TPM003
TPM003 (TG062) is a triple agonist of GLP-1R, GIPR and GCGR, with EC50 values of 33.9, 12.5 and 92.9 pM, respectively. TPM003 suppresses appetite, regulates blood glucose, enhances insulin sensitivity, reduces gastrointestinal intolerance, promotes hepatic lipid mobilization and increases energy expenditure. TPM003 induces weight loss, improves metabolic parameters, reverses hepatic steatosis and optimizes liver function markers. TPM003 is applicable for research on obesity and non-alcoholic steatohepatitis.
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- Formule: C238H370FN51O73S2
- Masse moléculaire:5196.91
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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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Activité biologique
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Chemical Information
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Activité biologique
Description
Parmacokinetics
| Species | Dose | Route | T1/2 | AUC0-inf | AUC0-t | Cmax | Tmax | F |
|---|---|---|---|---|---|---|---|---|
| Rat[1] | 1.0 mg/kg | i.v. | 21.5 h | 289.2 μg·h/mL | 265.3 μg·h/mL | / | / | / |
| Rat[1] | 3.0 mg/kg | s.c. | 26.4 h | 570.3 μg·h/mL | 410.5 μg·h/mL | 8.2 μg/mL | 24 h | 50.9 % |
| Cynomolgus Monkey[1] | 0.2 mg/kg | i.v. | 83.3 h | 302.1 μg·h/mL | 277.6 μg·h/mL | / | / | / |
| Cynomolgus Monkey[1] | 0.2 mg/kg | s.c. | 97.2 h | 228.9 μg·h/mL | 199.0 μg·h/mL | 1.8 μg/mL | 18 h | 75.7 % |
| Pig[1] | 0.16 mg/kg | i.v. | 101.9 h | 142.9 μg·h/mL | 140.8 μg·h/mL | / | / | / |
| Pig[1] | 0.16 mg/kg | s.c. | 129.0 h | 174.9 μg·h/mL | 170.4 μg·h/mL | 1.0 μg/mL | 32 h | 122.4 % |
In Vivo
TPM003 (10 nmol/kg; s.c.; single administration) exerts a sustained maximal weight loss effect in high-fat diet-induced obese male C57BL/6J mice[1].
TPM003 (10 nmol/kg; s.c.; once every 3 days for 21 days) induces a 30% reduction in body weight, potent suppression of food intake, and enhanced hepatic lipid clearance in high-fat diet-induced obese male C57BL/6J mice[1].
TPM003 (10 nmol/kg; s.c.; once daily or once every three days for 8 weeks) induces significant body weight loss and antifibrotic effects in mice induced by high-fat diet and CCl4[1].
TPM003 (1.0-3.0 mg/kg; s.c.; twice weekly for 4 weeks) induces reversible transient reductions in food intake and body weight in both male and female SD rats, with no serious adverse reactions[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, 8−10 weeks old)[1]
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Dosage:3 nmol/kg; 10 nmol/kg; 30 nmol/kg
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Administration:s.c.; single dose
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Result:Induced dose-dependent reductions in body weight, cumulative food intake, and fed blood glucose levels, with maximal effects within 96 hours post dosing.
Sustained body weight reduction effects until day 4 at 30 nmol/kg, when values returned to baseline.
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Animal Model:C57BL/6J (male, high-fat diet-induced obesity)[1]
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Dosage:10 nmol/kg
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Administration:s.c.; single dose
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Result:Induced pronounced reductions in body weight, cumulative food intake, and blood glucose levels within 1−3 days post injection.
Produced a greater maximal weight reduction than retatrutide, with effects sustained without early rebound (unlike tirzepatide, which showed rebound starting at day 4).
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Animal Model:C57BL/6J (male, high-fat diet-induced obesity)[1]
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Dosage:10 nmol/kg
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Administration:s.c.; every 3 days; 21 days
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Result:Achieved approximately 30% body weight reduction over the 21-day treatment period, with cumulative food intake suppressed to levels lower than tirzepatide-treated mice.
Reduced fasting blood glucose, plasma insulin, plasma alanine aminotransferase (ALT), blood triglycerides (TG), blood total cholesterol (TC), liver TG, and liver TC to levels approaching lean control values.
Showed the most substantial clearance of hepatic lipid droplets compared to retatrutide and tirzepatide via Oil Red O staining.
