Tirzepatide sodium
Based on 1 Customer Validation
Tirzepatide sodium (LY3298176 sodium) is a dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist. Tirzepatide sodium exerts anti-apoptotic and pro-differentiation effects via the pAkt/CREB/BDNF cascade and miRNA in neurons; in the heart, it promotes BCAA catabolism and inhibits the mTOR pathway by mediating the dephosphorylation of BCKDHA; meanwhile, it effectively reduces insulin and leptin levels and suppresses inflammatory responses at the systemic level. Tirzepatide sodium can be used for research on myocardial infarction, colon cancer, diabetes, diabetic cognitive impairment, neurodegeneration, diabetes-related neuropathy, and obesity.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C225H348N48O68.xNa
- Molecular Weight:4813.45 (free base)
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Speicherung:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
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Lösungsmittel & Löslichkeit
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
Biologische Aktivität
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GLP-1 |
mTOR |
Tirzepatide (LY3298176) (0.2 μM; 7 days) sodium has no effect on the proliferation of human neuroblastoma SHSY5Y cells exposed to normoglycemic or hyperglycemic conditions, and upregulates the expression of nerve growth markers, differentiation markers, and glucose transporters[2].
Tirzepatide (0.2 μM; 7 days) sodium reverses high glucose-induced apoptosis and significantly reduces the BAX/Bcl-2 protein ratio in SH-SY5Y cells[2].
Tirzepatide (35-100 nM; 96 h) sodium exerts no direct effect on the proliferation of MC38 mouse colon cancer cells in vitro[3].
Tirzepatide sodium binds to BCKDHA, a key enzyme in branched-chain amino acid (BCAA) catabolism[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human neuroblastoma SHSY5Y cells (exposed to normal glucose (25 mM) or high glucose (150 mM))
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Concentration:0.2 μM
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Incubation Time:7 days
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Result:Did not alter Ki-67 median fluorescence compared to untreated high glucose cells.
Had no significant effect on Ki-67 median fluorescence in normal glucose-exposed cells.
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Cell Line:human neuroblastoma SHSY5Y cells (exposed to normal glucose (25 mM) or high glucose (150 mM))
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Concentration:0.2 μM
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Incubation Time:7 days
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Result:Increased p-Akt protein levels (and p-Akt/AKT ratio), MAP2 protein levels, GAP43 protein level, and AGBL4 protein levels in normal glucose-exposed cells.
Prevented the high glucose-induced downregulation of p-Akt, MAP2, and GAP43 protein levels.
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Cell Line:human neuroblastoma SHSY5Y cells (exposed to normal glucose (25 mM) or high glucose (150 mM))
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Concentration:0.2 μM
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Incubation Time:7 days
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Result:Decreased miR-34a expression and increased miR-212 and miR-29c expression in normal glucose-exposed cells.
Reversed the high glucose-induced increase in miR-34a expression and reversed the high glucose-induced decrease in miR-212 and miR-29c expression in high glucose-exposed cells.
prevented the high glucose-induced downregulation of MAP2 and GAP43 mRNA expression in high glucose-exposed cells.
Did not affect AGBL4 mRNA or protein levels in high glucose-exposed cells.
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Cell Line:MC38 murine colorectal cancer cells
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Concentration:35, 70, 100 nM
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Incubation Time:96 h
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Result:Did not significantly alter proliferation rate of MC38 cells after 96 hours of incubation, as measured by cell number counts.
Tirzepatide sodium (1.35 mg/kg; i.p.; once weekly; for 15 weeks) induces mild metabolic and molecular changes in healthy rats without impairing spatial learning or memory abilities[1].
Tirzepatide sodium (10 nM/kg; s.c.; once daily; for 28 days) significantly reduces body weight, food intake, serum insulin and leptin levels, and indirectly inhibits tumor growth in a diet-induced obese (DIO) MC38 colon cancer mouse model[3].
Tirzepatide sodium (10 nM/kg; s.c.; once daily; for 14 days) significantly reduces body weight, food intake, serum insulin and leptin levels in diet-induced obese mouse models[3].
Tirzepatide (10 nM/kg/day; i.p.; once daily; for 14 consecutive days) exerts protective effects in a mouse model of myocardial infarction (MI) induced by coronary artery ligation, including reducing mortality, decreasing myocardial infarction size, promoting branched-chain amino acid (BCAA) catabolism, and facilitating early fibrotic repair[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague Dawley (male, 7-8 weeks old, 180-200 g, high-fat diet + streptozotocin injection)[1]
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Dosage:1.35 mg/kg
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Administration:i.p.; once weekly; 8 weeks
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Result:Significantly reduced fasting blood glucose and insulin levels.
Shortened escape latency and increased time spent in the target quadrant in the Morris water maze.
Decreased Aβ40 production and neuronal loss in the hippocampus.
Inhibited the mRNA expression of TNF-α, IL-6, IL-1β, and the phosphorylation of NF-κB.
