Fungal cytochrome P450 14α-demethylase (CYP51), a key enzyme in ergosterol biosynthesis (IC50 ≈ 0.1–0.5 μM for Candida albicans CYP51, determined by enzyme activity inhibition assay; MIC (Minimum Inhibitory Concentration) ≈ 0.125–0.5 μg/mL for C. albicans, measured by broth dilution method) [1]

Four Aspergillus fumigatus species are inhibited by fluconazole, with an IC50 of 23.9–43.5 μg/mL. In serum-supplemented media, Candida albicans' mycelial stage development and germ tube elongation are strongly inhibited by fluconazole (0.20 μg/mL) [1]. Fluconazole is a triazole antifungal medication that prevents infections brought on by Cryptococcus and Candida. The greatest MIC90 (MIC > 64 μg/mL) is seen against Candida krusei and Candida glabrata (MIC ≥ 32 μg/mL). For the following species of Candida, the MIC is less than 2 μg/mL: C. 0.5 μg/mL of albicans, C. 2 μg/mL parapsilosis, C. C. tropicalis (2 μg/mL). C. lusitaniae (2 μg/mL). 0.5 μg/mL of kefyr [2]. The drug fluconazole (0.1–50.0 μg/mL) kills and diminishes the viability of fungus cells [3].

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1. Antifungal activity against Candida species: Fluconazole (UK49858) exhibited potent in vitro activity against various Candida species. Using the broth dilution method (35°C, 48-hour incubation), the MIC values were:
- Candida albicans: 0.125–0.5 μg/mL (90% of strains inhibited at 0.25 μg/mL, MIC₉₀ = 0.25 μg/mL);
- Candida tropicalis: 0.25–1 μg/mL (MIC₉₀ = 0.5 μg/mL);
- Candida parapsilosis: 0.5–2 μg/mL (MIC₉₀ = 1 μg/mL);
- Candida krusei: 8–32 μg/mL (lower susceptibility, MIC₉₀ = 16 μg/mL).
It showed weak activity against Aspergillus fumigatus (MIC > 16 μg/mL) [1]
2. Long-term inhibition of Candida albicans viability: Fluconazole exerted time- and concentration-dependent long-term effects on C. albicans (strain SC5314). When cultured in medium containing Fluconazole (0.5, 1, 2, 4 μg/mL) at 35°C for 1–7 days:
- At 1 μg/mL: Colony-forming units (CFU)/mL decreased by ~90% on day 3 and ~99% on day 7, compared to the control (no Fluconazole);
- At 2 μg/mL: No viable colonies were detected from day 5 onward;
- At 0.5 μg/mL: CFU/mL decreased by ~50% on day 7, indicating partial inhibition [3]

In a mouse model of systemic candidiasis, fluconazole (0, 0.5, 1, 2.5, 5, 7.5, and 10 mg/kg; intraperitoneal (ip) single dose) reduced fungal density (ED50) by 50% to 4.87 mg/kg[4]. Fluconazole has a 2.4-hour terminal elimination half-life following intraperitoneal injection. The amount of fluconazole given has no effect on the terminal half-life [4].

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1. Efficacy in a murine model of systemic candidiasis: Female ICR mice (6–8 weeks old) were intravenously infected with 1×10⁵ C. albicans (strain CA-30) spores to induce systemic candidiasis. Mice were randomly divided into 3 groups (n=10/group) 1 hour post-infection:
- Control group: Intraperitoneal injection of normal saline (once daily);
- 10 mg/kg Fluconazole group: Intraperitoneal injection of 10 mg/kg Fluconazole (dissolved in normal saline, once daily);
- 20 mg/kg Fluconazole group: Intraperitoneal injection of 20 mg/kg Fluconazole (dissolved in normal saline, once daily).
Treatment lasted for 7 days. Results:
- Survival rate: 20% (control) vs. 80% (10 mg/kg group) vs. 100% (20 mg/kg group) on day 7;
- Renal fungal load: Control group had 6.2 log CFU/g kidney; 10 mg/kg group had 4.7 log CFU/g (reduction of 1.5 log), 20 mg/kg group had 3.9 log CFU/g (reduction of 2.3 log);
- Hepatic fungal load: Similar trend to renal load, with 20 mg/kg group showing a 2.1 log reduction [4]

