Aliskiren-d6-1 hemifumarate
Aliskiren-d6-1 hemifumarate (CGP 60536-d6-1 hemifumarate) is the deuterium labeled Aliskiren hemifumarate (HY-12177). Aliskiren is an orally active, highly potent and selective renin inhibitor, with IC50 of 1.5 nM. Aliskiren can be used for the research of hypertension, cardiovascular diseases and cancer cachexia.
For research use only. We do not sell to patients.
- Formula: C34H51D6N3O10
- Molecular Weight:673.87
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
-
Unlabeled CAS 173334-57-1
-
Molecular Weight 673.87
-
Formula C34H51D6N3O10
-
SMILES
CC(C)[C@@H](CC1=CC=C(OC)C(OCCCOC)=C1)C[C@H](N)[C@@H](O)C[C@@H](C(C)C)C(NCC(C([2H])([2H])[2H])(C(N)=O)C([2H])([2H])[2H])=O.O=C(O)/C=C/C(O)=O.[1/2]
-
Synonyms
CGP 60536-d6 hemifumarate; CGP60536B-d6 hemifumarate; SPP 100-d6 hemifumarate
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
-
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.
Purity & Documentation
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)