ESMOLOL HYDROCHLORIDE- esmolol hydrochloride injection, solution
Medical Purchasing Solutions, LLC
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HIGHLIGHTS OF PRESCRIBING INFORMATIONThese highlights do not include all the information needed to use ESMOLOL HYDROCHLORIDE INJECTION safely and effectively. See full prescribing information for ESMOLOL HYDROCHLORIDE INJECTION.
ESMOLOL HYDROCHLORIDE injection, for intravenous use Initial U.S. Approval: 1986 INDICATIONS AND USAGEEsmolol hydrochloride injection is a beta adrenergic blocker indicated for the short-term treatment of: DOSAGE AND ADMINISTRATION
DOSAGE FORMS AND STRENGTHS
CONTRAINDICATIONS
WARNINGS AND PRECAUTIONS
ADVERSE REACTIONSMost common adverse reactions (incidence >10%) are symptomatic hypotension (hyperhidrosis, dizziness) and asymptomatic hypotension
(6)
DRUG INTERACTIONSSee 17 for PATIENT COUNSELING INFORMATION. Revised: 7/2015 |
Esmolol hydrochloride injection is indicated for the rapid control of ventricular rate in patients with atrial fibrillation or atrial flutter in perioperative, postoperative, or other emergent circumstances where short term control of ventricular rate with a short-acting agent is desirable. Esmolol hydrochloride injection is also indicated in noncompensatory sinus tachycardia where, in the physician’s judgment, the rapid heart rate requires specific intervention. Esmolol hydrochloride injection is intended for short-term use.
Esmolol hydrochloride injection is indicated for the short-term treatment of tachycardia and hypertension that occur during induction and tracheal intubation, during surgery, on emergence from anesthesia and in the postoperative period, when in the physician’s judgment such specific intervention is considered indicated.
Use of esmolol hydrochloride injection to prevent such events is not recommended.
Esmolol hydrochloride injection is administered by continuous intravenous infusion with or without a loading dose. Additional loading doses and/or titration of the maintenance infusion (step-wise dosing) may be necessary based on desired ventricular response.
Table 1 Step-Wise Dosing
Step
| Action
|
1
| Optional loading dose (500 mcg per kg over 1 minute),
then 50 mcg per kg per min for 4 min |
2
| Optional loading dose if necessary, then 100 mcg per kg per min for 4 min
|
3
| Optional loading dose if necessary, then 150 mcg per kg per min for 4 min
|
4
| If necessary increase dose to 200 mcg per kg per min
|
In the absence of loading doses, continuous infusion of a single concentration of esmolol reaches pharmacokinetic and pharmacodynamic steady-state in about 30 minutes.
The effective maintenance dose for continuous and step-wise dosing is 50 to 200 mcg per kg per minute, although doses as low as 25 mcg per kg per minute have been adequate. Dosages greater than 200 mcg per kg per minute provide little added heart-rate lowering effect, and the rate of adverse reactions increases.
Maintenance infusions may be continued for up to 48 hours.
In this setting it is not always advisable to slowly titrate to a therapeutic effect. Therefore two dosing options are presented: immediate control and gradual control.
Immediate Control
Gradual Control
Maximum Recommended Doses
After patients achieve adequate control of the heart rate and a stable clinical status, transition to alternative antiarrhythmic drugs may be accomplished.
When transitioning from esmolol hydrochloride injection to alternative drugs, the physician should carefully consider the labeling instructions of the alternative drug selected and reduce the dosage of esmolol hydrochloride injection as follows:
1. Thirty minutes following the first dose of the alternative drug, reduce the esmolol hydrochloride infusion rate by one-half (50%).
2. After administration of the second dose of the alternative drug, monitor the patient's response, and, if satisfactory control is maintained for the first hour, discontinue the esmolol hydrochloride infusion.
Esmolol hydrochloride injection is available in a single dose vial. Esmolol hydrochloride injection is not compatible with Sodium Bicarbonate (5%) solution (limited stability) or furosemide (precipitation).
Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
Single Dose Vial
The Single Dose Vial may be used to administer a loading dosage by hand-held syringe while the maintenance infusion is being prepared.
