9/22 News More research is needed about TD 139

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Background: Parkinson’s disease (PD) is the most prevalent neurodegenerative motor disorder. The neuropathology is characterized by intraneuronal protein aggregates of alpha-synuclein and progressive degeneration of dopaminergic neurons within the substantia nigra. Previous studies have shown that extracellular alpha-synuclein aggregates can activate microglial cells, induce inflammation and contribute to the neurodegenerative process in PD. However, the signaling pathways involved in alpha-synuclein-mediated microglia activation are poorly understood. Galectin-3 is a member of a carbohydrate-binding protein family involved in cell activation and inflammation. Therefore, we investigated whether galectin-3 is involved in the microglia activation triggered by alpha-synuclein. Results: We cultured microglial (BV2) cells and induced cell activation by addition of exogenous alpha-synuclein monomers or aggregates to the cell culture medium. This treatment induced a significant increase in the levels of proinflammatory mediators including the inducible Nitric Oxide Synthase (iNOS), interleukin 1 Beta (IL-1beta) and Interleukin-12 (IL-12). We then reduced the levels of galectin-3 expression using siRNA or pharmacologically targeting galectin-3 activity using bis-(3-deoxy-3-(3-fluorophenyl-1H-1,2,3-triazol-1-yl)-beta-D-galactopyranosyl)-sulfane. Both approaches led to a significant reduction in the observed inflammatory response induced by alpha-synuclein. We confirmed these findings using primary microglial cells obtained from wild-type and galectin-3 null mutant mice. Finally, we performed injections of alpha-synuclein in the olfactory bulb of wild type mice and observed that some of the alpha-synuclein was taken up by activated microglia that were immunopositive for galectin-3. Conclusions: We show that alpha-synuclein aggregates induce microglial activation and demonstrate for the first time that galectin-3 plays a significant role in microglia activation induced by alpha-synuclein. These results suggest that genetic down-regulation or pharmacological inhibition of galectin-3 might constitute a novel therapeutic target in PD and other synucleinopathies.

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Reference:
Tetrahydropyran – Wikipedia,
Tetrahydropyran – an overview | ScienceDirect Topics

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Glycomimetic drugs have attracted increasing interest as unique targeting vectors or surrogates for endogenous biomolecules. However, it is generally difficult to determine the in vivo pharmacokinetic profile of these compounds. In this work, two galectin-3 inhibitors were radiolabeled with fluorine-18 and used as surrogate PET tracers of TD139 and GB1107. Both compounds are promising drugs for clinical applications. In vivo evaluation revealed that both surrogates strongly differed with respect to their biodistribution profile. The disaccharide (TD139 surrogate) was rapidly eliminated from blood while the monosaccharide (GB1107 surrogate) showed no sign of excretion. The data obtained allowed us to infer the different in vivo fate of TD139 and GB1107 and rationalize how different administration routes could boost efficacy. Whereas the fast excretion profile of the TD139 surrogate indicated that systemic application of disaccharides is unfavorable, the extended biological half-life of the GB1107 surrogate indicated that systemic administration is possible for monosaccharides.

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Reference:
Tetrahydropyran – Wikipedia,
Tetrahydropyran – an overview | ScienceDirect Topics

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The dynamic chemical diversity of the numerous elements, ions and molecules that constitute the basis of life provides wide challenges and opportunities for research. 1450824-22-2, Name is TD 139, molecular formula is C28H30F2N6O8S. In a Patent,once mentioned of 1450824-22-2, Recommanded Product: TD 139

Aspects of the invention relate to novel synthetic compounds for treatment of metabolic diseases partially associated with systemic insulin resistance caused by Galectin proteins binding and inhibiting insulin and TGFb1 receptors causing physiological disturbances in the insulin pathways.

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Reference:
Tetrahydropyran – Wikipedia,
Tetrahydropyran – an overview | ScienceDirect Topics

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Enzyme inhibitors cause a decrease in the reaction rate of an enzyme-catalyzed reaction by binding to a specific portion of an enzyme. Irreversible inhibitors are therefore the equivalent of poisons in heterogeneous catalysis. 1450824-22-2, C28H30F2N6O8S. A document type is Patent, introducing its new discovery., Reference of 1450824-22-2

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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Tetrahydropyran – Wikipedia,
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Aspects of the invention relate to novel synthetic compounds having a binding affinity with galectin proteins.

