 Chemical Structure.png)
Physicochemical Properties
| Molecular Formula | C20H15N2OSCL3 |
| Molecular Weight | 437.77 |
| Exact Mass | 435.997 |
| CAS # | 99592-32-2 |
| Related CAS # | Sertaconazole nitrate;99592-39-9 |
| PubChem CID | 65863 |
| Appearance | Typically exists as solid at room temperature |
| Density | 1.4±0.1 g/cm3 |
| Boiling Point | 614.1±55.0 °C at 760 mmHg |
| Flash Point | 325.2±31.5 °C |
| Vapour Pressure | 0.0±1.7 mmHg at 25°C |
| Index of Refraction | 1.675 |
| LogP | 7.49 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 6 |
| Heavy Atom Count | 27 |
| Complexity | 488 |
| Defined Atom Stereocenter Count | 0 |
| SMILES | C1=CC2=C(C(=C1)Cl)SC=C2COC(CN3C=CN=C3)C4=C(C=C(C=C4)Cl)Cl |
| InChi Key | JLGKQTAYUIMGRK-UHFFFAOYSA-N |
| InChi Code | InChI=1S/C20H15Cl3N2OS/c21-14-4-5-16(18(23)8-14)19(9-25-7-6-24-12-25)26-10-13-11-27-20-15(13)2-1-3-17(20)22/h1-8,11-12,19H,9-10H2 |
| Chemical Name | 1-[2-[(7-chloro-1-benzothiophen-3-yl)methoxy]-2-(2,4-dichlorophenyl)ethyl]imidazole |
| HS Tariff Code | 2934.99.9001 |
| Storage |
Powder-20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition | Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs) |
Biological Activity
| ln Vitro | Sertaconazole (0.03-40 µg/mL; 24 h) inhibits 150 yeast strains, including six species of Candida, whose arithmetic mean minimum inhibitory concentration (MIC) is 0.77 µg/mL [1]. In a time-dependent manner, p38 MAP kinase is activated by sertaconazole (1 µg/mL; 5, 10, 30, 60 min)[2]. Dependent on p38 activation, sertaconazole (1, 2 µg/mL; 6, 8, or 24 h) causes a twofold release of PGE2 via COX-2 in keratinocytes[2]. By depolymerizing interphase and spindle microtubules, cetaconazole (10, 20, 30, 40 µM; 24 h) promotes significant mitotic arrest, which results in chromosomal aggregation problems and an anti-proliferation effect[3]. In HeLa cells, sertaconazole (20, 40 µM; 24 h) causes apoptosis via the p53 pathway[3]. HeLa cell migration is inhibited by sertaconazole (20, 30 µM; 24, 48, and 72 h) in a concentration-dependent manner[3]. In A549 and H460 cells, sertaconazole (15, 30 µM; 24 h) initiates autophagy[4]. |
| ln Vivo | Sertaconazole (1% (w/v); applied once to the left ear) reduces TPA-induced otitis media in CD-1 mice[2]. |
| Cell Assay |
Cell Viability Assay[1] Cell Types: C. albicans, C. guilliermondii, C. krusei, C. parapsilosi, C. tropicalis, C. glabrata Tested Concentrations: 0.03-40 µg/m Incubation Duration: 24 h Experimental Results: Againsted 150 strains of yeasts (six Candida species) which included C albicans, C. guilliermondii, C. krusei, C. parapsilosi, C. tropicalis, C. glabrata species with arithmetic mean MIC values of 1.02, 0.51, 0.38, 0.31, 1.67 and 0.78 µg/mL, respectively. Western Blot Analysis[2] Cell Types: HaCaT cells Tested Concentrations: 1 µg/mL Incubation Duration: 5, 10, 30, 60 min Experimental Results: demonstrated activity of activating p38 MAP kinase and Hsp27 in a time-dependent manner. Western Blot Analysis[2] Cell Types: HaCaT cells Tested Concentrations: 1, 2 µg/mL Incubation Duration: 6 or 8 h Experimental Results: Induced 50% expression of COX-2 and resulted in a twofold increased in PGE2 release. Western Blot Analysis[2] Cell Types: siRNA-transfected HaCaT cells (without p38 MAP kinase expression) Tested Concentrations: 1 µg/mL Incubation Duration: 24 h Experimental Results: Mediated induction o |
| Animal Protocol |
Animal/Disease Models: CD-1 mice (TPA-induced ear edema model)[2]. Doses: 1% (w/v) Route of Administration: Apply to the left ear, once. Experimental Results: demonstrated a significant reduction of inflammation in mice by mediating PGE2 release. |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion Bioavailability is negligible. |
| Toxicity/Toxicokinetics |
Toxicity Summary Sertaconazole interacts with 14-α demethylase, a cytochrome P-450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Sertaconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms, inhibit purine uptake, and impair triglyceride and/or phospholipid biosynthesis. Protein Binding >99% to plasma |
| References |
