PRODUCTS

RYTHMODAN

Rythmodan is an organoammonium phosphate.
Rythmodan belongs to a group of medicines called anti-arrhythmic agents used to treat irregular heartbeats.
Rythmodan is available in both oral and intravenous forms and has a low degree of toxicity.

CAS Number: 3737-09-5
EC Number: 22059-60-5
Formula: C21H29N3O
Molar mass: 339.483 g·mol−1

Disopyramide PHOSPHATE, 22059-60-5, Norpace, Disopyramide PHOSPHATE SALT, Rythmodan, Norpace Cr, SC 7031 phosphate, Dirythmin sa, Diso-duriles, DisopyramidePhosphate, EINECS 244-756-1, SC 7031 (phosphate), NSC-756744, SC-13957, SC-7031 PHOSPHATE, CHEBI:4658, N6BOM1935W, 22059-60-5 (phosphate), SC 13957, Norpace (TN), 2-(1-(Ammoniocarbonyl)-3-(diisopropylammonio)-1-phenylpropyl)pyridinium phosphate, Disopyramid phosphate, 4-(diisopropylamino)-2-phenyl-2-(pyridin-2-yl)butanamide phosphate, 4-[di(propan-2-yl)amino]-2-phenyl-2-pyridin-2-ylbutanamide;phosphoric acid, alpha-(2-Diisopropylaminoethyl)-alpha-phenyl-2-pyridineacetamide phosphate, (+-)-alpha-(2-(Diisopropylamino)ethyl)-alpha-phenyl-2-pyridineacetamide phosphate (1:1), 2-Pyridineacetamide, alpha-(2-(bis(1-methylethyl)amino)ethyl)-alpha-phenyl-, phosphate, 2-Pyridineacetamide, alpha-(2-(bis(1-methylethyl)amino)ethyl)-alpha-phenyl-, phosphate (1:1), 2-Pyridineacetamide, alpha-(2-(diisopropylamino)ethyl)-alpha-phenyl-, phosphate, alpha-(2-(Diisopropylamino)ethyl)-alpha-phenyl-2-pyridineacetamide phosphate (1:1), 2-Pyridineacetamide, alpha-(2-(bis(1-methylethyl)amino)ethyl)-alpha-phenyl-, (+-)-, phosphate (1:1), SR-01000003039, Disopyramide (phosphate), UNII-N6BOM1935W, SCHEMBL41810, MLS000028431, SPECTRUM1500261, C21H29N3O.H3O4P, CHEMBL1201020, HMS501I11, DTXSID30944685, Disopyramide phosphate (JAN/USP), HMS1920I14, HMS2094K15, HMS2234B16, HMS3259J21, HMS3261C04, HMS3369L05, HMS3652M20, HMS3885J07, Pharmakon1600-01500261, Disopyramide PHOSPHATE [MI], XAA05960, Disopyramide PHOSPHATE [JAN], Tox21_500411, CCG-40209, Disopyramide PHOSPHATE [USAN], HY-12533A, NSC756744, Disopyramide PHOSPHATE [VANDF], AKOS040744844, Disopyramide PHOSPHATE [MART.], Disopyramide PHOSPHATE [USP-RS], Disopyramide PHOSPHATE [WHO-DD], LP00411, NC00683, NSC 756744, Disopyramide phosphate [USAN:BAN:JAN], NCGC00093836-01, NCGC00093836-02, NCGC00093836-03, NCGC00093836-04, NCGC00261096-01, SMR000058438, Disopyramide PHOSPHATE [ORANGE BOOK], LS-130131, Disopyramide PHOSPHATE [EP MONOGRAPH], Disopyramide phosphate [USAN:USP:BAN:JAN], EU-0100411, FT-0630479, S4143, SW196836-3, SW196836-4, Disopyramide PHOSPHATE [USP MONOGRAPH], C07740, D 6035, D00637, SR-01000003039-2, SR-01000003039-6, Q27106430, 4-(diisopropylamino)-2-phenyl-2-(2-pyridyl)butanamide, (R)-4-(diisopropylamino)-2-phenyl-2-(pyridin-2-yl)butanamide phosphate, 4-[di(propan-2-yl)amino]-2-phenyl-2-pyridin-2-ylbutanamide,phosphoric acid, 4-DIISOPROPYLAMINO-2-PHENYL-2-(2-PYRIDYL)BUTYRAMIDE PHOSPHATE, Disopyramide phosphate, European Pharmacopoeia (EP) Reference Standard, Disopyramide phosphate, United States Pharmacopeia (USP) Reference Standard, (+/-)-.ALPHA.