Chondramide A
* Please be kindly noted products are not for therapeutic use. We do not sell to patients.
| Category | Antibiotics |
| Catalog number | BBF-00322 |
| CAS | |
| Molecular Weight | 646.77 |
| Molecular Formula | C36H46N4O7 |
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Description
It is produced by the strain of Chondromyces crocatus. Chondramide A has anti-candida, Henson yeast, lipids yeast, ball-like yeast and other fungal activities, but has no anti-gram positive and negative bacteria activities.
Specification
| Synonyms | (3S)-3beta-Methoxy-4alpha-(4-hydroxyphenyl)-7beta-(1H-indole-3-ylmethyl)-8,10alpha,13beta,15,17beta,18beta-hexamethyl-1-oxa-5,8,11-triazacyclooctadeca-15-ene-2,6,9,12-tetraone; CHEBI:84380 |
| IUPAC Name | (3S,4S,7R,10S,13S,15E,17R,18R)-4-(4-hydroxyphenyl)-7-(1H-indol-3-ylmethyl)-3-methoxy-8,10,13,15,17,18-hexamethyl-1-oxa-5,8,11-triazacyclooctadec-15-ene-2,6,9,12-tetrone |
| Canonical SMILES | CC1CC(=CC(C(OC(=O)C(C(NC(=O)C(N(C(=O)C(NC1=O)C)C)CC2=CNC3=CC=CC=C32)C4=CC=C(C=C4)O)OC)C)C)C |
| InChI | InChI=1S/C36H46N4O7/c1-20-16-21(2)24(5)47-36(45)32(46-7)31(25-12-14-27(41)15-13-25)39-34(43)30(18-26-19-37-29-11-9-8-10-28(26)29)40(6)35(44)23(4)38-33(42)22(3)17-20/h8-16,19,21-24,30-32,37,41H,17-18H2,1-7H3,(H,38,42)(H,39,43)/b20-16+/t21-,22+,23+,24-,30-,31+,32+/m1/s1 |
| InChI Key | IEKCRWAFVYJECW-XYDQKOHOSA-N |
Properties
| Antibiotic Activity Spectrum | fungi |
Reference Reading
1. The actin targeting compound Chondramide inhibits breast cancer metastasis via reduction of cellular contractility
Magdalena H Menhofer, Rebekka Kubisch, Laura Schreiner, Matthias Zorn, Florian Foerster, Rolf Mueller, Joachim O Raedler, Ernst Wagner, Angelika M Vollmar, Stefan Zahler PLoS One. 2014 Nov 12;9(11):e112542. doi: 10.1371/journal.pone.0112542. eCollection 2014.
Background: A major player in the process of metastasis is the actin cytoskeleton as it forms key structures in both invasion mechanisms, mesenchymal and amoeboid migration. We tested the actin binding compound Chondramide as potential anti-metastatic agent. Methods: In vivo, the effect of Chondramide on metastasis was tested employing a 4T1-Luc BALB/c mouse model. In vitro, Chondramide was tested using the highly invasive cancer cell line MDA-MB-231 in Boyden-chamber assays, fluorescent stainings, Western blot and Pull down assays. Finally, the contractility of MDA-MB-231 cells was monitored in 3D environment and analyzed via PIV analysis. Results: In vivo, Chondramide treatment inhibits metastasis to the lung and the migration and invasion of MDA-MB-231 cells is reduced by Chondramide in vitro. On the signaling level, RhoA activity is decreased by Chondramide accompanied by reduced MLC-2 and the stretch induced guanine nucleotide exchange factor Vav2 activation. At same conditions, EGF-receptor autophosphorylation, Akt and Erk as well as Rac1 are not affected. Finally, Chondramide treatment disrupted the actin cytoskeleton and decreased the ability of cells for contraction. Conclusions: Chondramide inhibits cellular contractility and thus represents a potential inhibitor of tumor cell invasion.
2. Modulation of actin dynamics as potential macrophage subtype-targeting anti-tumour strategy
Carlo Pergola, Katrin Schubert, Simona Pace, Jana Ziereisen, Felix Nikels, Olga Scherer, Stephan Hüttel, Stefan Zahler, Angelika M Vollmar, Christina Weinigel, Silke Rummler, Rolf Müller, Martin Raasch, Alexander Mosig, Andreas Koeberle, Oliver Werz Sci Rep. 2017 Jan 30;7:41434. doi: 10.1038/srep41434.
Tumour-associated macrophages mainly comprise immunosuppressive M2 phenotypes that promote tumour progression besides anti-tumoural M1 subsets. Selective depletion or reprogramming of M2 may represent an innovative anti-cancer strategy. The actin cytoskeleton is central for cellular homeostasis and is targeted for anti-cancer chemotherapy. Here, we show that targeting G-actin nucleation using chondramide A (ChA) predominantly depletes human M2 while promoting the tumour-suppressive M1 phenotype. ChA reduced the viability of M2, with minor effects on M1, but increased tumour necrosis factor (TNF)α release from M1. Interestingly, ChA caused rapid disruption of dynamic F-actin filaments and polymerization of G-actin, followed by reduction of cell size, binucleation and cell division, without cellular collapse. In M1, but not in M2, ChA caused marked activation of SAPK/JNK and NFκB, with slight or no effects on Akt, STAT-1/-3, ERK-1/2, and p38 MAPK, seemingly accounting for the better survival of M1 and TNFα secretion. In a microfluidically-supported human tumour biochip model, circulating ChA-treated M1 markedly reduced tumour cell viability through enhanced release of TNFα. Together, ChA may cause an anti-tumoural microenvironment by depletion of M2 and activation of M1, suggesting induction of G-actin nucleation as potential strategy to target tumour-associated macrophages in addition to neoplastic cells.
3. Direct Interaction of Chivosazole F with Actin Elicits Cell Responses Similar to Latrunculin A but Distinct from Chondramide
Ireos Filipuzzi, Jason Ray Thomas, Verena Pries, David Estoppey, Michael Salcius, Christian Studer, Markus Schirle, Dominic Hoepfner ACS Chem Biol. 2017 Sep 15;12(9):2264-2269. doi: 10.1021/acschembio.7b00385. Epub 2017 Aug 15.
The microbial metabolite Chivosazole F has been described to affect the cytoskeleton and to inhibit actin polymerization in vitro. Applying orthogonal genomic and proteomics approaches, we now show for the first time that Chivosazole F exerts its effect by directly interacting with actin and demonstrate the cellular impact of Chivosazole F in an unbiased, genome-wide context in yeast and in mammalian cells. Furthermore, mutation-based resistance mapping identifies two SNPs located in the putative Chivosazole F binding site of actin. Comparing chemogenomic profiles and responses to the Chivosazole F-resistant SNPs shows a partially conserved mechanism of action for Chivosazole F and Latrunculin A, but clear divergence from Chondramide. In addition, C14orf80 is an evolutionarily highly conserved ORF, lacking any functional annotation. As editing of C14orf80 leads to Chivosazole F hyper-resistance, we propose a function for this gene product in counteracting perturbation of actin filaments.
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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 ╳
