Deziglipel
Based on 1 Customer Validation
Deziglipel (MKP10241) is an orally active GPR119 agonist (human EC50: 3.7 nM; IC50 > 7.2 μM). Deziglipel activates GPR119 to increase cAMP levels, promotes active GLP-1 release, reduces blood glucose and HbA1c, decreases body weight and feed intake, and resolves MASH via altered lipid, cytokine, and liver enzyme levels. Deziglipel shows low hERG channel inhibition, minimal CYP450 inhibition, no PXR activation, and no significant transporter inhibition. Deziglipel can be used for the research of type 2 diabetes mellitus, obesity, MASH/MASLD, and metabolic disorders.
Para uso exclusivo en investigación. No vendemos a pacientes.
- Pureza : 98.06%
- No. CAS: 2137977-29-6
- Fòrmula: C24H27FN6O3S2
- Peso molecular:530.64
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Almacenamiento:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Actividad biológica
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Chemical Information
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Solvente y solubilidad
- Protocolo
- Pureza y Documentación
- Referencias
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Help & FAQs
Actividad biológica
Descripciòn
In Vitro
Deziglipel (MKP10241) (0.3-1 μM; 1 h) enhances glucose-stimulated insulin secretion in HIT-T15 cells, with significant increases observed at 0.3 μM and 1 μM concentrations after 1 h incubation[1].
Deziglipel (3.7 nM; 1 h) potently activates GPR119 in CHO-hGPR119 cells, with an EC50 of 3.7 nM and a maximum efficacy of 74.1%[1].
Deziglipel (> 30 μM) exhibits minimal hERG channel inhibition, with an IC50 > 30 μM, indicating low potential for cardiotoxicity[1].
Deziglipel (> 7.2 μM) does not inhibit major CYP450 enzymes, with IC50 values > 7.2 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | AUC0-last | Tmax | Bioavailability | T1/2 | CL | Vss | Cmax |
|---|---|---|---|---|---|---|---|---|---|
| Mice[1] | 2 mg/kg | i.v. | / | / | / | 5.31 h | 5.71 mL/min/kg | 1.38 L/kg | / |
| Mice[1] | 10 mg/kg | p.o. | 14738.22 ng/mL·h | 0.50 h | 58 % | 5.3 h | / | / | 3700 ng/mL |
| Rat[1] | 2 mg/kg | i.v. | / | / | / | 11.95 h | 5.76 mL/min/kg | 3.96 L/kg | / |
| Rat[1] | 10 mg/kg | p.o. | 11722.5 ng/mL·h | 0.42 h | 46 % | / | / | / | / |
| Dog[1] | 2 mg/kg | i.v. | / | / | / | 20.72 h | 4.50 mL/min/kg | 6.62 L/kg | / |
| Dog[1] | 10 mg/kg | p.o. | 35300 ng/mL·h | 3.00 h | 60 % | / | / | / | / |
In Vivo
Deziglipel (51.25-102.45 mg/kg; p.o.; once daily for 56 days) reduces body weight, feed intake, lipid levels, and fat/liver weights in male DIO mice, with 102.45 mg/kg producing maximum body weight reduction and 35% feed intake reduction[1].
Deziglipel (30 mg/kg; p.o.; once daily for 112 days) improves glycemic control, reduces liver injury and inflammation markers, and lowers the NAFLD Activity Score in male STAM mice with MASH[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:db/db (male, 8-10 weeks of age)[1]
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Dosage:10 mg/kg; 30 mg/kg
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Administration:p.o.; once daily for 21 days
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Result:Produced glucose AUC reductions of 25% on day 1 and 38% on day 22 at 10 mg/kg relative to vehicle control.
Produced 12% reduction in FPG and 2.6% reduction in HbA1c after 21 days at 10 mg/kg relative to vehicle control.
Produced glucose AUC reductions of 31% on day 1 and 28% on day 22 at 30 mg/kg relative to vehicle control.
Produced 20% reduction in FPG and 3.0% reduction in HbA1c after 21 days at 30 mg/kg relative to vehicle control.
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Animal Model:C57BL/6J diet-induced obese (DIO) (male, 17-18 weeks of age, 11-12 weeks on high-fat diet)[1]
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Dosage:51.25 mg/kg; 102.45 mg/kg
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Administration:p.o.; once daily for 56 days
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Result:Inhibited body weight gain from day 1, reduced feed intake, decreased total cholesterol, LDL cholesterol, epididymal fat weight, subcutaneous fat pad weight, and liver weight, and increased plasma leptin levels at 51.25 mg/kg relative to vehicle control.
Produced significant body weight loss starting on day 10 (maximum reduction on day 14), prevented further weight gain throughout the study, reduced feed intake by a maximum of 35%, decreased total cholesterol, LDL cholesterol, epididymal fat weight, subcutaneous fat pad weight, and liver weight, and increased plasma leptin levels at 102.45 mg/kg relative to vehicle control.
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Animal Model:C57BL/6J STAM (male, metabolic dysfunction-associated steatohepatitis model)[1]
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Dosage:30 mg/kg
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Administration:p.o.; once daily for 112 days
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Result:Significantly reduced fasting blood glucose, plasma ALT levels, plasma TNF-α levels, plasma cholesterol levels, and plasma LDL levels relative to disease control.
Significantly reduced liver steatosis, inflammation, fibrosis, and the NAFLD Activity Score relative to disease control.
Ensayo clínico
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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No. CAS 2137977-29-6
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Appearance Solid
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Peso molecular 530.64
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Fòrmula C24H27FN6O3S2
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Color White to off-white
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SMILES
C[C@@H](C1CCN(CC1)C2=NC=C(C=N2)CC)OC(S3)=NN4C3=NC(C5=CC=C(C=C5F)S(C)(=O)=O)=C4
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Synonyms
MKP10241
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Solvente y solubilidad
In Vitro:
DMSO : 25 mg/mL (47.11 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Protocolo
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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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
Pureza y Documentación
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Ficha de datos (280 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Instrucciones de manejo (2659 KB)
Referencias
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 1.8845 mL | 9.4226 mL | 18.8452 mL | 47.1129 mL |
| 5 mM | 0.3769 mL | 1.8845 mL | 3.7690 mL | 9.4226 mL | |
| 10 mM | 0.1885 mL | 0.9423 mL | 1.8845 mL | 4.7113 mL | |
| 15 mM | 0.1256 mL | 0.6282 mL | 1.2563 mL | 3.1409 mL | |
| 20 mM | 0.0942 mL | 0.4711 mL | 0.9423 mL | 2.3556 mL | |
| 25 mM | 0.0754 mL | 0.3769 mL | 0.7538 mL | 1.8845 mL | |
| 30 mM | 0.0628 mL | 0.3141 mL | 0.6282 mL | 1.5704 mL | |
| 40 mM | 0.0471 mL | 0.2356 mL | 0.4711 mL | 1.1778 mL |
Deziglipel Related Classifications
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