Cart
sales@molnova.com
Angiotensinogen (1-14) ,Rat
CAS No. 110200-37-8
Angiotensinogen (1-14) ,Rat( ——— )
Catalog No. M40863 CAS No. 110200-37-8
Renin substrate, angiotensinogen (1-14), rat is a biological active peptide. (This peptide is derived from rat angiotensinogen amino acid residues 1-14. It is a synthetic renin substrate.)
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
| 25MG | Get Quote | Get Quote |
|
| 50MG | Get Quote | Get Quote |
|
| 100MG | Get Quote | Get Quote |
|
| 200MG | Get Quote | Get Quote |
|
| 500MG | Get Quote | Get Quote |
|
| 1G | Get Quote | Get Quote |
|
Biological Information
-
Product NameAngiotensinogen (1-14) ,Rat
-
NoteResearch use only, not for human use.
-
Brief DescriptionRenin substrate, angiotensinogen (1-14), rat is a biological active peptide. (This peptide is derived from rat angiotensinogen amino acid residues 1-14. It is a synthetic renin substrate.)
-
DescriptionRenin substrate, angiotensinogen (1-14), rat is a biological active peptide. (This peptide is derived from rat angiotensinogen amino acid residues 1-14. It is a synthetic renin substrate.)
-
In Vitro———
-
In Vivo———
-
Synonyms———
-
PathwayOthers
-
TargetOther Targets
-
Recptor———
-
Research Area———
-
Indication———
Chemical Information
-
CAS Number110200-37-8
-
Formula Weight1823.1
-
Molecular FormulaC89H123N21O21
-
Purity>98% (HPLC)
-
Solubility———
-
SMILES———
-
Chemical Name——
Shipping & Storage Information
-
Storage(-20℃)
-
ShippingWith Ice Pack
-
Stability≥ 2 years
Reference
molnova catalog
related products
-
7-Methoxy obtusifoli...
7-Methoxy obtusifolin (Compound 4) is a competitive tyrosinase inhibitor with an IC50 of 7.0 μM.
-
CHAPSO
CHAPSO is a nondenaturing, amphoteric descaler, a surface ionic active agent that can be used to solubilize membrane proteins and cleaved protein-protein interactions.
-
Citreorosein
Citreorosein is a cAMP phosphodiesterase inhibitor, it has anti-inflammatory effect, inhibits proinflammatory cytokines production through the inhibition of both MAPKs and AKT-mediated IκB kinase (IKK) phosphorylation and subsequent inhibition of transcription factor NF-κB activation.