Compatibility with Commonly Used Intravenous Fluids
Esmolol hydrochloride injection was tested for compatibility with ten commonly used intravenous fluids at a final concentration of 10 mg Esmolol Hydrochloride per mL. Esmolol hydrochloride injection was found to be compatible with the following solutions and was stable for at least 24 hours at controlled room temperature or under refrigeration:
Table 2 Esmolol Hydrochloride Injection Presentation
Product Name
| Esmolol Hydrochloride Injection
|
Total Dose
| 100 mg/10 mL
|
Esmolol Hydrochloride Concentration
| 10 mg/mL
|
Packaging
| 10 mL Vial
|
Esmolol hydrochloride injection is contraindicated in patients with:
Hypotension can occur at any dose but is dose-related. Patients with hemodynamic compromise or on interacting medications are at particular risk. Severe reactions may include loss of consciousness, cardiac arrest, and death. For control of ventricular heart rate, maintenance doses greater than 200 mcg per kg per min are not recommended. Monitor patients closely, especially if pretreatment blood pressure is low. In case of an unacceptable drop in blood pressure, reduce or stop esmolol hydrochloride. Decrease of dose or termination of infusion reverses hypotension, usually within 30 minutes.
Bradycardia, including sinus pause, heart block, severe bradycardia, and cardiac arrest have occurred with the use of esmolol hydrochloride. Patients with first-degree atrioventricular block, sinus node dysfunction, or conduction disorders may be at increased risk. Monitor heart rate and rhythm in patients receiving esmolol hydrochloride
[
see Contraindications (4)].
If severe bradycardia develops, reduce or stop esmolol hydrochloride.
Beta blockers, like esmolol hydrochloride, can cause depression of myocardial contractility and may precipitate heart failure and cardiogenic shock. At the first sign or symptom of impending cardiac failure, stop esmolol hydrochloride and start supportive therapy [ see Overdosage (10)].
Monitor vital signs closely and titrate esmolol hydrochloride slowly in the treatment of patients whose blood pressure is primarily driven by vasoconstriction associated with hypothermia.
Patients with reactive airways disease should, in general, not receive beta blockers. Because of its relative beta 1 selectivity and titratability, titrate esmolol hydrochloride to the lowest possible effective dose. In the event of bronchospasm, stop the infusion immediately; a beta 2 stimulating agent may be administered with appropriate monitoring of ventricular rate.
In patients with hypoglycemia, or diabetic patients (especially those with labile diabetes) who are receiving insulin or other hypoglycemic agents, beta blockers may mask tachycardia occurring with hypoglycemia, but other manifestations such as dizziness and sweating may not be masked.
Concomitant use of beta blockers and antidiabetic agents can enhance the effect of antidiabetic agents (blood glucose–lowering)
.
Infusion site reactions have occurred with the use of esmolol hydrochloride. They include irritation, inflammation, and severe reactions (thrombophlebitis, necrosis, and blistering), in particular when associated with extravasation
[
see Adverse Reactions (6.1)].
Avoid infusions into small veins or through a butterfly catheter.
If a local infusion site reaction develops, use an alternative infusion site and avoid extravasation.
Beta blockers may exacerbate anginal attacks in patients with Prinzmetal’s angina because of unopposed alpha receptor–mediated coronary artery vasoconstriction. Do not use nonselective beta blockers.
If esmolol hydrochloride is used in the setting of pheochromocytoma, give it in combination with an alpha-blocker, and only after the alpha-blocker has been initiated. Administration of beta-blockers alone in the setting of pheochromocytoma has been associated with a paradoxical increase in blood pressure from the attenuation of beta-mediated vasodilation in skeletal muscle.
In hypovolemic patients, esmolol hydrochloride can attenuate reflex tachycardia and increase the risk of hypotension.
In patients with peripheral circulatory disorders (including Raynaud’s disease or syndrome, and peripheral occlusive vascular disease), esmolol hydrochloride may aggravate peripheral circulatory disorders.
Severe exacerbations of angina, myocardial infarction, and ventricular arrhythmias have been reported in patients with coronary artery disease upon abrupt discontinuation of beta blocker therapy. Observe patients for signs of myocardial ischemia when discontinuing esmolol hydrochloride.
Heart rate increases moderately above pre-treatment levels 30 minutes after esmolol hydrochloride discontinuation.
