Mensacarcin - CAS 808750-39-2

Mensacarcin - CAS 808750-39-2 Catalog number: BADC-00839

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Mensacarcin is a bacterial metabolite that has been found in S. bottropensis and has anticancer activity. It strongly inhibits cell growth universally in cancer cell lines and potently induces apoptosis in melanoma cells. Mensacarcin targets to mitochondria, affects energy metabolism in mitochondria, and activates caspase-dependent apoptotic pathways.

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BADC-00839 -- $--
Mensacarcin is a bacterial metabolite that has been found in S. bottropensis and has anticancer activity. It strongly inhibits cell growth universally in cancer cell lines and potently induces apoptosis in melanoma cells. Mensacarcin targets to mitochondria, affects energy metabolism in mitochondria, and activates caspase-dependent apoptotic pathways.
Canonical SMILES
1.5±0.1 g/cm3
10 mm in DMSO
Flash Point
232.9±25.0 °C
Index Of Refraction
Vapor Pressure
0.0±2.1 mmHg at 25°C
In Vitro
Mensacarcin (0-100 μM; 24 hours) exhibits general cytostatic but type-specific cytotoxic effects for melanoma cells. Mensacarcin (2-50 μM; 15 hours) induces rapid apoptotic cell death in melanoma cells. Mensacarcin exhibits potent cytostatic properties (mean of 50% growth inhibition=0.2 μM) in almost all cell lines of the National Cancer Institute (NCI)-60 cell line screen and relatively selective cytotoxicity against melanoma cells. Mensacarcin is a highly oxygenated polyketide that was first isolated from soil-dwelling Streptomyces bacteria. Mensacarcin impairs mitochondrial function in melanoma cells. Cell Viability Assay Cell Line: SK-Mel-28 and SK-Mel-5 melanoma cells, HCT-116 colon cancer cells Concentration: 0.01, 0.1, 1, 10, 100 μM Incubation Time: 24 hours Result: Induced concentration- and time-dependent cell death in the two tested melanoma cell lines. HCT-116 colon carcinoma cells were strongly inhibited. Western Blot Analysis Cell Line: SK-Mel-28, SK-Mel-5 cells Concentration: 2, 10, 50 μM Incubation Time: 15 hours Result: Induced the formation of 89-kDa PARP-1 fragments as well as caspase-3 activation in SK-Mel-28 and SK-Mel-5 beginning between 6 and 15 h after exposure.
Solid Power
Shelf Life
-20℃ 3 years powder; -80℃ 2 years in solvent
Room temperature
Store at -20°C
Boiling Point
656.8±55.0 °C at 760 mmHg
1. Measurement of Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR) in Culture Cells for Assessment of the Energy Metabolism
Birte Plitzko, Sandra Loesgen Bio Protoc. 2018 May 20;8(10):e2850. doi: 10.21769/BioProtoc.2850.
Mammalian cells generate ATP by mitochondrial (oxidative phosphorylation) and non-mitochondrial (glycolysis) metabolism. Cancer cells are known to reprogram their metabolism using different strategies to meet energetic and anabolic needs ( Koppenol et al., 2011 ; Zheng, 2012). Additionally, each cancer tissue has its own individual metabolic features. Mitochondria not only play a key role in energy metabolism but also in cell cycle regulation of cells. Therefore, mitochondria have emerged as a potential target for anticancer therapy since they are structurally and functionally different from their non-cancerous counterparts (D'Souza et al., 2011). We detail a protocol for measurement of oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) measurements in living cells, utilizing the Seahorse XF24 Extracellular Flux Analyzer (Figure 1). The Seahorse XF24 Extracellular Flux Analyzer continuously measures oxygen concentration and proton flux in the cell supernatant over time ( Wu et al., 2007 ). These measurements are converted in OCR and ECAR values and enable a direct quantification of mitochondrial respiration and glycolysis. With this protocol, we sought to assess basal mitochondrial function and mitochondrial stress of three different cancer cell lines in response to the cytotoxic test lead compound mensacarcin in order to investigate its mechanism of action. Cells were plated in XF24 cell culture plates and maintained for 24 h. Prior to analysis, the culture media was replaced with unbuffered DMEM pH 7.4 and cells were then allowed to equilibrate in a non-CO2 incubator immediately before metabolic flux analysis using the Seahorse XF to allow for precise measurements of Milli-pH unit changes. OCR and ECAR were measured under basal conditions and after injection of compounds through drug injection ports. With the described protocol we assess the basic energy metabolism profiles of the three cell lines as well as key parameters of mitochondrial function in response to our test compound and by sequential addition of mitochondria perturbing agents oligomycin, FCCP and rotenone/antimycin A. Figure 1.Overview of seahorse experiment.
