acid secretion-in-1

Acid secretion-IN-1, a polycyclic compound, is synthesized for its application as an IDO inhibitor in synthetic experiments.

Thiazolidinone-Derivatives-1 抑制胃酸分泌，可用于研究胃和十二指肠溃疡的治疗。

gamma-preprotachykinin amide (72-92) acetate 是一种 21 个氨基酸的肽，属于速激肽 (TK) 家族，在其 C 末端序列中包括神经激肽 A (NKA)。它对中枢 NK-2 受体的亲和力高于 NKA；它对 NK-1 受体的亲和力较低，但是，它有效地刺激唾液分泌，这是由 NK-1 受体激活介导的。

BAA473 是胆汁酸类似物，是一种强效的吡喃类炎症小体激活剂。BAA473可通过激活髓样和肠上皮细胞中的炎症小体来诱导白细胞介素（ IL-18 ）的分泌。

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)

D-Trimannuronic acid is an alginate oligomer that originates from seaweed. It can induce TNF-α secretion by mouse macrophage cell lines, making it valuable in pain and vascular dementia research [1][2][3].

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).

N-Arachidonoyl taurine is an arachidonoyl amino acid. It is oxygenated by 12(S)- and 15(S)-lipoxygenase and is converted to 12-HETE-taurine (12-HETE-T) in murine resident peritoneal macrophages. N-Arachidonoyl taurine is an activator of the transient receptor potential vanilloid (TRPV) channels TRPV1 and TRPV4 (EC50s = 28 and 21 μM, respectively). It increases calcium flux in HIT-T15 pancreatic β-cells and INS-1 rat islet cells when used at a concentration of 10 μM and increases insulin secretion from 832 13 INS-1 pancreatic β-cells. The levels of N-arachidonoyl taurine are changed in mouse brain following administration of δ9-tetrahydrocannabinol (δ9-THC).

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.

GLP-1 amide is a peptide hormone cleaved from proglucagon in the pancreas.1,2 Mice lacking the glucagon receptor (Gcgr- -) have approximately nine-fold higher levels of total GLP-1 amide, including GLP-1 (1-36) amide and truncated GLP-1 (7-36) amide , in pancreatic tissue compared to wild-type mice.2References1. Schjoldager, B.T., Mortensen, P.E., Christiansen, J., et al. GLP-1 (glucagon-like peptide 1) and truncated GLP-1, fragments of human proglucagon, inhibit gastric acid secretion in humans. Dig. Dis. Sci. 34(5), 703-708 (1989).2. Gelling, R.W., Du, X.Q., Dichmann, D.S., et al. Lower blood glucose, hyperglucagonemia, and pancreatic α cell hyperplasia in glucagon receptor knockout mice. Proc. Natl. Acad. Sci. U.S.A. 100(3), 1438-1443 (2003). GLP-1 amide is a peptide hormone cleaved from proglucagon in the pancreas.1,2 Mice lacking the glucagon receptor (Gcgr- -) have approximately nine-fold higher levels of total GLP-1 amide, including GLP-1 (1-36) amide and truncated GLP-1 (7-36) amide , in pancreatic tissue compared to wild-type mice.2 References1. Schjoldager, B.T., Mortensen, P.E., Christiansen, J., et al. GLP-1 (glucagon-like peptide 1) and truncated GLP-1, fragments of human proglucagon, inhibit gastric acid secretion in humans. Dig. Dis. Sci. 34(5), 703-708 (1989).2. Gelling, R.W., Du, X.Q., Dichmann, D.S., et al. Lower blood glucose, hyperglucagonemia, and pancreatic α cell hyperplasia in glucagon receptor knockout mice. Proc. Natl. Acad. Sci. U.S.A. 100(3), 1438-1443 (2003).

1-Arachidonoyl lysophosphatidic acid is a phospholipid containing arachidonic acid at the sn-1 position. It has been found in rat brain as 37% of the arachidonic acid-containing lysophosphatidic acid (LPA) species and is a precursor to 1-arachidonoyl glycerol . 1-Arachidonoyl lysophosphatidic acid binds to the LPA2 EDG4 receptor with an EC50 value of approximately 10 nM. It prevents TNF-α and IL-6 secretion in wild-type but not Lpa2- - dendritic cells stimulated by LPS. It also decreases differentiation of HT-29 human colon carcinoma cells to goblet cells in the presence of sodium butyrate.

Gastrin-releasing peptide (GRP) is a neuropeptide that stimulates gastrin release. It binds to (Ki = 300 nM) and stimulates amylase secretion in rat pancreatic AR42J cells (EC50 = 0.3 nM). GRP increases proliferation of human liver carcinoma HepG2 and MHCC97H cells but does not affect the proliferation of normal HL-7702 liver cells at a concentration of 1 nM. In vivo, GRP (0.35 nmol/kg/h) increases both pancreatic exocrine secretion and pancreatic polypeptide (PP) release in rats. It dose-dependently stimulates gastrin, pancreatic amylase, lipase, bilirubin, and acid output and induces gallbladder contraction in humans when administered at doses ranging from 1 to 27 pmol/kg per hour.

