2. Disease Areas
  3. Blood or Cardio-cerebrovascular Disease
  4. Heart Disease
  5. Arrhythmias
  6. Disobutamide

Disobutamide (SC-31828) is an orally active, blood-brain barrier permeable cationic amphiphilic ditertiary amine piperidine ring compound with antiarrhythmic properties. Disobutamide induces lysosomal phospholipid accumulation, which triggers extensive cytoplasmic vacuolization and leads to cell death. Disobutamide prolongs multiple electrocardiographic intervals in canine hearts, induces cardiac arrest at high doses, and causes decreased retinal reflectivity. Disobutamide can be used in studies related to arrhythmias, and also serves as a model drug for investigating the storage mechanisms and toxicity thresholds of intracellular amphiphilic compounds.

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Disobutamide

Disobutamide Chemical Structure

CAS No. : 68284-69-5

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Disobutamide Related Antibodies

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Description

Disobutamide (SC-31828) is an orally active, blood-brain barrier permeable cationic amphiphilic ditertiary amine piperidine ring compound with antiarrhythmic properties. Disobutamide induces lysosomal phospholipid accumulation, which triggers extensive cytoplasmic vacuolization and leads to cell death. Disobutamide prolongs multiple electrocardiographic intervals in canine hearts, induces cardiac arrest at high doses, and causes decreased retinal reflectivity. Disobutamide can be used in studies related to arrhythmias, and also serves as a model drug for investigating the storage mechanisms and toxicity thresholds of intracellular amphiphilic compounds[1][2][3].

In Vitro

Disobutamide (1×10-4-10×10-4 M; 24 h) does not induce significant cytotoxicity (measured by LDH release) in rat urinary bladder carcinoma or rabbit aorta muscle cells at concentrations up to 10×10-4 M after 24 hours, but induces severe cytotoxicity in rat basophilic leukaemia cells at concentrations ≥4×10-4 M after 24 hours[1].
Disobutamide (10-3 M; 24 h) shows enhanced cellular uptake in rat urinary bladder carcinoma cells (RBT CC-8) with increased basicity of the culture medium, with clear cytoplasmic vacuoles forming at higher uptake levels[2].
Disobutamide (10-6-10-3 M; 30 min-6 hr) shows species-specific in vitro uptake by choroid plexus tissue, with highest uptake in rat choroid plexus, followed by monkey choroid plexus, then dog choroid plexus, and induces dose-dependent vacuolation in dog choroid plexus epithelial cells at concentrations ≥10-4 M[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Disobutamide Related Antibodies

Cell Cytotoxicity Assay[1]

Cell Line: rat urinary bladder carcinoma (RBT CC-8) cells, rabbit aorta muscle cells, rat basophilic leukaemia cells
Concentration: 1×10-4 M, 2×10-4 M, 4×10-4 M, 6×10-4 M, 8×10-4 M, 10×10-4 M
Incubation Time: 24 h
Result: Caused LDH release relative to total enzyme of ≤5.2% at all tested concentrations in rat urinary bladder carcinoma cells.
Caused LDH release relative to total enzyme ranging from 5.3% at 1×10-4 M to 31.2% at 10×10-4 M in rabbit aorta muscle cells, a magnitude not indicative of cytotoxicity.
Caused LDH release relative to total enzyme of 2.2% at 1×10-4 M, 18.7% at 2×10-4 M, and 84.4-89.9% at 4×10-4 M to 10×10-4 M in rat basophilic leukaemia cells, indicating significant cytotoxicity at concentrations ≥4×10-4 M.
In Vivo