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Animal Model:C57BL/6J (male, high-fat diet + carbon tetrachloride-induced NASH)[1]
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Dosage:10 nmol/kg
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Administration:s.c.; daily; 8 weeks
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Result:Produced a greater reduction in body weight compared to tirzepatide, reduced liver weight to levels approaching lean control values, and significantly decreased hepatic collagen deposition via Masson’s trichrome staining.
Induced significant reductions in key fibrosis markers: α-smooth muscle actin (α-SMA), fibronectin, and collagen type-I α-1 chain (COL1A1), with a significantly greater reduction in α-SMA expression compared to tirzepatide.
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Animal Model:C57BL/6J (male, Gubra Amylin NASH diet-induced NASH)[1]
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Dosage:10 nmol/kg
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Administration:s.c.; every 3 days; 8 weeks
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Result:Induced progressive, sustained body weight loss throughout the 8-week period (with no rebound, unlike retatrutide which showed partial rebound after week 3).
Significantly reduced the NAFLD Activity Score (NAS) compared to both retatrutide and tirzepatide, particularly in steatosis and hepatocellular ballooning components.
Reduced hepatic collagen deposition, COL1A1, and α-SMA expression, indicating robust suppression of hepatic fibrosis and inflammation.
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Animal Model:Sprague-Dawley (male, female, 8−10 weeks old)[1]
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Dosage:1.0 mg/kg; 3.0 mg/kg
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Administration:s.c.; twice weekly; 4 weeks
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Result:Induced transient reductions in food intake and body weight, with occasional emesis and mild diarrhea in a subset of animals; all effects were reversible upon treatment cessation.
No mortality, severe adverse events, overt serum biochemical pathological changes, or abnormal histological findings in key organs (thymus, spleen, mesenteric lymph nodes) were observed.
Chemical Information
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Masse moléculaire 5196.91
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Formule C238H370FN51O73S2
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SMILES
O=C([C@@H](N)CC1=CC=C(C=C1)O)NC(C)(C(N[C@H](C(NCC(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@@](CC)(C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(NC(C)(C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(NCC(NCC(N2CCC[C@H]2C(N[C@@H](CO)C(N[C@@H](CO)C(NCC(N[C@@H](C)C(N3CCC[C@H]3C(N4CCC[C@H]4C(N5CCC[C@H]5C(N[C@@H](CO)C(N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)CSC6)=O)CC(C)C)=O)CC(C)C)=O)CC7=CC=C(O)C=C7)=O)CCC(O)=O)=O)[C@H](CC)C)=O)CC8=CC=CC=C8)=O)CSCC(NCCN(C(CCC(NCCOCCOCC(NCCOCCOCC(NCCCC[C@@H](NC(CCCCCCCCCCCCCCCCCCC(O)=O)=O)C(O)=O)=O)=O)=O)=O)CCNC6=O)=O)=O)C)=O)CCC(N)=O)=O)C)=O)CCCCNC(C)=O)=O)CCCCN)=O)CC(O)=O)=O)CC(C)C)=O)C)=O)[C@H](CC)C)=O)CO)=O)CC9=CC=C(O)C=C9)=O)CC(O)=O)=O)CO)=O)[C@@H](C)O)=O)CC%10=C(C=CC=C%10)F)=O)[C@@H](C)O)=O)=O)CCC(N)=O)=O)C
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Synonyms
TG062
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
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Liver Histomorphometry
Liver histomorphometry is a quantitative histological approach used to measure structural alterations in hepatic tissue, including parenchymal loss, steatosis, fibrosis, and vascular remodeling, by combining stained tissue section analysis with stereological or computerized image-based measurements. Classical morphometric frameworks quantify volume fractions of liver compartments and fibrotic regions using systematic sampling and image analysis, enabling objective comparison of pathological changes across experimental groups. These approaches are widely applied in liver cirrhosis and fibrosis studies to reduce subjectivity in histological scoring and improve reproducibility of tissue evaluation. Recent methodological advances integrate automated image analysis and radiomics-based extraction of histological features from standard liver stains (e. g. , H&E and fibrotic stains), enabling quantitative correlation between morphometric features and fibrosis stages in non-alcoholic fatty live
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
TPM003 Related Classifications
HY-181709 Related Classifications
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