-(2-(DIISOPROPYLAMINO)ETHYL)-.ALPHA.-PHENYL-2-PYRIDINEACETAMIDE PHOSPHATE (1:1), 2-PYRIDINEACETAMIDE, .ALPHA.-(2-(BIS(1-METHYLETHYL)AMINO)ETHYL)-.ALPHA.-PHENYL-, (+/-)-, PHOSPHATE (1:1), 223-110-2 [EINECS], 2-pyridineacetamide, a-[2-[bis(1-methylethyl)amino]ethyl]-a-phenyl-, 2-Pyridineacetamide, α-(2-(bis(1-methylethyl)amino)ethyl)-α-phenyl-, 2-Pyridineacetamide, α-[2-[bis(1-methylethyl)amino]ethyl]-α-phenyl- [ACD/Index Name], 3737-09-5 [RN], 4-(Diisopropylamino)-2-phenyl-2-(2-pyridinyl)butanamid [German] [ACD/IUPAC Name], 4-(Diisopropylamino)-2-phenyl-2-(2-pyridinyl)butanamide [ACD/IUPAC Name], 4-(Diisopropylamino)-2-phényl-2-(2-pyridinyl)butanamide [French] [ACD/IUPAC Name], 4-(Diisopropylamino)-2-phenyl-2-(2-pyridyl)butyramide, 4-(Diisopropylamino)-2-phenyl-2-(pyridin-2-yl)butanamide, 4-(dipropan-2-ylamino)-2-phenyl-2-(pyridin-2-yl)butanamide, a-[2-(Diisopropylamino)ethyl]-a-phenyl-2-pyridineacetamide, a-[2-[Bis(1-methylethyl)amino]ethyl]a-phenyl-2-pyridineacetamide, disopiramida [Spanish] [INN], Disopyramide [French] [INN], Disopyramide [BAN] [INN] [JAN] [JP15] [USAN] [Wiki], Disopyramide, (R)-, Disopyramide, (S)-, disopyramidum [Latin] [INN], Isorythm, Lispine, MFCD00057366 [MDL number], Norpace [Trade name], Rythmodan [Trade name], α-[2-(DIISOPROPYLAMINO)ETHYL]-α-PHENYL-2-PYRIDINEACETAMIDE, α-Diisopropylaminoethyl-α-phenylpyridine-2-acetamide, дизопирамид [Russian] [INN], 丙吡胺 [Chinese] [INN], Disopyramide free base, NORPACE CR, Rythmodan-La, ξ-Disopyramide, [3737-09-5] [RN], 1309283-08-6 [RN], 2-Pyridineacetamide, α-(2-(diisopropylamino)ethyl)-α-phenyl-, 2-Pyridineacetamide, α-[2-(diisopropylamino)ethyl]-α-phenyl-, 2-Pyridineacetamide, α-[2-[bis(1-methylethyl)amino]ethyl]-α-phenyl-, 3737-09-5 (free base), 38236-46-3 [RN], 4-(diisopropylamino)-2-phenyl-2-(2-pyridyl)butanamide, 4-(diisopropylamino)-2-phenyl-2-pyridin-2-ylbutanamide, 4-[bis(methylethyl)amino]-2-phenyl-2-(2-pyridyl)butanamide, 4-[bis(propan-2-yl)amino]-2-phenyl-2-(pyridin-2-yl)butanamide, 4-[bis(propan-2-yl)amino]-2-phenyl-2-(pyridin-2-yl)butanimidic acid, 4-[di(propan-2-yl)amino]-2-phenyl-2-(pyridin-2-yl)butanamide, 4-[di(propan-2-yl)amino]-2-phenyl-2-pyridin-2-ylbutanamide, 492056 [Beilstein], 4-Diisopropylamino-2-phenyl-2-(2-pyridyl)-butyramide, 54687-36-4 [RN], 74464-83-8 [RN], 74464-84-9 [RN], BS-17145, DB00280, Dicorantil, Disopiramida, Disopiramida [INN-Spanish], Disopyramide-d5, Disopyramidum, Disopyramidum [INN-Latin], MFCD00069254 [MDL number], n-desalkyl Disopyramide, Norpace®, Ritmodan, Rythmodan P [Trade name], Rythmodan®, Searle 703, α-(2-(Diisopropylamino)ethyl)-α-phenyl-2-pyridineacetamide, α-(2-(Diisopropylamino)ethyl)-α-phenyl-2-pyridineacetamide, α-[2-[bis(1-methylethyl)amino]ethyl]-α-phenyl-2-pyridineacetamide, γ-Diisopropylamino-α-phenyl-α-(2-pyridyl)butyramide, γ-Diisopropylamino-α-phenyl-α-(2-pyridyl)butyramide, дизопирамид, 丙吡胺

