Clerosterol

Clerosterol
Product Name Clerosterol
CAS No.: 2364-23-0
Catalog No.: CFN90787
Molecular Formula: C29H48O
Molecular Weight: 412.7 g/mol
Purity: >=98%
Type of Compound: Steroids
Physical Desc.: Powder
Targets: Bcl-2/Bax | Caspase
Source: The herbs of Cleredendrum cwtophyllum Turcz.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Clerosterol as a precursor of cyasterone, isocyasterone and 29-norcyasterone in biosynthesis of phytoecdysteroids of Ajuga hairy roots. Clerosterol exerts its cytotoxic effect in A2058 human melanoma cells by caspases-dependent apoptosis.
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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.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

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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    The cytotoxic effects and mechanism of action of Clerosterol, isolated from the marine alga Codium fragile, were investigated in A2058 human melanoma cells.
    METHODS AND RESULTS:
    Clerosterol inhibited the growth of A2058 cells with an IC(50) of 150 µM and induced apoptotic cell death, as evidenced by DNA fragmentation, an increase in the number of sub-G(1) hypodiploid cells and the presence of apoptotic bodies. Clerosterol treatment caused the loss of mitochondrial membrane potential. Alterations in the expression of apoptosis-associated proteins in response to Clerosterol treatment included upregulation of Bax, downregulation of Bcl-2 and activation of caspases 3 and 9. The pan-caspase inhibitor treatment attenuated the expression of the active form of caspases and cell death induced by Clerosterol.
    CONCLUSIONS:
    The present results show that Clerosterol exerts its cytotoxic effect in A2058 human melanoma cells by caspases-dependent apoptosis.
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