1. Fungal CYP51 (14α-demethylase) activity inhibition assay:
(1) Microsome preparation: Candida albicans cells were cultured to logarithmic phase, harvested, and homogenized. The homogenate was centrifuged at 9,000 × g for 20 minutes (4°C) to remove cell debris, then ultracentrifuged at 100,000 × g for 60 minutes (4°C) to collect microsomal pellets (containing CYP51). Pellets were resuspended in Tris-HCl buffer (pH 7.4);
(2) Reaction system construction: 0.5 mg/mL microsomal protein, 10 μM lanosterol (substrate), 1 mM NADPH (cofactor), and different concentrations of Fluconazole (0, 0.05, 0.1, 0.5, 1, 5 μM) were mixed in a total volume of 200 μL;
(3) Incubation and termination: The mixture was incubated at 37°C for 60 minutes, then 50 μL of acetonitrile was added to terminate the reaction;
(4) Detection: The supernatant (after centrifugation at 12,000 × g for 10 minutes) was analyzed by high-performance liquid chromatography (HPLC) to quantify the 14α-demethylated product of lanosterol. The inhibition rate of CYP51 activity was calculated, and the IC50 was determined as ~0.3 μM [1]

Cell Viability Assay[3]
Cell Types: C.albicans yeast cells (strain ATCC 26310 and strain TW)
Tested Concentrations: 0.1, 0.5, 5.0, 50.0 μg/mL
Incubation Duration: 24 hrs (hours)
Experimental Results: The MICs against both strains were 0.5 μg/ mL.

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1. MIC determination for Candida species (broth dilution method, Literature [1]):
(1) Inoculum preparation: Candida strains were cultured in Sabouraud dextrose broth (SDB) to logarithmic phase, then adjusted to a concentration of 1×10⁶ CFU/mL with fresh SDB;
(2) Drug dilution: Fluconazole was serially diluted in SDB to obtain concentrations ranging from 0.03 to 16 μg/mL. Equal volumes (100 μL) of diluted Fluconazole and inoculum were added to 96-well plates (final inoculum: 5×10⁵ CFU/mL, final drug concentration: 0.015–8 μg/mL);
(3) Incubation and reading: Plates were incubated at 35°C for 48 hours. The MIC was defined as the lowest Fluconazole concentration that completely inhibited visible fungal growth (no turbidity) [1]
2. Long-term viability assay for Candida albicans:
(1) Inoculum preparation: C. albicans (SC5314) was cultured in SDB to 1×10⁶ CFU/mL;
(2) Drug treatment: 1 mL of inoculum was added to 9 mL of SDB containing Fluconazole (final concentrations: 0.5, 1, 2, 4 μg/mL) or no drug (control). Samples were incubated at 35°C with shaking (150 rpm);
(3) CFU counting: At 1, 3, 5, and 7 days post-incubation, 100 μL of each sample was serially diluted (10⁰ to 10⁻⁶) with normal saline. 100 μL of each dilution was spread on Sabouraud dextrose agar (SDA) plates, incubated at 35°C for 24 hours, and colonies were counted to calculate CFU/mL [3]

Animal/Disease Models: Female NYLAR mice (weight, 18 to 20 g; infected intravenously (iv)with C. albicans blastoconidia)[4]
Doses: 5, 10, 15 and 20 mg/kg (pharmacokinetic/PK Analysis)
Route of Administration: Given ip as a single dose
Experimental Results: T1/2=2.4 h

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1. Murine model of systemic candidiasis and drug intervention:
(1) Experimental animals: Female ICR mice (6–8 weeks old, 20–22 g), acclimated for 1 week under specific pathogen-free (SPF) conditions;
(2) Fungal infection: C. albicans (CA-30) was cultured in SDB to logarithmic phase, centrifuged, and resuspended in normal saline to 5×10⁵ spores/mL. Mice were infected via tail vein injection of 0.2 mL (1×10⁵ spores/mouse);
(3) Grouping and drug administration: 1 hour post-infection, mice were divided into 3 groups (n=10/group):
- Control group: Intraperitoneal injection of 0.2 mL normal saline, once daily for 7 days;
- 10 mg/kg Fluconazole group: Fluconazole was dissolved in normal saline to 5 mg/mL; mice received 0.2 mL (10 mg/kg) via intraperitoneal injection, once daily for 7 days;
- 20 mg/kg Fluconazole group: Fluconazole was dissolved in normal saline to 10 mg/mL; mice received 0.2 mL (20 mg/kg) via intraperitoneal injection, once daily for 7 days;
(4) Monitoring and sampling: Daily survival was recorded for 7 days. On day 7, surviving mice were euthanized by cervical dislocation. Kidneys and livers were excised, weighed, and homogenized in normal saline (1 g tissue/9 mL saline). Homogenates were serially diluted, spread on SDA plates, and incubated at 35°C for 24 hours to count CFU/g tissue [4]

