islets

BRD7389 是一种 RSK 家族激酶抑制剂，对 RSK1、RSK2 和 RSK3 的 IC50 分别为 1.5 μM、2.4 μM 和 1.2 μM。

BRD7552 是PDX1转录因子诱导剂，它能够上调人类原代胰岛和导管细胞中 PDX1 的表达，诱导 PDX1 启动子的表观遗传变化与转录激活一致，提高胰岛素表达。其中 PDX1 是参与胰腺发育和β细胞功能的关键转录因子。

AM-4668是一种具有口服利用度的GPR40（FFA1）激动剂，其优化过后降低了中枢神经系统（CNS）的渗透性，小鼠脑 血浆比值仅为0.02，在人类GPR40基因敲入小鼠中显著降低了血糖水平。

GLP-1(7-36), amide (MKC 253) 是一种生理性肠降血糖素，能够刺激胰岛素分泌。

AACOCF3（Arachidonyl trifluoromethyl ketone）是一种细胞可渗透的三氟甲基酮类花生四烯酸模拟物。它是一个强效且选择性的85-kDa胞质型磷脂酶A2（cPLA2）缓慢结合抑制剂。通过阻止钙离子载体挑战的血小板中花生四烯酸和12-羟基二十四碳五烯酸的生成，AACOCF3抑制了它们的合成。此外，AACOCF3还能抑制从分离的大鼠岛细胞中诱导的葡萄糖引起的胰岛素释放。鉴于其多样的应用，AACOCF3对心血管疾病研究具有潜在的应用价值。

Dimethyl DL-Glutamate (hydrochloride) 是一种细胞渗透性谷氨酸衍生物，可在孤立的胰岛和糖尿病动物模型中增强胰岛素释放以响应葡萄糖。

Galantide acetate 是一种特殊的甘丙肽受体 (galanin receptor) 拮抗剂，是一种由甘丙肽和 P 物质片段组成的肽段，在大鼠下丘脑可识别两类甘丙肽结合位点 (KD 分别小于 0.1 nM 和 ~6 nM)。Galantide 剂量依赖性 (IC50=1.0 nM) 拮抗甘丙肽介导的葡萄糖诱导的小鼠胰岛胰岛素分泌抑制。Galantide acetate 似乎与单一的 SP 受体群结合 (KD~40 nM)。

GKA50 stimulates insulin release from mouse islets of Langerhans and MIN6 cells. GKA50 shows significant glucose lowering in high fat fed female rats. GKA50 is a potent glucokinase activator (EC50=33 nM at 5 mM glucose).

Insulin B (20-30) is a peptide hormone produced by beta cells of the pancreatic islets, and it is considered to be the main anabolic hormone of the body. It is therefore an anabolic hormone, promoting the conversion of small molecules in the blood into la

Insulin B (22-30) is a peptide hormone produced by beta cells of the pancreatic islets, and it is considered to be the main anabolic hormone of the body. It is therefore an anabolic hormone, promoting the conversion of small molecules in the blood into la

BMS-986118 is a full agonist of GPR40, is a G-protein-coupled receptor expressed primarily in pancreatic islets and intestinal L-cells that has been a target of significant recent therapeutic interest for type II diabetes. Activation of GPR40 by partial a

WB403 is a TGR5 activator. WB403 significantly decreases fasting blood glucose, postprandial blood glucose and HbA1c, improves glucose tolerance in type 2 diabetic mice. WB403 increases pancreatic β-cells and restores the normal distribution pattern of α-

Neuromedin U (NMU) is a neuropeptide first demonstrated to drive smooth muscle contraction.1Translated as a 174 amino acid propeptide, NMU is cleaved to different lengths in different animals. It has diverse receptor-mediated rolesin vivo, as it regulates feeding, vasoconstriction, nociception, and bone remodeling and contributes to obesity, cancer and septic shock.2,2NMU-25 is the active form of NMU in humans. It binds with high affinity to receptors on human left ventricle and coronary artery (KDs = 0.26 and 0.11 nM, respectively), eliciting endothelium-independent vasoconstriction.3NMU-25 also suppresses glucose-stimulated insulin secretion in human islets, and this effect is lost in NMU R165W mutants, resulting in early-onset obesity.4 1.Mitchell, J.D., Maguire, J.J., and Davenport, A.P.Emerging pharmacology and physiology of neuromedin U and the structurally related peptide neuromedin SBritish Journal of Pharmacology15887-103(2009) 2.Greenwood, H.C., Bloom, S.R., and Murphy, K.G.Peptides and their potential role in the treatment of diabetes and obesityRev.Diabet.Stud.8(3)355-368(2011) 3.Mitchell, J.D., Maguire, J.J., Kuc, R.E., et al.Expression and vasoconstrictor function of anorexigenic peptides neuromedin U-25 and S in the human cardiovascular systemCardiovascular Research81353-361(2009) 4.Alfa, R.W., Park, S., Skelly, K.R., et al.Suppression of insulin production and secretion by a decretin hormoneCell Metabolism21(2)323-333(2015)

