AVE 0991 sodium salt
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
IC50: AVE 0991 and Ang-(1–7) competitively bind to bovine aortic endothelial cell membranes with IC50 values of 21 ± 35 and 220 ± 280 nM, respectively.
Angiotensin-(1–7) (Ang-[1–7]) acts as a crucial component of the renin-angiotensin system which can regulate and maintain the blood pressure by offsetting effects of Ang II, a typical vasoconstrictor in vivo. AVE 0991, a nonpeptide mimic of Ang-(1–7), performs as an agonist of angiotensin-(1-7) receptor. It plays an important role in exploring effects of Ang-(1-7) and evaluating the potential of Ang-(1-7) as a cardiovascular drug. 
In vitro: AVE 0991 was found to compete with Ang-(1-7) for bovine aortic endothelial cell membrane receptors with an IC50 of 21±35 nM. There was no significant difference in peak concentrations of NO and O2- released from AVE 0991 treated group and Ang-(1-7) treated group. However, the released amount of NO was approximately 5 times higher in AVE 0991 group than that in Ang-(1-7) group. Moreover, AVE 0091 significantly displaced the binding of I-Ang-(1-7) in both Mas-transfected monkey kidney cells (COS) and Mas-transfected Chinese hamster ovary (CHO) cells. 
In vivo: AVE 0091 at a dosage of 0.58 nmol/g resulted in a significant decrease in urinary volume, together with an increase in urinary osmolality in water-loaded C57BL/6 mice.  The antidiuretic effect of AVE was completely offset by the Ang II antagonists, which indicting a high specificity of AVE 0991. Since Ang II induced atherogenesis and ang-(1–7) offset Ang II action, it was proved that AVE 0991 blocked atherogenesis in apolipoprotein E (apoE)-knockout mice model. 
Clinical trial: So far, no clinical trial has been conducted.
Wiemer G, Dobrucki LW, Louka FR, Malinski T, Heitsch H. AVE 0991, a nonpeptide mimic of the effects of angiotensin-(1–7) on the endothelium. Hypertension. 2002 Dec; 40: 847-52.
 Pinheiro SV, Silva AC, Sampaio WO, Paula RD, Mendes EP, Bontempo ED, Pesquero JB, Walther T, Alenina N, Bader M, Bleich M and Santos RA. Nonpeptide AVE 0991 is an angiotensin-(1-7) receptor Mas agonist in the mouse kidney. Hypertension. 2004 Oct; 44(4):490-6.
Toton-Zuranska J, Gajda M, Pyka-Fosciak G, Kus K, Pawlowska M, Niepsuj A, Wolkow P, Olszanecki R, Jawien J and Korbut R. AVE 0991- angiotensin-(1-7) receptor agonist, inhibits atherogenesis in APOE-knockout mice. J Physiol Pharm. 2010, 61(2):181-183.
|Storage||Store at -20°C|
|Solubility||Soluble in DMSO|
|Chemical Name||sodium (Z)-N'-ethyl-N-((3-(4-((5-formyl-4-methoxy-2-phenyl-1H-imidazol-1-yl)methyl)phenyl)-5-isobutylthiophen-2-yl)sulfonyl)carbamimidate|