Ascochlorin

Ascochlorin

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Ascochlorin
Category Antibiotics
Catalog number BBF-00564
CAS 26166-39-2
Molecular Weight 404.93
Molecular Formula C23H29ClO4
Purity >98%

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Description

Ascochlorin is an antibiotic produced by Ascochyta viciae. It has anti-candida albicans activity. It can inhibit Newcastle disease virus and herpes simplex virus plaque formation in chicken embryo fibroblast culture.

Specification

Synonyms Ilicicolin D
Storage Store at -20°C
IUPAC Name 5-chloro-2,4-dihydroxy-6-methyl-3-[(2E,4E)-3-methyl-5-[(1R,2R,6R)-1,2,6-trimethyl-3-oxocyclohexyl]penta-2,4-dienyl]benzaldehyde
Canonical SMILES CC1CCC(=O)C(C1(C)C=CC(=CCC2=C(C(=C(C(=C2O)Cl)C)C=O)O)C)C
InChI InChI=1S/C23H29ClO4/c1-13(10-11-23(5)14(2)7-9-19(26)16(23)4)6-8-17-21(27)18(12-25)15(3)20(24)22(17)28/h6,10-12,14,16,27-28H,7-9H2,1-5H3/b11-10+,13-6+/t14-,16+,23+/m1/s1
InChI Key SETVRSKZJJWOPA-FLDGXQSCSA-N
Source Acremonium sp.

Properties

Appearance Colorless Needle Crystal
Antibiotic Activity Spectrum yeast
Boiling Point 556.9°C at 760 mmHg
Melting Point 153-154°C (dec.)
Density 1.199 g/cm3
Solubility Soluble in Mether, Ether, Acetone, Chloroform, Ethyl acetate, Ethanol

