Econazole: An imidazole derivative that is commonly used as a topical antifungal agent.Miconazole: An imidazole antifungal agent that is used topically and by intravenous infusion.Clotrimazole: An imidazole derivative with a broad spectrum of antimycotic activity. It inhibits biosynthesis of the sterol ergostol, an important component of fungal CELL MEMBRANES. Its action leads to increased membrane permeability and apparent disruption of enzyme systems bound to the membrane.Fenamates: Derivatives of orthoaminobenzoic acid that have a phenyl group bound to the orthoamino nitrogen. Members modulate ION CHANNELS and are used as ANTI-INFLAMMATORY AGENTS.Candidiasis, Vulvovaginal: Infection of the VULVA and VAGINA with a fungus of the genus CANDIDA.Antifungal Agents: Substances that destroy fungi by suppressing their ability to grow or reproduce. They differ from FUNGICIDES, INDUSTRIAL because they defend against fungi present in human or animal tissues.China: A country spanning from central Asia to the Pacific Ocean.Excipients: Usually inert substances added to a prescription in order to provide suitable consistency to the dosage form. These include binders, matrix, base or diluent in pills, tablets, creams, salves, etc.Nitrate Reductase: An enzyme that catalyzes the oxidation of nitrite to nitrate. It is a cytochrome protein that contains IRON and MOLYBDENUM.Technology, Pharmaceutical: The application of scientific knowledge or technology to pharmacy and the pharmaceutical industry. It includes methods, techniques, and instrumentation in the manufacture, preparation, compounding, dispensing, packaging, and storing of drugs and other preparations used in diagnostic and determinative procedures, and in the treatment of patients.Plasticizers: Materials incorporated mechanically in plastics (usually PVC) to increase flexibility, workability or distensibility; due to the non-chemical inclusion, plasticizers leach out from the plastic and are found in body fluids and the general environment.Diethylhexyl Phthalate: An ester of phthalic acid. It appears as a light-colored, odorless liquid and is used as a plasticizer for many resins and elastomers.Cosmetics: Substances intended to be applied to the human body for cleansing, beautifying, promoting attractiveness, or altering the appearance without affecting the body's structure or functions. Included in this definition are skin creams, lotions, perfumes, lipsticks, fingernail polishes, eye and facial makeup preparations, permanent waves, hair colors, toothpastes, and deodorants, as well as any material intended for use as a component of a cosmetic product. (U.S. Food & Drug Administration Center for Food Safety & Applied Nutrition Office of Cosmetics Fact Sheet (web page) Feb 1995)Tulipa: A plant genus of the family LILIACEAE. Members contain tuliposides and tulipalins and have been associated with allergic contact dermatitis in florists.Emergency Medicine: The branch of medicine concerned with the evaluation and initial treatment of urgent and emergent medical problems, such as those caused by accidents, trauma, sudden illness, poisoning, or disasters. Emergency medical care can be provided at the hospital or at sites outside the medical facility.Azoles: Five membered rings containing a NITROGEN atom.Polyenes: Hydrocarbons with more than one double bond. They are a reduced form of POLYYNES.Candida: A genus of yeast-like mitosporic Saccharomycetales fungi characterized by producing yeast cells, mycelia, pseudomycelia, and blastophores. It is commonly part of the normal flora of the skin, mouth, intestinal tract, and vagina, but can cause a variety of infections, including CANDIDIASIS; ONYCHOMYCOSIS; vulvovaginal candidiasis (CANDIDIASIS, VULVOVAGINAL), and thrush (see CANDIDIASIS, ORAL). (From Dorland, 28th ed)Candidiasis: Infection with a fungus of the genus CANDIDA. It is usually a superficial infection of the moist areas of the body and is generally caused by CANDIDA ALBICANS. (Dorland, 27th ed)Monomethylhydrazine: Hydrazine substituted by one methyl group.Ligands: A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)Pharmacology: The study of the origin, nature, properties, and actions of drugs and their effects on living organisms.Xylans: Polysaccharides consisting of xylose units.Cellulose: A polysaccharide with glucose units linked as in CELLOBIOSE. