Ascofuranone
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| Category | Antibiotics |
| Catalog number | BBF-00099 |
| CAS | 38462-04-3 |
| Molecular Weight | 420.93 |
| Molecular Formula | C23H29ClO5 |
| Purity | >98% |
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Description
Ascofuranone is an antibiotic produced by Ascochyta viciae. On the agar plate, it can inhibit the plaque formation of some viruses, and is not resistant to bacteria and other microorganisms. Oral administration in rats can reduce blood lipids.
Specification
| Storage | Store at -20°C |
| IUPAC Name | 5-chloro-3-[(2E,6E)-7-[(2S)-5,5-dimethyl-4-oxooxolan-2-yl]-3-methylocta-2,6-dienyl]-2,4-dihydroxy-6-methylbenzaldehyde |
| Canonical SMILES | CC1=C(C(=C(C(=C1Cl)O)CC=C(C)CCC=C(C)C2CC(=O)C(O2)(C)C)O)C=O |
| InChI | InChI=1S/C23H29ClO5/c1-13(7-6-8-14(2)18-11-19(26)23(4,5)29-18)9-10-16-21(27)17(12-25)15(3)20(24)22(16)28/h8-9,12,18,27-28H,6-7,10-11H2,1-5H3/b13-9+,14-8+/t18-/m0/s1 |
| InChI Key | VGYPZLGWVQQOST-JUERRSSISA-N |
Properties
| Appearance | Colorless needle Crystal |
| Antibiotic Activity Spectrum | viruses |
| Melting Point | 84-85°C |
| Solubility | Soluble in DMSO |
Reference Reading
1. Heterologous production of ascofuranone and ilicicolin A in Aspergillus sojae
Yasuko Araki, Yasutomo Shinohara, Seiichi Hara, Atsushi Sato, Ryoichi Sakaue, Keiko Gomi, Kiyoshi Kita, Kotaro Ito J Gen Appl Microbiol. 2022 Jun 20;68(1):10-16. doi: 10.2323/jgam.2021.08.001. Epub 2022 Apr 13.
Ascofuranone and its precursor, ilicicolin A, are secondary metabolites with various pharmacological activities that are produced by Acremonium egyptiacum. In particular, ascofuranone strongly inhibits trypanosome alternative oxidase and represents a potential drug candidate against African trypanosomiasis. However, difficulties associated with industrial production of ascofuranone by A. egyptiacum, specifically the co-production of ascochlorin, which inhibits mammalian respiratory chain complex III at low concentrations, has precluded its widespread application. Therefore, in this study, ascofuranone biosynthetic genes (ascA-E and H-J) were heterologously expressed in Aspergillus sojae, which produced very low-levels of endogenous secondary metabolites under conventional culture conditions. As a result, although we obtained transformants producing both ilicicolin A and ascofuranone, they were produced only when an adequate concentration of chloride ions was added to the medium. In addition, we succeeded in increasing the production of ilicicolin A, by enhancing the expression of the rate-determining enzyme AscD, using a multi-copy integration system. The heterologous expression approach described here afforded the production of both ascofuranone and ilicicolin A, allowing for their development as therapeutics.
2. Ascofuranone suppresses invasion and F-actin cytoskeleton organization in cancer cells by inhibiting the mTOR complex 1 signaling pathway
Yun-Jeong Jeong, Soon-Kyung Hwang, Junji Magae, Young-Chae Chang Cell Oncol (Dordr). 2020 Oct;43(5):793-805. doi: 10.1007/s13402-020-00520-w. Epub 2020 Jun 2.
Purpose: Ascofuranone is an antiviral antibiotic that is known to exert multiple anti-tumor effects, including cell cycle arrest, inhibition of mitochondrial respiration, and inhibition of angiogenesis. In this study, we investigated the molecular mechanisms underlying the anti-metastatic effects of ascofuranone in insulin-like growth factor-I (IGF-1)-responsive cancer cells. Methods: The inhibitory effect of ascofuranone on cancer cell migration and invasion was assessed using scratch wound healing and Matrigel invasion assays, respectively. F-actin cytoskeleton organization was assessed using FITC conjugated phalloidin staining. Target gene expression was evaluated using Western blotting and gene silencing was performed using siRNA transfections. Finally, the anti-metastatic effect of ascofuranone was investigated in vivo. Results: We found that ascofuranone suppressed IGF-1-induced cell migration, invasion and motility in multiple cancer cell lines. The effects of ascofuranone on actin cytoskeleton organization were found to be mediated by suppression of the mTOR/p70S6K/4EBP1 pathway. Ascofuranone inhibited IGF-1-induced mTOR phosphorylation and actin cytoskeleton organization via upregulation of AMPK and downregulation of Akt phosphorylation. It also selectively suppressed the IGF-1-induced mTOR complex (mTORC)1 by phosphorylation of Raptor, but did not affect mTORC2. Furthermore, we found that focal adhesion kinase (FAK) activation decreased in response to ascofuranone, rapamycin, compound C and wortmannin treatment. Finally, we found that ascofuranone suppressed phosphorylation of FAK and mTOR and dephosphorylation of Raptor in cancerous metastatic lung tissues in vivo. Conclusions: Our data indicate that ascofuranone suppresses IGF-1-induced cancer cell migration and invasion by blocking actin cytoskeleton organization and FAK activation through inhibition of the mTORC1 pathway, and reveal a novel anti-metastatic function of this compound.
3. Ascofuranone inhibits epidermal growth factor-induced cell migration by blocking epithelial-mesenchymal transition in lung cancer cells
Hyo-Weon Kim, Yun-Jeong Jeong, Soon-Kyung Hwang, Yoon-Yub Park, Yung Hyun Choi, Cheorl-Ho Kim, Junji Magae, Young-Chae Chang Eur J Pharmacol. 2020 Aug 5;880:173199. doi: 10.1016/j.ejphar.2020.173199. Epub 2020 May 18.
Ascofuranone, an isoprenoid antibiotic initially purified from a culture broth of Ascochyta viciae, has multiple anticancer effects. However, the impacts of ascofuranone on the epithelial-mesenchymal transition (EMT) and epidermal growth factor (EGF)-induced effects on human lung cancer cell lines have not been previously reported. Here, we show that ascofuranone exerts its anticancer effects by inhibiting the EGF-induced EMT and cell migration in human lung cancer cell lines. Ascofuranone significantly inhibited EGF-induced migration and invasion by lung cancer cells, and suppressed EGF-induced morphologic changes by regulating the expression of EMT-associated proteins. In addition, ascofuranone upregulated E-cadherin, and downregulated fibronectin, vimentin, Slug, Snail, and Twist. Inhibition of ERK/AKT/mTOR promoted EGF-induced E-cadherin downregulation and inhibited EGF-induced vimentin upregulation in response to ascofuranone, implying that inhibition of the EGF-induced EMT by ascofuranone was mediated by the ERK and AKT/mTOR pathways. Inhibition of c-Myc suppressed EGF-induced vimentin upregulation, suggesting the involvement of c-Myc. Collectively, these findings suggest that ascofuranone inhibits tumor growth by blocking the EGF-induced EMT through a regulatory mechanism involving ERK, AKT/mTOR, and c-Myc in lung 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 ╳
