rat y2 receptor

(R)-JNJ-31020028 is a high-affinity, selective brain-penetrant antagonist of the neuropeptide Y Y2 receptor, with pIC50 values of 8.07, 8.22, and 8.21 for human, rat, and mouse Y2 receptors, respectively.

JNJ-5207787 is a penetrates the blood-brain barrier neuropeptide Y Y2 receptor (Y2) antagonist. It is >100-fold selective versus human Y1, Y4, and Y5 receptors. JNJ-5207787 suppresses the binding of peptide YY with pIC50s of 7.0 and 7.1 for the human Y2 r

BIIE-0246是一种选择性的NPY2R拮抗剂，对大鼠[125I]PYY3-36位点的IC50=15 nM，能够在NPY刺激下降低 p-AKT S473、P-p44/42 MAPK 的表达。

JNJ-31020028是神经肽Y2受体选择性可脑渗透抑制剂，对人Y2和鼠源Y2受体pIC50值分别为8.07和8.22，其神经肽 Y2 受体的选择性比人 Y1/Y4/Y5 受体高 100 倍。

J-115814 is a potent feeding stimulant.

Neuropeptide Y (NPY) (3-36) is a C-terminal fragment of NPY, a neuropeptide involved in controlling appetite, blood pressure, cardiac contractility, and intestinal secretion. NPY (3-36) is an endogenous peptide produced by cleavage of NPY by dipeptidyl peptidase 4 (DPP-4). It binds selectively to the NPY receptor Y2 (Ki = 0.41 nM in CHP 234 cells) over the Y1 receptor, where it does not bind at concentrations up to 1 μM. NPY (3-36) (0.1 nM) increases migration of human umbilical vein endothelial cells (HUVECs) by 80% after 12 hours in an in vitro wound closure assay. NPY (3-36) corresponds to residues 3-36 of the human and rat protein sequence.

Neuropeptide Y (3-36) (human, rat) is a metabolite of neuropeptide Y (NPY) generated by dipeptidyl peptidase-4 (DPP4). Known as a selective Y2 receptor agonist, Neuropeptide Y (3-36) (human, rat) effectively reduces the release of norepinephrine via the Y2 receptor[1][2].

Peptide YY (13-36) (canine, mouse, porcine, rat) 是 Y2受体的激动剂。

Potent neuropeptide Y (NPY) Y5 receptor agonist (pEC50 values are 7.82, 6.28, 6.44 and > 6 at rat Y5, Y4, Y1 and Y2 receptors respectively) that displays > 26-fold, > 1000-fold and > 1000-fold selectivity over Y1, Y2 and Y4 receptors respectively. Induces

GEP44 是一种肽偏向的三重激动剂，针对胰高血糖素样肽 1 受体 (GLP-1R)、神经肽 Y1 受体 (Y1-R) 和神经肽 Y2 受体 (Y2-R)。该化合物通过抵消 Y1-R 和 GLP-1R 的激动作用，诱导大鼠和人类胰岛中 Y1-R 拮抗剂调控的 GLP-1R 依赖性胰岛素分泌刺激。GEP44 还促进肌肉组织中的胰岛素非依赖性 Y1-R 介导的葡萄糖摄取，显著减少饮食诱导的肥胖大鼠模型的食物摄入和体重。GEP44 可用于研究肥胖和 2 型糖尿病。