Rythmodan is an antiarrhythmic chemical used in the treatment of ventricular tachycardia.
Rythmodan is a sodium channel blocker and is classified as a Class 1a anti-arrhythmic agent.

Rythmodan has a negative inotropic effect on the ventricular myocardium and significantly reduces contractility.
Rythmodan also has an anticholinergic effect on the heart, which is responsible for many negative side effects.
Rythmodan is available in both oral and intravenous forms and has a low degree of toxicity.

Rythmodan is registered under the REACH Regulation and is manufactured in and / or imported to the European Economic Area, for intermediate use only.
Rythmodan is used at industrial sites and in manufacturing.

Rythmodan is an organoammonium phosphate.

Rythmodan is a class Ia antiarrhythmic agent with cardiac depressant properties.
Rythmodan exerts Rythmodan actions by blocking both sodium and potassium channels in cardiac membrane during phase 0 of the action potential.

This slows the impulse conduction through the AV node and prolongs the duration of the action potential of normal cardiac cells in atrial and ventricular tissues.
Rythmodan prolongs the QT interval and causes a widening of the QRS complex.

Rythmodan also possesses some anticholinergic and local anaesthetic properties.
Rythmodan is used in the treatment of supraventricular tachycardia.

A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine.
Rythmodan also possesses some anticholinergic and local anesthetic properties.

Rythmodan belongs to a group of medicines called anti-arrhythmic agents used to treat irregular heartbeats.
An irregular heartbeat is a condition in which your heart beats irregularly, too fast, or too slow.
Rythmodan helps slow the heart rate and prevent arrhythmias (abnormal heart rhythms).

Rythmodan sulphate contains Rythmodan, ie anti-arrhythmic agents.
Rythmodan helps bring irregular heartbeats to a normal rhythm by blocking certain electrical signals in the heart.
Irregular heartbeat treatment reduces the risk of blood clots, heart attack or stroke.

Rythmodan should be taken as prescribed by the doctor.
Your doctor may monitor EKGs and blood pressure during treatment to monitor your dose.

Some people may experience common side effects such as blurred or double vision, stomach pain, little or no urination, and low blood sugar.
Most of these side effects of Rythmodan do not require medical attention and will gradually improve over time.
However, if the side effects persist, please consult your doctor.

Please tell your doctor if you are known to be allergic to Rythmodan or any other medicines.
Rythmodan is not recommended for use in children.
Pregnant or breastfeeding women are advised to consult a doctor before taking Rythmodan.

Before taking Rythmodan, tell your doctor if you have kidney or liver disease, enlarged prostate, glaucoma (increased eye pressure) or low potassium levels in the blood (hypokalaemia).
Do not take Rythmodan if you are already taking other medicines to regulate your heartbeat.

Do not drive or operate machinery as Rythmodan may cause blurred vision, dizziness and low blood pressure.
Use Rythmodan with caution if you are elderly (over 65 years of age), have a low body weight, or have kidney or liver problems.

Rythmodan is used to treat certain irregular heartbeats).
Rythmodan is in a class of medications called antiarrhythmic drugs.
Rythmodan works by making your heart more resistant to abnormal activity.

Continuing Education Activity:
Rythmodan is a chemical used to treat heart rhythm abnormalities that can be life-threatening, such as ventricular tachycardia/fibrillation, or associated with increased morbidity and mortality, such as atrial fibrillation and hypertrophic cardiomyopathy.
This activity reviews several important aspects of this chemical, including indications, mechanism of action, applications, side effects, contraindications, monitoring, and toxicity.
This important knowledge of this chemical can improve interprofessional healthcare team outcomes.

Objectives:
Describe the mechanism of action of Rythmodan.
Describe possible side effects of Rythmodan.