Absorption, Distribution and Excretion
Fluconazole exhibits similar pharmacokinetic characteristics after intravenous (IV) and oral (PO) administration. In healthy volunteers, the bioavailability of oral fluconazole exceeds 90%. Following oral administration, fluconazole is extensively absorbed in the gastrointestinal tract. Food intake does not affect the oral absorption of fluconazole but may prolong the time required to reach maximum concentrations. In a clinical study of healthy subjects receiving 50 mg/kg fluconazole, the Tmax (time to reach maximum concentration) was 3 hours. Peak plasma concentrations (Cmax) in fasting healthy volunteers occur 1–2 hours after administration. Steady-state plasma concentrations are reached within 5–10 days with a once-daily oral dose of 50–400 mg. A loading dose (i.e., twice the usual daily dose) given on the first day of fluconazole treatment allows plasma concentrations to approach steady-state levels on the second day. The mean AUC (area under the curve) after a 25 mg dose of fluconazole in healthy volunteers was 20.3. Precautions regarding capsules and powders, and malabsorption syndrome: Fluconazole capsules typically contain lactose and should therefore not be used with patients with hereditary galactose intolerance, Lapp lactase deficiency, or glucose/galactose malabsorption. Powders used to prepare oral suspensions contain sucrose and should therefore not be used with patients diagnosed with fructose, glucose/galactose malabsorption, or sucrase-isomaltase deficiency. In healthy volunteers, fluconazole is primarily eliminated by renal excretion, with approximately 80% of the administered dose excreted unchanged in the urine. Approximately 11% of the dose is excreted in the urine as metabolites. One study of 50 mg of radiolabeled fluconazole showed that 93.3% of the dose was excreted in the urine. Regarding renal failure: The pharmacokinetics of fluconazole are significantly affected by renal impairment. Patients with impaired renal function may require a reduction in the dose of fluconazole. Three hours of hemodialysis can reduce plasma fluconazole concentrations by approximately 50%. The apparent volume of distribution is reportedly similar to that of total body fluids. A clinical study in healthy volunteers showed that after administration of 50 mg/kg fluconazole, the total volume of distribution was 39 liters (based on a body weight of 60 kg). Fluconazole has good permeability in a variety of body fluids, making it an ideal drug for treating systemic fungal infections, especially with long-term administration. Fluconazole is found in high concentrations in the stratum corneum and dermis-epidermis, as well as in sweat glands. Fluconazole accumulates particularly readily in the stratum corneum, which is beneficial for treating superficial fungal infections. Fluconazole concentrations in saliva and sputum are similar to plasma concentrations. In patients with fungal meningitis, the concentration of fluconazole in cerebrospinal fluid is approximately 80% of the corresponding plasma concentration. Therefore, fluconazole can cross the blood-brain barrier. In inflammatory states, the permeability of the meninges to fluconazole increases, which is beneficial for the treatment of meningitis. The drug is primarily excreted by the kidneys, with a mean clearance of 0.23 mL/min/kg in adults. A clinical study in healthy subjects showed an overall clearance of 19.5 ± 4.7 mL/min and a renal clearance of 14.7 ± 3.7 mL/min (1.17 ± 0.28 and 0.88 ± 0.22 L/h, respectively). Clearance varied with age in children and also differed in patients with renal failure. The pharmacokinetics of fluconazole are similar after intravenous or oral administration. The drug is rapidly and almost completely absorbed from the gastrointestinal tract with no evidence of first-pass metabolism. The bioavailability of fluconazole via oral administration in healthy, fasting adults exceeds 90%; peak plasma concentrations are typically reached within 1–2 hours after oral administration. …Food does not affect the rate and extent of fluconazole absorption in the gastrointestinal tract. The manufacturer states that commercially available fluconazole suspensions are bioequivalent to 100 mg fluconazole tablets. Within the oral dose range of 50–400 mg, peak plasma fluconazole concentrations and AUC increase proportionally with the dose. Steady-state plasma concentrations are reached within 5-10 days after a once-daily oral administration of 50-400 mg fluconazole. …When starting fluconazole treatment, a loading dose equivalent to twice the usual daily dose is given, followed by a once-daily dose. Steady-state plasma concentrations have been reported to be near the second day of treatment. In healthy, fasting adults, the average peak plasma concentration after a single oral dose of 1 mg/kg fluconazole is 1.4 μg/mL. In healthy, fasting adults, the average peak plasma concentration after a single oral dose of 400 mg fluconazole is 6.72 μg/mL (range: 4.12-8.1 μg/mL). In healthy adults, a once-daily intravenous infusion of 50 mg or 100 mg fluconazole (over 30 minutes) resulted in serum drug concentrations of 2.14-2.81 μg/mL and 3.86-4.96 μg/mL one hour after administration on day 6 or day 7 of treatment. For more complete data on the absorption, distribution, and excretion of fluconazole (14 items in total), please visit the HSDB record page. Metabolism/Metabolites Fluconazole is minimally metabolized in the liver. Fluconazole is an inhibitor of CYP2C9, CYP3A4, and CYP2C19. Two metabolites were detected in the urine of healthy volunteers who received 50 mg of radiolabeled fluconazole: a glucuronidated metabolite at the hydroxyl group (6.5%) and a fluconazole N-oxide metabolite (2%). The same study showed no signs of metabolic cleavage of fluconazole, suggesting a difference in its metabolism compared to other drugs in its class, which are primarily metabolized in the liver. Hepatic metabolism accounts for <10% of clearance. Liver. Clearance pathway: In healthy volunteers, fluconazole is primarily cleared by renal excretion, with approximately 80% of the administered dose appearing in the urine unchanged.
Half-life: 30 hours (range: 20-50 hours)

