Insulin Detemir
Modify Date: 2025-08-26 12:07:19
Insulin Detemir structure
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Common Name | Insulin Detemir | ||
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| CAS Number | 169148-63-4 | Molecular Weight | 5916.82198 | |
| Density | N/A | Boiling Point | N/A | |
| Molecular Formula | C267H402N64O76S6 | Melting Point | N/A | |
| MSDS | N/A | Flash Point | N/A | |
Use of Insulin DetemirInsulin Detemir is an artificial insulin, shows effect on controlling blood sugar levels. Insulin Detemir stimulates GLP-1 secretion as a consequence of enhanced Gcg expression by a mechanism involving activation of Akt- and/or extracellular signal-regulated kinase (ERK)-dependent-cat and CREB signaling pathways. Insulin Detemir can be used for type 2 diabetes research[1][2]. |
| Name | Levemir (tn) |
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| Description | Insulin Detemir is an artificial insulin, shows effect on controlling blood sugar levels. Insulin Detemir stimulates GLP-1 secretion as a consequence of enhanced Gcg expression by a mechanism involving activation of Akt- and/or extracellular signal-regulated kinase (ERK)-dependent-cat and CREB signaling pathways. Insulin Detemir can be used for type 2 diabetes research[1][2]. |
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| Related Catalog | |
| In Vitro | Insulin Detemir (d-INS) (100 nM; 0.5-4 h) increases Gcg mRNA expression in primary fetal rat intestinal cell (FRIC) cultures, and (100 nM; 5 min and 10 min) induces rapid phosphorylation of Akt, as well[1]. Insulin Detemir (100 nM; 5-120 min) increases β-catenin phosphorylation, its nuclear translocation, and enhances cAMP response element-binding protein (CREB) phosphorylation in a phosphatidylinositol 3-kinase and/or mitogen-activated protein kinase kinase/extracellular signal-regulated kinase-sensitive manner[1]. Western Blot Analysis[1] Cell Line: GLUTag cells Concentration: 100 nM Incubation Time: 0, 5, 10, 30, 60, and 120 min Result: Stimulated CREB, ERK1/2, Akt and its downstream glycogen synthase kinase (GSK)-3 phosphorylation at 5 min and 10 min. |
| In Vivo | Insulin Detemir (d-INS) (5 IU/kg; i.p.; once daily; 2 weeks) demonstrates weight-sparing effects compared with other insulin formulations, and shows a intestinal tissues preference, potentially involving the activation of insulin/-catenin/CREB signaling pathways[1]. Animal Model: Obese type 2 diabetic db/db mice[1] Dosage: 5 IU/kg Administration: Intraperitoneal injection; once daily for 2 weeks Result: Decreased body weight of the mice after 14-day daily injection of d-INS (5 IU/kg) significantly compared with those injected with the same dose of human Insulin or saline. Induced rapid phosphorylation of protein kinase B (Akt) in the gut L cells of normal mice. |
| References |
| Molecular Formula | C267H402N64O76S6 |
|---|---|
| Molecular Weight | 5916.82198 |
| InChIKey | UGOZVNFCFYTPAZ-IOXYNQHNSA-N |
| SMILES | CCCCCCCCCCCCCC(=O)NCCCCC(NC(=O)C1CCCN1C(=O)C(NC(=O)C(Cc1ccc(O)cc1)NC(=O)C(Cc1ccccc1)NC(=O)C(Cc1ccccc1)NC(=O)CNC(=O)C(CCCNC(=N)N)NC(=O)C(CCC(=O)O)NC(=O)CNC(=O)C1CSSCC(C(=O)NC(CC(N)=O)C(=O)O)NC(=O)C(Cc2ccc(O)cc2)NC(=O)C(CC(N)=O)NC(=O)C(CCC(=O)O)NC(=O)C(CC(C)C)NC(=O)C(CCC(N)=O)NC(=O)C(Cc2ccc(O)cc2)NC(=O)C(CC(C)C)NC(=O)C(CO)NC(=O)C2CSSCC(NC(=O)C(CCC(N)=O)NC(=O)C(CCC(=O)O)NC(=O)C(NC(=O)C(NC(=O)CN)C(C)CC)C(C)C)C(=O)NC(CSSCC(NC(=O)C(CC(C)C)NC(=O)C(Cc3c[nH]cn3)NC(=O)C(CCC(N)=O)NC(=O)C(CC(N)=O)NC(=O)C(NC(=O)C(N)Cc3ccccc3)C(C)C)C(=O)NCC(=O)NC(CO)C(=O)NC(Cc3c[nH]cn3)C(=O)NC(CC(C)C)C(=O)NC(C(C)C)C(=O)NC(CCC(=O)O)C(=O)NC(C)C(=O)NC(CC(C)C)C(=O)NC(Cc3ccc(O)cc3)C(=O)NC(CC(C)C)C(=O)NC(C(C)C)C(=O)N1)C(=O)NC(C(C)O)C(=O)NC(CO)C(=O)NC(C(C)CC)C(=O)N2)C(C)O)C(=O)O |