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Y1 receptor antagonist 1 Sale

(Synonyms: H 409-22 isomer) 目录号 : GC30945

Y1receptorantagonist1是H-409/22的一个异构体,是神经肽(neuropeptideY1)受体拮抗剂。

Y1 receptor antagonist 1 Chemical Structure

Cas No.:221697-09-2

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1 mg
¥4,280.00
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产品描述

Y1 receptor antagonist 1, an isomer of H-409/22, is a neuropeptide Y1 receptor antagonist.

Chemical Properties

Cas No. 221697-09-2 SDF
别名 H 409-22 isomer
Canonical SMILES O=C(N[C@@H](C(N[C@@H](C1=CC=C(O)C=C1)C)=O)CCCNC(N)=N)C(C2=CC=CC=C2)C3=CC=CC=C3
分子式 C28H33N5O3 分子量 487.59
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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1 mM 2.0509 mL 10.2545 mL 20.509 mL
5 mM 0.4102 mL 2.0509 mL 4.1018 mL
10 mM 0.2051 mL 1.0255 mL 2.0509 mL
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Research Update

Neuropeptide Y1 receptor antagonism protects β-cells and improves glycemic control in type 2 diabetes

Objectives: Loss of functional β-cell mass is a key factor contributing to poor glycemic control in advanced type 2 diabetes (T2D). We have previously reported that the inhibition of the neuropeptide Y1 receptor improves the islet transplantation outcome in type 1 diabetes (T1D). The aim of this study was to identify the pathophysiological role of the neuropeptide Y (NPY) system in human T2D and further evaluate the therapeutic potential of using the Y1 receptor antagonist BIBO3304 to improve β-cell function and survival in T2D. Methods: The gene expression of the NPY system in human islets from nondiabetic subjects and subjects with T2D was determined and correlated with the stimulation index. The glucose-lowering and β-cell-protective effects of BIBO3304, a selective orally bioavailable Y1 receptor antagonist, in high-fat diet (HFD)/multiple low-dose streptozotocin (STZ)-induced and genetically obese (db/db) T2D mouse models were assessed. Results: In this study, we identified a more than 2-fold increase in NPY1R and its ligand, NPY mRNA expression in human islets from subjects with T2D, which was significantly associated with reduced insulin secretion. Consistently, the pharmacological inhibition of Y1 receptors by BIBO3304 significantly protected β cells from dysfunction and death under multiple diabetogenic conditions in islets. In a preclinical study, we demonstrated that the inhibition of Y1 receptors by BIBO3304 led to reduced adiposity and enhanced insulin action in the skeletal muscle. Importantly, the Y1 receptor antagonist BIBO3304 treatment also improved β-cell function and preserved functional β-cell mass, thereby resulting in better glycemic control in both HFD/multiple low-dose STZ-induced and db/db T2D mice. Conclusions: Our results revealed a novel causal link between increased islet NPY-Y1 receptor gene expression and β-cell dysfunction and failure in human T2D, contributing to the understanding of the pathophysiology of T2D. Furthermore, our results demonstrate that the inhibition of the Y1 receptor by BIBO3304 represents a potential β-cell-protective therapy for improving functional β-cell mass and glycemic control in T2D.

Identification of a novel specific small-molecule melanocortin-2-receptor antagonist

The overproduction of adrenocorticotropic hormone (ACTH), in conditions such as Cushing's disease and congenital adrenal hyperplasia (CAH), leads to significant morbidity. Current treatment with glucocorticoids does not adequately suppress plasma ACTH, resulting in excess adrenal androgen production. At present, there is no effective medical treatment in clinical use that would directly block the action of ACTH. Such a therapy would be of great clinical value. ACTH acts via a highly selective receptor, the melanocortin-2 receptor (MC2R) associated with its accessory protein MRAP. ACTH is the only known naturally occurring agonist for this receptor. This lack of redundancy and the high degree of ligand specificity suggest that antagonism of this receptor could provide a useful therapeutic strategy in the treatment of conditions of ACTH excess. To this end, we screened an extensive library of low-molecular-weight drug-like compounds for MC2R antagonist activity using a high-throughput homogeneous time-resolved fluorescence cAMP assay in Chinese hamster ovary cells stably co-expressing human MC2R and MRAP. Hits that demonstrated MC2R antagonist properties were counter-screened against the β2 adrenergic receptor and dose-response analysis undertaken. This led to the identification of a highly specific MC2R antagonist capable of antagonising ACTH-induced progesterone release in murine Y-1 adrenal cells and having selectivity for MC2R amongst the human melanocortin receptors. This work provides a foundation for the clinical investigation of small-molecule ACTH antagonists as therapeutic agents and proof of concept for the screening and discovery of such compounds.

Neuropeptide Y1 receptor antagonist but not neuropeptide Y itself increased bone mineral density when locally injected with hyaluronic acid in male Wistar rats

Background/aim: The nervous system controls bone mass via both the central (CNS) and the peripheral (PNS) nervous systems. Intriguingly, neuropeptide Y (NPY) signaling occurs in both. Less is known on how the PNS stimulated NPY signaling controls bone metabolism. The objective of this study was to evaluate whether NPY or NPY1 receptor antagonist changes local bone mineral density (BMD) when injected into a Wistar rat tibia.
Materials and methods: Tibial intramedullary area of 24 wild type male Wistar rats (average weight = 350 ± 50 g, average age = 4 ± 0.5 months) were injected with NPY (1 × 10-5 M and 1 × 10-6 M) and NPY1 receptor antagonist (1 × 10-4 M) dissolved in hyaluronic acid (HA) separately. Tibiae were collected after one and two weeks. BMD was measured with dual-energy X-ray absorptiometry (DXA) and micro quantitative computer tomography (QCT). Histological changes were analyzed with light microscopy, Goldner's Masson trichrome (MT), and hematoxylin-eosin staining.
Results: According to DXA, the mean BMD of NPY dose 1 (1 × 10-5 M) was significantly lower than that of the control (HA applied) group and not significantly but still lower than that of the NPY dose 2 and NPY1 antagonist applied groups. QCT results indicated the same pattern statistically insignificantly in the trabecular area but not in the cortex of the bones. Histologically, only NPY1 antagonist applied tibiae revealed young spongiosis bone trabeculae formed in the borderline of the cortical bones. HA was remarkably biocompatible and late degrading in the tissues.
Conclusion: Local administration of NPY and NPY1 antagonists may hold regulating potential of BMD and bone formation. NPY1 antagonist caused new bone formation in trabecular bone when applied locally. NPY dissolved in HA however can be used to suppress bone formation.