUNGI: CLINICAL AND LABORATORIAL CORRELATIONS IN MEDICAL MYCOLOGY. Rev Inst Med Trop Sao Paulo. 2015 Sep;57 Suppl 19:57-64. doi: 10.1590/S0036-46652015000700011. [Article]
- Sun G, Thai SF, Lambert GR, Wolf DC, Tully DB, Goetz AK, George MH, Grindstaff RD, Dix DJ, Nesnow S: Fluconazole-induced hepatic cytochrome P450 gene expression and enzymatic activities in rats and mice. Toxicol Lett. 2006 Jun 20;164(1):44-53. doi: 10.1016/j.toxlet.2005.11.015. Epub 2006 Jan 6. [Article]
- Joseph-Horne T, Hollomon DW: Molecular mechanisms of azole resistance in fungi. FEMS Microbiol Lett. 1997 Apr 15;149(2):141-9. doi: 10.1111/j.1574-6968.1997.tb10321.x. [Article]
- Sheng C, Miao Z, Ji H, Yao J, Wang W, Che X, Dong G, Lu J, Guo W, Zhang W: Three-dimensional model of lanosterol 14 alpha-demethylase from Cryptococcus neoformans: active-site characterization and insights into azole binding. Antimicrob Agents Chemother. 2009 Aug;53(8):3487-95. doi: 10.1128/AAC.01630-08. Epub 2009 May 26. [Article]
- Devenport MH, Crook D, Wynn V, Lees LJ: Metabolic effects of low-dose fluconazole in healthy female users and non-users of oral contraceptives. Br J Clin Pharmacol. 1989 Jun;27(6):851-9. doi: 10.1111/j.1365-2125.1989.tb03449.x. [Article]
- Grossman NT, Pham CD, Cleveland AA, Lockhart SR: Molecular mechanisms of fluconazole resistance in Candida parapsilosis isolates from a U.S. surveillance system. Antimicrob Agents Chemother. 2015 Feb;59(2):1030-7. doi: 10.1128/AAC.04613-14. Epub 2014 Dec 1. [Article]
- Nasrollahi Z, Yadegari MH, Roudbar Mohammadi S, Roudbary M, Hosseini Poor M, Nikoomanesh F, Rajabi Bazl M: Fluconazole Resistance Candida albicans in Females With Recurrent Vaginitis and Pir1 Overexpression. Jundishapur J Microbiol. 2015 Sep 23;8(9):e21468. doi: 10.5812/jjm.21468. eCollection 2015 Sep. [Article]
- Debruyne D, Ryckelynck JP: Clinical pharmacokinetics of fluconazole. Clin Pharmacokinet. 1993 Jan;24(1):10-27. doi: 10.2165/00003088-199324010-00002. [Article]
- Manosuthi W, Chetchotisakd P, Nolen TL, Wallace D, Sungkanuparph S, Anekthananon T, Supparatpinyo K, Pappas PG, Larsen RA, Filler SG, Andes D: Monitoring and impact of fluconazole serum and cerebrospinal fluid concentration in HIV-associated cryptococcal meningitis-infected patients. HIV Med. 2010 Apr;11(4):276-81. doi: 10.1111/j.1468-1293.2009.00778.x. Epub 2009 Dec 8. [Article]
- Brammer KW, Coakley AJ, Jezequel SG, Tarbit MH: The disposition and metabolism of [14C]fluconazole in humans. Drug Metab Dispos. 1991 Jul-Aug;19(4):764-7. [Article]
- Elewski B, Tavakkol A: Safety and tolerability of oral antifungal agents in the treatment of fungal nail disease: a proven reality. Ther Clin Risk Manag. 2005 Dec;1(4):299-306. [Article]
- Fluconazole, Medsafe NZ data sheet [Link]
- EMA Summary of Product Characteristics: Diflucan (fluconazole) oral capsules [Link]
- FDA Approved Drug Products: Diflucan (fluconazole) [Link]
Clinical Trials
Manufacturers
- Pfizer chemicals div pfizer inc
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- Unique pharmaceutical laboratories
- Advanced Pharmaceutical Services Inc.
- Amerisource Health Services Corp.
- Apotex Inc.
- Apotheca Inc.
- APP Pharmaceuticals
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- A-S Medication Solutions LLC
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- Comprehensive Consultant Services Inc.
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- Dispensing Solutions
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- Glenmark Generics Ltd.
- Greenstone LLC
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- Hikma Pharmaceuticals
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- J.B. Chemicals & Pharmaceuticals
- Lake Erie Medical and Surgical Supply
- Medisca Inc.
- Murfreesboro Pharmaceutical Nursing Supply
- Mylan
- Northstar Rx LLC
- Novopharm Ltd.
- Nucare Pharmaceuticals Inc.
- Palmetto Pharmaceuticals Inc.
- Par Pharmaceuticals
- PCA LLC
- PD-Rx Pharmaceuticals Inc.
- Pfizer Inc.
- Pharmaceutical Utilization Management Program VA Inc.
- Physicians Total Care Inc.
- Preferred Pharmaceuticals Inc.
- Prepackage Specialists
- Prepak Systems Inc.
- Ranbaxy Laboratories
- Rebel Distributors Corp.
- Redpharm Drug
- Remedy Repack
- Resource Optimization and Innovation LLC
- Roxane Labs
- Sagent Pharmaceuticals
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- Taro Pharmaceuticals USA
- Teva Pharmaceutical Industries Ltd.
- UDL Laboratories
- West-Ward Pharmaceuticals
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PatentsNot AvailableStateSolidExperimental PropertiesPropertyValueSourcemelting point (°C)138-140 °C//www.chemspider.com/Chemical-Structure.3248.htmlboiling point (°C)579.8//www.lookchem.com/Fluconazole/water solubilityslightly soluble in waterFDA labellogP0.5//www.pfizer.ca/sites/g/files/g10050796/f/201806/Diflucan_PM_E_207077_12June2018.pdfpKa1.76//www.pfizer.ca/sites/g/files/g10017036/f/201410/DIFLUCAN(2).pdfPredicted PropertiesPredicted ADMET FeaturesPropertyValueProbabilityHuman Intestinal Absorption+0.9894Blood Brain Barrier+0.9382Caco-2 permeable+0.8867P-glycoprotein substrateNon-substrate0.6008P-glycoprotein inhibitor INon-inhibitor0.8782P-glycoprotein inhibitor IINon-inhibitor0.9004Renal organic cation transporterNon-inhibitor0.6461CYP450 2C9 substrateNon-substrate0.7898CYP450 2D6 substrateNon-substrate0.9116CYP450 3A4 substrateNon-substrate0.565CYP450 1A2 substrateNon-inhibitor0.6312CYP450 2C9 inhibitorNon-inhibitor0.5497CYP450 2D6 inhibitorNon-inhibitor0.809CYP450 2C19 inhibitorInhibitor0.532CYP450 3A4 inhibitorNon-inhibitor0.8196CYP450 inhibitory promiscuityLow CYP Inhibitory Promiscuity0.524Ames testNon AMES toxic0.548CarcinogenicityNon-carcinogens0.7298BiodegradationNot ready biodegradable1.0Rat acute toxicity2.4136 LD50, mol/kgNot applicablehERG inhibition (predictor I)Weak inhibitor0.8229hERG inhibition (predictor II)Non-inhibitor0.6614
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)