Anagliptin

SKU: orb1300040

Description

Anagliptin (SK-0403) is a highly potent and selective dipeptidyl peptidase-4 (DPP-4) inhibitor with an IC50 of 3.8 nM. It is a research compound used to study mechanisms and therapeutic potential for type 2 diabetes in both in vitro enzymatic assays and in vivo animal models.

Research Area

Protein Biochemistry

Key Properties

• CAS Number: 739366-20-2
• MW: 383.45
• Purity: >99.99% (May vary between batches)
• Formula: C₁₉H₂₅N₇O₂
• SMILES: Cc1cc2ncc(cn2n1)C(=O)NCC(C)(C)NCC(=O)N1CCC[C@H]1C#N
• Target: DPP-4,Proteasome
• Solubility: DMSO:50 mg/mL (130.4 mM);10% DMSO+40% PEG300+5% Tween 80+45% Saline:2 mg/mL (5.22 mM)

Bioactivity

• Target IC50:
  DPP8:68 nM |DPP9:60 nM|DPP4:3.8 nM
• In Vivo:
  Treatment with anagliptin for 16 wk significantly reduced accumulation of monocytes and macrophages in the vascular wall, SMC content in plaque areas, and oil red O-stained area around the aortic valve without affecting glucose tolerance or body weight. Serum DPP-4 concentrations were significantly higher in apoE-deficient mice than control mice, and the levels increased with aging, suggesting the involvement of DPP-4 in the progression of atherosclerosis. Anagliptin treatment significantly decreased the plasma total cholesterol (14% reduction, P < 0.01) and triglyceride levels (27% reduction, P < 0.01). Both low-density lipoprotein cholesterol and very low-density lipoprotein cholesterol were also decreased significantly by anagliptin treatment. Sterol regulatory element-binding protein-2 messenger ribonucleic acid expression level was significantly decreased at night in anagliptin-treated mice (15% reduction, P < 0.05). Anagliptin significantly suppressed sterol regulatory element-binding protein activity in HepG2 cells (21% decrease, P < 0.001).
• In Vitro:
  Soluble DPP-4 augmented cultured SMC proliferation, and anagliptin suppressed the proliferation by inhibiting ERK phosphorylation. In THP-1 cells, anagliptin reduced lipopolysaccharide-induced TNF-α production with inhibiting ERK phosphorylation and nuclear translocation of nuclear factor-κB. Quantitative analysis also showed that anagliptin reduced the area of atherosclerotic lesion in apoE-deficient mice.
• Animal Research:
  Male low-density lipoprotein receptor-deficient mice were administered 0.3% anagliptin in their diet. Plasma lipid levels were assayed and lipoprotein profile was analyzed using high-performance liquid chromatography. Hepatic gene expression was examined by deoxyribonucleic acid microarray and quantitative polymerase chain reaction analyses.

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Dipeptidyl Peptidase, DPP-4, DPP-8, DPP-9, DPP4, DPP, Anagliptin, atherosclerosis, Inhibitor, inhibit, lipid‐lowering, SK 0403, SK0403, SK-0403, smooth muscle cell, SMC

Compound Identifiers

PubChem CID

44513473