2. Cell Cycle/DNA Damage Vitamin D Related/Nuclear Receptor Metabolic Enzyme/Protease GPCR/G Protein Stem Cell/Wnt MAPK/ERK Pathway
  3. PPAR Bombesin Receptor ERK
  4. DSO-5a

DSO-5a is a potent, selective, orally active BB3 agonist. DSO-5a is a representative DMAKO-00 derivative compound. DSO-5a upregulates ppar-γ activity through BB3 and activates ERK1/2 phosphorylation. DSO-5a can be used in diabetes-related research.

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DSO-5a Chemical Structure

DSO-5a Chemical Structure

CAS No. : 2195411-63-1

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DSO-5a Related Antibodies

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PPARα PPARβ/δ PPARγ PPAR PPARδ

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ERK ERK1 ERK2 ERK5 ERK8

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Description

DSO-5a is a potent, selective, orally active BB3 agonist. DSO-5a is a representative DMAKO-00 derivative compound. DSO-5a upregulates ppar-γ activity through BB3 and activates ERK1/2 phosphorylation. DSO-5a can be used in diabetes-related research[1].

IC50 & Target[1]

PPARγ

 

In Vitro

DSO-5a (50 nM; 60min) induces IP-1 accumulation in hBB3-HEK cells with a pEC50 of 8.485 and a strong calcium response with a pEC50 of 7.964[1].
DSO-5a (500 nM; 60min) induces IP-1 accumulation in mBB3-HEK cells with a pEC50 of 7.262 and a strong calcium response with a pEC50 of 7.174[1].
DSO-5a (0-100 nM; 8min) causes a dose-dependent activation of ERK1/2 in hBB3-H1299 and mBB3-HEK cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

DSO-5a Related Antibodies

Western Blot Analysis[1]

Cell Line: hBB3-H1299 cells
Concentration: 0, 1,10,100 nM
Incubation Time: 8 min
Result: Caused a dose-dependent activation of ERK1/2 in hBB3-H1299 cells, which was completely blocked by Bantag-1.
In Vivo

DSO-5a (3-30 mg/kg; P.O.; 30 min) reduces blood glucose excursions in a dose-dependent manner in C57BL/6 mice[1].
DSO-5a (10 mg/kg/day; P.O.; 2-4 weeks) reduces the blood glucose concentration of diabetic db/db mice[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 mice[1]
Dosage: 3 mg/kg; 10 mg/kg; 30 mg/kg
Administration: Oral administration;30 min before glucose challenge (3 g/kg)
Result: Showed that the change rates of AUC at 3, 10 and 30 mg/kg were 5.03, 16.42 and 28.30%, respectively.
In BB3 knockout mice, DSO-5a failed to inhibit blood glucose drift.
Animal Model: Diabetic db/db mice[1]
Dosage: 10 mg/kg/day
Administration: Oral administration; 2-4 weeks
Result: After two weeks of treatment, the blood glucose excursion of db/db mice was significantly reduced.
After four weeks, fasting blood glucose levels, glycosylated serum protein (GSP), and HOMA-IR were significantly decreased in the DSO-5a treatment group.
Increased the protein expression of PPAR-gamma in white adipose tissue of db/db mice.
Molecular Weight

440.45

Formula

C23H24N2O7
CAS No.
SMILES

C=CC(C)(C(C(C=C1OC)=C(C2=C1/C(C=C/C2=N\O)=N/O)OC)OC(C3=CC=CO3)=O)C
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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DSO-5a Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

DSO-5a2195411-63-1PPARBombesin ReceptorERKPeroxisome proliferator-activated receptorsExtracellular signal regulated kinasesH1299 cellsC57BL/6 micediabetesHEK cellsDiabetic db/db miceInhibitorinhibitorinhibit

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