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations.Chromatography, High Pressure Liquid: Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.Pamphlets: Printed publications usually having a format with no binding and no cover and having fewer than some set number of pages. They are often devoted to a single subject.Patient Education as Topic: The teaching or training of patients concerning their own health needs.Skin Cream: A water-soluble medicinal preparation applied to the skin.Tinea: Fungal infection of keratinized tissues such as hair, skin and nails. The main causative fungi include MICROSPORUM; TRICHOPHYTON; and EPIDERMOPHYTON.Griseofulvin: An antifungal agent used in the treatment of TINEA infections.Dermatomycoses: Superficial infections of the skin or its appendages by any of various fungi.Trichophyton: A mitosporic fungal genus and an anamorphic form of Arthroderma. Various species attack the skin, nails, and hair.Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals.Nails: The thin, horny plates that cover the dorsal surfaces of the distal phalanges of the fingers and toes of primates.Nail Diseases: Diseases of the nail plate and tissues surrounding it. The concept is limited to primates.Beauty: Characteristics or attributes of persons or things which elicit pleasurable feelings.Fungi: A kingdom of eukaryotic, heterotrophic organisms that live parasitically as saprobes, including MUSHROOMS; YEASTS; smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi, commonly known as molds, refer to those that grow as multicellular colonies.Coriandrum: A plant genus of the family APIACEAE. The leaves are the source of cilantro and the seeds are the source of coriander, both of which are used in SPICES.Medicine, African Traditional: A system of traditional medicine which is based on the beliefs and practices of the African peoples. It includes treatment by medicinal plants and other materia medica as well as by the ministrations of diviners, medicine men, witch doctors, and sorcerers.Candidiasis, Oral: Infection of the mucous membranes of the mouth by a fungus of the genus CANDIDA. (Dorland, 27th ed)MycosesSoftware: Sequential operating programs and data which instruct the functioning of a digital computer.Drug Industry: That segment of commercial enterprise devoted to the design, development, and manufacture of chemical products for use in the diagnosis and treatment of disease, disability, or other dysfunction, or to improve function.Counterfeit Drugs: Drugs manufactured and sold with the intent to misrepresent its origin, authenticity, chemical composition, and or efficacy. Counterfeit drugs may contain inappropriate quantities of ingredients not listed on the label or package. In order to further deceive the consumer, the packaging, container, or labeling, may be inaccurate, incorrect, or fake.Fraud: Exploitation through misrepresentation of the facts or concealment of the purposes of the exploiter.Drugs, Chinese Herbal: Chinese herbal or plant extracts which are used as drugs to treat diseases or promote general well-being. The concept does not include synthesized compounds manufactured in China.Developing Countries: Countries in the process of change with economic growth, that is, an increase in production, per capita consumption, and income. The process of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures.Paeonia: A plant genus of the family Paeoniaceae, order Dilleniales, subclass Dilleniidae, class Magnoliopsida. These perennial herbs are up to 2 m (6') tall. Leaves are alternate and are divided into three lobes, each lobe being further divided into three smaller lobes. The large flowers are symmetrical, bisexual, have 5 sepals, 5 petals (sometimes 10), and many stamens.Quinolones: A group of derivatives of naphthyridine carboxylic acid, quinoline carboxylic acid, or NALIDIXIC ACID.Farnesyltranstransferase: An enzyme that catalyzes the synthesis of geranylgeranyl diphosphate from trans, trans-farnesyl diphosphate and isopentenyl diphosphate.Pancreatic Neoplasms: Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).DeoxycytidineAntineoplastic Combined Chemotherapy Protocols: The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.Maximum Tolerated Dose: The highest dose of a biologically active agent given during a chronic study that will not reduce longevity from effects other than carcinogenicity. (from Lewis Dictionary of Toxicology, 1st ed)Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