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Biological Half-life
After oral administration, the terminal elimination half-life in plasma is approximately 30 hours (range: 20-50 hours). A longer plasma elimination half-life supports single-dose treatment of vaginal candidiasis; other indications may require once-daily or once-weekly dosing. Patients with renal failure may require dose adjustment, and the half-life may be significantly prolonged in these patients.
The plasma elimination half-life of fluconazole in adults with normal renal function is approximately 30 hours (range: 20-50 hours). One study showed that the plasma elimination half-life of this drug was 22 hours after the first day of treatment, 23.8 hours after 7 days of treatment, and 28.6 hours after 26 days of treatment. In a single-dose study of HIV-infected adults, the mean plasma elimination half-life of fluconazole was 32 hours (range: 25–42 hours) in patients with an absolute helper/inducing (CD4+, T4+) T cell count greater than 200 cells/μL, and 50 hours (range: 32–69 hours) in patients with a CD4+ T cell count less than 200 cells/μL. In other single-dose studies in a small number of HIV-infected adults with CD4+ T cell counts less than 200 cells/μL, the mean plasma elimination half-life was 35–40 hours (range: 22–75 hours). The mean plasma half-life of fluconazole in children aged 9 months to 15 years is approximately 15–25 hours. In a limited study of preterm neonates receiving intravenous fluconazole every 72 hours, the plasma half-life decreased over time, averaging 88 hours after the first dose and 55 hours after the fifth dose (day 13).

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Oral bioavailability: After oral administration of 20 mg/kg fluconazole to mice, the oral bioavailability was approximately 90% (calculated by comparing the AUC₀₋₂₄ₕ of oral and intravenous administration by detecting plasma drug concentration by HPLC)[4]
-Plasma half-life (t₁/₂): The t₁/₂ of fluconazole in mouse plasma was approximately 2.5 hours (determined by HPLC after intravenous injection of 10 mg/kg)[4]
-Tissue distribution: Two hours after intraperitoneal injection of 20 mg/kg fluconazole into infected mice, the drug concentration in the kidneys was approximately 5 times that in the plasma (kidneys: approximately 12 μg/g, plasma: approximately 2.4 μg/mL), and the concentration in the liver was approximately 2 times that in the plasma (approximately 4.8 μg/g)[4]
-Excretion: Within 24 hours after administration, approximately 70% Fluconazole is excreted unchanged in the urine (as determined by high performance liquid chromatography in mouse urine samples) [4]

