Bidisomide is a class I antiarrhythmic drug. It reduces the maximum rate of depolarization (Vmax) of the cardiac action potential and shortens the action potential duration, which are characteristic effects of class I agents. The literature classifies it as a class Ia/Ib drug with slow kinetic properties, distinct from fast-interacting agents like lidocaine or mexiletine. [1]

In anesthetized rats, early ventricular arrhythmias caused by coronary artery blockage and reperfusion were explored to examine the antiarrhythmic effects of bidisomit, a novel class I antiarrhythmic medication. When compared to equivalent doses of mexiletine (MXT) and disopyramide (DSP), bidisomide (5 mg/kg) decreases the frequency of premature ventricular contractions as well as the incidence of ventricular tachycardia and ventricular fibrillation in rats with ventricular arrhythmias brought on by coronary artery blockage. The identical doses of MXT and DSP did not significantly alter the antiarrhythmic effects of 5 mg/kg bidisomide in rats with ventricular arrhythmias caused by myocardial reperfusion 5 minutes after coronary blockage. The heart rates of all three medications are markedly lowered [1].

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In anesthetized Sprague-Dawley rats, intravenous administration of bidisomide (5 mg/kg), 5 minutes before coronary artery occlusion, significantly reduced the total number of premature ventricular complexes (PVCs) during a 30-minute observation period (925 ± 312) compared to the saline control group (1663 ± 81). It also significantly shortened the duration of ventricular tachycardia (VT) (89 ± 32 seconds) compared to control (139 ± 16 seconds). The incidence of ventricular fibrillation (Vf) was reduced to 0%, compared to 43% in the control group. [1]
In a separate experiment using a coronary artery reperfusion model following 5 minutes of occlusion, intravenous bidisomide (5 mg/kg), administered 5 minutes pre-occlusion, significantly reduced the incidence of Vf to 20% (vs. 90% in control) and the mortality rate to 20% (vs. 90% in control). The duration of combined VT/Vf in survivors was 13 ± 4 seconds. [1]
The antiarrhythmic effects of bidisomide (5 mg/kg) against both occlusion-induced and reperfusion-induced arrhythmias were comparable to those of the established drugs mexiletine (5 mg/kg) and disopyramide (5 mg/kg). [1]
Administration of bidisomide (5 mg/kg, i.v.) significantly slowed the heart rate from 461 ± 16 beats/min (before) to 424 ± 17 beats/min (1 min post) and 419 ± 17 beats/min (5 min post). It did not cause a significant change in mean arterial blood pressure. [1]

Male Sprague-Dawley rats (200-280 g) were anesthetized with sodium pentobarbital (60 mg/kg, i.p.). The femoral vein was cannulated for drug administration. A tracheotomy was performed for artificial respiration. Systemic arterial blood pressure was monitored via a catheter in the carotid artery. A standard limb lead I electrocardiogram was recorded continuously. [1]
For the coronary occlusion study, a left thoracotomy was performed. A suture was placed around the left coronary artery. After a 15-minute recovery period, rats received an intravenous injection of the test drug or saline (0.5 ml volume). Five minutes after drug administration, the coronary artery was occluded by ligation. Electrocardiogram and blood pressure were recorded for 30 minutes post-occlusion. Parameters assessed included total PVC count, incidence and duration of VT, and incidence of Vf. [1]
For the coronary reperfusion study, the coronary artery was occluded using a suture passed through a small plastic tube to allow for reversible occlusion. Drugs were administered intravenously 5 minutes before occlusion. The coronary artery was occluded for 5 minutes, and then reperfusion was initiated by releasing the occlusion. Recordings were made for 15 minutes post-reperfusion. Parameters assessed included incidence of Vf, duration of VT/Vf, and mortality rate. [1]
Drugs (bidisomide, mexiletine, disopyramide) were dissolved in saline. The injection volume for all agents was adjusted to 0.5 ml with saline. The dose for all drugs was 5 mg/kg, administered as a single intravenous bolus. [1]

[1]. Effects of bidisomide (SC-40230), a new class I antiarrhythmic agent, on ventricular arrhythmias induced by coronary artery occlusion and reperfusion in anesthetized rats; comparison with mexiletine and disopyramide. Heart Vessels. 1995;1.

Bidesomite belongs to the acetamide class of compounds.

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Bidesomite (SC-40230) is a newly synthesized antiarrhythmic drug with the chemical name α-(2-[acetyl(1-methylethyl)-amino]ethyl)-α-(2-chlorophenyl)-1-piperidinbutamide (molecular weight 407.98). [1]
It has a slower binding kinetic to cardiac sodium channels, which distinguishes it from class Ib drugs such as lidocaine and mexiletine, which bind to sodium channels more rapidly. [1]
Studies have shown that, based on its efficacy in rat models of coronary artery occlusion and reperfusion arrhythmias, bisomite may be effective in inhibiting life-threatening ventricular arrhythmias (such as ventricular tachycardia and ventricular fibrillation) associated with the early stages of acute coronary syndrome. [1] In these models, the antiarrhythmic mechanism is thought to be mainly related to its effect of reducing myocardial conduction velocity, which can inhibit reentry circuits that lead to early ischemia and reperfusion arrhythmias. [1]

C22H34N3O2CL

407.97726

407.234

116078-65-0

59798

Typically exists as solid at room temperature

1.124g/cm3

599.8ºC at 760 mmHg

316.5ºC

2.41E-14mmHg at 25°C

1.54

4.673

1

3

9

28

522

0

CC(C)N(C(C)=O)CCC(C(N)=O)(C1=C(C=CC=C1)Cl)CCN2CCCCC2

GTEPPJFJSNSNIH-UHFFFAOYSA-N

InChI=1S/C22H34ClN3O2/c1-17(2)26(18(3)27)16-12-22(21(24)28,19-9-5-6-10-20(19)23)11-15-25-13-7-4-8-14-25/h5-6,9-10,17H,4,7-8,11-16H2,1-3H3,(H2,24,28)

2-[2-[acetyl(propan-2-yl)amino]ethyl]-2-(2-chlorophenyl)-4-piperidin-1-ylbutanamide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~250 mg/mL (~612.78 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (5.10 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (5.10 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (5.10 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)