Disobutamide (6-90 mg/kg/day; p.o.; daily; 14 days-52 weeks) induces dose/time-dependent, progressive cytoplasmic vacuolation across multiple dog cell types and organs without overt cellular injury, while also causing cardiac electrophysiologic effects and sudden death at high chronic doses, with a no-observed-adverse-effect threshold below 6 mg/kg/day for tapetal changes[2].
Disobutamide (10-300 mg/kg/day; p.o.; daily; 5 days-52 weeks) induces selective cytoplasmic vacuolation in Rattus norvegicus choroid plexus and epididymal epithelial cells at 300 mg/kg/day, causes lethal toxicity at the same dose with prolonged exposure, and induces hepatic phospholipidosis without cellular injury during long-term high-dose dosing[2].
Disobutamide (30-250 mg/kg; i.g.; daily; 4-35 days) induces dose-dependent lysosomal vacuolation (phospholipidosis) in multiple rat organs, with very severe choroid plexus epithelial vacuolation at 250 mg/kg, moderate changes at 100 mg/kg, and mild changes at 30 mg/kg, correlating[3].
Disobutamide (45 mg/kg; p.o.; daily; 35 days) induces vacuolation in multiple dog organs but not choroid plexus epithelium, while direct intraventricular administration (0.035 mg total dose; i.c.v.; single dose) causes choroid plexus epithelial vacuolation, linked to low drug penetration into CSF via oral dosing[3].
Disobutamide (90 mg/kg; i.g.; daily; 35 days) induces very severe choroid plexus epithelial vacuolation and dose-dependent vacuolation in other monkey organs, correlating with high choroid plexus drug concentration and increased CSF/serum ratio over time[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Jcl:SD rats (male and female, 5 weeks of age)[3]
Dosage: 30 mg/kg; 100 mg/kg; 250 mg/kg
Administration: i.g.; daily; 13 weeks (30, 100, 250 mg/kg); i.g.; single dose (100, 250 mg/kg); i.g.; daily; 4, 7, or 35 days (100, 250 mg/kg)
Result: Caused 10/16 males and 10/16 females to die of convulsions during weeks 1-9 at 250 mg/kg.
Reduced feed intake and depressed body weight gain in both sexes at 250 mg/kg.
Elevated total cholesterol in both sexes, phospholipid in males, and triglyceride in females at 250 mg/kg.
Decreased most organ weights in males, and thymus/spleen weights in females at 250 mg/kg.
Induced very severe vacuolation in choroid plexus epithelium, severe vacuolation in renal distal tubules and hepatocytes, moderate vacuolation in submaxillary gland, bronchus, uterine epithelium, cardiac muscle, coronary artery, and lung macrophages, slight vacuolation in stomach, small intestine, spleen macrophages, thymus macrophages, and bone marrow macrophages at 250 mg/kg.
Detected choroid plexus drug concentration of 11.8 mg/g, brain concentration of 26.2 μg/g, liver concentration of 604 μg/g, and kidney concentration of 403 μg/g after 35 days of 250 mg/kg dosing.
Caused muscle relaxation and prone position in females, slight feed intake decrease and body weight gain depression in males, slight thymus weight decrease in males, and slight vacuolation in submaxillary gland, bronchus, cardiac muscle, coronary artery, lung macrophages, thymus macrophages, and bone marrow macrophages at 100 mg/kg.
Induced large lysosome increase in choroid plexus epithelium after 4 days and vacuoles in large choroid plexus lysosomes after 7 days of 100 mg/kg dosing.
Caused slight thymus weight decrease in males and slight vacuolation in submaxillary gland, cardiac muscle, coronary artery, thymus macrophages, and bone marrow macrophages at 30 mg/kg.
Animal Model: Beagle dogs (female, 13-17 months of age; male and female, 10 months of age)[3]
Dosage: 45 mg/kg; 0.035 mg total dose
Administration: p.o.; daily; 35 days (45 mg/kg); i.c.v.; single dose (0.035 mg)
Result: Induced severe vacuolation in stomach, small intestine, renal distal tubules, and bronchial epithelium, moderate vacuolation in spleen macrophages, slight vacuolation in esophagus, submaxillary gland, iris pigment epithelium, hepatocytes, cardiac muscle, coronary artery, aorta, intestinal muscle cells, lung macrophages, thymus macrophages, and bone marrow macrophages at 45 mg/kg p.o.
Detected choroid plexus drug concentration of 0.124 mg/g, brain concentration of 12.2 μg/g, liver concentration of 468 μg/g, and kidney concentration of 653 μg/g after 35 days of 45 mg/kg p.o. dosing.
Caused numerous enlarged lysosomes (some with vacuoles) in choroid plexus epithelial cells 3 hours after 0.035 mg i.c.v. dosing.
Animal Model: Macaca fasciculata (female, adult age)[3]
Dosage: 90 mg/kg
Administration: i.g.; daily; 35 days
Result: Induced severe lymphocyte cytoplasmic vacuolation; one monkey showed elevated total cholesterol and phospholipid at 2 weeks.
Caused very severe vacuolation in choroid plexus epithelium, severe vacuolation in renal distal tubules and intestinal muscle cells, moderate vacuolation in stomach, small intestine, bronchial epithelium, uterine epithelium, hepatocytes, coronary artery, spleen macrophages, and bone marrow macrophages, slight vacuolation in esophagus, submaxillary gland, cardiac muscle, aorta, lung macrophages, and thymus macrophages.
Detected choroid plexus drug concentration of 30.233 mg/g, brain concentration of 18.7 μg/g, liver concentration of 1304 μg/g, and kidney concentration of 1092 μg/g after 35 days of dosing.
Showed higher CSF concentration at 24 hours and significantly higher CSF/serum ratio at 24 hours on day 35 compared to day 1.
Molecular Weight

408.02

Formula

C23H38ClN3O
CAS No.
SMILES

O=C(C(CCN(C(C)C)C(C)C)(CCN1CCCCC1)C2=CC=CC=C2Cl)N
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Disobutamide Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Disobutamide68284-69-5SC-31828SC31828SC 31828Othersrat basophilic leukaemia cellsphospholipidosisrat urinary bladder carcinoma cellscardiac arrhythmiaChinese hamster ovary tumour cellsmouse fibroblast cellscardiac antiarrhythmic propertieslysosomesblood-brain barrierchoroid plexus epithelial cellsInhibitorinhibitorinhibit

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