16891-85-3
Chemical Structure
Roridin E
- CAS No.: 16891-85-3
- Formula:C29H38O8
- Molecular Weight:514.61
IUPAC Name: (2S,4'E,9'R,10'E,12'Z,16'R,16a'S,18'R,19a'R,23a'R)-9'-((R)-1-hydroxyethyl)-5',16a',21'-trimethyl-6',7',16',16a',19a',22'-hexahydro-1'H,3'H,18'H,23'H-spiro[oxirane-2,17'-[16,18]methano[1,6,12]trioxacyclooctadecino[3,4-d]chromene]-3',14'(9'H)-dione
InChIKey: KEEQQEKLEZRLDS-FLGSVKSYSA-N
SMILES: C[C@@]12[C@]3(CO3)[C@@]4([H])C[C@@]1([H])OC(/C=C\C=C\[C@@]([C@H](O)C)([H])OCC/C(C)=C/C(OC[C@]25[C@](C=C(C)CC5)([H])O4)=O)=O
Biological Activity: Roridin E is a glucose-6-phosphatase (G6Pase) inhibitor and antibiotic, and is a metabolic byproduct of Roridin A (HY-N9599). Roridin E induces significant oxidative stress, characterized by depletion of glutathione in vivo, induction of hepatic lipid peroxidation, and inhibition of renal superoxide dismutase activity. Roridin E reduces blood glucose levels in rats, but exhibits acute toxicity (which is enhanced when co-administered with linoleic acid (HY-N0729)) and causes hepatotoxicity in male albino mice. Roridin E induces a decrease in total blood protein and increases in the levels of total lipids, γ-glutamyltransferase, alkaline phosphatase, and 5'-nucleotidase. Roridin E can be isolated from molds, and possesses cytostatic and antifungal activities similar to those of Verrucarin A (HY-107426) and Roridin A. Roridin E exhibits in vivo activity in rodents and is commonly used in hepatotoxicity-related studies[1][2][3].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
|
Roridin E | 99.89% | Roridin E is a glucose-6-phosphatase (G6Pase) inhibitor and antibiotic, and is a metabolic byproduct of Roridin A (HY-N9599). Roridin E induces significant oxidative stress, characterized by depletion of glutathione in vivo, induction of hepatic lipid peroxidation, and inhibition of renal superoxide dismutase activity. Roridin E reduces blood glucose levels in rats, but exhibits acute toxicity (which is enhanced when co-administered with linoleic acid (HY-N0729)) and causes hepatotoxicity in male albino mice. Roridin E induces a decrease in total blood protein and increases in the levels of total lipids, γ-glutamyltransferase, alkaline phosphatase, and 5'-nucleotidase. Roridin E can be isolated from molds, and possesses cytostatic and antifungal activities similar to those of Verrucarin A (HY-107426) and Roridin A. Roridin E exhibits in vivo activity in rodents and is commonly used in hepatotoxicity-related studies. | ||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
- [1]. Omar H E D M, et al. Acute toxicity of the mycotoxin roridin E on liver and kidney of rats[J]. Journal of Applied Animal Research, 1997, 12(2): 145-152.
- [2]. Qusti S Y, et al. Effect of Nigella sativa L. oil on roridin E toxin administration on liver of male mice[J]. Journal of Applied Animal Research, 2007, 31(2): 161-164.
- [3]. Böhner B, et al. Über die Isolierung von Verrucarin H, Verrucarin J, Roridin D und Roridin E aus Myrothecium‐Arten. Verrucarine und Roridine, 8. Mitteilung[J]. Helvetica Chimica Acta, 1965, 48(5): 1079-1087.
Keywords