Beta blockers, including esmolol hydrochloride, have been associated with increases in serum potassium levels and hyperkalemia. The risk is increased in patients with risk factors such as renal impairment. Intravenous administration of beta blockers has been reported to cause potentially life-threatening hyperkalemia in hemodialysis patients. Monitor serum electrolytes during therapy with esmolol hydrochloride.
Beta blockers, including esmolol hydrochloride, have been reported to cause hyperkalemic renal tubular acidosis. Acidosis in general may be associated with reduced cardiac contractility.
Beta-adrenergic blockade may mask certain clinical signs (e.g., tachycardia) of hyperthyroidism. Abrupt withdrawal of beta blockade might precipitate a thyroid storm; therefore, monitor patients for signs of thyrotoxicosis when withdrawing beta blocking therapy.
When using beta blockers, patients at risk of anaphylactic reactions may be more reactive to allergen exposure (accidental, diagnostic, or therapeutic).
Patients using beta blockers may be unresponsive to the usual doses of epinephrine used to treat anaphylactic or anaphylactoid reactions
[
see Drug Interactions (7)].
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice.
The following adverse reaction rates are based on use of esmolol hydrochloride in clinical trials involving 369 patients with supraventricular tachycardia and over 600 intraoperative and postoperative patients enrolled in clinical trials. Most adverse effects observed in controlled clinical trial settings have been mild and transient. The most important and common adverse effect has been hypotension [ see Warnings and Precautions (5.3)]. Deaths have been reported in post-marketing experience occurring during complex clinical states where esmolol hydrochloride was presumably being used simply to control ventricular rate [ see Warnings and Precautions (5.5)].
Table 3 Clinical Trial Adverse Reactions (Frequency ≥3%)
System Organ Class (SOC)
| Preferred MedDRA Term
| Frequency
|
VASCULAR DISORDERS
| Hypotension*
Asymptomatic hypotension Symptomatic hypotension (hyperhidrosis, dizziness) |
25% 12% |
GENERAL DISORDERS AND ADMINISTRATION SITE CONDITIONS
| Infusion site reactions
(inflammation and induration) | 8%
|
GASTROINTESTINAL DISORDERS
| Nausea
| 7%
|
NERVOUS SYSTEM DISORDERS
| Dizziness
Somnolence | 3%
3% |
* Hypotension resolved during esmolol hydrochloride infusion in 63% of patients. In 80% of the remaining patients, hypotension resolved within 30 minutes following discontinuation of infusion.
Clinical Trial Adverse Reactions (Frequency <3%)
Psychiatric Disorders
Confusional state and agitation (~2%)
Anxiety, depression and abnormal thinking (<1%)
Nervous System Disorders
Headache (~ 2%)
Paresthesia, syncope, speech disorder, and lightheadedness (<1%)
Convulsions (<1%), with one death
Vascular Disorders
Peripheral ischemia (~1%)
Pallor and flushing (<1%)
Gastrointestinal Disorders
Vomiting (~1%)
Dyspepsia, constipation, dry mouth, and abdominal discomfort have (<1%)
Renal and Urinary Disorders
Urinary retention (<1%)
In addition to the adverse reactions reported in clinical trials, the following adverse reactions have been reported in the post-marketing experience. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to estimate reliably their frequency or to establish a causal relationship to drug exposure.
