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Itraconazole

Itraconazole is a triazole antifungal medication used to treat a variety of fungal infections, including candidiasis, blastomycosis, histoplasmosis, and aspergillosis.
It works by inhibiting the synthesis of ergosterol, an essential component of the fungal cell membrane.
Itraconazole is availble in oral and intravenous formulations, and is known for its broad spectrum of activity and good tolerability profile.
Reserchers can leverage the PubCompare.ai platform to optimize their Itraconazole reserch, locateing protocols from literature, pre-printes, and patents, and utilizing AI-driven comparisons to identify the best protocols and products.
This powerful tool can enhance reproducibility and accuracy in Itraconazole reserch.

Most cited protocols related to «Itraconazole»

1
Modeling Induction and Inhibition Processes
Cited 8 times
Mathematical implementation of the induction and inhibition processes in general is specified in Section 1 of Appendix S1. The final rifampicin model was coupled to models of midazolam, alfentanil, itraconazole, and digoxin, to assess its DDI performance with CYP3A4 and P‐gp substrates. To describe the influence of rifampicin on these victim drugs, induction and simultaneous competitive inhibition of CYP3A4 and P‐gp by rifampicin have been added. Furthermore, inhibition of midazolam and digoxin elimination by itraconazole and by clarithromycin were modeled and compared to observed clinical data, evaluating the performance of these two victim drug models with two different CYP3A4 and P‐gp inhibitors. Inhibition of alfentanil metabolism by itraconazole or clarithromycin was not tested, as there are no clinical studies available to compare to.
All induction and inhibition processes were modeled using interaction parameter values either identified during the development of the perpetrator models if no experimental values could be found to parameterize their auto‐induction or auto‐inhibition (using multiple‐dose perpetrator studies only, without co‐administration of victim drugs), or taken from literature without further adjustment or fitting, as a means of further evaluation of the perpetrator and victim drug models.
Hanke N., Frechen S., Moj D., Britz H., Eissing T., Wendl T, & Lehr T. (2018). PBPK Models for CYP3A4 and P‐gp DDI Prediction: A Modeling Network of Rifampicin, Itraconazole, Clarithromycin, Midazolam, Alfentanil, and Digoxin. CPT: Pharmacometrics & Systems Pharmacology, 7(10), 647-659.
Publication 2018
Alfentanil Clarithromycin Cytochrome P-450 CYP3A4 Digoxin inhibitors Itraconazole Metabolism Midazolam Pharmaceutical Preparations Psychological Inhibition Rifampin
2
Antifungal Susceptibility Testing Protocol
Cited 7 times
Reference antifungal susceptibility testing of all 212 isolates was performed by BMD (broth microdilution) exactly as described in CLSI document M27-A2 [29 ] against fluconazole (Pfizer, Sao Paulo, Brazil), itraconazole (Janssen, Beerse, Belgium) and amphotericin B (Sigma, St. Louis, MO, USA). The isolates were incubated at 35°C and the presence or absence of growth, after 48 h, was observed by visual inspection. The MIC endpoint for amphotericin B was considered the lowest tested drug concentration able to prevent any visible growth, while the MIC for azoles was considered the lowest tested drug concentration causing a significant reduction (approximately 50%) in growth compared to the growth of the drug-free positive control [29 ]. MIC interpretations follow the CLSI breakpoints [29 ] for fluconazol (≤8 ug/ml, susceptible; 16-32 ug/ml, SDD, ≥64, resistant) and itraconazole (≤0.125 μg/ml, susceptible; 0.25-0.5 ug/ml, SDD, ≥1, resistant). For amphotericin B, due to a lack of consensus about the definition of this drug's MIC, previous interpretative breakpoints described elsewhere [30 (link)] were employed (≤1 ug/ml, susceptible, ≥2, resistant).
