Endocrinology/Hormones

This assay employs the competitive inhibition enzyme immunoassay technique. The microtiter plate provided in this kit has been pre-coated with Mouse MDA protein. Standards or samples are added to the appropriate microtiter plate wells then with a biotin-conjugated antibody specific to Mouse MDA. Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm ± 10nm. The concentration of Mouse MDA in the samples is then determined by comparing the OD of the samples to the standard curve.

The test principle applied in this kit is Sandwich enzyme immunoassay. The microtiter plate provided in this kit has been pre-coated with an antibody specific to Horse IGF1. Standards or samples are added to the appropriate microtiter plate wells then with a biotin-conjugated antibody specific to Horse IGF1. Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain Horse IGF1, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm ± 10nm. The concentration of Horse IGF1 in the samples is then determined by comparing the OD of the samples to the standard curve.

The test principle applied in this kit is Sandwich enzyme immunoassay. The microtiter plate provided in this kit has been pre-coated with an antibody specific to Rat VLDL. Standards or samples are added to the appropriate microtiter plate wells then with a biotin-conjugated antibody specific to Rat VLDL. Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain Rat VLDL, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm ± 10nm. The concentration of Rat VLDL in the samples is then determined by comparing the OD of the samples to the standard curve.

Relacorilant is an oral glucocorticoid receptor antagonist with Ki of 7.2 nM, potential for treating Cushing's syndrome.

SR17018 is an mu-opioid-receptor (MOR) agonist, binding with GTPγS, with an EC50 of 97 nM.

Cebranopadol (GRT6005) is an analgesic NOP and opioid receptor agonist with Kis of 0.9 nM, 0.7 nM, 2.6 nM, 18 nM for human NOP, μ-opioid (MOP), κ-opioid (KOP)

Pamoic acid is the orphan G protein-coupled receptor GPR35 agonist. Pamoic acid activates ERK and beta-arrestin2 and causes antinociceptive activity.

This is an incretin hormone that causes glucose dependent release of insulin by pancreatic beta cells. It is the cleavage product of GLP-1 (1-36) amide peptide.  This peptide, human GLP-1 (7–36), shares the same sequence with preproglucagon (78-107), amide, human.

ANP (9-22) is derived from the atrial natriuretic peptide (ANP) which is a cardiac hormone involved in maintaining cardio-renal homeostasis. This occurs through the activation of the guanylyl cyclase-coupled receptor, resulting in the increased concentration of cyclic guanylate monophosphate. Moreover its function in the processes of anti-proliferation and anti-angiogenesis allow it to take part in the cardiovascular remodelling process.ANP is a member of the natriuretic peptide family and it is encoded by the NPPA gene, located on chromosome 1. Once synthesized from the 151 amino acid pre-prohormone into its biologically active form, ANP is secreted by the atrial cardiomyocytes in the circulating forms: ANP (1-98) and ANP (99-126). This synthesis process involves the signal peptide being removed from the pre-prohormone resulting in proANP (1-126) which is converted into the circulating forms by the type II transmembrane serine protease Corin.

ANP (13-26) is derived from the atrial natriuretic peptide (ANP) which is a cardiac hormone involved in maintaining cardio-renal homeostasis. This occurs through the activation of the guanylyl cyclase-coupled receptor, resulting in the increased concentration of cyclic guanylate monophosphate. Moreover its function in the processes of anti-proliferation and anti-angiogenesis allow it to take part in the cardiovascular remodelling process.ANP is a member of the natriuretic peptide family and it is encoded by the NPPA gene, located on chromosome 1. Once synthesized from the 151 amino acid pre-prohormone into its biologically active form, ANP is secreted by the atrial cardiomyocytes in the circulating forms: ANP (1-98) and ANP (99-126). This synthesis process involves the signal peptide being removed from the pre-prohormone resulting in proANP (1-126) which is converted into the circulating forms by the type II transmembrane serine protease Corin.

Peptide derived from the Gastric inhibitory polypeptide (GIP), an inhibiting hormone of the secretin family of hormones. While GIP is a weak inhibitor of gastric acid secretion, its main role is to stimulate insulin secretion - in a glucose-dependent mechanism. Therefore, GIP is referred to as a glucose-dependent insulinotropic peptide.GIP is derived from a 153-amino acid pro-protein encoded by the GIP gene and circulates as a biologically active 42-amino acid peptide. It is synthesised by K cells, which are found in the mucosa of the duodenum and the jejunum of the gastrointestinal tract. GIP receptors are seven-transmembrane proteins found on β-cells in the pancreas. These β-cells are those that are able to simultaneously detect glucose and release insulin as a result to GIP binding.The clinical relevance of GIP is related to type 2 diabetes mellitus (T2DM)- studies have found that T2DM diabetics are unresponsive to GIP and have lower levels of GIP secretion after a meal when compared to non-diabetics. In research involving knockout mice, it was found that absence of the GIP receptors correlates with resistance to obesity.