Antibiotic. More potent and specific H+-ATPase inhibitor than bafilomycin A1 (Prod. No. BML-CM110). Inhibits acidification of organelles such as lysosomes and the Golgi apparatus. Blocks cell surface expression of viral glycoproteins without affecting their synthesis. Exhibits cytotoxic effects in a number of cell lines in a cell viability assay. Induces nitric oxide (NO) production. Inhibits Autophagy.
Product Details
| Alternative Name: | Folimycin |
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| Formula: | C46H75NO14 |
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| MW: | 866.1 |
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| Source: | Isolated from Streptomyces sp. |
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| CAS: | 80890-47-7 |
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| RTECS: | CB9732000 |
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| Purity: | ≥95% (HPLC) |
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| Appearance: | White to off-white solid (sub-milligram quantities will appear as clear film). |
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| Solubility: | Soluble in methanol, DMSO or acetonitrile; insoluble in water. |
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| Shipping: | Ambient Temperature |
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| Short Term Storage: | +4°C |
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| Long Term Storage: | -20°C |
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| Use/Stability: | Stable for at least 1 year after receipt when stored at -20°C. After reconstitution protect from light . Solutions are more stable when stored at -20°C. |
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| Regulatory Status: | RUO - Research Use Only |
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Product Literature References
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Comparative Proteomics Reveals Strain-Specific β-TrCP Degradation via Rotavirus NSP1 Hijacking a Host Cullin-3-Rbx1 Complex: S. Ding, et al.; PLoS Pathology
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Full Text
Identification of V-ATPase as a molecular sensor of SOX11-levels and potential therapeutic target for mantle cell lymphoma: V.K. Emruli, et al.; BMC Cancer
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Application(s): Transient knock-down of V-ATPase,
Abstract;
Full Text
Escape of HIV-1-infected dendritic cells from TRAIL-mediated NK cell cytotoxicity during NK-DC cross-talk--a pivotal role of HMGB1: M.T. Melki, et al.; PLoS Pathog.
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Full Text
Microautophagy of the nucleus coincides with a vacuolar diffusion barrier at nuclear-vacuolar junctions: R. Dawaliby, et al.; Mol. Biol. Cell
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Abstract;
Full Text
Degradation of oxidized proteins by autophagy during oxidative stress in Arabidopsis: Y. Xiong, et al.; Plant Physiol.
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Abstract;
Nitric oxide production by the vacuolar-type (H+)-ATPase inhibitors bafilomycin A1 and concanamycin A and its possible role in apoptosis in RAW 264.7 cells: J. Hong, et al.; J. Pharmacol. Exp. Ther.
319, 672 (2006),
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Organization of the biosynthetic gene cluster for the macrolide concanamycin A in Streptomyces neyagawaensis ATCC 27449: S.F. Haydock, et al.; Microbiology
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Abstract;
Full Text
Concanamycin A, the specific inhibitor of V-ATPases, binds to the V(o) subunit c: M. Huss, et al.; J. Biol. Chem.
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Abstract;
Characterization of the ATPase activity of P-glycoprotein from multidrug-resistant Chinese hamster ovary cells: F.J. Sharom, et al.; Biochem. J.
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Abstract;
Specific inhibitors of vacuolar type H(+)-ATPases induce apoptotic cell death: T. Nishihara, et al.; BBRC
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Folimycin (concanamycin A), a specific inhibitor of V-ATPase, blocks intracellular translocation of the glycoprotein of vesicular stomatitis virus before arrival to the Golgi apparatus: M. Muroi, et al.; Cell Struct. Funct.
18, 139 (1993),
Abstract;
Folimycin (concanamycin A), an inhibitor of V-type H(+)-ATPase, blocks cell-surface expression of virus-envelope glycoproteins: M. Muroi, et al.; BBRC
193, 999 (1993),
Abstract;
Inhibitory effect of modified bafilomycins and concanamycins on P- and V-type adenosinetriphosphatases: S. Drose, et al.; Biochemistry
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Abstract;
Involvement of the vacuolar H(+)-ATPases in the secretory pathway of HepG2 cells: M. Yilla, et al.; J. Biol. Chem.
268, 19092 (1993),
Abstract;
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Purification of vacuolar ATPase with bafilomycin C1 affinity chromatography: T.J. Rautiala, et al.; BBRC
194, 50 (1993),
Abstract;
Intravesicular acidification correlates with binding of ADP- ribosylation factor to microsomal membranes: S. Zeuzem, et al.; PNAS
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Abstract;
Structure and function of vacuolar class of ATP-driven proton pumps: M. Forgac; Physiol. Rev.
69, 765 (1989),
Abstract;
Bafilomycins: a class of inhibitors of membrane ATPases from microorganisms, animal cells, and plant cells: E.J. Bowman, et al.; PNAS
85, 7972 (1988),
Abstract;
Isolation and characterization of concanamycins A, B and C: H. Kinashi, et al.; J. Antibiot. (Tokyo)
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