Beta-adrenergic receptors (β2-adrenoceptors, IC50 = 32 ± 19 nmol/L for displacement of 125I-iodopindolol)
Sodium channels (cardiac)[1]

The growth of esophageal squamous cell carcinoma (ESCC) cells is inhibited by propafenone (5–25 μM) [3]. Propafenone reduces the potential of the mitochondrial membrane and decreases the expression of Bcl-xL and Bcl-2, which results in mitochondrial malfunction [3]. The anti-apoptotic proteins Bcl-xL and Bcl-2 were found to have their expression levels dramatically down-regulated in ESCC cells with propafenone (10 and 20 μ m) treatment. Additionally, propafenone can lower p-ERK expression [3].

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Propafenone displaced 125I-iodopindolol from β2-adrenoceptors on human lymphocytes in a concentration-dependent manner. The displacement curve was monophasic. The IC50 value for propafenone was 32 ± 19 nmol/L (Ki = 12 ± 4 nmol/L). In comparison, its metabolite N-desalkyl propafenone had an IC50 of 90 ± 38 nmol/L (Ki = 37 ± 15 nmol/L), and 5-hydroxy propafenone had an IC50 of 478 ± 154 nmol/L (Ki = 181 ± 61 nmol/L), indicating that the parent drug propafenone has the highest affinity for β2-adrenoceptors among the three compounds.[1]
In vitro studies readily demonstrate the beta-blocking actions of propafenone.[1]
As a sodium-channel blocking agent, propafenone is effective in managing atrial and ventricular arrhythmias.[1]

Tumor burden was significantly reduced by 69.2% when propafenone (20 mg/kg; intraperitoneally injected every other day) was administered [3]. Additionally, tumor cell proliferation was significantly reduced (average index dropped from 56.3±6.7% in the DMSO-treated group to 20.7±5.1% in the 10 mg/kg propafenone-treated group and from 20.7±5.1% in the 20 mg/kg propafenone-treated group to 11.3±4.0%. treatment group) [3].

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In 14 normal human subjects, treatment with propafenone (150, 225, and 300 mg every eight hours for five days each) produced beta-blockade, as measured by the reduction in tachycardia induced by isoproterenol boluses and treadmill exercise. The degree of beta-blockade varied with the metabolizer phenotype. At lower dosages (150 and 225 mg), subjects with the poor-metabolizer phenotype (n=5) exhibited significantly greater beta-blockade compared to those with the extensive-metabolizer phenotype (n=9). At the highest dose (300 mg), a similar degree of beta-blockade was observed in both groups.[1]
The beta-blocking effect of propafenone in vivo was correlated with its plasma concentration. A 10% reduction in maximal exercise heart rate was estimated to occur at plasma propafenone concentrations of approximately 3.12 ± 1.50 µmol/L (1065 ± 513 ng/mL) in extensive metabolizers and 3.30 ± 1.10 µmol/L (1126 ± 377 ng/mL) in poor metabolizers.[1]
Prolongation of the QRS complex, an in vivo marker of sodium-channel blockade, was more prominent at any given plasma concentration of propafenone in subjects with the extensive-metabolizer phenotype than in those with the poor-metabolizer phenotype, suggesting metabolites contribute to sodium-channel blockade.[1]

Cell proliferation assay[3]
Cell Types: Human esophageal squamous cell carcinoma lines KYSE30, KYSE150 and KYSE270
Tested Concentrations: 5, 10, 15, 20 and 25 μm
Incubation Duration: 24, 48 and 72 hrs (hours)
Experimental Results: Cells over time Proliferation gradually diminished in KYSE30, KYSE150 and KYSE270 cells, and cell proliferation was effectively inhibited with increasing concentration.

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Western Blot Analysis [3]
Cell Types: Human ESCC cell lines KYSE30, KYSE150 and KYSE270
Tested Concentrations: 0, 10 and 20 μm
Incubation Duration: 72 hrs (hours)
Experimental Results: A significant down-regulation of Bcl-xL and Bcl-2 expression levels was observed.