Comparison of the toxicity of fluconazole and other azole antifungal drugs to murine and human granulocyte-macrophage progenitor cells in vitro. (1/56)

We studied the inhibitory effects on colony formation by granulocyte-macrophage colony forming units (cfu-gm) of eight azole antifungal agents in vitro. All agents, except fluconazole, inhibited colony formation dose-dependently with 50% inhibitory concentrations (IC50) in the range of 0.78-49 micromol/L in cultures of murine and human bone marrow. For human cells, the IC50 values were 0.553 mg/L for itraconazole, 1.24 mg/L for saperconazole, 2.58 mg/L for clotrimazole, 5.33 mg/L for miconazole, 6.17 mg/L for econazole, 6.27 mg/L for ketoconazole and 8.38 mg/L for oxiconazole. The IC50 of itraconazole for human cfu-gm in vitro was similar to the plasma level of this drug recommended for systemic antifungal therapy (>0.5 mg/L) thus indicating the potential clinical relevance of our data. The IC50 of ketoconazole for human cfu-gm in vitro may be exceeded by plasma levels produced in vivo by high (> or =400 mg) doses, whereas fluconazole failed to reduce colony formation by 50% even at 100 mg/L, a concentration not reached in vivo even after extremely high doses (2000 mg/day). To most of the drugs studied, murine progenitor cells seemed to be less sensitive than the human ones. There was, however, a close correlation between the murine and human log IC50 values of the drugs (r2 = 0.964, P< 0.001), suggesting that cultures of murine bone marrow may be suitable to predict the in-vitro toxicity of azole antifungals to human cfu-gm.  (+info)

In-vitro resistance to azoles associated with mitochondrial DNA deficiency in Candida glabrata. (2/56)

A commercially available disk diffusion procedure was used in a large-scale study to evaluate the susceptibility of a wide range of Candida isolates to polyenes and azoles. With almost all isolates of C. glabrata resistant colonies were present within the inhibition zones for the azole compounds fluconazole, ketoconazole and miconazole, and less frequently for isoconazole, econazole and clotrimazole. Ten randomly selected isolates were cloned by limiting dilution and the susceptibility of the resulting strains to polyenes and azoles was determined. All strains presented a similar susceptibility pattern with sensitivity to polyenes and the presence of resistant colonies for all azole compounds except tioconazole. For each strain and each antifungal agent, one of these resistant colonies was subcultured and studied for antifungal susceptibility. All these colonies showed similar properties regardless of which antifungal agent allowed their selection, with increased sensitivity to polyenes and cross-resistance to the azole compounds except tioconazole. Similar results were obtained on Shadomy's modified medium and on synthetic medium. Likewise, determination of MICs by the Etest method confirmed the resistance to fluconazole. Comparative growth studies revealed a respiratory deficiency in the mutants caused by mitochondrial DNA (mtDNA) deletions. In addition, 'petite' mutants were obtained from a wild-type strain by exposure to ethidium bromide, and these respiratory mutants were shown to be resistant to azoles. These results demonstrate the relationship between mtDNA deficiency and resistance to azoles, and provide an interesting model to study the mechanisms of action of these antifungal agents.  (+info)

In vitro activities of ketoconazole, econazole, miconazole, and Melaleuca alternifolia (tea tree) oil against Malassezia species. (3/56)

The in vitro activities of ketoconazole, econazole, miconazole, and tea tree oil against 54 Malassezia isolates were determined by agar and broth dilution methods. Ketoconazole was more active than both econazole and miconazole, which showed very similar activities. M. furfur was the least susceptible species. M. sympodialis, M. slooffiae, M. globosa, and M. obtusa showed similar susceptibilities to the four agents.  (+info)

Positive and negative control of multidrug resistance by the Sit4 protein phosphatase in Kluyveromyces lactis. (4/56)

