| Stereochemistry | ABSOLUTE |
| Molecular Formula | C6H11NO2S |
| Molecular Weight | 161.222 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
N[C@@H](CSCC=C)C(O)=O
InChI
InChIKey=ZFAHNWWNDFHPOH-YFKPBYRVSA-N
InChI=1S/C6H11NO2S/c1-2-3-10-4-5(7)6(8)9/h2,5H,1,3-4,7H2,(H,8,9)/t5-/m0/s1
S-Allylcysteine (SAC), the most abundant organosulfur compound in aged garlic extract, has multifunctional activity via different mechanisms and neuroprotective effects that are exerted probably via its antioxidant or free radical scavenger action. Anticancer effects of SAC were reported in prostate cancer, breast cancer, oral cavity cancer, non-small cell lung cancer, neuroblastoma, and hepatocellular carcinoma through the restoration of E-cadherin, the reduction of Slug and matrix metalloproteinase (MMP) protein expression, and stimulating apoptotic pathways. In addition, recently was revealed, that SAC might have imperative implications for the deterrence and early treatment of type 2 diabetes by reducing the influx of glucose in the polyol pathway, thereby elevating the GSH level and reducing the activities of aldose reductase (AR) and sorbitol dehydrogenase (SDH).
Approval Year
PubMed
Patents
Sample Use Guides
in rats: Diabetes was induced in male albino Wistar rats by intraperitoneal administration of STZ (55 mg kg-1 bw-1) and NA (110 mg kg-1 bw-1). S-allylcysteine (SAC) (150 mg kg-1 bw-1) was orally administered to the rats with diabetes for 45 days to assess its effects on blood glucose, insulin, insulin resistance, glycated hemoglobin, aldose reductase (AR), sorbitol dehydrogenase (SDH), sorbitol, fructose, thiobarbituric acid-reactive substances (TBARS), hydroperoxide, hemoglobin and glutathione (GSH).
Route of Administration:
Oral
S-allylcysteine (SAC) suppressed proliferation and induced apoptosis in human ovarian cancer cells in vitro. SAC (1-100 mmol/L) inhibited the proliferation of A2780 cells in dose- and time-dependent manners (the IC50 value was approximately 25 mmol/L at 48 h, and less than 6.25 mmol/L at 96 h). Furthermore, SAC dose-dependently inhibited the colony formation of A2780 cells. Treatment of A2780 cells with SAC resulted in G1/S phase arrest and induced apoptosis, accompanied by decreased expression of pro-caspase-3, Parp-1 and Bcl-2, and increased expression of active caspase-3 and Bax. SAC treatment significantly reduced the migration of A2780 cells, and markedly decreased the protein expression of Wnt5a, p-AKT and c-Jun, which were the key proteins involved in proliferation and metastasis.
SUBSTANCE RECORD