Bruder-Nascimento A., Camargo C.H., Sugizaki M.F., Sadatsune T., Montelli A.C., Mondelli A.L, & Bagagli E. (2010). Species distribution and susceptibility profile of Candida species in a Brazilian public tertiary hospital. BMC Research Notes, 3, 1.
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Publication 2010
Amphotericin Amphotericin B Antifungal Agents Azoles Fluconazole Itraconazole MICB protein, human Substance Abuse Detection Susceptibility, Disease
3
Prophylactic Antiviral and Antifungal Regimen
Cited 6 times
Oral sulfamethoxazole and norfloxacin were given to all patients. Acyclovir was given daily from the beginning of conditioning therapy to engraftment, and it was then administered daily for 7 days every 2 weeks until 1 year after transplantation. Ganciclovir was given for 2 weeks before transplantation for prophylaxis of CMV infections, and was administered once again when CMV viremia occurred. Antifungal agents were administered 5 days before transplantation. Fluconazole (0.3 g/day) or itraconazole (0.4 g/kg.d) was used for up to +60 days post-transplantation in patients with no history of invasive fungal infection (IFI); those with a history of IFI received itraconazole (0.4 g/day), voriconazole (0.4 g/day), caspofungin (50 mg/day) or Am-Bisome (2 mg/kg.day) intravenously. Oral itraconazole or voriconazole was started when the peripheral white blood cell count exceeded 2.0 × 109/L and was discontinued after 90 days post-transplantation.
Xuan L., Huang F., Fan Z., Zhou H., Zhang X., Yu G., Zhang Y., Liu C., Sun J, & Liu Q. (2012). Effects of intensified conditioning on Epstein-Barr virus and cytomegalovirus infections in allogeneic hematopoietic stem cell transplantation for hematological malignancies. Journal of Hematology & Oncology, 5, 46.
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Publication 2012
Acyclovir Antifungal Agents Behavior Therapy Caspofungin Cytomegalovirus Infections Fluconazole Ganciclovir Infection Invasive Fungal Infections Itraconazole Leukocyte Count Norfloxacin Patients Sulfamethoxazole Transplantation Viremia Voriconazole
4
Physiologically-Based Pharmacokinetic Modeling
Cited 5 times
Models of rifampicin, itraconazole, clarithromycin, midazolam, alfentanil, and digoxin were built combining bottom‐up and top‐down techniques. To establish the models, an extensive literature search was conducted, collecting (i) physicochemical parameters, (ii) information on absorption, distribution, metabolism, and excretion processes, and (iii) clinical studies of intravenous and oral administration to healthy subjects in single‐dosing and multiple‐dosing regimens, covering the full dosing range published. All data used in this analysis has been taken from previously published human or preclinical studies.
The PBPK models were developed based on a healthy male European individual, 30 years of age, with a body weight of 73 kg, and a height of 176 cm. Physiological parameters, like organ volumes, blood flow rates, and surface permeabilities, are provided within the software.7 Absorption, distribution, metabolism, and excretion‐relevant proteins reported to govern the PK of a drug, such as metabolizing enzymes, transporters, or binding partners, were implemented into the models and tested. Whenever available and in accordance with literature protein expression, the PK‐Sim expression database reverse transcription‐polymerase chain reaction (RT‐PCR) profiles8 were used to define the relative tissue distribution of these proteins. For parameters that could not be informed from (in vitro) experimental data, parameter identification based on plasma concentration‐time profiles was performed using a subset of the available clinical studies (training dataset) for optimization. The decision of which studies to include into the training dataset was based on the number of studies available and the information contained in the different studies (dosing regimen, study size, sampling times, fraction excreted measurements, etc.).
