Disease relevance of Pevaryl

• In view of recent evidence that the imidazole antifungals econazole (EC) and miconazole (MC) inhibit TG-sensitive Ca(2+)-ATPase activity in normal rat thymocytes, we investigated the effect of these agents on intracellular Ca(2+) homeostasis and cell survival in WEHI7.2 mouse lymphoma cells and human CEMT-cell leukemia cells [1].
• The complexation of econazole with the mucoadhesive polycarbophil was found to significantly improve the therapeutic benefit of the drug in the topical treatment of experimental vaginal candidiasis in mice, while no difference in the antimycotic activity exerted by econazole and polycarbophil-econazole could be detected in vitro [2].
• In these trials, sulconazole generally displayed similar efficacy to clotrimazole, econazole and miconazole, although in a few studies sulconazole produced better and/or quicker improvement than clotrimazole or miconazole in small numbers of patients with tinea pedis [3].
• Liposomal econazole was successfully administered to tumor bearing mice at 50 mg/kg, and no significant toxicities attributable to econazole were observed [4].
• Breast cancer colonies were reduced 60-500-fold or more after exposure to econazole while hemopoietic colonies were typically reduced only 2-fold [5].

Psychiatry related information on Pevaryl

• The matched case-control pair analysis did not indicate any teratogenic potential of econazole use during the second and third months of gestation, i.e. in the critical period for most major congenital abnormalities [6].

High impact information on Pevaryl

• This activity was inhibited by the known aromatase inhibitors, 4-hydroxyandrostenedione and econazole [7].
• Imidazole antifungals Miconazole and Econazole induce apoptosis in mouse lymphoma and human T cell leukemia cells: regulation by Bcl-2 and potential role of calcium [1].
• Imidazole antimycotics, especially econazole and miconazole, were the most potent inhibitors (IC50 approximately equal to 10(-6) M) [8].
• Cell clones were derived by treatment of HL-60 cells with stepwise increasing concentrations of econazole (Ec), an imidazole antifungal that blocks Ca2+ influx and induces endoplasmic reticulum (ER) stress-related cell death in multiple mammalian cell types [9].
• The Ca2+ channel blockers, nickel and econazole, and the K+ channel blockers, tetraethylammonium chloride, apamin, and charybdotoxin, inhibit the granulysin-induced increase in intracellular Ca2+ ([Ca2+](i)), the decrease in intracellular K+, and apoptosis [10].

Chemical compound and disease context of Pevaryl

• Diazepam and econazole induce only hypodiploidy; pyrimethamine does not induce numerical chromosomal aberrations [11].
• The ability of bovine serum albumin to reverse the inhibitory action of econazole and the unsaturated fatty acid oleate on store-dependent Ca2+ inflow was examined in Ehrlich ascites tumour cells [12].
• Naftifine cream 1% versus econazole cream 1% in the treatment of tinea cruris and tinea corporis [13].
• The activity and tolerance of 200 mg clotrimazole vaginal tablets and 150 mg econazole vaginal ovules were compared in the treatment of vaginal candidiasis in a controlled multicenter (3 centers) study [14].
• Two hundred and thirty-five women with clinically and microbiologically proven candidal vaginitis were randomly allocated for treatment with either one topically applied vaginal tablet of 150 mg econazole (114 women) or one orally administered capsule of 150 mg fluconazole (121 women) [15].

Biological context of Pevaryl

• Virus induction could be blocked in a dose-dependent manner by the calcium channel blocker econazole [16].
• When applied extracellularly, this compound blocked Icrac in a concentration-dependent manner with onset kinetics comparable to econazole [17].
• Low doses of econazole inhibit both, TRPV6 dependent Ca(2+) signals and cell proliferation while BTP2, a potent inhibitor of Ca(2+) signals and cell proliferation in T-cells, neither influences TRPV6 dependent Ca(2+) signals nor cell proliferation of HEK-293 cells [18].
• Econazole (15-20 microM) had no consistent effect on afferent volleys, EPSPs or population spikes; but in seven out of nine slices, it prevented the induction of tetanic long-term potentiation (LTP) of field EPSPS [19].
• GVBD was resumed by econazole, one of the nitroimidazole derivatives which act as inhibitors of catalytic subunit of adenylate cyclase [20].

