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Sevoflurane, USP, volatile liquid for inhalation, a nonflammable and nonexplosive liquid administered by vaporization, is a halogenated general inhalation anesthetic drug. Sevoflurane, USP is fluoromethyl 2,2,2,-trifluoro-1-(trifluoromethyl) ethyl ether and its structural formula is:
| Sevoflurane, USP, Physical Constants are: | |
| Molecular weight | 200.05 |
| Boiling point at 760 mm Hg | 58.6°C |
| Specific gravity at 20°C | 1.520 - 1.525 |
| Vapor pressure in mm Hg | 157 mm Hg at 20°C |
| 197 mm Hg at 25°C | |
| 317 mm Hg at 36°C | |
| Distribution Partition Coefficients at 37°C: | |
| Blood/Gas | 0.63 - 0.69 |
| Water/Gas | 0.36 |
| Olive Oil/Gas | 47 - 54 |
| Brain/Gas | 1.15 |
| Mean Component/Gas Partition Coefficients at 25°C for Polymers Used Commonly in Medical Applications: | |
| Conductive rubber | 14.0 |
| Butyl rubber | 7.7 |
| Polyvinylchloride | 17.4 |
| Polyethylene | 1.3 |
Sevoflurane, USP is nonflammable and nonexplosive as defined by the requirements of International Electrotechnical Commission 601-2-13.
Sevoflurane, USP is a clear, colorless, liquid containing no additives. Sevoflurane, USP is not corrosive to stainless steel, brass, aluminum, nickel-plated brass, chrome-plated brass or copper beryllium. Sevoflurane, USP is nonpungent. It is miscible with ethanol, ether, chloroform, and benzene, and it is slightly soluble in water. Sevoflurane, USP is stable when stored under normal room lighting conditions according to instructions. No discernible degradation of Sevoflurane, USP occurs in the presence of strong acids or heat. When in contact with alkaline CO2 absorbents (e.g. Baralyme® and to a lesser extent soda lime) within the anesthesia machine, Sevoflurane, USP can undergo degradation under certain conditions. Degradation of Sevoflurane, USP is minimal, and degradants are either undetectable or present in non-toxic amounts when used as directed with fresh absorbents. Sevoflurane, USP degradation and subsequent degradant formation are enhanced by increasing absorbent temperature increased Sevoflurane, USP concentration, decreased fresh gas flow and desiccated CO2 absorbents (especially with potassium hydroxide containing absorbents e.g. Baralyme).
Sevoflurane, USP alkaline degradation occurs by two pathways. The first results from the loss of hydrogen fluoride with the formation of pentafluoroisopropenyl fluoromethyl ether, (PIFE, C4H2F6O), also known as Compound A, and trace amounts of pentafluoromethoxy isopropyl fluoromethyl ether, (PMFE, C5H6F6O). The second pathway for degradation of Sevoflurane, USP, which occurs primarily in the presence of desiccated CO2 absorbents, is discussed later.
In the first pathway, the defluorination pathway, the production of degradants in the anesthesia circuit results from the extraction of the acidic proton in the presence of a strong base (KOH and/or NaOH) forming an alkene (Compound A) from Sevoflurane, USP similar to formation of 2-bromo-2-chloro-1,1-difluoro ethylene (BCDFE) from halothane. Laboratory simulations have shown that the concentration of these degradants is inversely correlated with the fresh gas flow rate (See Figure 1).
Since the reaction of carbon dioxide with absorbents is exothermic, the temperature increase will be determined by quantities of CO2 absorbed, which in turn will depend on fresh gas flow in the anesthesia circle system, metabolic status of the patient, and ventilation. The relationship of temperature produced by varying levels of CO2 and Compound A production is illustrated in the following in vitro simulation where CO2 was added to a circle absorber system.
Compound A concentration in a circle absorber system increases as a function of increasing CO2 absorbent temperature and composition (Baralyme producing higher levels than soda lime), increased body temperature, and increased minute ventilation, and decreasing fresh gas flow rates. It has been reported that the concentration of Compound A increases significantly with prolonged dehydration of Baralyme. Compound A exposure in patients also has been shown to rise with increased Sevoflurane, USP concentrations and duration of anesthesia. In a clinical study in which Sevoflurane, USP was administered to patients under low flow conditions for ≥2 hours at flow rates of 1 Liter/minute, Compound A levels were measured in an effort to determine the relationship between MAC hours and Compound A levels produced. The relationship between Compound A levels and Sevoflurane, USP exposure are shown in Figure 2a.