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The affinity of propafenone and its metabolites for beta-adrenergic receptors was assessed using a radioligand binding assay on human lymphocytes. Lymphocytes were presumably isolated from human blood. The specific binding of the radioligand 125I-iodopindolol to β2-adrenoceptors on these cells was measured in the presence of increasing concentrations of propafenone, N-desalkyl propafenone, or 5-hydroxy propafenone. Displacement curves were generated, and IC50 values (concentration inhibiting 50% of specific binding) were determined. The dissociation constant (Ki) was also calculated. The shape of the curves was analyzed to be monophasic.[1]

Animal/Disease Models: Female BALB/c nude mice (6-8 weeks) carrying KYSE270 xenografts [3]
Doses: 10 mg/kg or 20 mg/kg
Route of Administration: intraperitoneal (ip) injection
Experimental Results:Significant effect on tumor growth Inhibitory xenografts.

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Tumor Xenograft Model: Female BALB/c nude mice (6-8 weeks old) were subcutaneously implanted with KYSE270 cells (5 × 10⁵ cells in a mixture of PBS and Matrigel) to establish tumor xenografts. When tumors reached approximately 5 mm in diameter, mice were randomly divided into control and treatment groups. The treatment groups received intraperitoneal injections of propafenone at doses of 10 mg/kg or 20 mg/kg every other day. The control group received vehicle only. Body weight and tumor size (measured every three days, volume calculated as length × width² / 2) were monitored. At the end of the study, tumors and vital organs (lungs, liver, kidneys) were collected for further analysis (immunohistochemistry, Western blot, histological examination). [3]

Absorption, Distribution and Excretion
Almost completely absorbed (90%) after oral administration. Due to significant first-pass metabolism, systemic bioavailability ranges from 5% to 50%. This wide variation in systemic bioavailability is related to two factors: the presence of food (food increases bioavailability) and dosage (3.4% bioavailability for a 150 mg tablet versus 10.6% for a 300 mg tablet). Approximately 50% of the pipandone metabolites are excreted in the urine after administration of immediate-release tablets. For patients with ventricular arrhythmias and a broad metabolic phenotype taking 337.5, 450, 675, or 900 mg of pipandone hydrochloride (immediate-release tablets) daily, the plasma 5-hydroxypipandone (5-OHP) to pipandone ratios are 45%, 40%, 24%, and 19%, respectively; while some patients with a weak metabolic phenotype have a higher relative proportion of 5-OHP in their plasma. High parent drug concentrations were observed at all doses, and 5-OHP was not detected. The ratio of N-depropylpicamenone (NDPP) to pipandone was similar in both fast and slow metabolizers (approximately 10% and 6%, respectively). In slow metabolizers, NDPP was the major metabolite, and 5-OHP may be undetectable. In healthy individuals with a fast metabolizer phenotype, after oral administration of 300 mg pipandone hydrochloride (immediate-release tablets) every 8 hours for 14 days, the mean plasma concentrations of pipandone, 5-OHP, and NDPP were 1010, 174, and 179 ng/mL, respectively. In an individual considered to have a weak metabolizer phenotype, after oral administration of the immediate-release tablets, the plasma concentrations of