Trichodion
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| Category | Enzyme inhibitors |
| Catalog number | BBF-02710 |
| CAS | |
| Molecular Weight | 238.24 |
| Molecular Formula | C12H14O5 |
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Description
Trichodion is originally isolated from Trichosporiella sp. It inhibits the expression of secretion alkaline phosphatase (SEAP) Reporter gene mediated by IFN-V with IC50 of 5-10 μg/mL, and it also inhibits the expression of human IFN-α promoter-driven Luciferase Reporter gene with IC50 of 2.5-5μg/mL.
Specification
| IUPAC Name | (3R,7S)-3-hydroxy-7-methyl-2-[(E)-prop-1-enyl]-2,3,6,7-tetrahydropyrano[2,3-b]pyran-4,5-dione |
| Canonical SMILES | CC=CC1C(C(=O)C2=C(O1)OC(CC2=O)C)O |
| InChI | InChI=1S/C12H14O5/c1-3-4-8-10(14)11(15)9-7(13)5-6(2)16-12(9)17-8/h3-4,6,8,10,14H,5H2,1-2H3/b4-3+/t6-,8?,10+/m0/s1 |
| InChI Key | ZHJAUCLFHVHSFH-CZNHCDSPSA-N |
Properties
| Appearance | Colorless Crystalline |
| Melting Point | 167-169°C |
Reference Reading
1. Trichodion, a new inhibitor of inflammatory signal transduction pathways from a Trichosporiella species
G Erkel FEBS Lett. 2000 Jul 21;477(3):219-23. doi: 10.1016/s0014-5793(00)01784-1.
In a search for new inhibitors of the IFN-gamma mediated signal transduction in HeLa S3 cells using secreted alkaline phosphatase (SEAP) as reporter gene, the novel pyran-dione trichodion was isolated from fermentations of the imperfect fungus Trichosporiella sp. 20-95. The compound inhibits the IFN-gamma mediated expression of the reporter gene with IC(50) values of 21-42 microM (5-10 microgram/ml). The NF-kappaB and AP-1 mediated expression of the reporter gene are inhibited with IC(50) values of 42-84 microM (10-20 microgram/ml) and 21 microM (5 microgram/ml) respectively. Western blotting with COX-2 and NOS II antibodies showed that the expression of both proinflammatory enzymes is almost completely inhibited at 21-42 microM (5-10 microgram/ml) in LPS/IFN-gamma stimulated J774 mouse macrophages. Studies on the mode of action of the compound revealed that the inhibition of the NF-kappaB dependent pathway is due to the stabilization of the IkappaB protein and the inhibition of the IFN-gamma dependent signaling is caused by an inhibition of the phosphorylation of the STAT1alpha transcription factor.
2. Globosumones A-C, cytotoxic orsellinic acid esters from the Sonoran desert endophytic fungus Chaetomium globosum
Bharat P Bashyal, E M Kithsiri Wijeratne, Stanley H Faeth, A A Leslie Gunatilaka J Nat Prod. 2005 May;68(5):724-8. doi: 10.1021/np058014b.
Three new esters of orsellinic acid, globosumones A-C (1-3), and three known compounds, orsellinic acid (4), orcinol, and trichodion (5), were isolated from Chaetomium globosum endophytic on Ephedrafasciculata (Mormon tea). The structures of the new compounds 1-3 were established spectroscopically, which included 2D NMR experiments and 1H NMR studies on Mosher's ester derivatives. All compounds were evaluated for inhibition of cell proliferation in a panel of four cancer cell lines, NCI-H460 (non-small cell lung cancer), MCF-7 (breast cancer), SF-268 (CNS glioma), and MIA Pa Ca-2 (pancreatic carcinoma), and normal human fibroblast cells (WI-38). Only globosumones A (1) and B (2) were found to be moderately active.
3. Glycogen synthase kinase-3beta suppression eliminates tumor necrosis factor-related apoptosis-inducing ligand resistance in prostate cancer
Xinbo Liao, Liping Zhang, J Brantley Thrasher, Jie Du, Benyi Li Mol Cancer Ther. 2003 Nov;2(11):1215-22.
Prostate cancer is a major health threat for American men. Therefore, the development of effective therapeutic options is an urgent issue for prostate cancer treatment. In this study, we evaluated the effect of glycogen synthase kinase-3beta (GSK-3beta) suppression on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in human prostate cancer cell lines. In the presence of lithium chloride (LiCl) or SB216763, the GSK-3beta inhibitors, TRAIL-induced cell death was dramatically enhanced, and the enhanced cell death was an augmented apoptotic response evidenced by increased Annexin V labeling and caspase-3 activation. GSK-3beta gene silencing mediated by a small interference RNA (siRNA) duplex also sensitized the cells to TRAIL, confirming the specificity of GSK-3beta suppression. Importantly, TRAIL stimulation increased GSK-3beta tyrosine phosphorylation at Y216, suggesting that GSK-3beta is activated by TRAIL. Furthermore, TRAIL sensitization was associated with increased proteolytic procession of caspase-8 and its downstream target BID, and z-IETD-FMK, the inhibitor specific to active caspase-8 totally blocked LiCl-induced TRAIL sensitization. Finally, Trichodion, a potent nuclear factor-kappaB (NF-kappaB) inhibitor, could not affect LiCl-induced TRAIL sensitization, although GSK-3beta inhibitors significantly blocked TRAIL-reduced NF-kappaB activity in prostate cancer cells. These results indicate that GSK-3beta suppression sensitizes prostate cancer cells to TRAIL-induced apoptosis that is dependent on caspase-8 activities but independent of NF-kappaB activation, and suggest that a mechanism involving GSK-3beta activation may be responsible for TRAIL resistance in prostate cancer cells.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