Compound A has been shown to be nephrotoxic in rats after exposures that have varied in duration from one to three hours. No histopathologic change was seen at a concentration of up to 270 ppm for one hour. Sporadic single cell necrosis of proximal tubule cells has been reported at a concentration of 114 ppm after a 3-hour exposure to Compound A in rats. The LC50 reported at 1 hour is 1050-1090 ppm (male-female) and, at 3 hours, 350-490 ppm (male-female).
An experiment was performed comparing Sevoflurane, USP plus 75 or 100 ppm Compound A with an active control to evaluate the potential nephrotoxicity of Compound A in non-human primates. A single 8-hour exposure of Sevoflurane, USP in the presence of Compound A produced single-cell renal tubular degeneration and single-cell necrosis in cynomolgus monkeys. These changes are consistent with the increased urinary protein, glucose level and enzymic activity noted on days one and three on the clinical pathology evaluation. This nephrotoxicity produced by Compound A is dose and duration of exposure dependent.
At a fresh gas flow rate of 1 L/min, mean maximum concentrations of Compound A in the anesthesia circuit in clinical settings are approximately 20 ppm (0.002%) with soda lime and 30 ppm (0.003%) with Baralyme in adult patients; mean maximum concentrations in pediatric patients with soda lime are about half those found in adults. The highest concentration observed in a single patient with Baralyme was 61 ppm (0.0061%) and 32 ppm (0.0032%) with soda lime. The levels of Compound A at which toxicity occurs in humans is not known.
The second pathway for degradation of Sevoflurane, USP occurs primarily in the presence of desiccated CO2 absorbents and leads to the dissociation of Sevoflurane, USP into hexafluoroisopropanol (HFIP) and formaldehyde. HFIP is inactive, non-genotoxic, rapidly glucuronidated and cleared by the liver. Formaldehyde is present during normal metabolic processes. Upon exposure to a highly desiccated absorbent, formaldehyde can further degrade into methanol and formate. Formate can contribute to the formation of carbon monoxide in the presence of high temperature that can be associated with desiccated Baralyme®. Methanol can react with Compound A to form the methoxy addition product pentafluromethoxy isopropyl fluoromethyl ether (PMFE). This compound can undergo further HF elimination to form additional compounds.
Sevoflurane, USP degradants were observed in the respiratory circuit of an experimental anesthesia machine using desiccated CO2 absorbents and maximum Sevoflurane, USP concentrations (8%) for extended periods of time (>2 hours). Concentrations of formaldehyde observed with desiccated soda lime in this experimental anesthesia respiratory circuit were consistent with levels that could potentially result in respiratory irritation. Although KOH containing CO2 absorbents are no longer commercially available, in the laboratory experiments, exposure of Sevoflurane, USP to the desiccated KOH containing CO2 absorbent, Baralyme, resulted in the detection of substantially greater degradant levels.
Sevoflurane, USP is an inhalational anesthetic agent for use in induction and maintenance of general anesthesia. Minimum alveolar concentration (MAC) of Sevoflurane, USP in oxygen for a 40-year-old adult is 2.1%. The MAC of Sevoflurane, USP decreases with age (see Dosage and Administration for details).
Because of the low solubility of Sevoflurane, USP in blood (blood/gas partition coefficient @ 37°C = 0.63-0.69), a minimal amount of Sevoflurane, USP is required to be dissolved in the blood before the alveolar partial pressure is in equilibrium with the arterial partial pressure. Therefore there is a rapid rate of increase in the alveolar (end-tidal) concentration (FA) toward the inspired concentration (FI) during induction.
In a study in which seven healthy male volunteers were administered 70% N2O/30% O2 for 30 minutes followed by 1.0% Sevoflurane, USP and 0.6% isoflurane for another 30 minutes the FA/FI ratio was greater for Sevoflurane, USP than isoflurane at all time points. The time for the concentration in the alveoli to reach 50% of the inspired concentration was 4-8 minutes for isoflurane and approximately 1 minute for Sevoflurane, USP.
FA/FI data from this study were compared with FA/FI data of other halogenated anesthetic agents from another study. When all data were normalized to isoflurane, the uptake and distribution of Sevoflurane, USP was shown to be faster than isoflurane and halothane, but slower than desflurane. The results are depicted in Figure 3.
The low solubility of Sevoflurane, USP facilitates rapid elimination via the lungs. The rate of elimination is quantified as the rate of change of the alveolar (end-tidal) concentration following termination of anesthesia (FA), relative to the last alveolar concentration (Fa0) measured immediately before discontinuance of the anesthetic. In the healthy volunteer study described above, rate of elimination of Sevoflurane, USP was similar compared with desflurane, but faster compared with either halothane or isoflurane. These results are depicted in Figure 4.
