Derrisaponin A
Derrisaponin A is an oleanane-type triterpenoid saponin and sweetener found in the stems of Derris eriocarpa, with sweetness intensity approximately 80 times that of Sucrose (HY-B1779) at 1% concentration. Derrisaponin A shows no acute toxic activity. Derrisaponin A can be used for research on hypertension, hyperglycemia, and obesity.
For research use only. We do not sell to patients.
- CAS No.: 1965272-21-2
- Formula: C56H88O26
- Molecular Weight:1177.28
-
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]
-
Biological Activity
-
Chemical Information
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
Biological Activity
Description
In Vitro
Derrisaponin A (Compound 2) (2 mg; 2 h) produces D-glucuronic acid (HY-N6612), D-galactose (HY-N0210), L-rhamnose (HY-N1420), and D-glucose (HY-B0389) upon acid hydrolysis[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:ICR mice (male and female, 3-4 weeks old, specific pathogen-free)[1]
-
Dosage:400 mg/kg bw
-
Administration:i.v.; single injection
-
Result:Observed transient diaphragm spasm in one mouse that resolved within 10 minutes post-injection.
Detected no other treatment-related clinical signs of toxicity, mortality, or gross pathological changes to internal organs over the 14-day observation period.
Determined the maximum tolerated dose (MTD) to be 400 mg/kg bw.
Chemical Information
-
CAS No. 1965272-21-2
-
Molecular Weight 1177.28
-
Formula C56H88O26
-
SMILES
C[C@]12[C@]3(C([C@@]4([H])[C@@](CC3)([C@@H](C[C@@](C)(C4)C(O)=O)OC(C)=O)C)=CC[C@]1([H])[C@@]5([C@@]([C@](C)([C@H](CC5)O[C@H]6[C@@H]([C@H]([C@@H]([C@H](O6)C(O)=O)O)O)O[C@H]7[C@@H]([C@H]([C@H]([C@H](O7)CO)O)O[C@@H]8O[C@@H]([C@H]([C@@H]([C@H]8O)O)O)CO)O[C@H]9[C@@H]([C@@H]([C@H]([C@@H](O9)C)O)O)O)CO)([H])CC2)C)C
-
Structure Classification
-
Initial Source
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
-
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)
Derrisaponin A Related Classifications
HY-N19794 Related Classifications
Powered by Bioz