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S-Allyl-L-cysteine Catalog No.GC30205

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Sample solution is provided at 25 µL, 10mM.

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Chemical Properties

Cas No. 21593-77-1 SDF Download SDF
Synonyms N/A
Chemical Name N/A
Canonical SMILES N[C@@H](CSCC=C)C(O)=O
Formula C6H11NO2S M.Wt 161.22
Solubility H2O : 33.33 mg/mL (206.74 mM; Need ultrasonic) Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
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**When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / CoA (available online).



S-Allyl-L-cysteine, one of the organosulfur compounds found in AGE, possess various biological effects including neurotrophic activity, anti-cancer activity, anti-inflammatory activity.

It is found that S-Allyl-L-cysteine could protect against amyloid-protein (A)-and tunicamycin-induced cell death in differentiated PC12 cells. Simultaneously applied S-Allyl-L-cysteine (1 μM) suppresses the cell death induced by Aβ25-35 and Aβ1-40 in a concentration-dependent manner, and neuronal integrity is almost completely retained. Simultaneously applied S-Allyl-L-cysteine significantly decreases the Aβ-induced level of ROS. The TEAC value of S-Allyl-L-cysteine is lower than that of oxidized GSH, and no antioxidant activity is observed. Intracellular GSH levels remains unaffected by treatment of neurons with S-Allyl-L-cysteine for 24 h. Furthermore, the increase in caspase-12 protein expression is suppressed by simultaneously adding 1 μM S-Allyl-L-cysteine [1]. S-Allyl-L-cysteine up to a concentration 1.0 mM does not exhibit any cytotoxic impact on morphology of myoblast and myotubes in culture observed under bright field microscope. TNF treatment leads to a significant decrease in the intracellular CK activity while S-Allyl-L-cysteine pre-treatment to TNF treated myotubes decreases the release of CK in media. S-Allyl-L-cysteine pre-treatment decreases the level of active form of this enzyme in S-Allyl-L-cysteine+TNF group. Similar observations are recorded at mRNA level for caspase-3. These results illustrate that S-Allyl-L-cysteine regulates apoptotic signals via suppressing the transcription and thus protein expression of caspase-3[2].

[1]. Kosuge Y, et al. S-allyl-L-cysteine selectively protects cultured rat hippocampal neurons from amyloid beta-protein- and tunicamycin-induced neuronal death. Neuroscience. 2003;122(4):885-95. [2]. Dutt V, et al. S-allyl cysteine inhibits TNFα-induced skeletal muscle wasting through suppressing proteolysis and expression of inflammatory molecules. Biochim Biophys Acta. 2018 Apr;1862(4):895-906.