Yasuda N, Lockhart S, Eger EI II, et al: Comparison of kinetics of Sevoflurane, USP and isoflurane in humans. Anesth Analg 72:316, 1991.
The effects of Sevoflurane, USP on the displacement of drugs from serum and tissue proteins have not been investigated. Other fluorinated volatile anesthetics have been shown to displace drugs from serum and tissue proteins in vitro. The clinical significance of this is unknown. Clinical studies have shown no untoward effects when Sevoflurane, USP is administered to patients taking drugs that are highly bound and have a small volume of distribution (e.g., phenytoin).
Sevoflurane, USP is metabolized by cytochrome P450 2E1, to hexafluoroisopropanol (HFIP) with release of inorganic fluoride and CO2. Once formed HFIP is rapidly conjugated with glucuronic acid and eliminated as a urinary metabolite. No other metabolic pathways for Sevoflurane, USP have been identified. In vivo metabolism studies suggest that approximately 5% of the Sevoflurane, USP dose may be metabolized.
Cytochrome P450 2E1 is the principal isoform identified for Sevoflurane, USP metabolism and this may be induced by chronic exposure to isoniazid and ethanol. This is similar to the metabolism of isoflurane and enflurane and is distinct from that of methoxyflurane which is metabolized via a variety of cytochrome P450 isoforms. The metabolism of Sevoflurane, USP is not inducible by barbiturates. As shown in Figure 5, inorganic fluoride concentrations peak within 2 hours of the end of Sevoflurane, USP anesthesia and return to baseline concentrations within 48 hours post-anesthesia in the majority of cases (67%). The rapid and extensive pulmonary elimination of Sevoflurane, USP minimizes the amount of anesthetic available for metabolism.
Cousins M.J., Greenstein L.R., Hitt B.A., et al: Metabolism and renal effects of enflurane in man. Anesthesiology 44:44; 1976* and Sevo-93-044+.
Legend:
Pre-Anesth. = Pre-anesthesia
Up to 3.5% of the Sevoflurane, USP dose appears in the urine as inorganic fluoride. Studies on fluoride indicate that up to 50% of fluoride clearance is nonrenal (via fluoride being taken up into bone).
Fluoride ion concentrations are influenced by the duration of anesthesia, the concentration of Sevoflurane, USP administered, and the composition of the anesthetic gas mixture. In studies where anesthesia was maintained purely with Sevoflurane, USP for periods ranging from 1 to 6 hours, peak fluoride concentrations ranged between 12 µM and 90 µM. As shown in Figure 6, peak concentrations occur within 2 hours of the end of anesthesia and are less than 25 µM (475 ng/mL) for the majority of the population after 10 hours. The half-life is in the range of 15-23 hours.
It has been reported that following administration of methoxyflurane, serum inorganic fluoride concentrations >50 µM were correlated with the development of vasopressin-resistant, polyuric, renal failure. In clinical trials with Sevoflurane, USP, there were no reports of toxicity associated with elevated fluoride ion levels.
Fluoride concentrations have been measured after single, extended, and repeat exposure to Sevoflurane, USP in normal surgical and special patient populations, and pharmacokinetic parameters were determined.
Compared with healthy individuals, the fluoride ion half-life was prolonged in patients with renal impairment, but not in the elderly. A study in 8 patients with hepatic impairment suggests a slight prolongation of the half-life. The mean half-life in patients with renal impairment averaged approximately 33 hours (range 21-61 hours) as compared to a mean of approximately 21 hours (range 10-48 hours) in normal healthy individuals. The mean half-life in the elderly (greater than 65 years) approximated 24 hours (range 18-72 hours). The mean half-life in individuals with hepatic impairment was 23 hours (range 16-47 hours). Mean maximal fluoride values (Cmax) determined in individual studies of special populations are displayed below.
| n = number of patients studied. | |||||
Fluoride Ion Estimates in Special Populations | |||||
| n | Age (yr) | Duration (hr) | Dose (MAC•hr) | Cmax (µM) | |
| PEDIATRIC PATIENTS | |||||
| Anesthetic | |||||
| Sevoflurane-O2 | 76 | 0 - 11 | 0.8 | 1.1 | 12.6 |
| Sevoflurane-O2 | 40 | 1 - 11 | 2.2 | 3.0 | 16.0 |
| Sevoflurane/N2O | 25 | 5 - 13 | 1.9 | 2.4 | 21.3 |
| Sevoflurane/N2O | 42 | 0 - 18 | 2.4 | 2.2 | 18.4 |
| Sevoflurane/N2O | 40 | 1 - 11 | 2.0 | 2.6 | 15.5 |
| ELDERLY | 33 | 65 - 93 | 2.6 | 1.4 | 25.6 |
| RENAL | 21 | 29 - 83 | 2.5 | 1.0 | 26.1 |
| HEPATIC | 8 | 42 - 79 | 3.6 | 2.2 | 30.6 |
| OBESE | 35 | 24 - 73 | 3.0 | 1.7 | 38.0 |
Changes in the depth of Sevoflurane, USP anesthesia rapidly follow changes in the inspired concentration.