Explains the importance of monitoring when using Rythmodan as an antiarrhythmic chemical.
Outline professional team strategies for improving care coordination and communication when using Rythmodan to maximize the benefits of this chemical and minimize Rythmodan side effects.

Indications:
In 1962, new antiarrhythmic drugs were needed apart from quinidine and procainamide, which were the main antiarrhythmic agents available at the time.
Rythmodan is the selected agent among more than 500 compounds synthesized for the research program of new antiarrhythmic agents.
The chemical structures of Rythmodan are similar to the synthetic muscarinic antagonist lacquer, which explains Rythmodan anticholinergic property.

Although Rythmodan is rarely used for heart rhythm abnormalities due to the availability of newer drugs that provide better efficacy and favorable side-effect profiles, Rythmodan is still the drug of choice for vagal-mediated atrial fibrillation such as sleep-induced or atrial fibrillation in athlete groups.
The effectiveness of Rythmodan in these conditions is due to Rythmodan anticholinergic activity, which abolishes the parasympathetic tone.

Rythmodan is also a third-line antiarrhythmic agent for a patient with coronary artery disease.
Also, a patient with left ventricular hypertrophy has impaired depolarization, which can induce torsade de pointes.

Therefore, antiarrhythmics that prolong the QT interval are avoided, but if sotalol or amiodarone is unsuccessful or unsuitable, Rythmodan may be an alternative.
In a patient with atrial fibrillation and hypertrophic obstructive cardiomyopathy (HOCM), Rythmodan is the agent of choice, other than amiodarone, as Rythmodan may decrease the left ventricular outflow tract (LVOT) gradient (off-label use).

Data from a multicenter study of the safety and efficacy of Rythmodan in obstructive cardiomyopathy showed that Rythmodan significantly reduced the SVOT gradient from 75+/- 33 to 40+/-32 mmHg in 78 patients (66% of study subjects) (P<0.0001). has shown. ) and raises the New York Heart Association functional class (NYHA FC) from 23+/-07 to 17+/-06 (P<0.0001).
When Rythmodan is used in combination with a non-dihydropyridine calcium channel blocker or beta blocker, they can effectively prevent recurrence of AF in HCOM patients.

Patients with ventricular premature beat (VPB) or premature ventricular complexes (PVC) may have a high symptom burden.
Rythmodan can be used in patients without structural heart disease, although Rythmodan efficacy is less than ablation.
In addition, based on a randomized, double-blind, placebo-controlled one-year follow-up study, Rythmodan (n=44) was effective in maintaining sinus rhythm after electro cardioversion for atrial fibrillation compared to placebo (n=46) and was significantly different (%) at one-month follow-up. 70 vs 39%) and continues after twelve months (54% vs 30%).

Uses of Rythmodan:
Rythmodan is used to treat certain types of serious (possibly fatal) irregular heartbeat (such as sustained ventricular tachycardia).
Rythmodan is used to restore normal heart rhythm and maintain a regular, steady heartbeat.

Rythmodan is known as an anti-arrhythmic drug.
Rythmodan works by blocking certain electrical signals in the heart that can cause an irregular heartbeat.
Treating an irregular heartbeat can decrease the risk for blood clots, and this effect can reduce your risk of heart attack or stroke.

Usage of Rythmodan:
Rythmodan comes as a capsule and an extended-release (long-acting) capsule to take by mouth.
Rythmodan capsules may be taken every 6 or 8 hours.

The extended-release capsule is usually taken every 12 hours.
Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand.

Take Rythmodan exactly as directed.
Do not take more or less of Rythmodan or take it more often than prescribed by your doctor.

Swallow the extended-release capsules; do not open, crush, or chew them.

Rythmodan helps control your condition but will not cure it.
Continue to take Rythmodan even if you feel well.
Do not stop taking Rythmodan without talking to your doctor.

Mechanism of action of Rythmodan:
Rythmodan's Class 1a activity is similar to that of quinidine in that Rythmodan targets sodium channels to inhibit conduction.
Rythmodan depresses the increase in sodium permeability of the cardiac myocyte during Phase 0 of the cardiac action potential, in turn decreasing the inward sodium current.

This results in an increased threshold for excitation and a decreased upstroke velocity.
Rythmodan prolongs the PR interval by lengthening both the QRS and P wave duration.