2. Biosynthesis of the Tricyclic Aromatic Type II Polyketide Rishirilide: New Potential Third Ring Oxygenation after Three Cyclization Steps
Ahmad Alali, Lin Zhang, Jianyu Li, Chijian Zuo, Dimah Wassouf, Xiaohui Yan, Philipp Schwarzer, Stefan Günther, Oliver Einsle, Andreas Bechthold Mol Biotechnol. 2021 Jun;63(6):502-514. doi: 10.1007/s12033-021-00314-x. Epub 2021 Mar 24.
Rishirilides are a group of PKS II secondary metabolites produced by Streptomyces bottropensis Gö C4/4. Biosynthetic studies in the past have elucidated early and late steps of rishirilide biosynthesis. This work is aiming to solve the remaining steps in the rishirilide biosynthesis. Inactivation of the cyclase gene rslC3 in Streptomyces bottropensis resulted in an interruption of rishirilide production. Instead, accumulation of the tricyclic aromatic galvaquinones was observed. Similar results were observed after deletion of rslO4. Closer inspection into RslO4 crystal structure in addition to site-directed mutagenesis and molecular dynamic simulations revealed that RslO4 might be responsible for quinone formation on the third ring. The RslO1 three-dimensional structure shows a high similarity to FMN-dependent luciferase-like monooxygenases such as the epoxy-forming MsnO8 which acts with the flavin reductase MsnO3 in mensacarcin biosynthesis in the same strain. The high sequence similarity between RslO2 and MsnO3 suggests that RslO2 provides RslO1 with reduced FMN to form an epoxide that serves as substrate for RslO5.
3. Bioenergetics underlying single-cell migration on aligned nanofiber scaffolds
Abinash Padhi, Alexander H Thomson, Justin B Perry, Grace N Davis, Ryan P McMillan, Sandra Loesgen, Elizabeth N Kaweesa, Rakesh Kapania, Amrinder S Nain, David A Brown Am J Physiol Cell Physiol. 2020 Mar 1;318(3):C476-C485. doi: 10.1152/ajpcell.00221.2019. Epub 2019 Dec 25.
Cell migration is centrally involved in a myriad of physiological processes, including morphogenesis, wound healing, tissue repair, and metastatic growth. The bioenergetics that underlie migratory behavior are not fully understood, in part because of variations in cell culture media and utilization of experimental cell culture systems that do not model physiological connective extracellular fibrous networks. In this study, we evaluated the bioenergetics of C2C12 myoblast migration and force production on fibronectin-coated nanofiber scaffolds of controlled diameter and alignment, fabricated using a nonelectrospinning spinneret-based tunable engineered parameters (STEP) platform. The contribution of various metabolic pathways to cellular migration was determined using inhibitors of cellular respiration, ATP synthesis, glycolysis, or glucose uptake. Despite immediate effects on oxygen consumption, mitochondrial inhibition only modestly reduced cell migration velocity, whereas inhibitors of glycolysis and cellular glucose uptake led to striking decreases in migration. The migratory metabolic sensitivity was modifiable based on the substrates present in cell culture media. Cells cultured in galactose (instead of glucose) showed substantial migratory sensitivity to mitochondrial inhibition. We used nanonet force microscopy to determine the bioenergetic factors responsible for single-cell force production and observed that neither mitochondrial nor glycolytic inhibition altered single-cell force production. These data suggest that myoblast migration is heavily reliant on glycolysis in cells grown in conventional media. These studies have wide-ranging implications for the causes, consequences, and putative therapeutic treatments aimed at cellular migration.

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