Home GPCR & G Protein Angiotensin Receptor antagonist Fimasartan

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Fimasartan Angiotensin Receptor antagonist

Cat.No.S4975

Fimasartan (Kanarb) is a non-peptide angiotensin II receptor antagonist (ARB) with noncompetitive, insurmountable binding with the AT1 receptor. It is used for the treatment of hypertension and heart failure.
Fimasartan Angiotensin Receptor antagonist Chemical Structure

Chemical Structure

Molecular Weight: 501.65

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Quality Control

Batch: S497501 DMSO]100 mg/mL]false]Ethanol]24 mg/mL]false]Water]Insoluble]false Purity: 99.75%
99.75

Solubility

In vitro
Batch:

DMSO : 100 mg/mL (199.34 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 24 mg/mL

Water : Insoluble

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In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 501.65 Formula

C27H31N7OS

 Storage (From the date of receipt)
CAS No. 247257-48-3 -- Storage of Stock Solutions

Synonyms Kanarb Smiles CCCCC1=NC(=C(C(=O)N1CC2=CC=C(C=C2)C3=CC=CC=C3C4=NNN=N4)CC(=S)N(C)C)C

Mechanism of Action

Targets/IC50/Ki
AT1 receptor
In vitro

Fimasartan is a selective AT1 receptor antagonist. The concentration that inhibits the binding of [125I]Ang II to the AT1 receptor from rat adrenal cortex by 50% (IC50) is 0.13 nM. This compound potently attenuates myocardial apoptotic death in reperfused rat heart and H9c2 cells. It could attenuate mitochondrial damage which is associated with minimizing the reduction in Bcl-2 and connected with the reduction in p53 and activation of Akt and GSK-3β, and inhibiting mitochondrial Ca2+ overload by suppressing the ICa,L and MCU.
In vivo

In various animal models including renal hypertensive rats, spontaneously hypertensive rats and Beagle dogs, fimasartan effectively reduces blood pressure in a dose-dependent manner following single or repeated oral and intravenous administration. This compound does not affect general behavior, respiratory rate or tidal volume in experimental animals, and shows no adverse findings in the human ether-a-go-go-related gene (hERG) test or monkey telemetry study. A number of general toxicity, carcinogenic toxicity, genetic toxicity, and developmental toxicity studies given either orally or intravenously in various species including mice, rats, monkeys and dogs are conducted and these preclinical results demonstrate the safety and tolerability of this chemical for long-term clinical use and offer sufficient safety margins to support the expected human therapeutic dose. It is rapidly absorbed following oral administration with the time to peak plasma concentration (Tmax) ranging 0.5-3 h and the terminal half-life (t1/2) being 5-16 h at doses of 20 to 480 mg in healthy subjects. Similar results are obtained in patients with hypertension, i.e., Tmax ranges 0.5-1.3 h and t1/2 is 7-10 h following this compound administration at doses 20-180 mg in the subsequent phase II study. The urinary excretion of this chemical is low, with the overall urinary excretion of unchanged drug over the first 24 h after dosing being less than 3% of the administered dose. It undergoes nonrenal elimination with minimal metabolism. This compound treatment before myocardial ischemia significantly attenuates reperfusion injury and apoptotic changes, possibly by suppressing mitochondrial damage during reperfusion. In various preclinical studies, including aortic balloon injury, myocardial infarct ischemia/reperfusion, doxorubicin cardiotoxicity, and ischemic stroke models, this chemical shows anti-inflammatory and organ-protecting effects.
References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02994745 Completed
Hypertension Hyperlipidemia
Boryung Pharmaceutical Co. Ltd
 December 23 2016 Phase 1
NCT02920047 Completed
Hypertension
Boryung Pharmaceutical Co. Ltd
 October 2016 Phase 1
NCT02995720 Completed
Hypertension Hyperlipidemia
Boryung Pharmaceutical Co. Ltd
 August 26 2016 Phase 1
NCT03231293 Completed
Hypertension|Ischemic Stroke|Transient Ischemic Attack
Boryung Pharmaceutical Co. Ltd
 July 28 2016 --

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