This effect is particularly well suited in the treatment of ventricular tachycardia as Rythmodan slows the action potential propagation through the atria to the ventricles.
Rythmodan does not act as a blocking agent for beta or alpha adrenergic receptors, but does have a significant negative inotropic effect on the ventricular myocardium.
As a result, the use of Rythmodan may reduce contractile force up to 42% at low doses and up to 100% in higher doses compared to quinidine.

Levites proposed a possible secondary mode of action for Rythmodan, against reentrant arrhythmias after an ischemic insult.
Rythmodan decreases the inhomogeneity between infarcted and normal myocardium refractory periods; in addition to lengthening the refractory period.

This decreases the chance of re-entry depolarization, because signals are more likely to encounter tissue in a refractory state which cannot be excited.
This provides a possible treatment for atrial and ventricular fibrillation, as Rythmodan restores pacemaker control of the tissue to the SA and AV nodes.

Pharmacology and Biochemistry of Rythmodan:

MeSH Pharmacological Classification:

Anti-Arrhythmia Agents:
Agents used for the treatment or prevention of cardiac arrhythmias.
They may affect the polarization-repolarization phase of the action potential, Rythmodan excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers.
Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.

Obstructive hypertrophic cardiomyopathy:
Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disease, occurring in 1:500 individuals in the general population.
Rythmodan is estimated that there are 600,000 individuals in the United States with hypertrophic cardiomyopathy.

The most common variant of HCM presents with left ventricular (LV) intracavitary obstruction due to systolic anterior motion of the mitral valve, and mitral-septal contact, diagnosed readily with echocardiography.
Pharmacologic treatment with negative inotropic drugs is first-line therapy.

Beta-blockers are used first, and while they improve symptoms of shortness of breath, chest pain and exercise intolerance, they do not reduce resting LV intraventricular pressure gradients and often are inadequate to control symptoms.
Many investigators and clinicians believe that Rythmodan controlled release is the most potent agent available for reducing resting pressure gradients and improving symptoms.

Rythmodan has been actively used for more than 30 years.
Rythmodan administration for obstructive HCM has a IB recommendation in the 2020 American Heart Association/American College of Cardiology Foundation guidelines for treatment of obstructive HCM.
A IB treatment recommendation indicates that a treatment is recommended, and may be useful, and beneficial.

Negative inotropes improve LV obstruction by decreasing LV ejection acceleration and hydrodynamic forces on the mitral valve.
Rythmodan's particular efficacy is due to Rythmodan potent negative inotropic effects; in head-to-head comparison, Rythmodan is more effective for gradient reduction than either beta-blocker or verapamil.

Rythmodan is most often administered with beta-blockade.
When used in patients resistant to beta-blockade, Rythmodan is effective in 60% of cases, reducing symptoms and gradient to the extent that invasive procedures such as surgical septal myectomy are not required.

Rythmodan, despite Rythmodan efficacy, has one main side effect that has limited Rythmodan use in the US, though Rythmodan has seen wider application in Canada, UK and Japan.
Vagal blockade predictably causes dry mouth, and in men with prostatism, may cause urinary retention.
Teichman et al. showed that pyridostigmine used in combination with Rythmodan substantially alleviates vagolytic side effects without compromising antiarrhythmic efficacy.

This combination has also been shown to be effective and safe in obstructive HCM in a large cohort of patients.
Some clinicians prescribe pyridostigmine sustained release (marketed in the US as Mestinon Timespan) to every patient begun on Rythmodan.
This combination increases acceptance of higher Rythmodan dosing, important since there is a dose-response correlation in obstructive HCM, higher doses yielding lower gradients.

Another concern about Rythmodan has been the hypothetical potential for inducing sudden death from Rythmodan type 1 anti-arrhythmic effects.
However, a multicenter registry and two recent cohort registries have largely reduced this concern, by showing sudden death rates lower than that observed from the disease itself.

These concerns about the drug must be viewed from the clinical perspective that Rythmodan is generally the last agent that is tried for patients before they are referred for invasive septal reduction with surgical septal myectomy (an open-heart operation) or alcohol septal ablation (a controlled heart attack).
Both of these invasive procedures have risk of morbidity and mortality.

For selected patients, a trial of oral Rythmodan is a reasonable approach before proceeding to invasive septal reduction.
Patients who respond to Rythmodan are continued on the drug.