Model selection was based on the ability of the model to describe (training dataset) and predict (test dataset) plasma concentration‐time profiles from all published clinical studies as well as fraction excreted unchanged to urine. Furthermore, physiological plausibility, precision and covariance of parameter estimates, and population predictions were assessed.
Hanke N., Frechen S., Moj D., Britz H., Eissing T., Wendl T, & Lehr T. (2018). PBPK Models for CYP3A4 and P‐gp DDI Prediction: A Modeling Network of Rifampicin, Itraconazole, Clarithromycin, Midazolam, Alfentanil, and Digoxin. CPT: Pharmacometrics & Systems Pharmacology, 7(10), 647-659.
Publication 2018
Administration, Oral Alfentanil Blood Circulation Body Weight Clarithromycin Digoxin Enzymes Europeans Healthy Volunteers Homo sapiens Itraconazole Males Membrane Transport Proteins Metabolism Midazolam Organ Volume Permeability Pharmaceutical Preparations physiology Plasma Proteins Reverse Transcriptase Polymerase Chain Reaction Rifampin Treatment Protocols Urine
5
Antifungal susceptibility testing protocol
Cited 5 times
Antifungal susceptibility was determined in flat bottom, 96-well microtiter plates (Sarstedt) using a modified broth microdilution protocol, as described [44] (link). Minimum inhibitor concentration (MIC) tests were set up in a total volume of 0.2 ml/well with 2-fold dilutions of caspofungin (CF, generously provided by Rochelle Bagatell). Echinocandin gradients were from 16 µg/ml down to 0 with the following concentration steps in µg/ml: 16, 8, 4, 2, 1, 0.5, 0.25, 0.125, 0.0625, 0.03125, 0.015625, and 0. Cell densities of overnight cultures were determined and dilutions were prepared such that ∼103 cells were inoculated into each well. Geldanamycin (GdA, A.G. Scientific, Inc.) and radicicol (RAD, A.G. Scientific, Inc.) were used to inhibit Hsp90 at the indicated concentrations, and cyclosporin A (CsA, CalBiochem) and FK506 (A.G. Scientific, Inc.) were used to inhibit calcineurin at the indicated concentrations. Dimethyl sulfoxide (DMSO, Sigma Aldrich Co.) was the vehicle for GdA, RAD, CsA, and FK506. Sterile water was the vehicle for CF. Plates were incubated in the dark at 30°C for the time period indicated, at which point plates were sealed and re-suspended by agitation. Absorbance was determined at 600 nm using a spectrophotometer (Molecular Devices) and was corrected for background from the corresponding medium. Each strain was tested in duplicate on at least two occasions. MIC data was quantitatively displayed with colour using the program Java TreeView 1.1.3 (http://jtreeview.sourceforge.net).
Clinical antifungal MICs were determined using broth microdilution with RPMI 1640 broth for amphotericin, fluconazole, ketoconazole, itraconazole, voriconazole, and caspofungin following Clinical and Laboratory Standards Institute document M27-A3 [56] . Visual MIC endpoints were read after 24 hours of incubation at 35°C for caspofungin and after 48 hours of incubation for all other drugs. Complete inhibition was used to determine amphotericin endpoints; 50% inhibition (compared to growth control) was used for caspofungin and 80% inhibition was used for the other drugs.
Singh-Babak S.D., Babak T., Diezmann S., Hill J.A., Xie J.L., Chen Y.L., Poutanen S.M., Rennie R.P., Heitman J, & Cowen L.E. (2012). Global Analysis of the Evolution and Mechanism of Echinocandin Resistance in Candida glabrata. PLoS Pathogens, 8(5), e1002718.
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Publication 2012
Amphotericin Antifungal Agents Calcineurin Cardiac Arrest Caspofungin Cell Culture Techniques Cells Clinical Laboratory Services Cyclosporine Echinocandins FK-506 Fluconazole geldanamycin HSP90 Heat-Shock Proteins Itraconazole Ketoconazole Medical Devices Minimum Inhibitory Concentration monorden Pharmaceutical Preparations Psychological Inhibition Sterility, Reproductive Strains Sulfoxide, Dimethyl Susceptibility, Disease Technique, Dilution Voriconazole

