MedChemExpress LLC (MCE)

MedChemExpress - Model Methylisothiazolinone - 2682-20-4

Methylothiazolinone is a bacterial and fungal inhibitor and preservative, as well as a sensitizer. Methylisothiazolinone can activate matrix metalloproteinases (MMPs) in human bronchial epithelial cells to induce apoptosis and inflammatory response. Methylisothiazolinone can promote the development of atopic dermatitis in mice by disrupting Th2/Th17 related immune responses. Methylisothiazolinone can cause mitochondrial damage in the endothelium of rat cerebral blood vessels[1][2][4].

Methylisothiazolinone

MCE China：Methylisothiazolinone

Brand：MedChemExpress (MCE)

Cat. No.HY-W010520

CAS：2682-20-4

Purity：99.37%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Methylothiazolinone is a bacterial and fungal inhibitor and preservative, as well as a sensitizer. Methylisothiazolinone can activate matrix metalloproteinases (MMPs) in human bronchial epithelial cells to induce apoptosis and inflammatory response. Methylisothiazolinone can promote the development of atopic dermatitis in mice by disrupting Th2/Th17 related immune responses. Methylisothiazolinone can cause mitochondrial damage in the endothelium of rat cerebral blood vessels.

In Vitro：Methylisothiazolinone (0-8 μg/mL, 24 h) induces cell apoptosis and inflammatory response by activating matrix metalloproteinases (MMPs) in human bronchial epithelial cells[1]. Methylisothiazolinone (0-2.5 μg/mL, 1 h) can cause mitochondrial damage in brain endothelial cells[2].

In Vivo：Methylisothiazolinone (0.15 mg/kg; once; i.v.) can increase the susceptibility of rat cerebral vascular endothelium to endogenous pathological stimuli and lead to mitochondrial damage[2]. Methylisothiazolinone (20 or 40 μL; handling skin (20 μL), days 1 and 8; intranasal instillation (40 μL), day 15) can cause sensitization in asthmatic mice when handled on the skin[3]. Methylisothiazolinone (0.1875 mg/kg CMIT/MIT; once daily; 15 days; epidermal contact) promotes the development of atopic dermatitis in mice through Th2/Th17 related immune response dysregulation[4].

References：

[1]. Park EJ, et al. Methylisothiazolinone induces apoptotic cell death via matrix metalloproteinase activation in human bronchial epithelial cells. Toxicol In Vitro. 2020 Feb;62:104661. [Content Brief]

[2]. Kim D, et al. Functional and dynamic mitochondrial damage by chloromethylisothiazolinone/methylisothiazolinone (CMIT/MIT) mixture in brain endothelial cell lines and rat cerebrovascular endothelium. Toxicol Lett. 2022 Aug 1;366:45-57. [Content Brief]

[3]. Devos FC, et al. Methylisothiazolinone: dermal and respiratory immune responses in mice. Toxicol Lett. 2015 Jun 15;235(3):179-88. [Content Brief]

[4]. Go HN, et al. Effects of chloromethylisothiazolinone/methylisothiazolinone (CMIT/MIT) on Th2/Th17-related immune modulation in an atopic dermatitis mouse model. Sci Rep. 2020 Mar 5;10(1):4099. [Content Brief]

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