In the Sevoflurane, USP clinical program, the following recovery variables were evaluated:
Some of these variables are summarized as follows:
| n = number of patients with recording of events. | ||
Induction and Recovery Variables for Evaluable Pediatric Patients in Two Comparative Studies: | ||
| Time to End-Point (min) | Sevoflurane Mean ± SEM | Halothane Mean ± SEM |
| Induction | 2.0 ± 0.2 (n=294) | 2.7 ± 0.2 (n=252) |
| Emergence | 11.3 ± 0.7 (n=293) | 15.8 ± 0.8 (n=252) |
| Response to command | 13.7 ± 1.0 (n=271) | 19.3 ± 1.1 (n=230) |
| First analgesia | 52.2 ± 8.5 (n=216) | 67.6 ± 10.6 (n=150) |
| Eligible for recovery discharge | 76.5 ± 2.0 (n=292) | 81.1 ± 1.9 (n=246) |
| n = number of patients with recording of recovery events. | ||
Recovery Variables for Evaluable Adult Patients in Two Comparative Studies: Sevoflurane versus Isoflurane | ||
| Time to Parameter: (min) | Sevoflurane Mean ± SEM | Isoflurane Mean ± SEM |
| Emergence | 7.7 ± 0.3 (n=395) | 9.1 ± 0.3 (n=348) |
| Response to command | 8.1 ± 0.3 (n=395) | 9.7 ± 0.3 (n=345) |
| First analgesia | 42.7 ± 3.0 (n=269) | 52.9 ± 4.2 (n=228) |
| Eligible for recovery discharge | 87.6 ± 5.3 (n=244) | 79.1 ± 5.2 (n=252) |
| n = number of patients with recording of events. | |||
| |||
| Meta-Analyses for Induction and Emergence Variables for Evaluable Adult Patients in Comparative Studies: Sevoflurane versus Propofol | |||
| Parameter | No. of Studies | Sevoflurane Mean ± SEM | Propofol Mean ± SEM |
| Mean maintenance anesthesia exposure | 3 | 1.0 MAC•hr ± 0.8 (n=259) | 7.2 mg/kg/hr ± 2.6 (n=258) |
| Time to induction: (min) | 1 | 3.1 ± 0.18* (n=93) | 2.2 ± 0.18† (n=93) |
| Time to emergence: (min) | 3 | 8.6 ± 0.57 (n=255) | 11.0 ± 0.57 (n=260) |
| Time to respond to command: (min) | 3 | 9.9 ± 0.60 (n=257) | 12.1 ± 0.60 (n=260) |
| Time to first analgesia: (min) | 3 | 43.8 ± 3.79 (n=177) | 57.9 ± 3.68 (n=179) |
| Time to eligibility for recovery discharge: (min) | 3 | 116.0 ± 4.15 (n=257) | 115.6 ± 3.98 (n=261) |
Sevoflurane, USP was studied in 14 healthy volunteers (18-35 years old) comparing Sevoflurane-O2(Sevo/O2) to Sevoflurane-N2O/O2 (Sevo/N2O/O2) during 7 hours of anesthesia. During controlled ventilation, hemodynamic parameters measured are shown in Figures 7-10:
Sevoflurane, USP is a dose-related cardiac depressant. Sevoflurane, USP does not produce increases in heart rate at doses less than 2 MAC.
A study investigating the epinephrine induced arrhythmogenic effect of Sevoflurane, USP versus isoflurane in adult patients undergoing transsphenoidal hypophysectomy demonstrated that the threshold dose of epinephrine (i.e., the dose at which the first sign of arrhythmia was observed) producing multiple ventricular arrhythmias was 5 mcg/kg with both Sevoflurane, USP and isoflurane. Consequently, the interaction of Sevoflurane, USP with epinephrine appears to be equal to that seen with isoflurane.