Most recents protocols related to «Itraconazole»

1
Pharmacokinetics of Mitapivat Sulfate with Itraconazole or Rifampin
Not available on PMC !

Example 2

Twenty-eight (28) healthy, adult male and female (non-childbearing potential) subjects were enrolled in the study in total; 14 subjects in each study part (Parts 1 and 2). A minimum of 8 female subjects were enrolled in the study (i.e., a minimum of 4 female subjects per study part). Each subject participated in either Part 1 or Part 2, but not both.

Part 1

On Day 1 of Treatment Period 1, a single oral dose of 20 mg mitapivat sulfate was administered. Serial blood samples for plasma assay of mitapivat concentrations and its CYP3A4 metabolite, referred to herein as the “Metabolite” (structure below),

[Figure (not displayed)]
were collected from predose to 120 hours following administration of mitapivat sulfate. In Treatment Period 2, an oral dose of 200 mg itraconazole was administered once daily (QD) for 9 consecutive days (Day 1 through Day 9 of Treatment Period 2) with a single oral dose of 20 mg mitapivat sulfate coadministered on Day 5. Serial blood samples for plasma assay of mitapivat and the Metabolite concentrations were collected from predose to 120 hours following coadministration of mitapivat sulfate and itraconazole on Day 5.

In Treatment Period 1, mitapivat sulfate was administered orally with approximately 240 mL of water. In Treatment Period 2, on Days 1 to 4, itraconazole was administered alone immediately followed by approximately 220 mL of water, and on Day 5, itraconazole was administered first (no water) and was immediately followed by mitapivat sulfate administration with approximately 220 mL of water. Study drugs (mitapivat sulfate and itraconazole) were administered following an overnight fast of at least 10 hours on Day 1 of Treatment Period 1 (mitapivat sulfate only) and Day 5 of Treatment Period 2 (mitapivat sulfate and itraconazole), and subjects remained fasted for 4 hours after dosing. On all other dosing days, itraconazole was administered following a predose fast of at least 4 hours and subjects remained fasted for at least 2 hours after dosing.

Part 2

On Day 1 of Treatment Period 1, a single oral dose of 50 mg mitapivat sulfate was administered. Serial blood samples for plasma assay of mitapivat and the Metabolite concentrations were collected from predose to 120 hours following administration of mitapivat sulfate. In Treatment Period 2, an oral dose of 600 mg rifampin was administered QD for 12 consecutive days (Day 1 through Day 12 of Treatment Period 2) with a single oral dose of 50 mg mitapivat sulfate coadministered on Day 8. Serial blood samples for plasma assay of mitapivat sulfate and the Metabolite concentrations were collected from predose to 120 hours following coadministration of mitapivat and rifampin on Day 8.

In Part 2, study drugs were administered with approximately 240 mL of water on all dosing days including the coadministration of mitapivat sulfate and rifampin on Day 8 of Treatment Period 2. Mitapivat sulfate and rifampin was administered following an overnight fast of at least 10 hours on Day 1 of Treatment Period 1 (mitapivat sulfate only) and Day 8 of Treatment Period 2 (both mitapivat sulfate and rifampin) and subjects remained fasted for 4 hours after dosing. On all other dosing days, rifampin was administered following a predose fast of at least 4 hours and subjects remained fasted for at least 2 hours after dosing. There was a washout period of 7 days between the mitapivat sulfate dose in Treatment Period 1 and the first itraconazole (Part 1) or rifampin (Part 2) dose in Treatment Period 2. All study drugs were consumed within 5 minutes for both Part 1 and Part 2.