Cardiac Disorders
Cardiac arrest, Coronary arteriospasm
Skin and Subcutaneous Tissue Disorders
Angioedema, Urticaria, Psoriasis
Concomitant use of esmolol hydrochloride with other drugs that can lower blood pressure, reduce myocardial contractility, or interfere with sinus node function or electrical impulse propagation in the myocardium can exaggerate esmolol hydrochloride’s effects on blood pressure, contractility, and impulse propagation. Severe interactions with such drugs can result in, for example, severe hypotension, cardiac failure, severe bradycardia, sinus pause, sinoatrial block, atrioventricular block, and/or cardiac arrest. In addition, with some drugs, beta blockade may precipitate increased withdrawal effects. (See clonidine, guanfacine, and moxonidine below.) Esmolol hydrochloride should therefore be used only after careful individual assessment of the risks and expected benefits in patients receiving drugs that can cause these types of pharmacodynamic interactions, including but not limited to:
Pregnancy Category C. Esmolol hydrochloride has been shown to produce increased fetal resorptions with minimal maternal toxicity in rabbits when given in doses approximately 8 times the maximum human maintenance dose (300 mcg/kg/min). There are no adequate and well-controlled studies in pregnant women. Esmolol hydrochloride should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Teratogenicity studies in rats at intravenous dosages of esmolol hydrochloride up to 3000 mcg/kg/min (10 times the maximum human maintenance dosage) for 30 minutes daily produced no evidence of maternal toxicity, embryotoxicity or teratogenicity, while a dosage of 10,000 mcg/kg/min produced maternal toxicity and lethality. In rabbits, intravenous dosages up to 1000 mcg/kg/min for 30 minutes daily produced no evidence of maternal toxicity, embryotoxicity or teratogenicity, while 2500 mcg/kg/min produced minimal maternal toxicity and increased fetal resorptions.
Although there are no adequate and well-controlled studies in pregnant women, use of esmolol in the last trimester of pregnancy or during labor or delivery has been reported to cause fetal bradycardia, which continued after termination of drug infusion. Esmolol hydrochloride should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from esmolol hydrochloride, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
The safety and effectiveness of esmolol hydrochloride in pediatric patients have not been established.
Clinical studies of esmolol hydrochloride did not include sufficient numbers of subjects aged 65 and over to determine whether they responded differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should usually start at the low end of the dosing range, reflecting greater frequency of decreased renal or cardiac function and of concomitant disease or other drug therapy.
No special precautions are necessary in patients with hepatic impairment because esmolol hydrochloride is metabolized by red-blood cell esterases [ see Clinical Pharmacology (12.3)].
No dosage adjustment is required for esmolol in patients with renal impairment receiving a maintenance infusion of esmolol 150 mcg/kg for 4 hours. There is no information on the tolerability of maintenance infusions of esmolol using rates in excess of 150 mcg/kg or maintained longer than 4 hours [ see Clinical Pharmacology (12.3)].
Overdoses of esmolol hydrochloride can cause cardiac and central nervous system effects. These effects may precipitate severe signs, symptoms, sequelae, and complications (for example, severe cardiac and respiratory failure, including shock and coma), and may be fatal. Continuous monitoring of the patient is required.
Because of its approximately 9-minute elimination half-life, the first step in the management of toxicity should be to discontinue the esmolol hydrochloride infusion. Then, based on the observed clinical effects, consider the following general measures
.
Bradycardia:
Consider intravenous administration of atropine or another anticholinergic drug or cardiac pacing.
Cardiac Failure
Consider intravenous administration of a diuretic or digitalis glycoside. In shock resulting from inadequate cardiac contractility, consider intravenous administration of dopamine, dobutamine, isoproterenol, or inamrinone. Glucagon has been reported to be useful.
Symptomatic hypotension
Consider intravenous administration of fluids or vasopressor agents such as dopamine or norepinephrine.
Bronchospasm
Consider intravenous administration of a beta
2 stimulating agent or a theophylline derivative.
Massive accidental overdoses of esmolol hydrochloride have resulted from dilution errors. Some of these overdoses have been fatal while others resulted in permanent disability. Bolus doses in the range of 625 mg to 2.5 g (12.5 to 50 mg/kg) have been fatal. Patients have recovered completely from overdoses as high as 1.75 g given over one minute or doses of 7.5 g given over one hour for cardiovascular surgery. The patients who survived appear to be those whose circulation could be supported until the effects of esmolol hydrochloride resolved.
