(-)-Syringaresinol

(-)-Syringaresinol
Product Name (-)-Syringaresinol
CAS No.: 6216-81-5
Catalog No.: CFN92500
Molecular Formula: C22H26O8
Molecular Weight: 418.4 g/mol
Purity: >=98%
Type of Compound: Lignans
Physical Desc.: Powder
Targets: Cdk | p21 | Bcl-2/Bax | Caspase | PARP | P450 (e.g. CYP17)
Source: The rhizomes of Polygonatum kingianum
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $268/5mg
(-)-Syringaresinol inhibits the proliferation of human promyelocytic HL-60 cells through G(1) arrest and induction of apoptosis, may be a potential chemotherapeutic agent for the treatment of cancer.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Int Immunopharmacol. 2008 Jul;8(7):967-73.
    (-)-Syringaresinol inhibits proliferation of human promyelocytic HL-60 leukemia cells via G1 arrest and apoptosis.[Pubmed: 18486907]
    We examined the effect of (-)-Syringaresinol, a furofuran-type lignan isolated from Daphne genkwa, on cell cycle regulation in HL-60 human promyelocytic leukemia cells in vitro.
    METHODS AND RESULTS:
    (-)-Syringaresinol decreased the viability of HL-60 cells by inducing G(1) arrest followed by apoptosis in a dose- and time-dependent manner. The G(0)/G(1) phase of the cell cycle is regulated by cyclin-dependent kinases (Cdk), cyclins and cyclin-dependent kinase inhibitors (Cdki). We show by western blot analysis, that the (-)-Syringaresinol-induced G(1) arrest was mediated through the increased expression of Cdki proteins (p21(cip1/waf1) and p27(kip1)) with a simultaneous decrease in cdk2, cdk4, cdk6, cyclin D(1), cyclin D(2), and cyclin E expression. The induction of apoptosis after treatment with (-)-Syringaresinol for 24 h was demonstrated by morphological changes, DNA fragmentation, altered ratio of Bax/Bcl-2, cleavage of poly(ADP-ribose) polymerase and flow cytometry analysis. (-)-Syringaresinol also induced cytochrome c release and activation of caspase-3 and caspase-9. To our knowledge, this is the first time that (-)-Syringaresinol has been reported to potently inhibit the proliferation of human promyelocytic HL-60 cells through G(1) arrest and induction of apoptosis.
    CONCLUSIONS:
    These findings suggest that (-)-Syringaresinol may be a potential chemotherapeutic agent for the treatment of cancer.
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