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Fimasartan skeletal.svg
Clinical data
Trade namesKanarb
ATC code
  • 2-(2-Butyl-4-methyl-6-oxo-1-{[2'-(1H-tetrazol-5-yl)-4-biphenylyl]methyl}-1,6-dihydro-5-pyrimidinyl)-N,N-dimethylethanethioamide
CAS Number
PubChem CID
CompTox Dashboard (EPA)
Chemical and physical data
Molar mass501.65 g·mol−1
3D model (JSmol)
  • CCCCC1=NC(=C(C(=O)N1CC2=CC=C(C=C2)C3=CC=CC=C3C4=NN=NN4)CC(=S)N(C)C)C
  • InChI=1S/C27H31N7OS/c1-5-6-11-24-28-18(2)23(16-25(36)33(3)4)27(35)34(24)17-19-12-14-20(15-13-19)21-9-7-8-10-22(21)26-29-31-32-30-26/h7-10,12-15H,5-6,11,16-17H2,1-4H3,(H,29,30,31,32)

Fimasartan is a non-peptide angiotensin II receptor antagonist (ARB) used for the treatment of hypertension and heart failure.[1][2] Through oral administration, fimasartan blocks angiotensin II receptor type 1 (AT1 receptors), reducing pro-hypertensive actions of angiotensin II, such as systemic vasoconstriction and water retention by the kidneys.[3] Concurrent administration of fimasartan with diuretic hydrochlorothiazide has shown to be safe in clinical trials.[1] Fimasartan was approved for use in South Korea on September 9, 2010, and is available under the brand name Kanarb through Boryung Pharmaceuticals, who are presently seeking worldwide partnership.[4]

Mechanism of action

Fimasartan acts on the kidney's rennin-angiotensin cascade, which begins when renin release from the kidney causes the breakdown of angiotensinogen into angiotensin I. Angiotensin-converting enzyme (ACE) then catalyzes the reaction that forms angiotensin II, which acts on AT1 receptors on the blood vessels, heart, and kidneys.[5] On blood vessels, the AT1 receptor is coupled to an intracellular pathway that causes smooth muscle contraction (vasoconstriction) of blood vessels.[6]

In blocking the AT1 receptor, fimasartan inhibits vasoconstriction, favouring vasodilation. At the kidney and adrenal gland, AT1 blockage and prevention of aldosterone formation increase excretion of water and salt by the kidneys, which decreases overall blood volume.[7] At the heart, AT1 blockage decreases contractility and the stimulatory effects of the sympathetic nervous system.[4] Collectively, fimasartain leads to a reduction in blood pressure and alleviation of hypertensive symptoms. ARBs like fimasartan have also shown to be protective against stroke, myocardial infarction, and heart failure.[8] Fimasartan has been shown to reduce cardiac hypertrophy, fibrosis, remodelling, and unnecessary cell proliferation via blockage of AT1 activation [4][9] conceivably through decreased Endothelin 1 production, a result of AT1 activation.[10] Fimastartan can also block TGF-β1 production (also AT1 dependent), which contributes to fibrosis and ventricular damage post-infarct.[11] After ARB administration, mice showed improved prognosis after a myocardial infarction,[9] though further studies still need to be done to assess fimasartan's specific effects on decreasing cardiovascular damage.

Side effects

Side effects In clinical trials, fimasartan was well tolerated in all patients. However, higher dosing (360 mg/day) was accompanied by increased dizziness (most likely due to the momentary decrease in blood pressure) and headaches in a low number of patients.[1] Other side effects such as diarrhea, syncope, and cold feet were also experienced in a low number of subjects, which all resolved without medical intervention.[1]


Fimasartan is rapidly absorbed and has minimal accumulation in the body 7 days after administration.[1] Fimasartan possesses a half-life of 9 to 16 hours,[1] appropriate for daily dosing. Fimasartan was found to be effective in fasted or fed states, with a variety of dosing regimens. In trials, the maximum effects of the drug occurred slightly after the maximum plasma concentration (T-max) was achieved,[1] which occurs 30 minutes to 3 hours after dosing.[12] Fimasartan was found mostly in unmetabolized form in the plasma and in bile excretions. Urinary elimination of the drug was low, at less than 3% 24 hours after administration, entailing that the fimasartan does not undergo renal excretion.[1]

Society and culture

Brand names

The drug is also available in Russia as Канарб (Kanarb).[13] Fimasartan is being marketed in India under the brand name of Fimanta and Fimagen through Ajanta Pharma Ltd.