Those who continue to have disabling symptoms or who experience side effects are promptly referred for septal reduction.
Using such a stepped strategy, investigators have reported that survival does not differ from that observed in the age-matched normal United States population.

Extracardiac effects:
Atropine like effects (anticholinergic)
Dry mouth
Constipation
Urinary retention – Rythmodan should not be given to patients with symptomatic prostatism.
Blurred vision
Glaucoma
Rash
Agranulocytosis

Additionally, Rythmodan may enhance the hypoglycaemic effect of gliclazide, insulin, and metformin.

Metabolism of Rythmodan:
Rythmodan can cause hypoglycemia, perhaps due to increased secretion of insulin, and can also potentiate the effects of conventional hypoglycemic drugs.
This effect may be due to Rythmodan chief metabolite mono-N dealkylRythmodan, since many of the reported cases of hypoglycemia have been in patients with renal impairment, in which the metabolite accumulates.

In six subjects who were being considered for treatment with Rythmodan, serum glucose concentrations were measured at 13, 15, 17, and 19 hours after supper, with no further food, with and without the added administration of two modified-released tablets of Rythmodan 150 mg with supper and 12 hours later.
Rythmodan significantly reduced the serum glucose concentration at all measurement times by an average of 0.54 mmol/l.
The fall in serum glucose concentration was not related to the serum concentration of Rythmodan or the serum creatinine concentration; Rythmodan was greater in older patients and in underweight patients.

Hypoglycemia has also been reported in a 70-year-old woman with type 2 diabetes mellitus taking Rythmodan.

Clinical data of Rythmodan:
Trade names: Norpace
AHFS/Drugs.com: Monograph
MedlinePlus: a682408
Pregnancy category: AU: B2
Routes ofadministration: Oral, intravenous
ATC code: C01BA03 (WHO)

Legal status:
UK: POM (Prescription only)
US: ℞-only

Pharmacokinetic data of Rythmodan:
Bioavailability: High
Protein binding: 50% to 65% (concentration-dependent)
Metabolism: Hepatic (CYP3A4-mediated)
Elimination half-life: 6.7 hours (range 4 to 10 hours)
Excretion: Renal (80%)

Identifiers of Rythmodan:
IUPAC name: (RS)-4-(Diisopropylamino)-2-phenyl-2-(pyridin-2-yl)butanamide
CAS Number: 3737-09-5
PubChem CID: 3114
IUPHAR/BPS: 7167
DrugBank: DB00280
ChemSpider: 3002
UNII: GFO928U8MQ
KEGG: D00303
ChEBI: CHEBI:4657
ChEMBL: ChEMBL517
CompTox Dashboard (EPA): DTXSID1045536
ECHA InfoCard: 100.021.010

Properties of Rythmodan:
Formula: C21H29N3O
Molar mass: 339.483 g·mol−1
Melting point: 94.5 to 95 °C (202.1 to 203.0 °F)
SMILES: O=C(N)C(c1ncccc1)(c2ccccc2)CCN(C(C)C)C(C)C
InChI: InChI=1S/C21H29N3O/c1-16(2)24(17(3)4)15-13-21(20(22)25,18-10-6-5-7-11-18)19-12-8-9-14-23-19/h5-12,14,16-17H,13,15H2,1-4H3,(H2,22,25)
Key:UVTNFZQICZKOEM-UHFFFAOYSA-N

Molecular Weight: 437.5 g/mol
Hydrogen Bond Donor Count: 4
Hydrogen Bond Acceptor Count: 7
Rotatable Bond Count: 8
Exact Mass: 437.20795813 g/mol
Monoisotopic Mass: 437.20795813 g/mol
Topological Polar Surface Area: 137Å²
Heavy Atom Count: 30
Complexity: 459
Isotope Atom Count: 0
Defined Atom Stereocenter Count: 0
Undefined Atom Stereocenter Count: 1
Defined Bond Stereocenter Count: 0
Undefined Bond Stereocenter Count: 0
Covalently-Bonded Unit Count: 2
Compound Is Canonicalized: Yes

Names of Rythmodan:

Regulatory process names:

Disopyramide

IUPAC names:
4-(diisopropylamino)-2-phenyl-2-pyridin-2-ylbutanamide
4-[bis(propan-2-yl)amino]-2-phenyl-2-(pyridin-2-yl)butanamide
Disopyramide

Other identifiers:
3737-09-5