Diabetes 서비스
인슐린 분비 감소(insufficient insulin secretion) 및 인슐린 감수성(Insulin Sensitivity) 저하와 같은 발병 원인을 기준으로 개발된 서비스
Eurofins Discovery
| Eurofins DiscoverX(Eurofins Discovery) 공식 대리점 
INTRODUCTION
Diabetes Panel은 인슐린 분비 감소(insufficient insulin secretion) 및 인슐린 감수성(Insulin Sensitivity) 저하와 같은 발병 원인을 기준으로 개발된 서비스입니다. 임상결과에서 치료 효과를 보였던 Target을 토대로 2종류(①Insulin Release Panel ②Insulin Sensitivity Panel)의 서비스를 제공하고 있습니다.
Diabetes 서비스를 통해서 개발하고 있는 후보 약물의 MOA 및 multi-target effects를 확인할 수 있습니다.
서비스 종류 및 샘플 준비 방법
| 서비스 유형 | Insulin Sensitivity Panel | Insulin Release Panel |
| Target 수 | 7 | 11 |
| 실험농도 | 선택 가능 | 선택 가능 |
| Sample Volume | 50 µL, 10 mM stock | 350 µL, 10 mM stock |
| 실험 조건(변경할 경우)에 따라 필요 Sample Volume이 달라질 수 있습니다. | ||
| 반복실험횟수 | Duplicate | Duplicate |
| TAT | 15 Days | 20 Days |
| 서비스 장소 | 대만(Panlabs) | |
서비스 상세
Insulin Sensitivity Panel
| Class | Target | Item# | Biological Relevance |
| Kinase | AMPK | 199100-0 | AMPK is the center of energy metabolism that regulates glucose uptake, glucose, and lipid metabolism. The first line antidiabetic drug metformin, which is an indirect AMPK activator, is widely prescribed for T2D patients. |
| INSR | 243000 | INSR activation causes the translocation of GLUT4 to the cellular membrane. This enhances glucose uptake and metabolism. Abnormally expressed INSR is highly associated with insulin resistance. | |
| GSK3β | 176500 | GSK3β inhibition enhances glycogenesis and glucose metabolism. GSK3β signaling pathway is highly correlated with diabetes complications such as diabetic neuropathy. | |
| NHR | PPARγ | 267500 | PPARγ activation improves insulin sensitivity by increasing glucose uptake through GLUT4 in muscle and reducing free fatty acid by lipogenesis. This enhances the utilization of glucose. |
| Phosphatase | PTP1B | 192010 | PTP1B Inhibition suppresses activated INSR and Leptin receptors, leading to insulin sensitivity improvement. |
| Deacetylase | SIRT1 | 199102-0 | SIRT1 activation inhibits PTP1B activity and thus increases insulin sensitivity. SIRT1 activation also enhances insulin secretion. |
| Dehydrogenase | 11β-HSD1 | 125710 | Abnormal high cortisol level is highly associated with insulin resistance and diabetes. 11β-HSD1 catalyzes the conversion of cortisone to cortisol. 11β-HSD1 inhibition reduces cortisol level and results in insulin sensitivity improvement. |
Insulin Release Panel
| Class | Target | Item# | Biological Relevance |
| GPCR | GLP1R | 231710 | GLP1R activation increases insulin secretion in a glucose-dependent manner and reduces glycaemia by inhibiting glucagon secretion. |
| GIPR | 312970-0 | The combination of GLP1 and GIP analogues improves glycaemic control and weight loss. Chimeric peptides that mimic GIP and GLP1 have been developed for diabetes treatment | |
| GPR40 | 311810-0 | PR40 activation stimulates intestinal secretion of GLP1 and GIP with pancreatic secretion of insulin in a glucosedependent manner. | |
| NPY1R | 257010 | NPY1R activation may particularly contribute to insulin secretion after weight loss surgery for T2D. The analogues of PYY(1-36), a selective NPY1R agonist, have been designed for diabetes treatment. | |
| GCGR | 231680 | GCGR antagonists that inhibit glucagon actions can counter high glycaemia in diabetes. Several GLP1R/GCGR dual agonists and GLP1R/GCGR/GIPR tri-agonists have been developed for diabetes treatment. | |
| Kinase | GCK | 199101-0 | GCK activation promotes hepatic glucose uptake, glycogen synthesis, and enhances glucose-stimulated insulin secretion from the pancreas. |
| Peptidase | DPP4 | 199007 | DPP4 plays a key role in the clearance of GLP1. DPP4 inhibition has been well-established for glycaemic control improvement in T2D patients. |
| Ion Channel | KATP | 265600 | Inhibition of pancreatic KATP channels leads to depolarization and increases intracellular calcium levels, resulting in insulin release. |
| Transporter | IBAT | 314100-1 | IBAT inhibition prevents bile acid reabsorption, which leads to GLP1 secretion and GLP1R activation. |
| SGLT1 | 355710-1 | SGLT1 inhibition delays glucose absorption in the small intestine and colon, resulting in glucose reduction, insulin secretion, and glycaemic control improvement. | |
| Phenotypic | Insulin Release |
331500-0 | Pancreatic islet beta cell line HIT-T15 is used to assess the ability to stimulate insulin release by test compounds. |
Related Service
Glucose Uptake
| Class | Target | Item# | Biological Relevance |
| Phenotypic | Glucose Uptake | 320020 | Skeletal muscle is a major organ for glucose uptake. Skeletal muscle cell line L6 is used to examine the 2-Deoxyglucose uptake ability of test compounds. |
서비스 절차
서비스 문의