Reference Reading

1. Ascochlorin inhibits growth factor-induced HIF-1α activation and tumor-angiogenesis through the suppression of EGFR/ERK/p70S6K signaling pathway in human cervical carcinoma cells
Hyeun-Wook Chang, Yun-Jeong Jeong, Yoon-Yub Park, Hyun-Ji Cho, Jae-Moon Shin, Ji-Hak Jeong, Jeong-Han Kang, Il-Kyung Chung, Junji Magae, Kwan-Kyu Park J Cell Biochem . 2012 Apr;113(4):1302-13. doi: 10.1002/jcb.24001.
Ascochlorin, a non-toxic prenylphenol compound derived from the fungus Ascochyta viciae, has been shown recently to have anti-cancer effects on various human cancer cells. However, the precise molecular mechanism of this anti-cancer activity remains to be elucidated. Here, we investigated the effects of ascochlorin on hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) expression in human epidermoid cervical carcinoma CaSki cells. Ascochlorin inhibited epidermal growth factor (EGF)-induced HIF-1α and VEGF expression through multiple potential mechanisms. First, ascochlorin selectively inhibited HIF-1α expression in response to EGF stimulation, but not in response to hypoxia (1% O(2)) or treatment with a transition metal (CoCl(2)). Second, ascochlorin inhibited EGF-induced ERK-1/2 activation but not AKT activation, both of which play essential roles in EGF-induced HIF-1α protein synthesis. Targeted inhibition of epidermal growth factor receptor (EGFR) expression using an EGFR-specific small interfering RNA (siRNA) diminished HIF-1α expression, which suggested that ascochlorin inhibits HIF-1α expression through suppression of EGFR activation. Finally, we showed that ascochlorin functionally abrogates in vivo tumor angiogenesis induced by EGF in a Matrigel plug assay. Our data suggest that ascochlorin inhibits EGF-mediated induction of HIF-1α expression in CaSki cells, providing a potentially new avenue of development of anti-cancer drugs that target tumor angiogenesis.
2. Ascochlorin, an isoprenoid antibiotic, induces G1 arrest via downregulation of c-Myc in a p53-independent manner
Young-Chae Chang, Ji-Hak Jeong Biochem Biophys Res Commun . 2010 Jul 16;398(1):68-73. doi: 10.1016/j.bbrc.2010.06.037.
Numerous anti-cancer agents inhibit cell cycle progression via a p53-dependent mechanism; however, many of these carcinostatic substances are toxic. Here, we show that ascochlorin, an isoprenoid antibiotic, is a non-toxic anti-cancer agent that induces G1 arrest via the induction of p21(WAF1/CIP1) in a c-Myc, but not a p53, dependent manner. Ascochlorin has a broad spectrum of anti-tumor and anti-metastatic activities, but the molecular mechanism by which it inhibits cell cycle progression of cancer cells remains to be elucidated. We demonstrated that cytostatic G1 arrest by ascochlorin is mainly associated with the upregulation of p21(WAF1/CIP1), and the downregulation of c-Myc. Furthermore, we used a chromatin immunoprecipitation assay, RNA interference, and p53-deficient cells to verify that p21(WAF1/CIP1) induction by ascochlorin is related to transcriptional repression of c-Myc. Ascochlorin abolished pRB hyperphosphorylation, which resulted in the inactivation of E2F transcriptional activity. These results suggest that ascochlorin induces G1 arrest via the p53-independent suppression of c-Myc. Thus, we reveal a role for ascochlorin in inhibiting tumor growth via G1 arrest, and identify a novel regulatory mechanism for c-Myc.
3. Ascochlorin induces caspase-independent necroptosis in LPS-stimulated RAW 264.7 macrophages
Junyoung Park, Hee-Do Kim, Young-Chae Chang, Sook-Hyun Lee, Cheorl-Ho Kim, Young-Choon Lee, Choong-Hwan Kwak, Junji Magae, Tae-Wook Chung J Ethnopharmacol . 2019 Jul 15;239:111898. doi: 10.1016/j.jep.2019.111898.
Ethnopharmacological relevance:Plant-specific fungus of natural compound of Ascochyta viciae has traditionally been used in the treatment of sleeping sickness and tumors. The anti-tumor activities of the compounds obtained from Pisum sativum L were evaluated in this study.Aim of the study:In this study, during the prolonged incubation, treatment of the LPS-stimulated tumor-like macrophage RAW 264.7 cells with ASC exhibited the shift of anti-inflammatory behavior to a type of necroptotic cell death named necroptosis.Materials and methods:Ascochlorin (ASC) purified from plant-specific fungus Ascochyta viciae is a natural compound with the trimethyl oxocyclohexyl structure and an anti-cancer and antibiotic agent. The fungus contributes to the Ascochyta blight disease complex of pea (Pisum sativum L). RAW 264.7 cells have been stimulated with LPS and treated with ASC. Cell viability of the LPS-treated RAW 264.7 cells and bone marrow-derived macrophage (BMDM) cells were examined. Flow cytometry analysis with 7AAD and Annexin V was examined for the apoptotic or necroptosis/late-apoptosis. Cleaved caspase-3, -7 and -8 as well as cleaved PARP were assessed with a caspase inhibitor, z-VAD-fmk. LPS-responsible human leukemic U937 and colon cancer SW480 and HT-29 cells were also examined for the cell viabilities.Results:Flow cytometry analysis after Annexin V and 7AAD double staining showed that ASC alone induces apoptosis in RAW 264.7 cells, while it induces necroptosis/late-apoptosis in LPS-treated RAW 264.7 cells. 7AAD and Annexin V positive populations were increased in the LPS-treated cells with ASC. Although viability of LPS-treated cells with ASC was decreased, the amounts of cleaved caspase-3, -7 and -8 as well as cleaved PARP were reduced when compared with ASC-treated cells. Upon ASC treatment, the cleaved caspase-8 level was not changed, however, cleaved caspase-3, -7, and PARP were reduced in LPS-stimulated RAW 264.7 cells treated with ASC, claiming a caspase-8 independent necroptosis of ASC. Furthermore, ASC and LPS-cotreated cells which a caspase inhibitor, z-VAD-fmk, was pretreated, showed the decreased cell viability compared with control cells without the inhibitor. Cell viability of RAW 264.7 cells co-treated with ASC and LPS when treated with z-VAD was decreased. In the LPS-responsible human leukemic U937 and colon cancer SW480 and HT-29 cells, cell viabilities were decreased by 10 μM ASC.Conclusion:Prolonged stimulation of ASC with LPS induces the necroptosis in RAW cells. Activated immune cells may share the susceptibility of antitumor agents with the cancer cells.

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Tip: Chemical formula is case sensitive. C22H30N4O c22h30n40
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