US11878049B1. Mitapivat therapy and modulators of cytochrome P450 (2024-01-23). Agios Pharmaceuticals, Inc. [US]. Inventors: Varsha Venkatachalam Iyer [US], Chandra Agarwal Prakash [US], Hua Yang [US].
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Patent 2024
Adult Biological Assay Cytochrome P-450 CYP3A4 Cytochrome P-450 CYP3A4 Inducers Cytochrome P-450 CYP3A4 Inhibitors Drug Interactions Females Itraconazole Males mitapivat mitapivat sulfate Plasma Rifampin
2
Investigating BI 425809's CYP Inhibition
To investigate the potential of BI 425809 to reversibly inhibit the major human CYPs, CYP-selective substrates (phenacetin 60 μM [CYP1A2], bupropion 80 μM [CYP2B6], amodiaquine 2 μM [CYP2C8], diclofenac 5 μM [CYP2C9], S-mephenytoin 80 μM [CYP2C19], dextromethorphan 5 μM [CYP2D6], midazolam 2 μM, and testosterone 50 μM [CYP3A4/5]) were incubated with human liver microsomes and BI 425809 (0.015, 0.046, 0.137, 0.411, 1.23, 3.70, 11.1, 33.3, and 100 μM). For positive control reactions, BI 425809 was replaced with a CYP-selective inhibitor (α-naphthoflavone [CYP1A2], ticlopidine [CYP2B6], montelukast [CYP2C8], sulfaphenazole [CYP2C9], benzylnirvanol [CYP2C19], quinidine [CYP2D6], and itraconazole [CYP3A4/5]). Substrate metabolites were quantified with liquid chromatography–tandem mass spectrometry using gradient elution (mobile phase for amodiaquine metabolite—A, 5 mM ammonium formate in water/formic acid [100:0.1, v/v]; B, acetonitrile/formic acid [100:0.1, v/v]; mobile phase for all other substrate metabolites—A, water/formic acid [100:0.1, v/v]; B, acetonitrile/formic acid [100:0.1, v/v]) on a Synergi Hydro RP column (50 × 2.0 mm, 4 μm; Phenomenex) with positive electrospray ionization.
IC50 values were obtained using a 3-parameter dose-response, 4-parameter dose-response, or normalized dose-response model; model comparisons were performed in Prism 6 (GraphPad Inc) to determine the optimal model for each data set. A least-squares fitting approach was used, and the Hill slope was not constrained for the 4-parameter model.
Desch M., Schlecker C., Hohl K., Liesenfeld K.H., Chan T., Müller F., Wunderlich G., Keller S., Ishiguro N, & Wind S. (2023). Pharmacokinetic-Interactions of BI 425809, a Novel Glycine Transporter 1 Inhibitor, With Cytochrome P450 and P-Glycoprotein Substrates: Findings From In Vitro Analyses and an Open-Label, Single-Sequence Phase I Study. Journal of Clinical Psychopharmacology, 43(2), 113-121.
Publication 2023
acetonitrile Amodiaquine BI 425809 Bupropion Cardiac Arrest CYP1A2 protein, human CYP2C8 protein, human CYP2C19 protein, human Cytochrome P-450 CYP2D6 Cytochrome P-450 CYP3A4 Dextromethorphan Diclofenac formic acid formic acid, ammonium salt Homo sapiens Itraconazole Liquid Chromatography Mephenytoin Microsomes, Liver Midazolam montelukast Phenacetin prisma Quinidine Sulfaphenazole Tandem Mass Spectrometry Testosterone Ticlopidine
3
Diagnosis and Treatment of Adrenal Disorders
The diagnosis of autoimmune PAI was made on the basis of normal, atrophic adrenal glands without calcification and an absence of evidence of current or previous tuberculosis. 21-hydroxylase (21-OH) antibodies were measured in all suspected patients. AH was diagnosed by findings of enlarged adrenal glands on radiology and demonstration of Histoplasma by staining and/or culture of adrenal tissue. Diagnosis of AT was made by the findings of enlarged adrenal glands, granulomas on histology and positive culture or genetic testing for M tuberculosis. Where adrenal biopsy or FNA was not feasible (n = 3) or non-diagnostic (n = 3), AT was diagnosed by a response to anti-tuberculous drugs with resolution of fever and toxemia or documentary evidence of current or previous tuberculosis at other sites. Four patients (4.5%) with enlarged glands could not be classified.
Patients with AH were treated with oral itraconazole (600 mg/day for 3 days, followed by 400 mg/day), with or without parenteral amphotericin B, according to guidelines (20 (link)). Itraconazole was continued for a period of 12–18 months. Patients with AT were treated with four drugs (isoniazid, rifampicin, pyrazinamide and ethambutol) for 2 months followed by isoniazid and rifampicin for a further 4 months. All patients received physiological doses of glucocorticoids (prednisolone (82 patients, dose 2.5–5 mg/day in two divided doses) and hydrocortisone (7 patients,15–25 mg/day in three divided doses)) and fludrocortisone (50–125 µg/day). The dose of prednisolone or hydrocortisone was doubled for the duration of rifampicin use, which is known to induce acceleration of cortisol metabolism. Advice on stress dosing was provided at every visit.
