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Candesartan Cilexetil Angiotensin Receptor antagonist

Cat.No.S2037

Candesartan Cilexetil (TCV-116) is an angiotensin II receptor antagonist with IC50 of 0.26 nM, used in the treatment of hypertension.
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Quality Control

Batch: Purity: 99.98%
99.98

Solubility

In vitro
Batch:

DMSO : 122 mg/mL (199.78 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 4 mg/mL

Water : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 610.66 Formula

C33H34N6O6

Storage (From the date of receipt)
CAS No. 145040-37-5 Download SDF Storage of Stock Solutions

Synonyms TCV-116 SMILES CCOC1=NC2=CC=CC(=C2N1CC3=CC=C(C=C3)C4=CC=CC=C4C5=NNN=N5)C(=O)OC(C)OC(=O)OC6CCCCC6

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Mechanism of Action

Targets/IC50/Ki
Ang II receptor
0.26 nM
In vitro
Candesartan blocks the effects of angiotensin II at the angiotensin II type 1 (AT1) receptor. Candesartan cilexetil is a prodrug that is activated to candesartan by ester hydrolysis during gastrointestinal absorption.
In vivo
Candesartan improves the functional markers in a dose-dependent manner and also upregulates Ang (1-7), ACE2 and mas1 in the myocardium of DCM rats. Candesartan reduces various ER stress and apoptosis markers and the number apoptotic cells in the Candesartan treated rats. Candesartan cilexetil shows angiotensin-II blocking action in a dose-dependent manner in rats with dilated cardiomyopathy. Candesartan cilexetil reduces the left ventricular end-diastolic pressure and heart weight/body weight ratio, the area of myocardial fibrosis and expressions of transforming growth factor-beta1 and collagen-III mRNA. Candesartan cilexetil (1 mg/kg, p.o.) and enalapril (10 mg/kg, p.o.) reduces blood pressure to the same extent 5 hours after administration on the 1st and the 7th day. Candesartan cilexetil significantly increases renal blood flow without any changes in the cardiac index. TCV-116 and enalapril also tends to increase splanchnic blood flow following the 1st dose but not the 7th dose. Candesartan cilexetil is absorbed from the small intestine and hydrolyzed completely to the pharmacologically active metabolite M-I during absorption process.
References
  • [4] http://www.ncbi.nlm.nih.gov/pubmed/ 9127812
  • [5] https://pubmed.ncbi.nlm.nih.gov/8767349/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2025-12-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT05826912 ENROLLING_BY_INVITATION
Traumatic Brain Injury
University of California, San Francisco
2024-08-01 PHASE2
NCT05920005 COMPLETED
Hypertension
Hospital Israelita Albert Einstein
2023-08-22 PHASE3
NCT05122182 TERMINATED
COVID-19; SARS-CoV2 Infection
University of Sydney
2022-01-07 PHASE2
NCT03847506 COMPLETED
Hypertension, Hyperlipidemia
HK inno.N Corporation
2018-07-05 PHASE4
NCT02047019 WITHDRAWN
Hypertension
Bayer
2017-12-01 PHASE3
NCT04012307 COMPLETED
Bioequivalence
Pharmtechnology LLC
2019-07-11 PHASE1

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