pipandone, 5-hydroxyacetone (5-OHP), and NDPP were 1048 ng/mL, undetectable, and 219 ng/mL, respectively. Following administration of pipandoxane hydrochloride extended-release capsules, plasma concentrations of 5-OHP and NDPP are typically 40% and 10% lower than the plasma concentration of pipandoxane, respectively. The concentration patterns of pipandoxane and its metabolites in plasma during long-term oral pipandoxane treatment depend primarily on genetically determined metabolic phenotypes, and secondarily on hepatic blood flow and enzyme function. In individuals with normal hepatic and renal function, steady-state plasma concentrations of the parent drug and its metabolites are reached within 4-5 days after oral administration of pipandoxane (immediate-release tablets). Plasma concentrations of 5-hydroxypipandoxane (5-OHP) and N-depropylpipandoxane (NDPP) are typically 20% lower than those of pipandoxane on average. Slower metabolizers taking 675-900 mg of pipandoxane hydrochloride (immediate-release tablets) daily have plasma pipandoxane concentrations 1.5-2 times higher than those with faster metabolizers; at lower doses, plasma pipandoxane concentrations in individuals with weaker metabolic capacity may be more than five times higher than those in individuals with stronger metabolic capacity. The significant individual variability in pipandone pharmacokinetics observed in individuals with high metabolic capacity is primarily attributed to first-pass hepatic metabolism and nonlinear pharmacokinetics. Individual variability in pipandone pharmacokinetic parameters increases after both single and multiple doses of pipandone hydrochloride extended-release capsules. The fact that inter-individual variability in pipandone pharmacokinetics is significantly smaller in individuals with low metabolic capacity than in those with high metabolic capacity suggests that this difference may not be due to the drug formulation but rather to CYP2D6 polymorphism. In healthy individuals, a single oral dose (300 or 450 mg immediate-release tablet) or intravenous injection (35–50 mg) of pipandone hydrochloride produces similar peak plasma concentrations (278 ng/mL and 295 ng/mL, respectively). However, 5-hydroxypipandone (5-OHP) or N-depropylpipandone (NDPP) was not detected in plasma after intravenous injection in these individuals. Because 5-OHP and NDPP possess significant clinical antiarrhythmic activity, the efficacy of pipandone may vary depending on whether it is administered orally or intravenously. Significant individual variability exists in plasma concentrations following administration of the same dose of pipandone and its metabolites. In healthy individuals, after a single oral dose of pipandone hydrochloride immediate-release tablets (300–450 mg), the mean peak plasma concentrations of 5-hydroxyacetone (5-OHP) and dihydroacetone phosphate (NDPP) were 101–288 ng/mL and 8–40 ng/mL, respectively. In patients with a wide range of metabolic phenotypes, pipandone, 5-OHP, and NDPP all exhibit nonlinear pharmacokinetic characteristics, although the pharmacokinetic deviations of 5-OHP and NDPP are smaller. The pharmacokinetic characteristics of pipandone, 5-hydroxyacetone, and N-depropylacetone appear to be significantly unaffected by age or sex. For more complete data on the absorption, distribution, and excretion of pipandone (15 metabolites), please visit the HSDB records page.