Gunna S., Singh M., Pandey R., Marak R.S., Aggarwal A., Mohanta B., Yu L, & Bhatia E. (2023). Etiology, clinical characteristics and mortality among Indian patients with Addison’s disease. Endocrine Connections, 12(3), e220439.
Publication 2023
Acceleration Adrenal Glands Amphotericin B Antibodies Atrophy Biopsy Calcinosis Drug Fever Ethambutol Fludrocortisone Glucocorticoids Granuloma Histoplasma Hydrocortisone Isoniazid Itraconazole Metabolism Mycobacterium tuberculosis Parenteral Nutrition Patients Pharmaceutical Preparations physiology Prednisolone Pyrazinamide Rifampin Steroid 21-Monooxygenase Tissues Toxemia Tuberculosis X-Rays, Diagnostic
4
Antifungal Susceptibility of Filamentous Fungi
In vitro susceptibility testing was performed using broth microdilution for filamentous fungi according to EUCAST guidelines with concentrations ranging from 0.016 µg/mL to 8 µg/mL. The antifungals used were amphotericin B (AmB), voriconazole (VRC), itraconazole (ITC), posaconazole (POS), and anidulafungin (ANI), all purchased from Sigma-Aldrich, reconstituted in DMSO and stored frozen at −80 °C until use. The MICs were determined in flat-bottomed 96-well plates with conidial suspensions prepared in RPMI 1640 supplemented with 2% glucose, buffered with MOPS, and adjusted to a final concentration of 5 × 105 CFU/mL, as previously described [39 ]. Inoculated plates were incubated for 72 h at 35 °C. MICs were spectroscopically determined at 405 nm using a spectrophotometer (NEPHELOstar, BMG Labtech) as the antifungal concentration that resulted in 90% (AmB) or 50% growth inhibition (VRC, ITC, POS, ISA).
Guegan H., Poirier W., Ravenel K., Dion S., Delabarre A., Desvillechabrol D., Pinson X., Sergent O., Gallais I., Gangneux J.P., Giraud S, & Gastebois A. (2023). Deciphering the Role of PIG1 and DHN-Melanin in Scedosporium apiospermum Conidia. Journal of Fungi, 9(2), 134.
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Publication 2023
Amphotericin B Anidulafungin Antifungal Agents Conidia Freezing Fungus, Filamentous Glucose Itraconazole Minimum Inhibitory Concentration morpholinopropane sulfonic acid posaconazole Psychological Inhibition Sulfoxide, Dimethyl Susceptibility, Disease Voriconazole
5
Antimicrobial Susceptibility Testing Protocol
Both the antibacterials and antifungals were evaluated for their activity, as per the standard protocol of the Clinical and Laboratory Standards Institute, using an overnight grown bacterial/fungal suspension as described earlier [8 (link),9 (link),12 (link),46 (link)]. The minimum inhibitory concentration (MIC) required for inhibiting the growth of the microorganisms was determined for each of the antibacterials (Aminoglycosides: Amikacin, Gentamicin, and Tobramycin; β-lactam: Ampicillin; Cephalosporins: Cefuroxime, Ceftriaxone, Cefepime, and Cefazolin; Fluoroquinolones: Gatifloxacin, Moxifloxacin, Ciprofloxacin and Ofloxacin; Amphenicols: Chloramphenicol; Macrolide: Azithromycin; Nitroimidazole: Metronidazole; Lincosamide: Clindamycin and Lincomycin; Tetracycline: Monocycline) and the antifungal drugs (Amphotericin B, Caspofungin, Fluconazole, Itraconazole, Natamycin and Voriconazole). The susceptibility tests were determined in triplicate.
Shivaji S., Nagapriya B, & Ranjith K. (2023). Differential Susceptibility of Mixed Polymicrobial Biofilms Involving Ocular Coccoid Bacteria (Staphylococcus aureus and S. epidermidis) and a Filamentous Fungus (Fusarium solani) on Ex Vivo Human Corneas. Microorganisms, 11(2), 413.
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Publication 2023
Amikacin Aminoglycosides Amphenicol Amphotericin B Ampicillin Anti-Bacterial Agents Antifungal Agents Azithromycin Bacteria Caspofungin Cefazolin Cefepime Ceftriaxone Cefuroxime Cephalosporins Chloramphenicol Ciprofloxacin Clindamycin Clinical Protocols Fluconazole Fluoroquinolones Gatifloxacin Gentamicin Itraconazole Lactams Lincomycin Lincosamides Macrolides Metronidazole Minimum Inhibitory Concentration Moxifloxacin Natamycin Nitroimidazoles Ofloxacin Susceptibility, Disease Tetracycline Tobramycin Voriconazole

