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Diallyl trisulfide


Catalogue Number : AV-AK0087
Specification : 98%
CAS number : 2050-87-5
Formula : C6H10S3
Molecular Weight : 178.34
PUBCHEM ID : 16315
Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Botanical Source

Structure Type







1.1±0.1 g/cm3


Flash Point

87.8±25.2 °C

Boiling Point

229.5±43.0 °C at 760 mmHg

Melting Point


InChl Key

WGK Germany


HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:2050-87-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




Diallyl trisulfide (DATS) is a secondary metabolite of allicin, a volatile organosulfur flavoring compound generated by the crushing of garlic. These compounds have various medicinal effects such as antiplatelet activity. In this study, we demonstrated for the first time the cellular mechanism involved in the inhibition of platelet aggregation by DATS and dipropyl trisulfide (DPTS), which is a saturated analogue of DATS. Washed murine platelets were incubated with these sulfides, and platelet aggregation was evaluated by light transmission aggregometry. The amount of reaction products produced by DATS, DPTS, and glutathione (GSH) was measured using liquid chromatography-mass spectrometry. Compared with DPTS, DATS potently inhibited platelet aggregation induced by thrombin, U46619, and collagen. N-Ethylmaleimide (NEM), which is commonly used to modify sulfhydryl groups, also suppressed platelet aggregation. The reactivity of DATS with GSH was higher than that of DPTS. These data suggested that DATS inhibited platelet aggregation through the reaction of sulfhydryl groups.


diallyl trisulfide; garlic; glutathione; platelet aggregation; sulfhydryl group.


Diallyl Trisulfide Inhibits Platelet Aggregation through the Modification of Sulfhydryl Groups


Takashi Hosono 1 2, Asuka Sato 1, Natsumi Nakaguchi 1, Yori Ozaki-Masuzawa 2, Taiichiro Seki 1 2

Publish date

2020 Feb 12;




Anaplastic thyroid cancer (ATC) is the most aggressive thyroid cancer. Current approaches including surgery, chemotherapy and therapeutic drugs provide limited benefits for ATC patients. Diallyl trisulfide (DATS) has been documented as a promising anti-cancer agent for various carcinomas. However, its role in ATC tumorigenesis remained unclear. Our results showed that DATS treatment at 12.5, 25 and 50 μM decreased the viability of 8505C cells both in a time- and dose-dependent manner. The phosphorylation of H2A.X, which is a DNA damage marker, was induced by DATS both in a dose- and time-dependent manner. Moreover, DATS mediated the DNA damage through the phosphorylation of ATM but not ATR. DATS also induced G2/M cell-cycle arrest followed by the translocation of Cdc25C from the nucleus to the cytoplasm. Further results showed that DATS induced mitochondrial apoptosis in 8505C cells, evidenced by Hoechst/PI double staining, PI-Annexin V assay and western blot. Taken altogether, our findings demonstrated that DATS induced G2/M cell-cycle arrest and mitochondrial apoptosis by triggering DNA damage in ATC 8505C cells, which shed light on a novel therapeutic approach for ATC treatment.


Diallyl trisulfide induces G2/M cell-cycle arrest and apoptosis in anaplastic thyroid carcinoma 8505C cells


Jiangxia Zheng 1, Xian Cheng 2, Shichen Xu 2, Li Zhang 2, Jie Pan 3, Huixin Yu 2, Jiandong Bao 2, Rongrong Lu 3

Publish date

2019 Nov 1;




Therapeutic angiogenesis is essential for rescuing necrotic tissues in cases of ischemic disease. The exogenous hydrogen sulfide (H2S) donor, diallyl trisulfide (DATS), has been investigated as a therapeutic agent that promotes angiogenesis. However, the short half-life of generated H2S limits its therapeutic efficacy. In an attempt to overcome this difficulty, a poly(D,L-lactic-co-glycolic acid) microparticle system that contains DATS (DATS@MPs) is prepared as an in situ depot for the controlled release of H2S, providing slow release and long-term effectiveness. The results of in vitro investigations indicate that the slow-released DATS from the DATS@MPs depot yields a longer intracellular production of H2S than that from a free DATS depot. The intracellular generation of H2S favors the translocation of the transcription factor, Nrf2, from the cytosol to nuclei, potentially upregulating the gene expressions of antioxidant enzymes, ultimately increasing cellular resistance to oxidative stress. Intramuscular injection of the slow-releasing H2S donor depot DATS@MPs in an ischemic limb that is experimentally generated in a mouse model promotes therapeutic angiogenesis and protects cells from apoptosis and tissues from necrosis, ultimately salvaging the limb. These analytical results reveal that DATS@MPs is potentially useful in H2S-based therapy for treating ischemic diseases.


Critical limb ischemia; Drug delivery; H(2)S donor; Oxidative stress; Therapeutic angiogenesis.


An in situ slow-releasing H 2 S donor depot with long-term therapeutic effects for treating ischemic diseases


Meng-Hsuan Hsieh 1, Hung-Wen Tsai 2, Kun-Ju Lin 3, Zheng-Yu Wu 1, Hsin-Yi Hu 1, Yen Chang 4, Hao-Ji Wei 5, Hsing-Wen Sung 6

Publish date

2019 Nov;