Verrucarin A
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| Category | Antibiotics |
| Catalog number | BBF-03441 |
| CAS | 3148-09-2 |
| Molecular Weight | 502.55 |
| Molecular Formula | C27H34O9 |
| Purity | 95% |
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Description
It is produced by the strain of Myrothecium verrucaria NRRL 3003. Verrucarin A has the effect of anti-Gram-negative bacteria and fungi, inhibiting Newcastle disease virus, tobacco Mosaic virus, and S-37 sarcoma and Yoshida sarcoma in animals.
Specification
| Synonyms | Muconomycin A; Antibiotic 379Y; VER A; (4S,5R,10E,12Z,16R,16aS,17S,18R,19aR,23aR)-4-hydroxy-5,16a,21-trimethyl-4,5,6,7,16,16a,22,23-octahydro-3H,18H,19aH-spiro[16,18-methano[1,6,12]trioxacyclooctadecino[3,4-d]chromene-17,2'-oxirane]-3,9,14-trione; NSC 126728 |
| Storage | Store at-20°C |
| IUPAC Name | (1R,3R,8R,12S,13R,18E,20Z,24R,25S,26S)-12-hydroxy-5,13,25-trimethylspiro[2,10,16,23-tetraoxatetracyclo[22.2.1.03,8.08,25]heptacosa-4,18,20-triene-26,2'-oxirane]-11,17,22-trione |
| Canonical SMILES | CC1CCOC(=O)C=CC=CC(=O)OC2CC3C4(C2(C5(CCC(=CC5O3)C)COC(=O)C1O)C)CO4 |
| InChI | InChI=1S/C27H34O9/c1-16-8-10-26-14-33-24(31)23(30)17(2)9-11-32-21(28)6-4-5-7-22(29)36-18-13-20(35-19(26)12-16)27(15-34-27)25(18,26)3/h4-7,12,17-20,23,30H,8-11,13-15H2,1-3H3/b6-4+,7-5-/t17-,18-,19-,20-,23+,25-,26-,27+/m1/s1 |
| InChI Key | NLUGUZJQJYVUHS-IDXDZYHTSA-N |
Properties
| Appearance | Colorless Flake Crystal |
| Antibiotic Activity Spectrum | Gram-negative bacteria; fungi; neoplastics (Tumor); viruses |
| Boiling Point | 747.4°C at 760 mmHg |
| Melting Point | >360°C |
| Density | 1.32 g/cm3 |
| Solubility | Soluble in ethanol, methanol, DMSO |
Reference Reading
1.Verrucarin A enhances TRAIL-induced apoptosis via NF-κB-mediated Fas overexpression.
Jayasooriya RG1, Moon DO, Yun SG, Choi YH, Asami Y, Kim MO, Jang JH, Kim BY, Ahn JS, Kim GY. Food Chem Toxicol. 2013 May;55:1-7. doi: 10.1016/j.fct.2012.12.045. Epub 2013 Jan 7.
We investigated whether verrucarin A (VA) sensitizes HepG2 hepatoma cells to tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-mediated apoptosis. We found that VA alone induces little apoptosis, but when combined with TRAIL (VA/TRAIL), it triggered significant apoptosis, causing little or no toxicity in normal mouse splenocytes. VA/TRAIL-induced cell death is involved in the loss of mitochondrial transmembrane potential and the consequent activation of caspases. Because nuclear factor (NF)-κB inhibition has been known as a critical target in TRAIL-mediated apoptosis, we also investigated the role of NF-κB in VA/TRAIL treatment. We found that VA upregulated the DNA binding activity of NF-κB, but that the antioxidants glutathione and N-acetyl-l-cysteine, as well as NF-κB inhibitor MG132, and mutant-IκB (m-IκB) transfection, significantly downregulated VA/TRAIL-induced cell death by inhibiting caspase-3 and NF-κB activities. Transfection of mutant-eIF2α also resulted in a decrease in VA/TRAIL-induced cell death by inhibiting of caspase-3, but not NF-κB activity.