The nuclear gene encoding the Sit4 protein phosphatase was identified in the budding yeast Kluyveromyces lactis. K. lactis cells carrying a disrupted sit4 allele are resistant to oligomycin, antimycin, ketoconazole, and econazole but hypersensitive to paromomycin, sorbic acid, and 4-nitroquinoline-N-oxide (4-NQO). Overexpression of SIT4 leads to an elevation in resistance to paromomycin and to lesser extent tolerance to sorbic acid, but it has no detectable effect on resistance to 4-NQO. These observations suggest that the Sit4 protein phosphatase has a broad role in modulating multidrug resistance in K. lactis. Expression or activity of a membrane transporter specific for paromomycin and the ABC pumps responsible for 4-NQO and sorbic acid would be positively regulated by Sit4p. In contrast, the function of a Pdr5-type transporter responsible for ketoconazole and econazole extrusion, and probably also for efflux of oligomycin and antimycin, is likely to be negatively regulated by the phosphatase. Drug resistance of sit4 mutants was shown to be mediated by ABC transporters as efflux of the anionic fluorescent dye rhodamine 6G, a substrate for the Pdr5-type pump, is markedly increased in sit4 mutants in an energy-dependent and FK506-sensitive manner.  (+info)

Effect of cytochrome P-450 inhibitors econazole, bifonazole and clotrimazole on prostanoid formation. (5/56)

1. The present study was carried out to clarify the effect of the imidazole antimycotics econazole, bifonazole and clotrimazole on prostanoid biosynthesis. Osteoblast-like MC3T3-E1 cells stimulated by endothelin-1, melittin, ionomycin or arachidonic acid showed diminished prostaglandin E(2) (PGE(2)) production upon pretreatment with econazole. Following pretreatment with bifonazole, stimulation with ionomycin or arachidonic acid also resulted in decreased PGE(2) formation. Clotrimazole inhibited ionomycin but not arachidonic acid stimulated PGE(2) synthesis in MC3T3-E1 cells. 2. The results observed in osteoblast-like UMR-106 cells pretreated with econazole, bifonazole or clotrimazole and stimulated by arachidonic acid were similar with the exception of clotrimazole which was a more effective inhibitor of PGE(2) biosynthesis than in MC3T3-E1 cells. 3. Upon treatment with arachidonic acid thromboxane B(2) (TXB(2)) production in human platelets was abolished completely at concentrations of the three imidazole antimycotics higher than 5 microM (IC(50)<1 microM). 4. These data were confirmed by a direct assay using purified ram seminal vesicle prostaglandin H(2) synthase-1 (PGHS-1), which clearly showed inhibitory properties of econazole (IC(50) 4.7+/-2.3 microM), bifonazole (IC(50) 9.4+/-0.8 microM) and clotrimazole (IC(50) 4.4+/-0.6 microM). 5. Summarizing, these results indicate an inhibitory effect of econazole, bifonazole and clotrimazole on PGHS-1, varying in its potency dependent on the cell system used. In addition TXB(2) formation is affected at doses even lower than those needed to suppress PGE(2) biosynthesis.  (+info)

Activity of the Kluyveromyces lactis Pdr5 multidrug transporter is modulated by the Sit4 protein phosphatase. (6/56)

A possible role for posttranslational modifications in regulating the activity of ATP-binding cassette (ABC) transporters has not been well established. In this study, the drug efflux ABC transporter gene KlPDR5 was isolated from the budding yeast Kluyveromyces lactis, and it was found that the encoded KlPdr5 drug pump is posttranslationally regulated by the type 2A-related Ser/Thr protein phosphatase, Sit4p. The KlPdr5 transporter is a protein of 1,525 amino acids sharing 63.8% sequence identity with its Saccharomyces cerevisiae counterpart, ScPdr5p. Overexpression of the KlPDR5 gene confers resistance to oligomycin, antimycin, econazole, and ketoconazole, whereas cells with a disrupted allele of KlPDR5 are hypersensitive to the drugs and have a decreased capacity to carry out efflux of the anionic fluorescent dye rhodamine 123. It was found that a chromosomal disruption of KlPDR5 abolishes the drug-resistant phenotype associated with sit4 mutations and that a synergistic hyperresistance to the drugs can be created by overexpressing KlPDR5 in sit4 mutants. These data strongly indicate that the multidrug-resistant phenotype of sit4 mutants is mediated by negatively modulating the activity of KlPdr5p. As the transcriptional level of KlPDR5 and the steady-state level of KlPdr5p are not significantly affected by mutations in SIT4, the regulation by Sit4p appears to be a posttranslational process.  (+info)

