DeDPP4
DeDPP4 is a DPP-4 PROTAC degrader. DeDPP4 induces sustained elevation of glucagon-like peptide-1 (GLP-1), enhances glucose tolerance, causes persistent reduction of blood glucose, and achieves long-term blood glucose regulation in animal models of type 2 diabetes. DeDPP4 mediates dose-dependent DPP-4 depletion in cancer cells, and also targets and degrades DPP-4 in the liver and adipose tissues of animal models with type 2 diabetes. DeDPP4 can be used for the research of type 2 diabetes and non-small cell lung cancer.
(Pink: DPP-4 ligand (HY-A0023A); Blue: Cereblon ligand (HY-W763812); Black: linker (HY-W067489)).
For research use only. We do not sell to patients.
- Formula: C36H38N8O8
- Molecular Weight:710.74
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Storage:
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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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
All PROTACs Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
Cereblon |
DPP-4 |
In Vitro
DeDPP4 (10 μg/mL; 4 h) can be internalized into A549 cells via the endocytic pathway, and intracellular fluorescence is detectable after incubation at 10 μg/mL for 4 h[1].
DeDPP4 (0-1250 nM, 24-48 h) induces dose- and time-dependent degradation of DPP-4 in A549 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:A549 human nonsmall cell lung cancer cells
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Concentration:0, 5, 25, 125, 625, 1250 nM (24 h incubation); 0, 1, 2, 3, 5, 10 μM (24 h incubation); 500 nM (4-48 h incubation); 2 μM (1-48 h incubation)
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Incubation Time:24 h (5-1250 nM, 1-10 μM); 4-48 h (500 nM); 1-48 h (2 μM)
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Result:Induced dose-dependent DPP-4 degradation in A549 cells, with pronounced efficacy at concentrations above 625 nM;
Showed a slight hook effect at 1-10 μM.
Induced time-dependent degradation, with increasing efficiency over 48 h at both 500 nM and 2 μM, consistent with PROTAC-mediated degradation kinetics.
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Cell Line:A549 human nonsmall cell lung cancer cells
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Concentration:500 nM
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Incubation Time:24 h
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Result:Caused a marked decrease in red DPP-4 fluorescence intensity in treated cells compared to the control group.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:leptin receptor-deficient (db/db) (10-week-old, male)[1]
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Dosage:5 mg/kg (4-week study); 10 mg/kg (single-dose efficacy study; 4-week study)
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Administration:i.v.; every 2 days; 4 weeks (5 mg/kg, 10 mg/kg 4-week study); i.v.; single dose (10 mg/kg efficacy longevity study)
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Result:Maintained reduced blood glucose levels for over 60 h, with sustained hypoglycemia observed for up to 48 h (10 mg/kg single dose).
Reduced fasting blood glucose levels more effectively than 5 mg/kg DeDPP4, and lowered hemoglobin A1c (HbA1c) levels to ~7% after 4 weeks of treatment (10 mg/kg).
Reduced blood glucose to 10.6 mmol/L within 60 min during OGTT, with a significantly lower area under the blood glucose curve (AUC) than the model group (10 mg/kg).
Reduced the homeostasis model assessment of insulin resistance (HOMA-IR) more effectively than alogliptin, and preserved pancreatic β-cell function (HOMA-β) (10 mg/kg).
Significantly increased serum glucagon-like peptide-1 (GLP-1) levels compared to alogliptin (10 mg/kg).
Reduced serum levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and free fatty acids (FFA) more effectively than 5 mg/kg DeDPP4 or alogliptin, while increasing high-density lipoprotein cholesterol (HDL-C) (10 mg/kg).
Significantly reduced serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and creatinine (CREA) levels (10 mg/kg).
Preserved pancreatic islet morphology with increased β-cell mass and reduced α/β cell ratio (10 mg/kg).
Induced a greater reduction in hepatic DPP-4 protein levels than 5 mg/kg DeDPP4 (10 mg/kg).
Chemical Information
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Molecular Weight 710.74
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Formula C36H38N8O8
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SMILES
O=C(N[C@H]1CN(C(N2CC3=CC=CC=C3C#N)=CC(N(C2=O)C)=O)CCC1)CCOCCNC4=CC=CC(C5=O)=C4C(N5[C@@H](CC6)C(NC6=O)=O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
DeDPP4 Related Classifications
HY-182336 Related Classifications
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