BVT-0091-M0011 mgCHF 130.00
BVT-0091-M0055 mgCHF 420.00
|Source/Host Chemicals||Isolated from Streptomyces parvulus.|
|Purity Chemicals||≥98% (HPLC)|
|Appearance||Yellow to brown powder.|
|Solubility||Soluble in DMSO or methanol; insoluble in water.|
|Identity||Determined by 1H-NMR.|
|Declaration||Manufactured by BioViotica.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
|Handling Advice||Protect from light.|
Stable for at least 1 year after receipt when stored at -20°C.
After reconstitution protect from light at -20°C.
|Product Specification Sheet|
- Apoptosis and endoplasmic reticulum stress-mediated cell death inducer.
- Potent, selective and competitive cell permeable rasfarnesyltransferase inhibitor (IC50 = 30 nM).
- Does not affect geranylgeranyltransferase (IC50 = 180 µM).
- Inhibition is competitive with respect to farnesyl pyrophosphate and non-competitive with respect to Ras.
- Neutral sphingomyelinase inhibitor.
- Blocks insulin-induced MAP kinase activation in rat cardiac myocytes (19 µM).
- Targets protein phosphatase 1α (PP1α) and reduces hydrogen peroxide.
- Corrects aberrant splicing of the muscle chloride channel Clcn1 in myotonic dystrophy type 1 (DM1).
- Shows potential anti-inflammatory activity.
- Irreversible human thioredoxin reductase 1 (TrxR-1) inhibitor (IC50=272nM) and inducer of NADPH oxidase activity. Acts very likely as a Michael acceptor to the nucleophilic Sec residue in the C-terminal redox center of TrxR-1 which yields a SecTRAP (selenium compromised thioredoxin reductase-derived apoptotic proteins), which promotes both apoptosis and necrosis via oxidative stress and increased intracellular reactive oxygen species (ROS) production.
- Identification of Rasfarnesyltransferase inhibitors by microbial screening: M. Hara et al.; PNAS 90, 2281 (1993)
- Inhibitors of Rasfarnesyltransferases: F. Tamanoi; TIBS 18, 349 (1993), (Review)
- Farnesyltransferase inhibitors: Ras research yields a potential cancer therapeutic: J.B. Gibbs, et al.; Cell 77, 175 (1994)
- Protein kinase C, but not tyrosine kinases or Ras, plays a critical role in angiotensin II-induced activation of Raf-1 kinase and extracellular signal-regulated protein kinases in cardiac myocytes: Y. Zou et al.; J. Biol. Chem. 271, 33592 (1996)
- Manumycin inhibits ras signal transduction pathway and induces apoptosis in COLO320-DM human colon tumour cells: A. Di Paolo, et al.; Br. J. Cancer 82, 905 (2000)
- Manumycin A and its analogues are irreversible inhibitors of neutral sphingomyelinase: C. Arenz, et al.; ChemBioChem 2, 141 (2001)
- Enhancement of manumycin A-induced apoptosis by methoxyamine in myeloid leukemia cells: M. She, et al.; Leukemia 19, 595 (2005)
- Binding of manumycin A inhibits IkappaB kinase beta activity: M. Bernier, et al.; J. Biol. Chem. 281, 2551 (2006)
- A yeast-based genomic strategy highlights the cell protein networks altered by FTase inhibitor peptidomimetics: G. Porcu, et al.; Mol. Cancer 9:197 (2010)
- Targeting farnesyl-transferase as a novel therapeutcstrategy for mevalonate kinase defiency: In vitro and in vivo approaches: L. De Leo, et al.; Pharmacol. Res. 61, 506 (2010)
- Manumycin A corrects aberrant splicing of Clcn1 in myotonic dystrophy type 1 (DM1) mice: K. Oana, et al.; Sci. Rep. 3, 2142 (2013)
- Manumycin induces apoptosis in prostate cancer cells: J.G. Li, et al., Onco Targets Ther. 7, 771 (2014)
- The natural tumorcide Manumycin-A targets protein phosphatase 1α and reduces hydrogen peroxide to induce lymphoma apoptosis. G.B. Carey, et al.; Exp. Cell. Res. 332, 136 (2015)
- Manumycin A from a new streptomyces strain induces endoplasmic reticulum stress-mediated cell death through specificity protein 1 signaling in human oral squamous cell carcinoma: C.J. Jae, et al.; Int. J. Oncol. 47, 1954 (2015)
- Manumycin A downregulates release of proinflammatory cytokines from TNF alpha stimulated human monocytes: E. Cecrdlova, et al.; Immunol. Lett. 169, 8 (2016)
- Manumycin A Is a Potent Inhibitor of Mammalian Thioredoxin Reductase-1 (TrxR-1): A. Tuladhar & K.S. Rein; ACS Med. Chem. Lett. 9, 318 (2018)