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Losartan Angiotensin Receptor antagonist

Cat.No.S5067

Losartan(DuP-753) is a selective, orally administered, nonpeptide blocker of angiotensin II type 1 (AT1) receptor used to treat high blood pressure, diabetic kidney disease, heart failure, and left ventricular enlargement.
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Quality Control

Batch: Purity: 99.99%
99.99

Solubility

In vitro
Batch:

DMSO : 84 mg/mL (198.62 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 422.91 Formula

C22H23ClN6O

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 114798-26-4 -- Storage of Stock Solutions

Synonyms DuP-753 SMILES CCCCC1=NC(=C(N1CC2=CC=C(C=C2)C3=CC=CC=C3C4=NNN=N4)CO)Cl

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Mechanism of Action

Targets/IC50/Ki
AT1 receptor
20 nM
In vitro

In vitro, losartan competes with the binding of angiotensin II to AT1 receptors; the concentration that inhibits 50% of the binding of angiotensin II (IC50) is 20 nmol/L. This compound increases AMPK phosphorylation in a time- and dose-dependent manner in VSMCs. It also increases ACC phosphorylation, a major downstream target protein in the AMPK signaling cascade, and LKB1 phosphorylation, which is an upstream kinase of AMPK. It increases p53 and p21 expression in a time-dependent manner, whereas the levels of p27 are not changed. This chemical suppresses Ang II-induced Rb phosphorylation, as well as cyclin D and cyclin E expression which are required for cell cycle progression. The mechanism of growth suppression by this compound is therefore G0/G1 cell cycle arrest which is reversed by AMPK inhibition, such as compound C or AMPK siRNA, but not by apoptosis.

In vivo

Losartan has a major active metabolite, EXP 3174. Administered intravenously, this compound is 10 to 20 times more potent than losartan and has a longer duration of action than this chemical. However, the oral bioavailability of EXP 3174 is very low. This compound has a bioavailability of about 33%, the half-life averages 2 h (6-9 hours), and the rate of protein binding is 98.7% when dosed at 50-100 mg/d. Treatment with this compound ameliorates the loss in the number and function of endothelial progenitor cells (EPCs) in hypertensive rats.

References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2026-04-21)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00162474 RECRUITING
Healthy
Hadassah Medical Organization
2003-09
NCT07762703 NOT_YET_RECRUITING
Triple-Negative Breast Cancer (TNBC)
BreakBio Corp
2026-09 PHASE1; PHASE2
NCT07762716 NOT_YET_RECRUITING
Glioblastoma (GBM)
BreakBio Corp
2026-09 PHASE1; PHASE2
NCT06933706 RECRUITING
Multi-ligament Knee Injury
Brigham and Women's Hospital
2025-10-01 PHASE2
NCT07099859 RECRUITING
Heart Valve Diseases; Left Ventricle Remodeling; Aortic Regurgitation Disease; Heart Failure Congestive; Natriuretic Peptide, Brain
Vitor Emer Egypto Rosa
2025-07-01 PHASE4
NCT07160361 NOT_YET_RECRUITING
Carcinoma, Hepatocellular
Second Affiliated Hospital of Xi'an Jiaotong University
2025-10-01 PHASE4

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