2.Verrucarin A, a protein synthesis inhibitor, induces growth inhibition and apoptosis in breast cancer cell lines MDA-MB-231 and T47D.
Palanivel K1, Kanimozhi V, Kadalmani B, Akbarsha MA. Biotechnol Lett. 2013 Sep;35(9):1395-403. doi: 10.1007/s10529-013-1238-y. Epub 2013 May 21.
Verrucarin A (VA), a protein synthesis inhibitor, derived from the pathogen fungus Myrothecium verrucaria, inhibits growth of leukemia cell lines and activates caspases and apoptosis and inflammatory signaling in macrophages. We have investigated VA-induced growth inhibition in breast cancer cells MDA-MB-231 and T47D and, particularly, the mechanism of VA-induced apoptosis. VA treatment brought about apoptotic cell death in a dose- and time-dependent manner which was associated with chromatin condensation, cell shrinkage, nuclear fragmentation and intracellular ROS production. Mitochondrial membrane depolarization, activation of caspase-3, down-regulation of Bcl-2 expression and up-regulation of Bax and p53 expression were observed. VA thus affects the viability of both the breast cancer cells by triggering ROS-mediated intrinsic mechanism of apoptosis.
3.Verrucarin A sensitizes TRAIL-induced apoptosis via the upregulation of DR5 in an eIF2α/CHOP-dependent manner.
Moon DO1, Asami Y, Long H, Jang JH, Bae EY, Kim BY, Choi YH, Kang CH, Ahn JS, Kim GY. Toxicol In Vitro. 2013 Feb;27(1):257-63. doi: 10.1016/j.tiv.2012.09.001. Epub 2012 Sep 12.
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is one of the most promising candidates for new cancer therapeutics. However, resistance to TRAIL in some cancers remains a current problem in recent. The protein-folding compartment of the endoplasmic reticulum (ER) is particularly sensitive to disturbances, which, if severe, may trigger apoptosis. Therefore, we examined whether verrucarin A (VA) sensitize TRAIL-induced apoptosis in cancer cells by induction of ER stress. We first found that VA induces a major molecule of ER stress, CCAAT/enhancer binding protein homologous protein (CHOP)-dependent DR5 induction and subsequently increases TRAIL-induced cleavage of caspases and PARP in TRAIL-resistant Hep3B cells. Importantly, the transient knockdown using siRNA for CHOP abrogated VA-induced DR5 expression and attenuated TRAIL-induced apoptosis. Treatment with VA also increased the levels of phosphorylation of eukaryotic translation initiation factor-2α (eIF2α), which is a common cellular response of ER stress.
4.Verrucarin A induces apoptosis through ROS-mediated EGFR/MAPK/Akt signaling pathways in MDA-MB-231 breast cancer cells.
Palanivel K1, Kanimozhi V, Kadalmani B, Akbarsha MA. J Cell Biochem. 2014 Nov;115(11):2022-32. doi: 10.1002/jcb.24874.
The present study was carried out to elucidate the mechanisms underlying Verrucarin A (VA)-induced cytotoxicity in human breast cancer cell line MDA-MB-231. VA inhibited the growth of MDA-MB-231 cells by induction of reactive oxygen species (ROS)-dependent mitochondrial apoptosis. Elevation of ROS production, associated with changes in Bax/Bcl-2 ratio, led to loss of mitochondrial membrane potential (Δψm) and cytochrome c release in VA-treated cells. Release of cytochrome c from mitochondria to cytosol triggered activation of caspase-3, PARP cleavage, DNA fragmentation, and finally apoptotic cell death. Furthermore, VA-induced apoptosis was accompanied by the activation of p38MAPK and inhibition of phosphorylation of EGFR as well as of Akt and ERK1/2. However, pre-treatment with n-acetyl cysteine, an ROS scavenger, and SB202190, a p38MAPK inhibitor, significantly inhibited VA-induced ROS generation, EGFR inhibition, p38MAPK activation and apoptosis.
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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 ╳