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Metabolism/Metabolites
Pipandone is primarily metabolized in the liver, where it is rapidly and extensively metabolized into two active metabolites: 5-hydroxypipandone and N-depropylpipandone. These metabolites have antiarrhythmic activity comparable to pipandone, but at concentrations less than 25% of pipandone's concentration.
In individuals with a broad metabolic phenotype, pipandone is metabolized in the liver into two active metabolites and at least nine other metabolites. The two active metabolites, 5-hydroxypipandone (5-OHP) and N-depropylpipandone (NDPP), are formed from the parent drug via hydroxylation and dealkylation, respectively. Pipandone is hydroxylated to 5-OHP by the cytochrome P-450 isoenzyme CYP2D6 (a genetically controlled enzyme). NDPP formation is catalyzed by different isoenzymes CYP1A2 and CYP3A4. Differences in the metabolism of R- and S-propapfenone have been observed in animals and humans treated with single enantiomers of this drug, which are related to their stereoselective interactions with the CYP2D6 isoenzyme. Following oral administration of 250 mg R- or S-propapfenone hydrochloride to adults with a fast-metabolizing phenotype, the mean elimination half-life, clearance, and volume of distribution of R-propapfenone were shorter than those of S-propapfenone, while the AUC was larger; however, these stereoselective effects were not observed in adults with a slow-metabolizing phenotype who received different enantiomers. In vitro and in vivo studies have shown that the R-enantiomer is cleared faster than the S-enantiomer via the 5-hydroxylation pathway (CYP2D6). This results in a higher ratio of S- to R-enantiomers at steady state. Although both enantiomers have the same sodium channel blocking potency, the S-enantiomer exhibits stronger β-adrenergic antagonism than the R-enantiomer. Following administration of propafenone hydrochloride (immediate-release tablets or extended-release capsules), the observed AUC ratio of S-enantiomers to R-enantiomers (S/R ratio) was approximately 1.7. After administration of 225, 325, or 425 mg extended-release capsules, the S/R ratio was dose-independent. Furthermore, the observed S/R ratios were similar across metabolic genotypes and after long-term administration. Propafenone is primarily metabolized in two modes. These modes are determined by an individual's ability to metabolize the drug via hepatic oxidative pathways. The ability to oxidatively metabolize propafenone depends on an individual's ability to metabolize dehydroisoquinoline (dehydroisoquinoline phenotype). The dehydroisoquinoline phenotype, or the observed propafenone metabolite pattern, can be used to determine an individual's propafenone metabolic phenotype. Individuals who extensively metabolize propafenone via oxidative pathways exhibit a strong metabolic phenotype, while those with impaired ability to metabolize the drug via this pathway exhibit a weak metabolic phenotype. Approximately 90–95% of Caucasians exhibit a strong metabolic phenotype, with the remainder exhibiting a weak metabolic phenotype. In patients with a poor metabolic phenotype, propafenone metabolism is characterized by a linear dose-concentration relationship and a relatively long terminal elimination half-life. Compared to individuals with a high metabolic capacity, these individuals have elevated plasma propafenone concentrations and are more prone to β-adrenergic blockade and adverse drug reactions. Known metabolites of propafenone include 5-hydroxypropafenone and N-depropylpropafenone. Biological half-life: 2-10 hours. For adults with a high metabolic capacity and normal renal and hepatic function, the average elimination half-life of propafenone after a single or multiple oral doses of immediate-release tablets is approximately 1-3 hours (range: 2-10 hours). For adults with a poor metabolic capacity, the average half-life of propafenone is approximately 8-13 hours (range: 6-36 hours). The half-life of a single oral dose of 300 mg of immediate-release pipandoxine hydrochloride is 3.5 hours; the half-life of a daily dose of 300 mg of pipandoxine hydrochloride for 1 month and 3 months is 6.7 hours and 5.8 hours, respectively. The steady-state plasma elimination half-life of pipandoxine is prolonged in slower metabolizers, averaging 17.2 hours (range: 10–32 hours), while it is 5.5 hours (range: 2–10 hours) in faster metabolizers. Pipandoxine is metabolized polymorphically in the human body and is mainly mediated by the hepatic cytochrome P450 isoenzyme P-450dbl (CYP2D6). Approximately 7% of the U.S. population is a metabolically inefficient individual with insufficient activity of this enzyme. [1]
Pipandoxine can be bioconverted into two main active metabolites: 5-hydroxypipandoxine and N-dealkylpipandoxine (N-depropylpipandoxine). The formation of 5-hydroxypipandoxine is catalyzed by CYP2D6. [1]
In individuals with poor metabolic capacity, the biotransformation of pipandone to 5-hydroxypipandone was severely impaired. This resulted in significantly higher steady-state concentrations of parent pipandone and N-desalkylpipandone in plasma compared to individuals with good metabolic capacity, while the concentration of 5-hydroxypipandone was significantly lower or undetectable. For example, after taking 150 mg every 8 hours, the trough concentration of pipandone in plasma was 0.56 ± 0.54 µmol/L in fast metabolizers and 3.18 ± 0.76 µmol/L in slow metabolizers. 5-hydroxypipandone was not detected in slow metabolizers. [1]
In fast metabolizers, the plasma concentration of pipandone increased disproportionately with dose, suggesting saturation of the CYP2D6 metabolic pathway. In slow metabolizers, the plasma concentration of pipandone increased more linearly with dose. [1]
In slow metabolizers, the metabolism of pipandone may be diverted to N-dealkylation, as evidenced by elevated N-dealkylpipandone levels in this group. [1]

