Design, synthesis and evaluation of N-acetyl glucosamine (NAG)-PEG-doxorubicin targeted conjugates for anticancer delivery.

Efficacy of anticancer drug is limited by the severe adverse effects induced by drug; therefore the crux is in designing delivery systems targeted only to cancer cells. Toward this objectives, we propose, synthesis of poly(ethylene glycol) (PEG)-doxorubicin (DOX) prodrug conjugates consisting N-acetyl glucosamine (NAG) as a targeting moiety. Multicomponent system proposed here is characterized by (1)H NMR, UV spectroscopy, and HPLC.

PEG-conjugated highly dispersive multifunctional magnetic multi-walled carbon nanotubes for cellular imaging.

We report synthesis of a highly versatile multicomponent nanosystem by covalently decorating the surface of multiwalled carbon nanotubes (CNTs) by magnetite nanoparticles (Fe(3)O(4)), poly(ethylene glycol) (PEG), and fluorophore fluorescein isothiocyanate (FITC). The resulting Fe(3)O(4)-PEG-FITC-CNT nanosystem demonstrates high dispersion ability in an aqueous medium, magnetic responsiveness, and fluorescent capacity. Transmission electron microscopy images revealed that Fe(3)O(4) nanoparticles were well anchored onto the surfaces of the CNT.

Novel diarylheptanoids as inhibitors of TNF-α production.

Synthesis and anti-inflammatory activity of novel diarylheptanoids [5-hydroxy-1-phenyl-7-(pyridin-3-yl)-heptan-3-ones and 1-phenyl-7-(pyridin-3-yl)hept-4-en-3-ones] as inhibitors of tumor necrosis factor-α (TNF-α) production is described in the present article. The key reactions involve the formation of a β-hydroxyketone by the reaction of substituted 4-phenyl butan-2-ones with pyridine-3-carboxaldehyde in presence of LDA and the subsequent dehydration of the same to obtain the α,β-unsaturated ketones. Compounds 4i, 5b, 5d, and 5g significantly inhibit lipopolysaccharide (LPS)-induced TNF-α production from human peripheral blood mononuclear cells in a dose-dependent manner.

A preferential p110alpha/gamma PI3K inhibitor attenuates experimental inflammation by suppressing the production of proinflammatory mediators in a NF-kappaB-dependent manner.

A promising therapeutic approach to diminish pathological inflammation is to inhibit the increased production and/or biological activity of proinflammatory cytokines (e.g., TNF-alpha, IL-6).