Fimasartan

Fimasartan structure

Fimasartan is an innovative non-peptide angiotensin II receptor antagonist (ARB) heralded for its efficacy in managing hypertension and heart failure. This agent finds its therapeutic basis by targeting and inhibiting the Angiotensin II receptor type 1 (AT1 receptors). As a result, it significantly reduces the pathological effects of angiotensin II, predominantly systemic vasoconstriction and water retention mediated by the kidneys.

Clinical Approvals and Branding

In South Korea, on September 9th, 2010, Fimasartan received regulatory approval and is presently marketed under the brand name Kanarb by Boryung Pharmaceuticals. Keen on expanding its global footprint, Boryung Pharmaceuticals is actively exploring international partnerships.

Mechanism of Action

The therapeutic efficacy of Fimasartan can be attributed to its action on the renin-angiotensin cascade of the kidneys:

• Renin release from the kidney induces the conversion of angiotensinogen to angiotensin I.
• Angiotensin I is subsequently transformed to angiotensin II through the catalytic activity of Angiotensin-converting enzyme (ACE).
• Angiotensin II interacts with AT1 receptors, notably in the blood vessels, heart, and kidneys.
  • Within blood vessels, AT1 receptor activation promotes smooth muscle contraction, causing vasoconstriction.
  • In the kidneys and adrenal gland, AT1 receptor activation stimulates aldosterone synthesis, leading to water and salt retention.
  • AT1 receptor stimulation in the heart enhances contractility and the effects of the sympathetic nervous system.

By antagonizing the AT1 receptor, Fimasartan promotes vasodilation, enhances renal excretion of water and salt, and suppresses cardiac contractility. The collective outcomes lead to a notable reduction in blood pressure, providing symptomatic relief in hypertension. Furthermore, ARBs, including Fimasartan, have demonstrated potential protective effects against myocardial infarction, stroke, and heart failure. On a cellular level, Fimasartan has been implicated in reducing cardiac hypertrophy, fibrosis, remodeling, and unwarranted cell proliferation. This is potentially mediated by inhibiting AT1 activation, which subsequently reduces Endothelin 1 production. Additionally, Fimasartan may inhibit TGF-β1 production, contributing to reduced fibrosis and ventricular damage post-myocardial infarction.

Clinical Safety and Side Effects

In clinical settings, Fimasartan showcased a favorable tolerability profile. Nonetheless, at higher doses (360 mg/day), a minority of patients reported:

• Dizziness (presumably a transient reduction in blood pressure).
• Headaches.
• Diarrhea.
• Syncope.
• Cold extremities.

All observed side effects were self-limiting, resolving without the need for medical interventions.

Pharmacological Profile

Fimasartan boasts a rapid absorption rate and demonstrates minimal bioaccumulation seven days post-administration. Its half-life ranges between 9 to 16 hours, making it suitable for daily dosing. Fimasartan's efficacy remains consistent, irrespective of food intake, and exhibits a flexible dosing regimen. Its pharmacokinetic studies reveal that the peak therapeutic effect ensues shortly after achieving maximum plasma concentration (T-max), which typically occurs between 30 minutes to 3 hours post-dosing. Fimasartan predominantly exists in its unmetabolized form in the plasma, and its primary route of excretion is via bile. Renal excretion is minimal, with less than 3% of the drug eliminated through urine 24 hours post-administration.

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