Simenda
Simenda Uses, Dosage, Side Effects, Food Interaction and all others data.
Simenda increases calcium sensitivity to myocytes by binding to troponin C in a calcium dependent manner. This increases contractility without raising calcium levels. It also relaxes vascular smooth muscle by opening adenosine triphosphate sensitive potassium channels. Simenda is used to manage acutely decompensated congestive heart failure.
Simenda is a new Ca2+-sensitizing inotropic agent. Ca2+ sensitizers represent a new class of inotropic agents, which overcome the disadvantages associated with currently available inotropic agents in as they are not associated with an increased risk of arrhythmias, cell injury and death due to Ca2+ overload in myocardial cells; they do not increase the activation energy; and they have the potential to reverse contractile dysfunction under pathophysiologic conditions, such as acidosis or myocardial stunning. Simenda has not been approved for use in the U.S. or Canada.
| Trade Name | Simenda |
| Generic | Levosimendan |
| Levosimendan Other Names | Levosimendán, Lévosimendan, Levosimendan, Levosimendanum |
| Weight | 12.5mg |
| Type | Injection |
| Formula | C14H12N6O |
| Weight | Average: 280.2847 Monoisotopic: 280.107259036 |
| Protein binding | 98% bound to plasma protein. |
| Groups | Approved, Investigational |
| Therapeutic Class | |
| Manufacturer | Lupin |
| Available Country | India |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Simenda is a calcium sensitizer indicated to treat acutely decompensated severe chronic heart failure.
For short term treatment of acutely decompensated severe chronic heart failure (CHF). Also being investigated for use/treatment in heart disease.
Simenda is also used to associated treatment for these conditions: Acute Decompensated Heart Failure (ADHF), Acute Decompensation of Chronic Heart Failure, Acute Heart Failure (AHF), Chronic Heart Failure (CHF), Acute Decompensated Chronic Heart Failure, Acute post-surgical heart failure, Heart failure post-myocardial infarction, Severe Decompensated Chronic Heart Failure, Positive cardiac inotropic effect, Intravenous inotropic therapy
How Simenda works
Simenda appears to increase myofilament calcium sensitivity by binding to cardiac troponin C in a calcium-dependent manner. This stabilizes the calcium-induced conformational change of troponin C, thereby (1) changing actin-myosin cross-bridge kinetics apparently without increasing the cycling rate of the cross-bridges or myocardial ATP consumption, (2) increasing the effects of calcium on cardiac myofilaments during systole and (3) improving contraction at low energy cost (inotropic effect). Calcium concentration and, therefore, sensitization decline during diastole, allowing normal or improved diastolic relaxation. Simenda also leads to vasodilation through the opening of ATP-sensitive potassium channels. By these inotropic and vasodilatory actions, levosimendan increases cardiac output without increasing myocardial oxygen demand. Simenda also has a selective phosphodiesterase (PDE)-III inhibitory action that may contribute to the inotropic effect of this compound under certain experimental conditions. It has been reported that levosimendan may act preferentially as a Ca2+ sensitizer at lower concentrations, whereas at higher concentrations its action as a PDE-III inhibitor becomes more prominent in experimental animals and humans.
Elimination Route
The bioavailability of oral levosimendan is 85 ± 6% in healthy volunteers and 84 ± 4% in patients.
Half Life
Eliminination half-life is approximately 1 hour.
Innovators Monograph
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