Hepatotoxicity
In clinical trials, propafenone was associated with a low incidence of elevated serum transaminases and alkaline phosphatase. Since its approval and widespread use, propafenone has been associated with rare cases of clinically significant liver injury, with at least a dozen cases reported in the literature. Patients typically develop jaundice and pruritus 2 to 8 weeks after starting propafenone, with serum enzyme elevations usually presenting as mixed (Case 1) or cholestatic (Case 2). Immune allergies and autoimmune features are uncommon. Although jaundice may persist for a long time, patients usually recover within 1 to 3 months, and there have been no reported cases of acute liver failure, chronic hepatitis, or bile duct disappearance syndrome due to the use of this drug. Probability Score: B (Rare but may lead to clinically significant liver injury). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation Limited information suggests that low concentrations of propafenone in breast milk are observed when mothers take up to 900 mg of propafenone daily. If the mother needs to take propafenone, breastfeeding does not need to be stopped. Until more data is available, breastfeeding women should use propafenone with caution, especially when breastfeeding newborns or premature infants.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
No published information found as of the revision date.

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Protein binding rate
97%

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Drug interactions
While there are currently no specific pharmacokinetic drug interaction studies, the manufacturer of propafenone notes that this drug should not be used concurrently with other drugs that prolong the QT interval, including certain phenothiazines, cisapride, benprimidil (currently not marketed in the US), tricyclic antidepressants, or macrolide antibiotics.
While there are currently no specific pharmacokinetic drug interaction studies, the manufacturer of ritonavir notes that ritonavir should not be used concurrently with propafenone. Because certain cardiovascular drugs, including propafenone, can cause significantly elevated plasma concentrations of these drugs and may produce serious and/or life-threatening side effects, they should not be used concurrently with propafenone. This pharmacokinetic interaction may occur due to ritonavir's high affinity for several cytochrome P-450 (CYP) isoenzymes (e.g., CYP3A, CYP2D6, CYP1A2) involved in propafenone metabolism. Elevated serum theophylline concentrations have been reported in patients receiving theophylline in combination with propafenone, and some clinicians recommend close monitoring of serum theophylline concentrations and electrocardiograms in patients receiving such combination therapy. The manufacturer notes that concomitant use of propafenone with local anesthetics (e.g., during pacemaker implantation, surgery, or dental procedures) may increase the risk of adverse neurological reactions. For more complete data on propafenone interactions (24 items in total), please visit the HSDB record page.

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Non-human toxicity values
LD50 Dogs intravenous injection 10 mg/kg propafenone hydrochloride/
Rat intravenous injection LD50: 18,800 μg/kg / propafenone hydrochloride/
Rat oral LD50: 700 mg/kg / propafenone hydrochloride/

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It has been reported that the incidence of side effects increases significantly when the plasma trough concentration of propafenone exceeds 2.64 µmol/L (900 ng/mL). Such high concentrations are more common in subjects with poor metabolism phenotypes. [1]
The clinically significant β-receptor blocking effect of propafenone may be considered a side effect in some cases (e.g., in asthmatic patients), but it is not stable in vivo and is more pronounced in poorly metabolized individuals due to higher accumulation of the parent drug. [1]
Although β-receptor blocking effects were observed, no changes in FEV1 (a pulmonary function indicator) were found in the normal subjects studied. [1]

[1]. The role of genetically determined polymorphic drug metabolism in the beta-blockade produced by propafenone. N Engl J Med. 1990 Jun 21;322(25):1764-8.

[2]. Effects of propafenone on K currents in human atrial myocytes. Br J Pharmacol. 1999 Mar;126(5):1153-62.

[3]. Propafenone suppresses esophageal cancer proliferation through inducing mitochondrial dysfunction. Am J Cancer Res. 2017 Nov 1;7(11):2245-2256.

Therapeutic Uses
Antiarrhythmic Drug
Propafenone hydrochloride immediate-release tablets are used to prolong the recurrence time of symptomatic, disabling paroxysmal supraventricular tachycardia (PSVT) (e.g., AV nodal reentrant tachycardia or AV reentrant tachycardia (Woo-Parkinson-White syndrome)) and symptomatic, disabling paroxysmal atrial fibrillation/atrial flutter (PAF) in patients without organic heart disease. Although comparative studies are limited, propafenone appears to be comparable to other antiarrhythmic drugs (e.g., quinidine, disopyramide, flecainide, procainamide, sotalol) in preventing PAF recurrence and maintaining sinus rhythm after successful atrial fibrillation cardioversion. /US Product Label Includes/
When administered in extended-release capsule form, propafenone is used to prolong the recurrence time of symptomatic paroxysmal atrial fibrillation in patients without organic heart disease. ²⁸⁹The safety and efficacy of propafenone extended-release capsules in patients with isolated paroxysmal supraventricular tachycardia or atrial flutter have not been established. /Included on US product label/
Propafenone hydrochloride (immediate-release tablets) are administered orally for the suppression and prevention of recurrence of recorded life-threatening ventricular arrhythmias (e.g., sustained ventricular tachycardia, ventricular fibrillation). Based on the results of the Cardiac Arrhythmia Suppression Trial (CAST), the US Food and Drug Administration (FDA), manufacturers, and many clinicians recommend that treatment with antiarrhythmic drugs (including propafenone) should be reserved for the suppression and prevention of recorded ventricular tachycardias deemed life-threatening by a clinician. /Included on US product label/
For more complete data on the therapeutic uses of disopyramine (one of 10), please visit the HSDB record page.

