30364-60-4Relevant articles and documents
Preparation and properties of gelatin films incorporated with N-hydroxysuccinimide-activated end-bit binary acid
Zhuang, Chen,Tao, Fu-Rong,Cui, Yue-Zhi
, p. 505 - 514 (2016/03/08)
A series of novel cross-linkers, N-hydroxysuccinimide (NHS)-activated end-bit binary acid (NHS-C4, C5, C6, C8, C10, C14), were synthesised to modify gelatin films and the crosslinking effects were compared. Homogeneous films with the exception of the film crosslinked by NHS-C14 were observed and the thickness was measured using a scanning electron microscope. The section feature influenced by different film-treatment conditions was also recorded. The differential scanning calorimetry results indicated higher thermal stability. The water contact angles confirmed enhanced hydrophobicity. NHS-C6, which was used as a probe crosslinker, exhibited the best crosslinking effect that the content of the free -NH2 achieved was the lowest out of all the crosslinkers. The biodegradation results of gelatin films modified by NHS-C6 exhibited better degradation-resistance and excellent stability. In addition, the optimal experimental conditions were 45°C for 12 h when [NHS-C6]/[-NH2] = 2.5.
NOVEL CELL-PERMEABLE SUCCINATE COMPOUNDS
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Page/Page column 67; 68, (2015/11/03)
The present invention provides novel cell-permeable succinates and cell permeable precursors of succinate aimed at increasing ATP-production in mitochondria. The main part of ATP produced and utilized in the eukaryotic cell originates from mitochondrial oxidative phosphorylation, a process to which high-energy electrons are provided by the Kreb's cycle. Not all Kreb's cycle intermediates are readily permeable to the cellular membrane, one of them being succinate. The provision of the novel cell permeable succinates is envisaged to allow passage over the cellular membrane and thus the cell permeable succinates can be used to enhance mitochondrial ATP-output.
COMPOUNDS AND METHODS FOR INHIBITING NHE-MEDIATED ANTIPORT IN THE TREATMENT OF DISORDERS ASSOCIATED WITH FLUID RETENTION OR SALT OVERLOAD AND GASTROINTESTINAL TRACT DISORDERS
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Page/Page column 291, (2010/08/04)
The present disclosure is directed to corn- pounds and methods for the treatment of disorders associated with fluid retention or salt overload, such as heart failure (in particular, congestive heart failure), chronic kidney disease, end-stage renal disease, liver disease, and peroxisome proliferator-activated receptor (PPAR) gamma agonist-induced fluid retention. The present disclosure is also directed to compounds and methods for the treatment of hypertension. The present disclosure is also directed to compounds and methods for the treatment of gastrointestinal tract disorders, including the treatment or reduction of pain associated with gastrointestinal tract disorders. The methods generally comprise administering to a mammal in need thereof a pharmaceutically effective amount of a compound, or a pharmaceutical composition comprising such a compound, that is designed to be substantially active in the gastrointestinal (GI) tract to inhibit NHE-mediated antiport of sodium ions and hydrogen ions therein. More particularly, the method comprises administering to a mammal in need thereof a pharmaceutically effective amount of a compound, or a pharmaceutical composition comprising such a compound, that inhibits NHE-3, -2 and/ or -8 mediated antiport of sodium and/or hydrogen ions in the GI tract and is designed to be substantially impermeable to the layer of epithelial cells, or more specifically the epithelium of the GI tract. As a result of the compound being substantially impermeable, it is not absorbed and is thus essentially systemically non-bioavailable, so as to limit the exposure of other internal organs (e.g., liver, heart, brain, etc.) thereto. The present disclosure is still further directed to a method wherein a mammal is administered such a compound with a fluid-absorbing polymer, such that the combination acts as described above and further provides the ability to sequester fluid and/or salt present in the GI tract