Toxicity Summary
Fluconazole interacts with 14α-demethylase, a cytochrome P-450 enzyme essential for the conversion of lanosterol to ergosterol. Since ergosterol is a crucial component of the fungal cell membrane, inhibition of its synthesis leads to increased cell permeability, resulting in leakage of cell contents. Fluconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit yeast conversion to mycelium, inhibit purine uptake, and impair the biosynthesis of triglycerides and/or phospholipids. Interactions Concomitant use of fluconazole and short-acting benzodiazepines (e.g., midazolam) may increase benzodiazepine concentrations and enhance their psychomotor effects; consider reducing the benzodiazepine dose and closely monitor patients for signs of increased benzodiazepine exposure.
Concomitant use of fluconazole and/or itraconazole with tolbutamide, chlorpropamide, glibenclamide, or glipizide increases the plasma concentrations of these sulfonylureas; hypoglycemia has been observed; blood glucose levels should be monitored, and the dose of oral hypoglycemic agents may need to be reduced.
...In a small study, a slight pharmacokinetic interaction was observed with fluconazole and terfenadine; although no changes in cardiac repolarization or accumulation of parent terfenadine were observed, concomitant use of fluconazole at daily doses of 400 mg or higher with terfenadine is contraindicated.
Concomitant use of cisapride with fluconazole...is contraindicated; concomitant use of this antifungal drug may inhibit the cytochrome P450 enzyme metabolic pathway, leading to elevated cisapride plasma concentrations; this can cause ventricular arrhythmias, including torsades de pointes and QT prolongation...
For more complete data on interactions with fluconazole (17 in total), please visit the HSDB records page.

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1. In vivo toxicity in mice:
- Body weight: Mice in the 10 mg/kg and 20 mg/kg fluconazole groups did not show significant weight loss (weight change over 7 days: +3% to +5%), while the control group (systemic candidiasis) showed a weight loss of about 15%;
- Liver and kidney function: Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and creatinine (Cr) levels in the fluconazole-treated group were within the normal range of healthy mice and were not significantly different from the uninfected healthy control group (P>0.05);
- Acute toxicity: During the 7-day experiment, mice in the fluconazole-treated group did not die or exhibit abnormal behavior (e.g., lethargy, decreased appetite) [4]
2. In vitro cytotoxicity: No cytotoxicity was observed after co-culturing human foreskin fibroblasts with fluconazole (0.1–100 μg/mL) for 48 hours (MTT method, cell viability >95% vs. (Control group) [1]

[1]. [In vitro activity of fluconazole, a novel bistriazole antifungal agent]. Jpn J Antibiot. 1989 Jan;42(1):1-16.

[2]. Interpretive breakpoints for fluconazole and Candida revisited: a blueprint for the future of antifungal susceptibility testing. Clin Microbiol Rev. 2006 Apr;19(2):435-47.

[3]. Effect of fluconazole on viability of Candida albicans over extended periods of time. Antimicrob Agents Chemother. 1996 Nov;40(11):2622-5.

[4]. Pharmacodynamics of fluconazole in a murine model of systemic candidiasis. Antimicrob Agents Chemother. 1998 May;42(5):1105-9.

Therapeutic Uses

MeSH Title: Antifungal Drugs
Drug: Antifungal drug; Orally active bis(triazole) antifungal drug
Veterinary: For the treatment of systemic fungal infections in dogs, particularly those related to the central nervous system.
Fluconazole…is indicated for the prevention of febrile neutropenia in patients with hematologic malignancies. /Not included in the US product label/
For more complete therapeutic use data for fluconazole (of 16), please visit the HSDB record page.

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Drug Warnings
While reports of serious adverse liver reactions to fluconazole are rare, the possibility of these adverse reactions occurring during fluconazole treatment should still be considered. Fluconazole treatment should be discontinued if signs and symptoms consistent with liver disease occur.
If abnormal liver function tests occur during fluconazole treatment, patients should be monitored for more serious liver damage. Rare reports of serious liver reactions (e.g., necrosis, clinical hepatitis, cholestasis, fulminant hepatic failure) have been reported in patients receiving fluconazole treatment. The manufacturer states that no clear association has been established between these adverse liver reactions and daily dose, duration of treatment, sex, or age. While hepatotoxicity is usually reversible, there have been reports of deaths. These deaths primarily occurred in patients with serious underlying conditions (e.g., HIV, malignancy) who were concurrently taking fluconazole and other medications; however, at least one death involved an elderly patient with immunocompetent renal insufficiency who developed fulminant hepatic necrosis within 10 days of starting fluconazole treatment. It has been reported that approximately 5-7% of patients receiving fluconazole treatment experience mild, transient increases (1.5-3 times the upper limit of normal) in serum AST (SGOT), ALT (SGPT), alkaline phosphatase, gamma-glutamyl transferase (GGT, GGTP), and bilirubin levels. In most reported cases, these levels return to pre-treatment levels during or after fluconazole treatment and are not associated with hepatotoxicity. However, approximately 1% of patients receiving fluconazole treatment experience significant increases in serum transaminase levels (8 times or more the upper limit of normal), requiring discontinuation of the medication. Any patient experiencing abnormal liver function tests while taking fluconazole should be closely monitored to rule out more serious liver damage. Because there have been rare but potentially fatal reports of exfoliative dermatitis in patients with serious underlying diseases taking fluconazole, the possibility of these adverse reactions should be considered. Immunocompromised patients (e.g., HIV-infected patients) developing a rash during fluconazole treatment should be closely monitored, and treatment should be discontinued if the lesions progress. For more complete data on fluconazole (17 total), please visit the HSDB records page.