Esmolol hydrochloride injection is a beta adrenergic receptor blocker with a very short duration of action (elimination half-life is approximately 9 minutes). Esmolol Hydrochloride is:
Esmolol hydrochloride injection is a clear, colorless to light yellow, sterile, nonpyrogenic solution of esmolol hydrochloride. The formulation for esmolol hydrochloride injection is described in the table below:
Table 4 Esmolol Hydrochloride Injection Formulation
| Esmolol Hydrochloride Injection
|
Esmolol Hydrochloride USP
| 10 mg/mL
|
Water for Injection USP
| Q.S. to volume of 10 mL
|
Sodium Acetate Trihydrate USP
| 2.8 mg/mL
|
Glacial Acetic Acid USP
| 0.546 mg/mL
|
Sodium Hydroxide
| Q.S. to adjust pH to 4.5-5.5
|
Hydrochloric Acid
| Q.S. to adjust pH to 4.5-5.5
|
Q.S. = Quantity sufficient
Esmolol hydrochloride is a beta 1-selective (cardioselective) adrenergic receptor blocking agent with rapid onset, a very short duration of action, and no significant intrinsic sympathomimetic or membrane stabilizing activity at therapeutic dosages. Its elimination half-life after intravenous infusion is approximately 9 minutes. Esmolol hydrochloride inhibits the beta 1 receptors located chiefly in cardiac muscle, but this preferential effect is not absolute and at higher doses it begins to inhibit beta 2 receptors located chiefly in the bronchial and vascular musculature.
Clinical pharmacology studies in normal volunteers have confirmed the beta blocking activity of esmolol hydrochloride, showing reduction in heart rate at rest and during exercise, and attenuation of isoproterenol-induced increases in heart rate. Blood levels of esmolol hydrochloride have been shown to correlate with extent of beta blockade. After termination of infusion, substantial recovery from beta blockade is observed in 10 to 20 minutes. The acid metabolite of esmolol exihibits negligible pharmacological activity.
In human electrophysiology studies, esmolol hydrochloride produced effects typical of a beta blocker; a decrease in the heart rate, increase in sinus cycle length, prolongation of the sinus node recovery time, prolongation of the AH interval during normal sinus rhythm and during atrial pacing, and an increase in antegrade Wenckebach cycle length.
In patients undergoing radionuclide angiography, esmolol hydrochloride, at dosages of 200 mcg/kg/min, produced reductions in heart rate, systolic blood pressure, rate pressure product, left and right ventricular ejection fraction and cardiac index at rest, which were similar in magnitude to those produced by intravenous propranolol (4 mg). During exercise, esmolol hydrochloride produced reductions in heart rate, rate pressure product and cardiac index which were also similar to those produced by propranolol, but esmolol hydrochloride produced a significantly larger fall in systolic blood pressure. In patients undergoing cardiac catheterization, the maximum therapeutic dose of 300 mcg/kg/min of esmolol hydrochloride produced similar effects and, in addition, there were small, clinically insignificant increases in the left ventricular end diastolic pressure and pulmonary capillary wedge pressure. At 30 minutes after the discontinuation of esmolol hydrochloride infusion, all of the hemodynamic parameters had returned to pretreatment levels.
The relative cardioselectivity of esmolol hydrochloride was demonstrated in 10 mildly asthmatic patients. Infusions of esmolol hydrochloride 100, 200 and 300 mcg/kg/min produced no significant increases in specific airway resistance compared to placebo. At 300 mcg/kg/min, esmolol hydrochloride produced slightly enhanced bronchomotor sensitivity to dry air stimulus. These effects were not clinically significant, and esmolol hydrochloride was well tolerated by all patients. Six of the patients also received intravenous propranolol, and at a dosage of 1 mg, two experienced significant, symptomatic bronchospasm requiring bronchodilator treatment. One other propranolol-treated patient also experienced dry air-induced bronchospasm. No adverse pulmonary effects were observed in patients with COPD who received therapeutic dosages of esmolol hydrochloride for treatment of supraventricular tachycardia (51 patients) or in perioperative settings (32 patients).
Esmolol is rapidly metabolized by hydrolysis of the ester linkage, chiefly by the esterases in the cytosol of red blood cells and not by plasma cholinesterases or red cell membrane acetylcholinesterase. Total body clearance in man was found to be about 20 L/kg/hr, which is greater than cardiac output; thus the metabolism of esmolol is not limited by the rate of blood flow to metabolizing tissues such as the liver or affected by hepatic or renal blood flow. Esmolol has a rapid distribution half-life of about 2 minutes and an elimination half-life of about 9 minutes.