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Drug Warning
A long-term, multicenter, randomized, double-blind study conducted at the National Heart, Lung, and Blood Institute (CAST) in patients with asymptomatic, non-life-threatening ventricular arrhythmias (with a history of myocardial infarction more than 6 days but less than 2 years ago) found that patients treated with encainide or flecainide (class 1C antiarrhythmics) had a higher rate of death or cardiac arrest reversal (7.7%; 56/730) compared to the placebo group (3.0%; 22/725). The mean duration of treatment with encainide or flecainide in this study was ten months. The applicability of the CAST results to other populations (e.g., patients without recent myocardial infarction) or to other antiarrhythmic drugs is uncertain; however, it is currently advisable to consider any class 1C antiarrhythmic drug with significant risks in patients with structural heart disease.
Given the lack of any evidence that these drugs improve survival, antiarrhythmic drugs should generally be avoided in patients with non-life-threatening ventricular arrhythmias, even if the patient experiences uncomfortable but non-life-threatening symptoms or signs. The most common adverse reactions of propafenone involve the gastrointestinal, cardiovascular, and central nervous systems, and are usually dose-related. In clinical trials, approximately 20% of propafenone patients required discontinuation of treatment. Among patients receiving treatment for ventricular arrhythmias, the most common reasons for discontinuation (i.e., more than 1% of patients) were proarrhythmias (4.7%), nausea and/or vomiting (3.4%), dizziness (2.4%), dyspnea (1.6%), congestive heart failure (1.4%), and ventricular tachycardia (1.2%). In clinical trials, the most common (i.e., incidence exceeding 1%) reasons for discontinuation in patients receiving propafenone for supraventricular arrhythmias were nausea and/or vomiting (2.9%), wide QRS complex tachycardia (1.9%), dizziness (1.7%), fatigue (1.5%), dysgeusia (1.3%), and asthenia (1.3%). In US clinical trials of propafenone for ventricular arrhythmias, reported adverse neurological reactions included dizziness and/or lightheadedness, fatigue/drowsiness in 6% of patients, and headache in 5%. Among patients receiving propafenone for ventricular arrhythmias, 2% reported asthenia, ataxia, insomnia, or anxiety, and 1% reported tremor or drowsiness. Pain or balance disorders have been reported in patients with ventricular arrhythmias receiving propafenone. At least one patient treated with propafenone reported transient total amnesia, which resolved within hours of discontinuation of the drug. Rare cases of peripheral neuropathy have also been reported with propafenone treatment, characterized by intermittent tingling and squeezing pain in the hands and feet, and hyperesthesia in the extremities, which resolved upon discontinuation of the drug. For more complete (31) data on propafenone warnings, please visit the HSDB record page.

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Pharmacodynamics
Propafenone is a Class 1C antiarrhythmic drug with local anesthetic activity that directly stabilizes the myocardial cell membrane. It is used to treat atrial and ventricular arrhythmias. Propafenone reduces myocardial excitability by inhibiting sodium channels, limiting sodium ion entry into myocardial cells. The local anesthetic activity of propafenone is roughly equivalent to that of procaine.

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Propafenone is a Class Ic antiarrhythmic drug with sodium channel blocking activity and a structure similar to propranolol. It is used to treat atrial and ventricular arrhythmias. [1]
The degree of β-receptor blockade during propafenone treatment varies from person to person, mainly depending on the polymorphism of the CYP2D6 gene, which affects drug metabolism. Slower metabolizers experience enhanced β-receptor blockade due to higher exposure to the parent drug, which is the main mediator of this effect. [1]
The β-receptor blockade of propafenone may contribute to its antiarrhythmic efficacy, but it may also lead to certain side effects. [1]
The sodium channel blocking effect of propafenone is caused by the combined action of the parent drug and its active metabolite 5-hydroxypropafenone, the latter having equal or stronger potency in this regard. [1]

C21H27NO3

341.45

341.199

54063-53-5

Propafenone hydrochloride;34183-22-7;(S)-Propafenone;107381-32-8;Propafenone-d7 hydrochloride;1219799-06-0;Propafenone-d5 hydrochloride;1346605-05-7

4932

White to off-white solid powder

1.096 g/cm3

171 - 174ºC

268ºC

1.557

3.632

2

4

11

25

368

0

JWHAUXFOSRPERK-UHFFFAOYSA-N

InChI=1S/C21H27NO3/c1-2-14-22-15-18(23)16-25-21-11-7-6-10-19(21)20(24)13-12-17-8-4-3-5-9-17/h3-11,18,22-23H,2,12-16H2,1H3

1-[2-[2-hydroxy-3-(propylamino)propoxy]phenyl]-3-phenylpropan-1-one

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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