Pharmacological modulation of monovalent cation currents through the epithelial Ca2+ channel ECaC1. (7/56)

1. The recent identification of the epithelial Ca(2+) channel, ECaC1, represents a major step forward in our knowledge of renal Ca(2+) handling. ECaC1 constitutes the rate-limiting apical Ca(2+) entry mechanism of active, transcellular Ca(2+) reabsorption. This unique highly selective Ca(2+) channel shares a low but significant homology with transient receptor potential (TRP) channels and vanilloid receptors (VR). 2. We have studied the pharmacological modulation of currents through ECaC1 heterologously expressed in HEK 293 cells. Monovalent cation currents were measured by use of the whole cell patch clamp technique in cells dialysed with 10 mM BAPTA or 10 mM EGTA to prevent the fast Ca(2+) dependent inactivation of ECaC1. 3. Several modulators were tested, including inorganic cations, putative store-operated Ca(2+) entry (SOC) blockers, the vanilloid receptor (VR-1) blocker capsazepine, protein tyrosine kinase blockers, calmodulin antagonists and ruthenium red. 4. Ruthenium red and econazole appeared to be the most effective inhibitors of currents through ECaC1, with IC(50) values of 111 nM and 1.3 microM, respectively, whereas the selective SOC inhibitor, SKF96365, was nearly ineffective. 5. The divalent cation current block profile for ECaC1 is Pb(2+)=Cu(2+) >Zn(2+) >Co(2+) >Fe(2+) with IC(50) values between 1 and approximately 10 microM. 6. In conclusion, ECaC activity is effectively inhibited by various compounds including ruthenium red, antimycotic drugs and divalent cations, which might be useful tools for pharmacological manipulation and several disorders related to Ca(2+) homeostasis could benefit from such developments.  (+info)

Sustained ER Ca2+ depletion suppresses protein synthesis and induces activation-enhanced cell death in mast cells. (8/56)

Depletion of Ca(2+) from the endoplasmic reticulum (ER) induces large increases in cytoplasmic Ca(2+), mitochondrial Ca(2+) loading, protein synthesis inhibition, and cell death. To clarify the connections among these events, we have evaluated the effect of Ca(2+) mobilizing agents thapsigargin (Tg), econazole (Ec), and the growth factor Steel Factor (SLF) on bone marrow-derived mast cells (BMMCs). BMMC Ca(2+) stores were found to consist of a Tg-sensitive ER compartment, the Tg-insensitive SIC store, and mitochondrial stores. Low levels of Ec interfered with Tg-stimulated mitochondrial loading while promoting progressive leakage of Ca(2+) from the ER. Low levels of Ec completely reversed Tg toxicity while higher levels blocked store-operated influx and induced cell death in a SLF-enhanced manner. Both Ec and Tg inhibited protein synthesis, however, only SLF plus Tg or very high levels of Ec were able to significantly stimulate EIF-2alpha phosphorylation. Cycloheximide only partially protected BMMCs from Tg toxicity yet strongly synergized with Ec to induce cell death. These results therefore indicate that although both Tg and Ec deplete ER Ca(2+) levels, Ec-induced cell death results from sustained protein synthesis inhibition while Tg toxicity results primarily from mitochondrial Ca(2+) overload and secondarily from ER stress associated with Ca(2+) depletion.  (+info)