Using an appropriate loading dose, steady-state blood levels of esmolol hydrochloride for dosages from 50 to 300 mcg/kg/min are obtained within five minutes. Steady-state is reached in about 30 minutes without the loading dose. Steady-state blood levels of esmolol increase linearly over this dosage range and elimination kinetics are dose-independent over this range. Steady-state blood levels are maintained during infusion but decrease rapidly after termination of the infusion. Because of its short half-life, blood levels of esmolol can be rapidly altered by increasing or decreasing the infusion rate and rapidly eliminated by discontinuing the infusion.
Consistent with the high rate of blood-based metabolism of esmolol, less than 2% of the drug is excreted unchanged in the urine. Within 24 hours of the end of infusion, the acid metabolite of esmolol in urine accounts for approximately 73 to 88% of the dosage.
Metabolism of esmolol results in the formation of the corresponding free acid and methanol. The acid metabolite has been shown in animals to have negligible activity, and in normal volunteers its blood levels do not correspond to the level of beta blockade. The acid metabolite has an elimination half-life of about 3.7 hours and is excreted in the urine with a clearance approximately equivalent to the glomerular filtration rate.
After a 4 hours maintenance infusion of 150 mcg/kg, the plasma concentrations of esmolol are similar in subjects with normal renal function and in patients with ESRD on dialysis. The half-life of the acid metabolite of esmolol hydrochloride, which is primarily excreted unchanged by the kidney, is increased about 12-fold to 48 hours in patients with ESRD. The peak concentrations of the acid metabolite are doubled in ESRD.
Methanol blood levels, monitored in subjects receiving esmolol hydrochloride for up to 6 hours at 300 mcg/kg/min and 24 hours at 150 mcg/kg/min, approximated endogenous levels and were less than 2% of levels usually associated with methanol toxicity.
Esmolol hydrochloride has been shown to be 55% bound to human plasma protein, while the acid metabolite is only 10% bound.
Because of its short term usage no carcinogenicity, mutagenicity, or reproductive performance studies have been conducted with esmolol.
Supraventricular Tachycardia
In two multicenter, randomized, double-blind, controlled comparisons of esmolol hydrochloride with placebo and propranolol, maintenance doses of 50 to 300 mcg/kg/min of esmolol hydrochloride were found to be more effective than placebo and about as effective as propranolol, 3 to 6 mg given by bolus injections, in the treatment of supraventricular tachycardia, principally atrial fibrillation and atrial flutter. The majority of these patients developed their arrhythmias postoperatively. About 60 to 70% of the patients treated with esmolol hydrochloride developed either a 20% reduction in heart rate, a decrease in heart rate to less than 100 bpm, or, rarely, conversion to normal sinus rhythm and about 95% of these patients did so at a dosage of 200 mcg/kg/min or less. The average effective dosage of esmolol hydrochloride was approximately 100 mcg/kg/min in the two studies. Other multicenter baseline-controlled studies gave similar results. In the comparison with propranolol, about 50% of patients in both the esmolol hydrochloride and propranolol groups were on concomitant digoxin. Response rates were slightly higher with both beta blockers in the digoxin-treated patients.
In all studies significant decreases of blood pressure occurred in 20 to 50% of patients, identified either as adverse reaction reports by investigators, or by observation of systolic pressure less than 90 mmHg or diastolic pressure less than 50 mmHg. The hypotension was symptomatic (mainly hyperhidrosis or dizziness) in about 12% of patients, and therapy was discontinued in about 11% of patients, about half of whom were symptomatic. Hypotension was more common with esmolol hydrochloride (53%) than with propranolol (17%). The hypotension was rapidly reversible with decreased infusion rate or after discontinuation of therapy with esmolol hydrochloride. For both esmolol hydrochloride and propranolol, hypotension was reported less frequently in patients receiving concomitant digoxin.
Physicians should inform patients of the risks associated with esmolol hydrochloride:
Manufactured for:
AuroMedics Pharma LLC
6 Wheeling Road
Dayton, NJ 08810
Manufactured by:
Aurobindo Pharma Limited
IDA, Pashamylaram - 502307
India
ESMOLOL HYDROCHLORIDE
esmolol hydrochloride injection, solution |
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Labeler - Medical Purchasing Solutions, LLC (601458529) |
Establishment | |||
Name | Address | ID/FEI | Business Operations |
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Medical Purchasing Solutions, LLC | 601458529 | repack(71872-7049) |