[1]. In-vitro antifungal activity of sertaconazole, econazole, and bifonazole against Candida spp. J Antimicrob Chemother. 1995 Oct;36(4):713-6. [2]. Anti-inflammatory activity of sertaconazole nitrate is mediated via activation of a p38-COX-2-PGE2 pathway. J Invest Dermatol. 2008 Feb;128(2):336-44. [3]. Sertaconazole induced toxicity in HeLa cells through mitotic arrest and inhibition of microtubule assembly. Naunyn Schmiedebergs Arch Pharmacol. 2021 Jun;394(6):1231-1249. [4]. Sertaconazole provokes proapoptotic autophagy via stabilizing TRADD in nonsmall cell lung cancer cells. MedComm (2020). 2021 Dec 16;2(4):821-837. |
| Additional Infomation |
1-{2-[(7-chloro-1-benzothiophen-3-yl)methoxy]-2-(2,4-dichlorophenyl)ethyl}imidazole is a member of the class of imidazoles that carries a 2-[(7-chloro-1-benzothiophen-3-yl)methoxy]-2-(2,4-dichlorophenyl)ethyl group at position 1. It is a dichlorobenzene, an ether, a member of imidazoles and a member of 1-benzothiophenes. Sertaconazole nitrate is an antifungal medication of the imidazole class. It is available in topical formulations for the treatment of skin infections such as athlete's foot. Sertaconazole is an Azole Antifungal. Sertaconazole is a synthetic imidazole derivative, containing a benzothiophene ring, with antifungal, antibacterial, anti-inflammatory and anti-pruritic activity. Besides its ability to inhibit the synthesis of ergosterol, the benzothiophene ring of sertaconazole is able to insert into the fungal cell wall instead of tryptophan. This increases the permeability of the cell wall. In addition, sertaconazole suppresses the release of cytokines. Sertaconazole is only found in individuals that have used or taken this drug. Sertaconazole nitrate is an antifungal medication of the imidazole class. It is available as a cream to treat skin infections such as athlete's foot. [Wikipedia] Sertaconazole interacts with 14-alpha demethylase, a cytochrome P-450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Sertaconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms, inhibit purine uptake, and impair triglyceride and/or phospholipid biosynthesis. See also: Sertaconazole Nitrate (has salt form). Drug Indication For the topical treatment of interdigital tinea pedis in immunocompetent patients 12 years of age and older, caused by Trichophyton rubrum, Trichophyton mentagrophytes, and Epidermophyton floccosum. FDA Label Mechanism of Action Sertaconazole interacts with 14-α demethylase, a cytochrome P-450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Sertaconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms, inhibit purine uptake, and impair triglyceride and/or phospholipid biosynthesis. Pharmacodynamics Sertaconazole is an imidazole/triazole type antifungal agent. Sertaconazole is a highly selective inhibitor of fungal cytochrome P-450 sterol C-14 α-demethylation via the inhibition of the enzyme cytochrome P450 14α-demethylase. This enzyme converts lanosterol to ergosterol, and is required in fungal cell wall synthesis. The subsequent loss of normal sterols correlates with the accumulation of 14 α-methyl sterols in fungi and may be partly responsible for the fungistatic activity of fluconazole. Mammalian cell demethylation is much less sensitive to fluconazole inhibition. Sertaconazole exhibits in vitro activity against Cryptococcus neoformans and Candida spp. Fungistatic activity has also been demonstrated in normal and immunocompromised animal models for systemic and intracranial fungal infections due to Cryptococcus neoformans and for systemic infections due to Candida albicans. |
Solubility Data
| Solubility (In Vitro) | May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples |
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples. Injection Formulations (e.g. IP/IV/IM/SC) Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] *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. Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline) Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline) Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline) Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil) Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Oral Formulations Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). Oral Formulation 3: Dissolved in PEG400 Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose Oral Formulation 6: Mixing with food powders Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.2843 mL | 11.4215 mL | 22.8430 mL | |
| 5 mM | 0.4569 mL | 2.2843 mL | 4.5686 mL | |
| 10 mM | 0.2284 mL | 1.1422 mL | 2.2843 mL |