Fusarochromanone
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| Category | Mycotoxins |
| Catalog number | BBF-01468 |
| CAS | 104653-89-6 |
| Molecular Weight | 292.33 |
| Molecular Formula | C15H20N2O4 |
| Purity | >98% |
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Description
Produced by the strain of Fusarium equiseti. Fusarochromanone causes Tibial chondrodysplasia in animals and is associated with kashin-Beck's disease in children.
Specification
| Synonyms | Fusarochromenone; 4H-1-Benzopyran-4-one, 5-amino-6-(3-amino-4-hydroxy-1-oxobutyl)-2,3-dihydro-2,2-dimethyl-; 5-Amino-6-(3-amino-4-hydroxy-1-oxobutyl)-2,3-dihydro-2,2-dimethyl-4H-1-benzopyran-4-one |
| IUPAC Name | 5-amino-6-(3-amino-4-hydroxybutanoyl)-2,2-dimethyl-3H-chromen-4-one |
| Canonical SMILES | CC1(CC(=O)C2=C(O1)C=CC(=C2N)C(=O)CC(CO)N)C |
| InChI | InChI=1S/C15H20N2O4/c1-15(2)6-11(20)13-12(21-15)4-3-9(14(13)17)10(19)5-8(16)7-18/h3-4,8,18H,5-7,16-17H2,1-2H3 |
| InChI Key | COSICWYFCAPPJB-UHFFFAOYSA-N |
Properties
| Boiling Point | 547°C at 760 mmHg |
| Melting Point | 132-134°C |
| Density | 1.267 g/cm3 |
Reference Reading
1. TNBC Therapeutics Based on Combination of Fusarochromanone with EGFR Inhibitors
Natalie Carroll, Reneau Youngblood, Alena Smith, Ana-Maria Dragoi, Brian A Salvatore, Elahe Mahdavian Biomedicines. 2022 Nov 12;10(11):2906. doi: 10.3390/biomedicines10112906.
Fusarochromanone is an experimental drug with unique and potent anti-cancer activity. Current cancer therapies often incorporate a combination of drugs to increase efficacy and decrease the development of drug resistance. In this study, we used drug combinations and cellular phenotypic screens to address important questions about FC101's mode of action and its potential therapeutic synergies in triple negative breast cancer (TNBC). We hypothesized that FC101's activity against TNBC is similar to the mTOR inhibitor, everolimus, because FC101 downregulates the phosphorylation of two mTOR substrates, S6K and S6. Since everolimus synergistically enhances the anti-cancer activities of two known EGFR inhibitors (erlotinib or lapatinib) in TNBC, we performed analogous studies with FC101. Phenotypic cellular assays helped assess whether FC101 acts similarly to everolimus, in both single and combination treatments with the two inhibitors. FC101 outperformed all other single treatments in both cell proliferation and viability assays. However, unlike everolimus, FC101 produced a sustained decrease in cell viability in drug washout studies. None of the other drugs were able to maintain comparable effects upon removal. Although we observed slightly additive effects when the TNBC cells were treated with FC101 and the two EGFR inhibitors, those effects were not truly synergistic in the manner displayed with everolimus.
2. Biological activities of fusarochromanone: a potent anti-cancer agent
Elahe Mahdavian, Phillip Palyok, Steven Adelmund, Tara Williams-Hart, Brian D Furmanski, Yoon-Jee Kim, Ying Gu, Mansoureh Barzegar, Yang Wu, Kaustubh N Bhinge, Gopi K Kolluru, Quincy Quick, Yong-Yu Liu, Christopher G Kevil, Brian A Salvatore, Shile Huang, John L Clifford BMC Res Notes. 2014 Sep 3;7:601. doi: 10.1186/1756-0500-7-601.
Background: Fusarochromanone (FC101) is a small molecule fungal metabolite with a host of interesting biological functions, including very potent anti-angiogenic and direct anti-cancer activity. Results: Herein, we report that FC101 exhibits very potent in-vitro growth inhibitory effects (IC50 ranging from 10nM-2.5 μM) against HaCat (pre-malignant skin), P9-WT (malignant skin), MCF-7 (low malignant breast), MDA-231 (malignant breast), SV-HUC (premalignant bladder), UM-UC14 (malignant bladder), and PC3 (malignant prostate) in a time-course and dose-dependent manner, with the UM-UC14 cells being the most sensitive. FC101 induces apoptosis and an increase in proportion of cells in the sub-G1 phase in both HaCat and P9-WT cell lines as evidenced by cell cycle profile analysis. In a mouse xenograft SCC tumor model, FC101 was well tolerated, non-toxic, and achieved a 30% reduction in tumor size at a dose of 8 mg/kg/day. FC101 is also a potent anti-angiogenenic agent. At nanomolar doses, FC101 inhibits the vascular endothelial growth factor-A (VEGF-A)-mediated proliferation of endothelial cells. Conclusions: Our data presented here indicates that FC101 is an excellent lead candidate for a small molecule anti-cancer agent that simultaneously affects angiogenesis signaling, cancer signal transduction, and apoptosis. Further understanding of the underlying FC101's molecular mechanism may lead to the design of novel targeted and selective therapeutics, both of which are pursued targets in cancer drug discovery.
3. Fusarochromanone-induced reactive oxygen species results in activation of JNK cascade and cell death by inhibiting protein phosphatases 2A and 5
Ying Gu, Mansoureh Barzegar, Xin Chen, Yang Wu, Chaowei Shang, Elahe Mahdavian, Brian A Salvatore, Shanxiang Jiang, Shile Huang Oncotarget. 2015 Dec 8;6(39):42322-33. doi: 10.18632/oncotarget.5996.
Recent studies have shown that fusarochromanone (FC101), a mycotoxin, is cytotoxic in a variety of cell lines. However, the molecular mechanism underlying its cytotoxicity remains elusive. Here we found that FC101 induced cell death in COS7 and HEK293 cells in part by activating JNK pathway. This is evidenced by the findings that inhibition of JNK with SP600125 or expression of dominant negative c-Jun partially prevented FC101-induced cell death. Furthermore, we observed that FC101-activated JNK pathway was attributed to induction of reactive oxygen species (ROS). Pretreatment with N-acetyl-L-cysteine (NAC), a ROS scavenger and antioxidant, suppressed FC101-induced activation of JNK and cell death. Moreover, we noticed that FC101 inhibited the serine/threonine protein phosphatases 2A (PP2A) and 5 (PP5) in the cells, which was abrogated by NAC. Overexpression of PP2A or PP5 partially prevented FC101-induced activation of JNK and cell death. The results indicate that FC101-induced ROS inhibits PP2A and PP5, leading to activation of JNK pathway and consequently resulting in cell death.
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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 ╳