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Reference:
Tetrahydropyran – Wikipedia,
Tetrahydropyran – an overview | ScienceDirect Topics

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Balanced chemical reaction does not necessarily reveal either the individual elementary reactions by which a reaction occurs or its rate law.COA of Formula: C28H30F2N6O8S. In my other articles, you can also check out more blogs about 1450824-22-2

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Aspects of the invention relate to novel synthetic compounds for treatment of metabolic diseases partially associated with systemic insulin resistance caused by Galectin proteins binding and inhibiting insulin and TGFb1 receptors causing physiological disturbances in the insulin pathways.

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Reference:
Tetrahydropyran – Wikipedia,
Tetrahydropyran – an overview | ScienceDirect Topics

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Related Products of 1450824-22-2, Chemistry can be defined as the study of matter and the changes it undergoes. You’ll sometimes hear it called the central science because it is the connection between physics and all the other sciences, starting with biology.1450824-22-2, Name is TD 139, molecular formula is C28H30F2N6O8S. In a patent, introducing its new discovery.

Background: Parkinson’s disease (PD) is the most prevalent neurodegenerative motor disorder. The neuropathology is characterized by intraneuronal protein aggregates of alpha-synuclein and progressive degeneration of dopaminergic neurons within the substantia nigra. Previous studies have shown that extracellular alpha-synuclein aggregates can activate microglial cells, induce inflammation and contribute to the neurodegenerative process in PD. However, the signaling pathways involved in alpha-synuclein-mediated microglia activation are poorly understood. Galectin-3 is a member of a carbohydrate-binding protein family involved in cell activation and inflammation. Therefore, we investigated whether galectin-3 is involved in the microglia activation triggered by alpha-synuclein. Results: We cultured microglial (BV2) cells and induced cell activation by addition of exogenous alpha-synuclein monomers or aggregates to the cell culture medium. This treatment induced a significant increase in the levels of proinflammatory mediators including the inducible Nitric Oxide Synthase (iNOS), interleukin 1 Beta (IL-1beta) and Interleukin-12 (IL-12). We then reduced the levels of galectin-3 expression using siRNA or pharmacologically targeting galectin-3 activity using bis-(3-deoxy-3-(3-fluorophenyl-1H-1,2,3-triazol-1-yl)-beta-D-galactopyranosyl)-sulfane. Both approaches led to a significant reduction in the observed inflammatory response induced by alpha-synuclein. We confirmed these findings using primary microglial cells obtained from wild-type and galectin-3 null mutant mice. Finally, we performed injections of alpha-synuclein in the olfactory bulb of wild type mice and observed that some of the alpha-synuclein was taken up by activated microglia that were immunopositive for galectin-3. Conclusions: We show that alpha-synuclein aggregates induce microglial activation and demonstrate for the first time that galectin-3 plays a significant role in microglia activation induced by alpha-synuclein. These results suggest that genetic down-regulation or pharmacological inhibition of galectin-3 might constitute a novel therapeutic target in PD and other synucleinopathies.

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Reference:
Tetrahydropyran – Wikipedia,
Tetrahydropyran – an overview | ScienceDirect Topics

Brief introduction of TD 139

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Aspects of the invention relate to novel synthetic compounds having a binding affinity with galectin proteins.

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Reference£º
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Tetrahydropyran – an overview | ScienceDirect Topics

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Glycomimetic drugs have attracted increasing interest as unique targeting vectors or surrogates for endogenous biomolecules. However, it is generally difficult to determine the in vivo pharmacokinetic profile of these compounds. In this work, two galectin-3 inhibitors were radiolabeled with fluorine-18 and used as surrogate PET tracers of TD139 and GB1107. Both compounds are promising drugs for clinical applications. In vivo evaluation revealed that both surrogates strongly differed with respect to their biodistribution profile. The disaccharide (TD139 surrogate) was rapidly eliminated from blood while the monosaccharide (GB1107 surrogate) showed no sign of excretion. The data obtained allowed us to infer the different in vivo fate of TD139 and GB1107 and rationalize how different administration routes could boost efficacy. Whereas the fast excretion profile of the TD139 surrogate indicated that systemic application of disaccharides is unfavorable, the extended biological half-life of the GB1107 surrogate indicated that systemic administration is possible for monosaccharides.

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

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