1-Methyl-4-imidazoleacetic acid (MIMA) is a stable metabolite of histamine that is produced by the oxidation of the primary metabolite, N-methylhistamine. Urinary levels of MIMA are commonly measured to evaluate histamine secretion, particularly in the context of systemic mastocytosis.

Esomeprazole magnesium salt is a potent and orally active proton pump inhibitor that effectively reduces acid secretion in gastric parietal cells by inhibiting the H+, K+-ATPase. This compound has shown promise for the research and treatment of symptomatic gastroesophageal reflux disease [1][2][3].

Esomeprazole potassium salt ((S)-Omeprazole potassium salt) is an effective and orally active proton pump inhibitor that works by inhibiting the H+, K+-ATPase enzyme in the gastric parietal cells, leading to a reduction in acid secretion. It is a promising compound for investigating symptomatic gastroesophageal reflux disease [1] [2] [3].

Esomeprazole hemistrontium, also known as (S)-Omeprazole, is a potent and orally active proton pump inhibitor that effectively reduces acid secretion by inhibiting the H+, K+-ATPase in gastric parietal cells. This compound exhibits promising potential for research in symptomatic gastroesophageal reflux disease [1] [2] [3].

MK-8666 Tris is a partial GPCR (G-protein-coupled receptor) agonist that is coordinated with the action of GPR40. GPR40, also known as free fatty acid (FFA) receptor 1 modulates fatty acid-induced insulin secretion in pancreatic beta cells and in intestinal enteroendocrine cells. Thus, MK-8666 Tris has been investigated for treatment of type 2 diabetes mellitus and has been shown to robustly lower glucose without negative effects.

MK-8666 is a partial GPCR (G-protein-coupled receptor) agonist that is coordinated with the action of GPR40. GPR40, also known as free fatty acid (FFA) receptor 1 modulates fatty acid-induced insulin secretion in pancreatic beta cells and in intestinal enteroendocrine cells. Thus, MK-8666 has been investigated for treatment of type 2 diabetes mellitus and has been shown to robustly lower glucose without negative effects.

Flufenamic acid-d4 is intended for use as an internal standard for the quantification of flufenamic acid by GC- or LC-MS. Flufenamic acid is a non-steroidal anti-inflammatory drug (NSAID) and COX inhibitor (IC50s = 3 and 9.3 µM for human COX-1 and COX-2, respectively). Flufenamic acid inhibits TNF-α-induced increases in COX-2 levels and NF-κB activation in HT-29 colon cancer cells in a concentration-dependent manner. It inhibits calcium influx induced by fMLP or A23187 in human polymorphonuclear leukocytes (PMN) with IC50 values of 29 and 14 µM, respectively. Flufenamic acid also activates various ion channels, including transient receptor potential canonical 6 (TRPC6) and the large-conductance calcium-activated potassium channel (KCa1.1). It also inhibits various ion channels, including TRPC3 and the cystic fibrosis transmembrane conductance regulator (CFTR). Flufenamic acid (20 mg kg) reduces increases in intestinal fluid secretion and intestinal barrier disruption in mice ......

Amylin, amide, human TFA 是一种含有37个氨基酸的胰腺多肽，与胰岛素共同分泌，对代谢和维持葡萄糖稳态具有重要作用。该化合物能够抑制胰高血糖素的分泌，延缓胃排空速度，同时作为增加饱腹感的因子。

Spexin TFA, a potent agonist for galanin receptor 2 3 (GAL2 GAL3) with EC50 values of 45.7 and 112.2 nM respectively, shows no significant activity towards galanin receptor 1. As an endogenous peptide promoting satiety, it reduces long chain fatty acid uptake by adipocytes and lowers food consumption in diet-induced obese mice and rats. Additionally, it moderates LH secretion in goldfish and demonstrates anxiolytic effects in vivo.

[Tyr0]Gastric Inhibitory Peptide(23-42), human，属于葡萄糖依赖性促胰岛素多肽（GIP）类，具有抑制胃酸分泌并促进胰岛素释放的功能。它在糖尿病和肥胖症的研究中有应用价值。

Pyruvate carboxylase是一种催化反应中丙酮酸与HCO3−和MgATP进行依赖性羧化生成草酰乙酸的含生物素酶。它在调控肝脏糖异生、脂肪细胞脂肪酸合成及胰腺β细胞胰岛素分泌方面，对全身能量平衡发挥关键作用。

Xenin-8 TFA为Xenin的C端八肽段，同时是其生物活性片段。该化合物隶属于神经降压素 xenopsin家族多肽中。它能激发基础胰岛素的分泌并剂量依赖性地加强胰岛素对葡萄糖反应(EC50=0.16 nM)。