860480P
Avanti
C10 bisphosphonate
Avanti Polar Lipids 860480P, powder
Synonym(s):
1-aminodecane-1,1-bisphosphonic acid
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About This Item
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form
powder
packaging
pkg of 1 × 500 μg (860480P-500ug)
manufacturer/tradename
Avanti Polar Lipids 860480P
lipid type
bioactive lipids
sphingolipids
shipped in
dry ice
storage temp.
−20°C
SMILES string
[NH3+]C(P([O-])(O)=O)(P(O)(O)=O)CCCCCCCCC
Related Categories
Application
C10 bisphosphonate is suitable for use as an inhibitor for acid sphingomyelinase.
Biochem/physiol Actions
C10 bisphosphonate, with prolonged carbon chain, is an inhibitor for acid sphingomyelinase and may be a treatment option for inflammatory lung diseases, cystic fibrosis and atherosclerosis. It interacts with the divalent metal ions and forms bidentate complexes. Bisphosphonates are inhibitors of end reaction in pathways. It is an inhibitor of cytosolic farnesyl diphosphate (FDP) synthase (geranyl diphosphate (GDP) and geranylgeranyl diphosphate (GGDP) synthase and isoprene pathway. Bisphosphonates have antimicrobial functionality and inhibits the growth of Entamoeba histolytica and Plasmodium falciparum.
Packaging
5 mL Amber Glass Screw Cap Vial (860480P-500ug)
Legal Information
Avanti Research is a trademark of Avanti Polar Lipids, LLC
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Certificates of Analysis (COA)
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Acid sphingomyelinase promotes mitochondrial dysfunction due to glutamate-induced regulated necrosis
Journal of Lipid Research, 59(2), 312-329 (2018)
Potent and selective inhibition of acid sphingomyelinase by bisphosphonates
Angewandte Chemie (International Edition in English), 48(41), 7560-7563 (2009)
Bisphosphonate inhibitors reveal a large elasticity of plastidic isoprenoid synthesis pathway in isoprene-emitting hybrid aspen
Plant Physiology, 168(2), 532-548 (2015)
Effects of bisphosphonates on the growth of Entamoeba histolytica and Plasmodium species in vitro and in vivo
Journal of Medicinal Chemistry, 47(1), 175-187 (2004)
Nature medicine, 14(4), 382-391 (2008-04-01)
Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here
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