  1. ^ a b c d e f g h Lee HY, Oh BH (July 2016). "Fimasartan: A New Angiotensin Receptor Blocker". Drugs. 76 (10): 1015–22. doi:10.1007/s40265-016-0592-1. PMID 27272555.
  2. ^ Pradhan A, Gupta V, Sethi R (July 2019). "Fimasartan: A new armament to fight hypertension". Journal of Family Medicine and Primary Care. 8 (7): 2184–2188. doi:10.4103/jfmpc.jfmpc_300_19. PMC 6691418. PMID 31463228.
  3. ^ DeMello WC, Re RN (2009). "Systemic versus local renin angiotensin systems. An overview.". In DeMello WC, Frohlich ED (eds.). Renin angiotensin system and cardiovascular disease. New York, NY: Humana Press. pp. 1–5. ISBN 978-1-60761-186-8.
  4. ^ a b c "Fimasartan". American Journal Cardiovascular Drugs. 11 (4): 249–252. 2011. doi:10.2165/11533640-000000000-00000.
  5. ^ Burnier M (February 2001). "Angiotensin II type 1 receptor blockers". Circulation. 103 (6): 904–12. doi:10.1161/01.cir.103.6.904. PMID 11171802.
  6. ^ Wynne BM, Chiao CW, Webb RC (2009). "Vascular Smooth Muscle Cell Signaling Mechanisms for Contraction to Angiotensin II and Endothelin-1". Journal of the American Society of Hypertension. 3 (2): 84–95. doi:10.1016/j.jash.2008.09.002. PMC 2704475. PMID 20161229.
  7. ^ Klabunde RE (15 March 2007). "Angiotensin Receptor Blockers (ARBs)". CV Pharmacology.
  8. ^ Neal B, MacMahon S, Chapman N (December 2000). "Effects of ACE inhibitors, calcium antagonists, and other blood-pressure-lowering drugs: results of prospectively designed overviews of randomised trials. Blood Pressure Lowering Treatment Trialists' Collaboration". Lancet. 356 (9246): 1955–64. doi:10.1016/s0140-6736(00)03307-9. PMID 11130523.
  9. ^ a b Harada K, Sugaya T, Murakami K, Yazaki Y, Komuro I (November 1999). "Angiotensin II type 1A receptor knockout mice display less left ventricular remodeling and improved survival after myocardial infarction". Circulation. 100 (20): 2093–9. doi:10.1161/01.cir.100.20.2093. PMID 10562266.
  10. ^ Phillips PA (July 1999). "Interaction between endothelin and angiotensin II". Clinical and Experimental Pharmacology & Physiology. 26 (7): 517–8. doi:10.1046/j.1440-1681.1999.03069.x. PMID 10405777.
  11. ^ Sun Y, Zhang JQ, Zhang J, Ramires FJ (August 1998). "Angiotensin II, transforming growth factor-beta1 and repair in the infarcted heart". Journal of Molecular and Cellular Cardiology. 30 (8): 1559–69. doi:10.1006/jmcc.1998.0721. PMID 9737942.
  12. ^ Gu N, Kim BH, Lim KS, Kim SE, Nam WS, Yoon SH, Cho JY, Shin SG, Jang IJ, Yu KS (July 2012). "The effect of fimasartan, an angiotensin receptor type 1 blocker, on the pharmacokinetics and pharmacodynamics of warfarin in healthy Korean male volunteers: a one-sequence, two-period crossover clinical trial". Clinical Therapeutics. 34 (7): 1592–600. doi:10.1016/j.clinthera.2012.06.004. PMID 22727611.
  13. ^ "Kanarb (fimasartan) film-coated tablets. Registration Certificate". Russian State Register of Medicines (in Russian). JSC R-Pharm. Retrieved 1 September 2020.