Anatomical context of Pevaryl

• These observations indicate that (1) cytochrome P-450 does not mediate store-regulated calcium influx, and (2) econazole probably inhibits store-regulated calcium influx by an alternative mechanism, such as interaction with plasma membrane calcium channels [21].
• 5. Clotrimazole, econazole, miconazole and CN- also significantly inhibited intracellular free Ca2+ signals and cell shortening in rat single ventricular myocytes [22].
• The effect of Stp on the entry of Ca2+ in activated (mAb C305) Jurkat lymphocytes was dose-related and was not the result of a direct inhibition of plasma membrane Ca2+ channels based on an absence of effect on the Tg-dependent entry of Ca2+ and the use of Ca2+ channel blockers (econazole and Ni2+) [23].
• RESULTS: Econazole (Ec) and ketotifen (Ke) were variably effective against human and murine leukemia cell lines after 24 hours of incubation [24].
• 3. Econazole dialysed from the pipette into the cytosol at concentrations ranging from 0.1 to 30 microM did not reduce Icrac, or quantitatively affect Icrac block by extracellularly applied econazole [17].

Associations of Pevaryl with other chemical compounds

• 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) [25].
• Immunoblot analyses revealed that administration of either ketoconazole or clotrimazole caused a approximately 4-5-fold increase in mEH levels, whereas either miconazole or econazole resulted in a approximately 7-fold increase in mEH at day 3 after treatment [26].
• We show the direct interactions of azoles with purified MAC-CYP51 by absorbance and electron paramagnetic resonance spectroscopy, and determine the minimum inhibitory concentrations (MICs) of econazole, ketoconazole, itraconazole, fluconazole, and voriconazole against MAC [27].
• Use of decimal assay for additivity to demonstrate synergy in pair combinations of econazole, nikkomycin Z, and ibuprofen against Candida albicans in vitro [28].
• Sertaconazole showed a higher antifungal activity than that of the other antimycotics, tested in vitro which was statistically significant (P < 0.001), as well as a lower resistance rate than that of econazole, bifonazole and ketoconazole [29].

Gene context of Pevaryl

• We observed that thapsigargin (TG) stimulated MAPK activation by store-operated calcium (SOC) influx via opening of calcium release-activated calcium (CRAC) channels as tyrphostin-A9, a CRAC channel blocker, and two SOC influx inhibitors, econazole and SKF-96365, diminished the action of the former [30].
• 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 [31].
• SK&F 96365 and econazole but not GdCl(3) inhibited PACAP-induced CA release [32].
• The agonist-evoked calcium plateau was inhibited in a dose-dependent manner by the Cl-channel blocker NPPB, by the divalent cation Ni2+ and by the imidazole antimycotic econazole [33].
• Inhibition of TRPM2 channels by the antifungal agents clotrimazole and econazole [34].

Analytical, diagnostic and therapeutic context of Pevaryl

• Stopped-flow fluorimetry indicated that econazole had no detectable effect on the early time course of agonist-evoked Mn2+ entry or rises in [Ca2+]i. These data confirm the existence of a Ca2+ entry pathway in human platelets which is activated by depletion of the intracellular Ca2+ stores [35].
• The total econazole absorbed into the supporting bed cotton ball in the test group was nearly 200-fold greater than that in the control group (p = 0.008) over the 14-day period [36].
• We further evaluated the effect of econazole on breast cancer cells present in mobilized hemopoietic cells obtained from patients undergoing high dose chemotherapy with autologous stem cell support [5].
• A Parenteral Econazole Formulation Using a Novel Micelle-to-Liposome Transfer Method: In Vitro Characterization and Tumor Growth Delay in a Breast Cancer Xenograft Model [4].
• Patients received a single course of econazole given as 1 vaginal pessary (150 mg) on 3 consecutive days [37].

References