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Animal Model:Sprague Dawley (male, 7-8 weeks old, 180-200 g, normal diet-fed)[1]
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Dosage:1.35 mg/kg
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Administration:i.p.; once weekly; 8 weeks
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Result:Induced a slight reduction in fasting blood glucose levels.
Slightly increased body weight.
Did not alter swimming speed in Morris water maze testing.
Caused minor reductions in hippocampal APP and BACE1 levels.
Had no significant effect on hippocampal Aβ40 levels or neuron density.
Slightly increased hippocampal PSD95 and SYT1 expression.
Increased density of stubby, mushroom-like, long, and filopodia-like dendritic spines.
Slightly reduced hippocampal mRNA levels of TNF-α, IL-6, and IL-1β.
Decreased phosphorylated NF-κB-positive cell percentage and phosphorylated IKKα levels.
Increased hippocampal p-IRS-1-S307, p-PI3K, p-AKT, p-GSK3β, and GSK3β levels.
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Animal Model:C57BL/6 (male; diet-induced obesity via high-fat diet feeding)[3]
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Dosage:10 nM/kg
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Administration:s.c.; once daily; 14 days
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Result:Reduced body weight relative to vehicle controls.
Reduced circulating glucose, insulin, leptin, and c-peptide levels in both fed and fasted states.
Eliminated the positive correlation between body weight and serum insulin levels seen in vehicle-treated controls.
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Animal Model:C57BL/6 (male; diet-induced obesity via high-fat diet feeding; subcutaneous allograft of MC38 colon cancer cells)[3]
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Dosage:10 nM/kg
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Administration:s.c.; once daily; 28 days
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Result:Caused a significant decrease in food intake and body weight.
Lowered glucose, insulin, leptin, and c-peptide levels in both fed and fasted states.
Significantly reduced MC38 tumor volume compared to the control group.
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Animal Model:C57BL/6J wild-type (12-week-old male/female; myocardial infarction model via permanent left descending coronary artery ligation or concurrent low-BCAA diet intervention)[4]
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Dosage:10 nM/kg/day
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Administration:i.p.; once daily; 14 days (starting day 1 post-MI)
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Result:Significantly improved long-term survival and reduced the incidence of cardiac rupture.
Decreased myocardial infarct size and improved left ventricular systolic function (increased LVEF).
Bound to BCKDHA and reduced its S293 phosphorylation, enhancing enzyme activity to promote cardiac BCAA catabolism and inhibit abnormal mTOR pathway activation.
Chemical Information
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Appearance Solid
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Molecular Weight 4813.45 (free base)
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Formel C225H348N48O68.xNa
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Synonyms
LY3298176 sodium
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Sequence
Tyr-{Aib}-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Tyr-Ser-Ile-{Aib}-Leu-Asp-Lys-Ile-Ala-Gln-{C20 diacid-gamma-Glu-(AEEA)2-Lys}-Ala-Phe-Val-Gln-Trp-Leu-Ile-Ala-Gly-Gly-Pro-Ser-Ser-Gly-Ala-Pro-Pro-Pro-Ser-NH2
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Sequence Shortening
Y-{Aib}-EGTFTSDYSI-{Aib}-LDKIAQ-{C20 diacid-gamma-Glu-(AEEA)2-Lys}-AFVQWLIAGGPSSGAPPPS-NH2
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Lösungsmittel & Löslichkeit
H2O : 50 mg/mL (Need ultrasonic)
Reinheit & Dokumentation
Verweise
[1]. Guo X, et al. Tirzepatide ameliorates spatial learning and memory impairment through modulation of aberrant insulin resistance and inflammation response in diabetic rats. Frontiers in pharmacology. 2023;14:1146960. [Content Brief]
[2]. Fontanella RA, et al. Tirzepatide prevents neurodegeneration through multiple molecular pathways. Journal of translational medicine. 2024 Jan 29;22(1):114. [Content Brief]
[4]. Chen M, et al. Glucose-dependent insulinotropic polypeptide/glucagon-like peptide 1 receptor agonist tirzepatide promotes branched chain amino acid catabolism to prevent myocardial infarction in non-diabetic mice. Cardiovascular research. 2025 Apr 29;121(3):454-467. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Tirzepatide sodium Related Classifications
HY-P1731C Related Classifications
Powered by Bioz
- Tirzepatide
- LY3298176
- LY 3298176
- LY-3298176
- GLP Receptor
- Insulin Receptor
- Apoptosis
- mTOR
- MC38 murine colorectal cancer cells
- GIPR
- BCKDHA
- mTOR signaling pathway
- glucagon-like peptide 1 receptor
- glucose-dependent insulinotropic polypeptide receptor
- branched-chain keto acid dehydrogenase E1 subunit α
- GLP-1R
- myocardial infarction
- SHSY5Y human neuroblastoma cells
- Inhibitor
- inhibitor
- inhibit