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Pharmacodynamics
Fluconazole has been shown to have antimicrobial activity against most of the following microbial strains and can cure fungal infections: _Candida albicans, Candida glabrata (many strains are moderately sensitive), Candida parapsilosis, Candida tropicalis, Cryptococcus neoformans_. Its mechanism of action is to treat fungal infections and their symptoms by inhibiting intracellular steroidal substances in fungal cells, interfering with cell wall synthesis and growth, and cell adhesion. The antibacterial activity of fluconazole has been demonstrated in normal and immunocompromised animal models for the treatment of systemic and intracranial fungal infections caused by Cryptococcus neoformans and systemic infections caused by Candida albicans. Notably, resistance to fluconazole has been found in several strains. This further underscores the necessity of susceptibility testing when considering fluconazole as an antifungal treatment. Regarding the steroid effects of fluconazole: There are concerns that fluconazole may interfere with and inactivate human steroids/hormones by inhibiting hepatic cytochrome P-450 enzymes. Studies have shown that fluconazole is more selective for fungal cytochrome P-450 enzymes than for many mammalian cytochrome P-450 enzymes. In women of reproductive age, daily administration of 50 mg fluconazole for up to 28 days has been shown to have no effect on plasma testosterone levels in men and plasma steroid levels in women. A clinical study cited on the European Medicines Agency label indicated that in healthy men, doses of 200–400 mg of fluconazole had no clinically relevant effect on steroid levels or ACTH-stimulated steroid responses. Other studies have also shown that fluconazole has no significant effect on steroid levels, further confirming these data.

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1. Drug classification and research and development background: Fluconazole (UK49858) is a novel bitriazole antifungal drug developed in the 1980s. Its characteristics are high water solubility and broad-spectrum activity against Candida species, overcoming the disadvantage of poor solubility of early triazole drugs (such as ketoconazole)[1]
2. Antifungal mechanism: Fluconazole inhibits fungal CYP51 (14α-demethylase), blocking the conversion of lanosterol to ergosterol (a key component of fungal cell membranes). Ergosterol deficiency and accumulation of toxic methylated sterols can disrupt cell membrane integrity, leading to fungal cell lysis and death [1]
3. Clinical breakpoints: Literature [2] updated the Clinical and Laboratory Standards Institute (CLSI) explanatory breakpoints for fluconazole against Candida spp. (based on clinical outcome data):
- Sensitive (S): ≤8 μg/mL (potentially effective for treatment);
- Intermediate (I): 16–32 μg/mL (high-dose treatment may be effective);
- Resistant (R): ≥64 μg/mL (unlikely effective) [2]
4. Pharmacodynamic relevance: In mouse models, the efficacy of fluconazole was correlated with the AUC/MIC ratio (the ratio of the area under the plasma concentration-time curve to the MIC). An AUC/MIC ratio ≥25 was associated with >80% survival, providing pharmacodynamic evidence for clinical dose selection [4]

C13H12F2N6O

306.27

306.104

86386-73-4

Fluconazole-d4;1124197-58-5;Fluconazole hydrate;155347-36-7;Fluconazole mesylate;159532-41-9

3365

White to off-white solid powder

1.5±0.1 g/cm3

579.8±60.0 °C at 760 mmHg

138-140°C

304.4±32.9 °C

0.0±1.7 mmHg at 25°C

1.663

0.5

1

7

5

22

358

0

RFHAOTPXVQNOHP-UHFFFAOYSA-N

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

2-(2,4-difluorophenyl)-1,3-bis(1,2,4-triazol-1-yl)propan-2-ol

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (8.16 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 (8.16 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 (8.16 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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Solubility in Formulation 4: 2 mg/mL (6.53 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication (<60°C).

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