  • Natamycin (5%) and econazole (2%) eye drops were started on a half-hourly basis, while itraconazole (1%) eye ointment was applied three times a day. (asm.org)
  • Read the Patient Information Leaflet and Instructions for Use if available from your pharmacist before you start using econazole and each time you get a refill. (cysticacnecauses.net)
  • Wash and dry the infected area of skin before you apply econazole. (patient.info)
  • Most cases reported product application with use under occlusion, genital application, or application to a large body surface area which may increase the systemic absorption of Econazole LP. Monitoring of International Normalized Ratio (INR) and/or prothrombin time may be indicated especially for patients who apply econazole to large body surface areas, in the genital area, or under occlusion. (sdrugs.com)
  • tell your doctor and pharmacist if you are allergic to econazole or any other drugs. (medlineplus.gov)
  • Because many drugs are excreted in human milk, caution should be exercised when Econazole LP is administered to a nursing woman. (sdrugs.com)
  • To get a free discount card for econazole and most other prescription drugs, click 'Free Card' at the top of the page. (helprx.info)
  • This study evaluated the preformulation transungual permeability of econazole nitrate and formulation development of a transungual topical patch utilizing penetration enhancers in combination with econazole nitrate to optimize the delivery and penetration through the nail . (temple.edu)
  • Percutaneous delivery of econazole using microemulsion as vehicle: formulation, evaluation and vesicle-skin interaction. (semanticscholar.org)
  • Polymeric nanosponges as an alternative carrier for improved retention of econazole nitrate onto the skin through topical hydrogel formulation. (semanticscholar.org)
  • Before using econazole, thoroughly clean and dry the affected area, then apply just enough of the medication to cover the site, gently massage it into the skin until it disappears. (helprx.info)
  • Sebazole Shampoo (Econazole Nitrate/Sulphur as Sodium Thiosulphate/Sodium Salicylate/Chloroxylenol) should not be applied to skin that is broken or severely damaged. (4nrx-uk.md)
  • It was selected as the nail permeation enhancer and skin penetration enhancer for econazole nitrate . (temple.edu)
Imidazole
Imidazole (blackhawksjerseyshop.com)
ECONAZOLE
ECONAZOLE (24seven.com.np)
Can You Use Econazole Nitrate Cream For Acne 2018 - Cystic Acne Causes
Can You Use Econazole Nitrate Cream For Acne 2018 - Cystic Acne Causes (cysticacnecauses.net)
Econazole nitrate cream for nail fungus - Herbal Revitol Stretch Mark Prevention - Aug 14, 2017
Econazole nitrate cream for nail fungus - Herbal Revitol Stretch Mark Prevention - Aug 14, 2017 (stretchmarkprevention.herbalyzer.com)
PEVISONCRM
PEVISONCRM (minapharm.com)
Econazole | The Merck Index Online
Econazole | The Merck Index Online (rsc.org)
Econazole (Topical Route) Description and Brand Names - Mayo Clinic
Econazole (Topical Route) Description and Brand Names - Mayo Clinic (mayoclinic.org)
Tinea Faciei Medication: Antifungal agents
Tinea Faciei Medication: Antifungal agents (emedicine.medscape.com)
DailyMed - ECONAZOLE NITRATE cream
DailyMed - ECONAZOLE NITRATE cream (dailymed.nlm.nih.gov)
Past, Present, and Future of Antifungal Drug Development | Springer for Research & Development
Past, Present, and Future of Antifungal Drug Development | Springer for Research & Development (rd.springer.com)
Https://www.medicalnewstoday.com/articles/261244.php
Https://www.medicalnewstoday.com/articles/261244.php (medicalnewstoday.com)
Econazole Nitrate Manufacturers, Suppliers & Exporters in India
Econazole Nitrate Manufacturers, Suppliers & Exporters in India (indianyellowpages.com)
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How Long Does It Take for Fluconazole to Work? | Reference.com
How Long Does It Take for Fluconazole to Work? | Reference.com (reference.com)
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Where is the capillary tube and bulb in a thermometer (answers.com)
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Mycotic Keratitis Due to Aspergillus nomius | Journal of Clinical Microbiology (jcm.asm.org)
Cytochrome P-450 CYP3A Inhibitors (strong) - DrugBank
Cytochrome P-450 CYP3A Inhibitors (strong) - DrugBank (drugbank.ca)
Ringworm (Tinea Corporis) Condition, Treatments, and Pictures for Parents - Overview | skinsight
Ringworm (Tinea Corporis) Condition, Treatments, and Pictures for Parents - Overview | skinsight (skinsight.com)