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Methods and kits using a pharmaceutical composition for use in inhibiting ocular angiogenesis or fibrosis are provided herein, such that composition includes a pharmaceutically suitable carrier or diluent and an amount of the inhibitor composition effective to inhibit the angiogenesis or the fibrosis by inhibiting expression and/or activity of a galectin protein or a portion thereof.

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The reactant in an enzyme-catalyzed reaction is called a substrate. Enzyme inhibitors cause a decrease in the reaction rate of an enzyme-catalyzed reaction.I hope my blog about 1450824-22-2 is helpful to your research., Safety of TD 139

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Discovery of glycan-competitive galectin-3-binding compounds that attenuate lung fibrosis in a murine model and that block intracellular galectin-3 accumulation at damaged vesicles, hence revealing galectin-3?glycan interactions involved in fibrosis progression and in intracellular galectin-3 activities, is reported. 3,3?-Bis-(4-aryltriazol-1-yl)thiodigalactosides were synthesized and evaluated as antagonists of galectin-1, -2, -3, and -4 N-terminal, -4 C-terminal, -7 and -8 N-terminal, -9 N-terminal, and -9 C-terminal domains. Compounds displaying low-nanomolar affinities for galectins-1 and -3 were identified in a competitive fluorescence anisotropy assay. X-ray structural analysis of selected compounds in complex with galectin-3, together with galectin-3 mutant binding experiments, revealed that both the aryltriazolyl moieties and fluoro substituents on the compounds are involved in key interactions responsible for exceptional affinities towards galectin-3. The most potent galectin-3 antagonist was demonstrated to act in an assay monitoring galectin-3 accumulation upon amitriptyline-induced vesicle damage, visualizing a biochemically/medically relevant intracellular lectin?carbohydrate binding event and that it can be blocked by a small molecule. The same antagonist administered intratracheally attenuated bleomycin-induced pulmonary fibrosis in a mouse model with a dose/response profile comparing favorably with that of oral administration of the marketed antifibrotic compound pirfenidone.

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Galectins have been recognized as potential novel therapeutic targets for the numerous fundamental biological processes in which they are involved. Galectins are key players in homeostasis, and as such their expression and function are finely tuned in vivo. Thus, their modes of action are complex and remain largely unexplored, partly because of the lack of dedicated tools. We thus designed galectin inhibitors from a lactosamine core, functionalized at key C2 and C3? positions by aromatic substituents to ensure both high affinity and selectivity, and equipped with a spacer that can be modified on demand to further modulate their physico-chemical properties. As a proof-of-concept, galectin-3 was selectively targeted. The efficacy of the synthesized di-aromatic lactosamine tools was shown in cellular assays to modulate collective epithelial cell migration and to interfere with actin/cortactin localization.

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A catalyst don`t appear in the overall stoichiometry of the reaction it catalyzes, but it must appear in at least one of the elementary reactions in the mechanism for the catalyzed reaction. Quality Control of: TD 139Quality Control of: TD 139, , Name is TD 139, molecular formula is C28H30F2N6O8S. In a patent, introducing its new discovery.

The present invention relates to a compound of the general formula (I): The compound of formula (I) is suitable for treating pulmonary fibrosis, such as Idiopathic pulmonary fibrosis in a mammal. Furthermore the present invention concerns a method of monitoring development or progression of pulmonary fibrosis in a human subject, a method of monitoring or predicting exacerbation of symptoms in a human subject with pulmonary fibrosis as well as a method for treatment of pulmonary fibrosis, such as Idiopathic pulmonary fibrosis in a human subject having a galectin-3 level indicative of pulmonary fibrosis or exacerbation of symptoms.

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Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease characterized by scarring of the lung interstitium that likely occurs because of repetitive wounding of the alveolar epithelium, followed by incomplete healing of the injury. IPF is a disease of high, unmet medical need due to an exceptionally poor prognosis combined with a lack of effective treatment options capable of altering its progression. There is an urgent need for the development of novel pharmacological agents capable of providing significant efficacy while modifying the natural course of the disease. Herein, we describe emerging targets for the treatment of IPF and progress in the development of small-molecule modulators against them. Targets for which there is limited pharmacologic validation or against which only biologic modalities exist are excluded.

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Aspects of the invention relate to novel synthetic compounds having a binding affinity with galectin proteins for the treatment of systemic insulin resistance disorders.

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[Problem] for the treatment of pulmonary fibrosis, safety and good tolerability compound, a compound of the pharmaceutical composition, the composition and method of administration. [Solution] a method for the treatment of pulmonary fibrosis in human use, the compound represented by the formula below, said compound-containing pharmaceutical compositions, the administration of dry powder inhaler or by administration of the composition and method. The compound is, the narrowest portion of human lung tissue, especially small bronchi and alveoli, which dosing 1 1, 1 1 amount times, preferably 0.15 – 50 mg. [Drawing] no (by machine translation)

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[Problem] to be utilized in the synthesis of various derivatives of sugar derivative-galactopyranoside. (I) formula [solution] galactopyranoside derivatives is shown. (R1 R (=O) is a-C5 Substituted phenyl groups bonded to each other or methylene; R2 As the […]; R3 Is H, methyl, Cl or nitro; R4 The bromo group or a phenylthio)[Drawing] no (by machine translation)

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CONJUGATES

A conjugate is disclosed. The conjugate may comprise a targeting unit for delivery to a target tissue, and a Galectin inhibitor for inhibiting Galectin interaction within the target tissue, wherein the Galectin inhibitor is conjugated to the targeting unit.

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Galectins have been recognized as potential novel therapeutic targets for the numerous fundamental biological processes in which they are involved. Galectins are key players in homeostasis, and as such their expression and function are finely tuned in vivo. Thus, their modes of action are complex and remain largely unexplored, partly because of the lack of dedicated tools. We thus designed galectin inhibitors from a lactosamine core, functionalized at key C2 and C3? positions by aromatic substituents to ensure both high affinity and selectivity, and equipped with a spacer that can be modified on demand to further modulate their physico-chemical properties. As a proof-of-concept, galectin-3 was selectively targeted. The efficacy of the synthesized di-aromatic lactosamine tools was shown in cellular assays to modulate collective epithelial cell migration and to interfere with actin/cortactin localization.

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Reference£º
Tetrahydropyran – Wikipedia,
Tetrahydropyran – an overview | ScienceDirect Topics