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Diallyl Tetrasulfide (Synonyms: ICD-1585)

رقم الكتالوجGC45992

An organosulfur compound with diverse biological activities

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Diallyl Tetrasulfide التركيب الكيميائي

Cas No.: 2444-49-7

الحجم السعر المخزون الكميّة
5mg
167٫00
متوفر
25mg
536٫00
متوفر

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Sample solution is provided at 25 µL, 10mM.

Description Chemical Properties Product Documents Related Products

Diallyl tetrasulfide is an organosulfur compound that has been found in A. sativum and has diverse biological activities, including antimicrobial, antioxidant, and anticancer properties.[1],[2],[3],[4] It is active against the bacteria S. aureus and methicillin-resistant S. aureus (MRSA; MICs = 0.5 and 2 mg/L, respectively), as well as the fungi C. albicans, C. krusei, C. glabrata, A. niger, A. flavus, and A. fumigatus (MICs = 0.5, 4, 2, 1, 2, and 4 mg/L, respectively).[1] It reduces cadmium-induced increases in hepatic levels of thiobarbituric acid reactive substances (TBARS) and increases cadmium-induced decreases in the hepatic activity of superoxide dismutase (SOD1), catalase, GST, and glucose-6-phosphate dehydrogenase (G6PDH) in rats when administered at a dose of 40 mg/kg.[2] Diallyl tetrasulfide is cytotoxic to MCF-7 breast cancer cells (IC50 = 92 μM) and reduces tumor growth in a BGC-823 mouse xenograft model when administered at doses of 20, 30, and 40 mg/kg for 32 days.[3],[4]

Reference:
[1]. Tsao, S.-M., and Yin, M.-C. In-vitro antimicrobial activity of four diallyl sulphides occurring naturally in garlic and Chinese leek oils. J. Med. Microbiol. 50(7), 646-649 (2001).
[2]. Murugavel, P., and Pari, L. Effects of diallyl tetrasulfide on cadmium-induced oxidative damage in the liver of rats. Hum. Exp. Toxicol. 26(6), 527-534 (2007).
[3]. Viry, E., Anwar, A., Kirsch, G., et al. Antiproliferative effect of natural tetrasulfides in human breast cancer cells is mediated through the inhibition of the cell division cycle 25 phosphatases. Int. J. Oncol. 38(4), 1103-1111 (2011).
[4]. Jiang, X.-Y., Zhu, X.-S., Xu, H.-Y., et al. Diallyl trisulfide suppresses tumor growth through the attenuation of Nrf2/Akt and activation of p38/JNK and potentiates cisplatin efficacy in gastric cancer treatment. Acta Pharmacol. Sin. 38(7), 1048-1058 (2017).

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