Top products related to «Itraconazole»

1
Itraconazole by Merck Group
Sourced in United States, Germany, France, United Kingdom, Brazil, Hungary, India
Itraconazole is a broad-spectrum antifungal agent used in the treatment of various fungal infections. It functions by inhibiting the synthesis of ergosterol, a critical component of the fungal cell membrane, thereby disrupting the integrity and function of the fungal cell.
2
Amphotericin b by Merck Group
Sourced in United States, Germany, United Kingdom, Spain, Italy, Brazil, France, Japan, Poland, Austria, Australia, Switzerland, Macao, Canada, Belgium, Ireland, China, Sao Tome and Principe, Hungary, India, Sweden, Israel, Senegal, Argentina, Portugal
Amphotericin B is a laboratory reagent used as an antifungal agent. It is a macrolide antibiotic produced by the bacterium Streptomyces nodosus. Amphotericin B is commonly used in research and biomedical applications to inhibit the growth of fungi.
3
Fluconazole by Merck Group
Sourced in United States, Germany, United Kingdom, Brazil, Italy, Canada, Japan, Sao Tome and Principe, Hungary, Poland, France, Ireland, Spain, China, India
Fluconazole is a pharmaceutical product manufactured by Merck Group. It is an antifungal medication used to treat a variety of fungal infections. The core function of Fluconazole is to inhibit the growth and proliferation of fungal pathogens.
4
Voriconazole by Merck Group
Sourced in United States, Germany, China, Brazil, France, United Kingdom, Japan, Spain, Italy
Voriconazole is a laboratory product used as an antifungal agent. It is a synthetic triazole compound that inhibits the fungal enzyme lanosterol 14-alpha-demethylase, which is essential for the synthesis of ergosterol, a vital component of fungal cell membranes.
5
Posaconazole by Merck Group
Sourced in United States, Germany, United Kingdom, Japan, Spain, France, India, Belgium
Posaconazole is a laboratory product manufactured by Merck Group. It is an antifungal agent used in research and development applications.
6
Itraconazole by Johnson & Johnson
Sourced in Belgium, United States, China, Spain, United Kingdom, Brazil
Itraconazole is a synthetic antifungal agent used in the treatment of various fungal infections. It acts by inhibiting the synthesis of ergosterol, a crucial component of the fungal cell membrane. Itraconazole is available in various formulations, including capsules, oral solution, and intravenous solution.
7
Caspofungin by Merck Group
Sourced in United States, Germany, Hungary, Ireland, Spain, India, France, Japan, Canada, United Kingdom, Belgium
Caspofungin is an antifungal medication developed by Merck. It is a semi-synthetic lipopeptide that acts as an echinocandin, inhibiting the synthesis of 1,3-beta-D-glucan, an essential component of the fungal cell wall. Caspofungin is primarily used to treat invasive candidiasis and invasive aspergillosis.
8
Dimethyl sulfoxide (dmso) by Merck Group
Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, India, Canada, Switzerland, Japan, Australia, Spain, Poland, Belgium, Brazil, Czechia, Portugal, Austria, Denmark, Israel, Sweden, Ireland, Hungary, Mexico, Netherlands, Singapore, Indonesia, Slovakia, Cameroon, Norway, Thailand, Chile, Finland, Malaysia, Latvia, New Zealand, Hong Kong, Pakistan, Uruguay, Bangladesh
DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
9
Ketoconazole by Merck Group
Sourced in United States, Germany, India, Sao Tome and Principe, United Kingdom, Macao, Israel
Ketoconazole is a laboratory product manufactured by Merck Group. It is an antifungal agent used for research and development purposes. The core function of Ketoconazole is to inhibit the synthesis of ergosterol, a key component of fungal cell membranes.
10
Voriconazole by Pfizer
Sourced in United States, Belgium, United Kingdom, Germany
Voriconazole is a medication used in the treatment of invasive fungal infections. It functions as an antifungal agent that inhibits the enzyme lanosterol 14-alpha-demethylase, which is essential for the synthesis of ergosterol, a vital component of the fungal cell membrane. This mechanism disrupts the integrity of the fungal cell membrane, leading to cell death.

More about "Itraconazole"

triazole, antifungal, candidiasis, blastomycosis, histoplasmosis, aspergillosis, ergosterol, oral, intravenous, PubCompare.ai, Amphotericin B, Fluconazole, Voriconazole, Posaconazole, Caspofungin, DMSO, Ketoconazole, fungal infection, treatment