Saralasin

Saralasin ([Sar1, Ala8] Angiotensin II) is an octapeptide analog of angiotensin II. Saralasin is a competitive angiotensin II receptor antagonist with a Ki value of 0.32 nM for 74% of the binding sites, and has partial agonist activity as well. Saralasin can be used for the research of renovascular hypertension, renin-dependent (angiotensinogenic) hypertension[1][3][6].

Product Specifications

CAS Number

[34273-10-4]

Product Name Alternative

[Sar1, Ala8] Angiotensin II

UNSPSC

12352209

Target

Angiotensin Receptor

Type

Peptides

Related Pathways

GPCR/G Protein

Applications

COVID-19-immunoregulation

Field of Research

Inflammation/Immunology; Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/saralasin.html

Purity

99.46

Solubility

DMSO : 50 mg/mL (ultrasonic)

Smiles

C[C@@H](C(O)=O)NC([C@H]1N(C([C@H](CC2=CNC=N2)NC([C@H](C(C)C)NC([C@H](CC3=CC=C(C=C3)O)NC([C@H](C(C)C)NC([C@H](CCCNC(N)=N)NC(CNC)=O)=O)=O)=O)=O)=O)CCC1)=O

Molecular Formula

C42H65N13O10

Molecular Weight

912.05

References & Citations

[1]P Schelling, et al. Effects of angiotensin II and angiotensin II antagonist saralasin on cell growth and renin in 3T3 and SV3T3 cells. J Cell Physiol. 1979 Mar;98 (3) :503-13. |[2]Jeremy H Kim, et al. Pressure-overload-induced angiotensin-mediated early remodeling in mouse heart. PLoS One. 2017 May 2;12 (5) :e0176713. |[3]Maziar Mohammad Akhavan, et al. A non-radioactive method for angiotensin II receptor binding studies using the rat liver. J Pharmacol Toxicol Methods. 2006 May-Jun;53 (3) :206-14. |[4]M Mikuni, et al. Saralasin-induced inhibition of ovulation in the in vitro perfused rat ovary is not replicated by the angiotensin II type-2 receptor antagonist PD123319. Am J Obstet Gynecol. 1998 Jul;179 (1) :35-40. |[5]Siu Po Ip, et al. Saralasin, a nonspecific angiotensin II receptor antagonist, attenuates oxidative stress and tissue injury in cerulein-induced acute pancreatitis. Pancreas. 2003 Apr;26 (3) :224-9. |[6]Campbell WB, et al. Saralasin-induced renin release: its blockade by prostaglandin synthesis inhibitors in the conscious rat. Hypertension. 1979;1 (6) :637‐642.