舍他康唑（0.03-40 µg/mL；24 h）可抑制 150 种酵母菌株，包括 6 种念珠菌，其算术平均最低抑制浓度（MIC）为 0.77 µg/mL [1]。 p38 MAP 激酶以时间依赖性方式被舍他康唑（1 µg/mL；5、10、30、60 分钟）激活[2]。根据 p38 的激活，舍他康唑（1、2 µg/mL；6、8 或 24 小时）会通过角质形成细胞中的 COX-2 导致 PGE2 双重释放 [2]。通过解聚间期和纺锤体微管，十六康唑（10、20、30、40 µM；24 小时）可促进显着的有丝分裂停滞，从而导致染色体聚集问题和抗增殖作用[3]。在 HeLa 细胞中，舍他康唑（20、40 µM；24 小时）通过 p53 途径引起细胞凋亡[3]。舍他康唑（20、30 µM；24、48 和 72 小时）以浓度依赖性方式抑制 HeLa 细胞迁移[3]。在 A549 和 H460 细胞中，舍他康唑（15、30 µM；24 小时）启动自噬[4]。

舍他康唑（1%（w/v）；施用于左耳一次）可减少 CD-1 小鼠中 TPA 诱发的中耳炎[2]。

细胞活力测定[1]
细胞类型：白色念珠菌、吉里蒙念珠菌、克柔念珠菌、近平滑念珠菌、热带念珠菌、光滑念珠菌
测试浓度： 0.03-40 µg/m
孵育时间： 24 小时
实验结果： 针对 150 株酵母（六种念珠菌），包括白色念珠菌、吉里蒙念珠菌、克柔念珠菌、近平滑念珠菌、热带念珠菌、光滑念珠菌，算术平均 MIC 值分别为 1.02、0.51、0.38、0.31、1.67 和 0.78 µg/mL。

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蛋白质印迹分析[2]
细胞类型： HaCaT 细胞
测试浓度： 1 µg/mL
孵育时间：5、10、30、60 分钟
实验结果：以时间依赖性方式证明激活 p38 MAP 激酶和 Hsp27 的活性。

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蛋白质印迹分析[2]
细胞类型： HaCaT 细胞
测试浓度： 1, 2 µg/mL
孵育时间：6 或 8 小时
实验结果：诱导 COX-2 表达 50%，导致 PGE2 释放增加两倍。

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蛋白质印迹分析[2]
细胞类型： siRNA 转染的 HaCaT 细胞（无 p38 MAP 激酶表达）
测试浓度： 1 µg/mL
孵育时间： 24 小时
实验结果： 介导诱导 o

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.

Absorption, Distribution and Excretion
Bioavailability is negligible.

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.

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Protein Binding
>99% to plasma

[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.

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).

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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

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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.

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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.

C20H15N2OSCL3

437.77

435.997

99592-32-2

Sertaconazole nitrate;99592-39-9

65863

Typically exists as solid at room temperature

1.4±0.1 g/cm3

614.1±55.0 °C at 760 mmHg

325.2±31.5 °C

0.0±1.7 mmHg at 25°C

1.675

7.49

55.29

0

3

6

27

488

0

C1=CC2=C(C(=C1)Cl)SC=C2COC(CN3C=CN=C3)C4=C(C=C(C=C4)Cl)Cl

JLGKQTAYUIMGRK-UHFFFAOYSA-N

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

1-[2-[(7-chloro-1-benzothiophen-3-yl)methoxy]-2-(2,4-dichlorophenyl)ethyl]imidazole

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)

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

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。