FKGK 18 is an inhibitor of group VIA (GVIA) calcium-independent phospholipase A2 (iPLA2). It inhibits GVIA iPLA2 by 99.9% at 0.091 mole fraction in a mixed micelle activity assay and is selective for GVIA iPLA2 over GIVA cPLA2 and GV sPLA2 where it shows 80.8 and 36.8% inhibition, respectively. FKGK 18 inhibits iPLA2β activity in cytosolic extracts from INS-1 cells overexpressing iPLA2β (IC50 = ~50 nM) as well as iPLA2γ activity in mouse heart membrane fractions (IC50s = ~1-3 μM). It inhibits glucose-induced increases in prostaglandin E2 production and insulin secretion in human pancreatic islets when used at a concentration of 10 μM and inhibits thapsigargin-induced apoptosis in INS-1 cells overexpressing iPLA2β in a concentration-dependent manner. FKGK 18 (20 mg/kg, 3 times per week) reduces blood glucose levels in an intraperitoneal glucose tolerance test, decreases the incidence of diabetes, and increases serum insulin levels in non-obese diabetic (NOD) mice.

Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004). Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3 References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004).

AP39 free base 是一种线粒体靶向 H（2）S 供体，可提高猪胰岛在培养中的存活率。AP39 free base 通过 AMPK-ULK1-FUNDC1 通路调节线粒体自噬，抑制细胞焦亡，并改善阿霉素诱导的心肌纤维化。

5(6)-EET is a fully racemic version of the enantiomeric forms biosynthesized from arachidonic acid by cytochrome P450 enzymes. In solution, 5(6)-EET degrades into 5,6-DiHET and 5(6)-δ-lactone, which can be converted to 5(6)-DiHET and quantified by GC-MS. In neuroendocrine cells, such as the anterior pituitary and pancreatic islets, 5(6)-EET has been implicated in the mobilization of calcium and hormone secretion. 5(6)-EET is an inhibitor of T-type voltage-gated calcium channels (Cav3) that inhibits isoforms Cav3.1, Cav3.2 (IC50 = 0.54 μM), and Cav3.3 and decreases nifedipine-resistant phenylephrine-induced vasoconstriction in isolated mouse mesenteric arteries via Cav3.2 blockade when used at a concentration of 3 μM. In addition, it is a substrate of COX-1 and COX-2, as measured by oxygen consumption and product formation assays when used at a concentration of 50 μM. (±)5(6)-EET is provided as a mixture of the free acid and lactone.

GKA50 quarterhydrate 是一种有效的葡萄糖激酶激活剂，其 EC50 值为 33 nM。GKA50 quarterhydrate 是一种啮齿动物和人类胰岛中 β 细胞代谢的葡萄糖样激活剂，也是一种 Ca2+依赖性胰岛素分泌调节剂。GKA50 quarterhydrate 能够刺激小鼠胰岛分泌胰岛素，可以显著降低高脂喂养的雌性大鼠血糖。

ATM-1001 is an inhibitor of the cancer-associated tropomyosin 3.1 (Tpm3.1), suppressing glucose-stimulated insulin secretion (GSIS) from the pancreatic islets.

PF-04671536 is a highly potent and selective inhibitor of phosphodiesterase 8B (PDE8B) phosphodiesterase 8A (PDE8A). In primary human pancreatic islets, PF-04671536 increases insulin secretion in a glucose-dependent manner.

MS4 is a novel glucocorticoid receptor (GR) agonist with anti-inflammatory activity and displaying reduced impact on islets.

Phospholipid-PEG-Biotin (MW 1000) 和 Phospholipid-PEG-Biotin (MW 3400) 均为磷脂与生物素通过线性聚乙二醇(PEG)连接桥接得到的衍生物。其中，Phospholipid-PEG-Biotin (MW 3400) 能够与亲和抗体发生相互作用，适用于脂质体和细胞表面的修饰，以及胰岛细胞移植领域。

Phospholipid-PEG-Biotin (MW 2000) 是一种PROTAClinker，属于 PEG 类。可用于合成PROTAC 分子。Phospholipid 是一类含有亲水“头”和疏水“尾”的脂类；PEG 是一种低毒性的亲水水溶性聚合物；生物素是一种酶辅因子，可用于标记蛋白质。

Phospholipid-PEG-Biotin (MW 3400) 为一种通过线性PEG链接剂桥接磷脂和生物素的磷脂聚乙二醇衍生物。该化合物能够与亲和抗体进行相互作用，并可用于脂质体及细胞表面的修饰，也适用于胰岛细胞移植。