Sevoflurane, USP was administered to a total of 3185 patients prior to Sevoflurane, USP NDA submission. The types of patients are summarized as follows:
Patients Receiving Sevoflurane, USP in Clinical Trials | |
| Type of Patients | Number Studied |
| ADULT | 2223 |
| Cesarean Delivery | 29 |
| Cardiovascular and patients at risk of myocardial ischemia | 246 |
| Neurosurgical | 22 |
| Hepatic impairment | 8 |
| Renal impairment | 35 |
| PEDIATRIC | 962 |
Clinical experience with these patients is described below.
The efficacy of Sevoflurane, USP in comparison to isoflurane, enflurane, and propofol was investigated in 3 outpatient and 25 inpatient studies involving 3591 adult patients. Sevoflurane, USP was found to be comparable to isoflurane, enflurane, and propofol for the maintenance of anesthesia in adult patients. Patients administered Sevoflurane, USP showed shorter times (statistically significant) to some recovery events (extubation, response to command, and orientation) than patients who received isoflurane or propofol.
Sevoflurane, USP has a nonpungent odor and does not cause respiratory irritability. Sevoflurane, USP is suitable for mask induction in adults. In 196 patients, mask induction was smooth and rapid, with complications occurring with the following frequencies: cough, 6%; breathholding, 6%; agitation, 6%; laryngospasm, 5%.
Sevoflurane, USP was compared to isoflurane and propofol for maintenance of anesthesia supplemented with N2O in two studies involving 786 adult (18-84 years of age) ASA Class I, II, or III patients. Shorter times to emergence and response to commands (statistically significant) were observed with Sevoflurane, USP compared to isoflurane and propofol.
| n = number of patients with recording of recovery events. | ||||
Recovery Parameters in Two Outpatient Surgery Studies: | ||||
| Sevoflurane/N2O | Isoflurane/N2O | Sevoflurane/N2O | Propofol/N2O | |
| Mean Maintenance Anesthesia Exposure ± SD | 0.64 ± 0.03 MAC•hr (n=245) | 0.66 ± 0.03 MAC•hr (n=249) | 0.8 ± 0.5 MAC•hr (n=166) | 7.3 ± 2.3 mg/kg/hr (n=166) |
| Time to Emergence (min) | 8.2 ± 0.4 (n=246) | 9.3 ± 0.3 (n=251) | 8.3 ± 0.7 (n=137) | 10.4 ± 0.7 (n=142) |
| Time to Respond to Commands (min) | 8.5 ± 0.4 (n=246) | 9.8 ± 0.4 (n=248) | 9.1 ± 0.7 (n=139) | 11.5 ± 0.7 (n=143) |
| Time to First Analgesia (min) | 45.9 ± 4.7 (n=160) | 59.1 ± 6.0 (n=252) | 46.1 ± 5.4 (n=83) | 60.0 ± 4.7 (n=88) |
| Time to Eligibility for Discharge from Recovery Area (min) | 87.6 ± 5.3 (n=244) | 79.1 ± 5.2 (n=252) | 103.1 ± 3.8 (n=139) | 105.1 ± 3.7 (n=143) |
Sevoflurane, USP was compared to isoflurane and propofol for maintenance of anesthesia supplemented with N2O in two multicenter studies involving 741 adult ASA Class I, II or III (18-92 years of age) patients. Shorter times to emergence, command response, and first post-anesthesia analgesia (statistically significant) were observed with Sevoflurane, USP compared to isoflurane and propofol.
| n = number of patients with recording of recovery events. | ||||
Recovery Parameters in Two Inpatient Surgery Studies: Least Squares Mean ± SEM | ||||
| Sevoflurane/N2O | Isoflurane/N2O | Sevoflurane/N2O | Propofol/N2O | |
| Mean Maintenance Anesthesia Exposure ± SD | 1.27 MAC•hr ± 0.05 (n=271) | 1.58 MAC•hr ± 0.06 (n=282) | 1.43 MAC•hr ± 0.94 (n=93) | 7.0 mg/kg/hr ± 2.9 (n=92) |
| Time to Emergence (min) | 11.0 ± 0.6 (n=270) | 16.4 ± 0.6 (n=281) | 8.8 ± 1.2 (n=92) | 13.2 ± 1.2 (n=92) |
| Time to Respond to Commands (min) | 12.8 ± 0.7 (n=270) | 18.4 ± 0.7 (n=281) | 11.0 ± 1.20 (n=92) | 14.4 ± 1.21 (n=91) |
| Time to First Analgesia (min) | 46.1 ± 3.0 (n=233) | 55.4 ± 3.2 (n=242) | 37.8 ± 3.3 (n=82) | 49.2 ± 3.3 (n=79) |
| Time to Eligibility for Discharge from Recovery Area (min) | 139.2 ± 15.6 (n=268) | 165.9 ± 16.3 (n=282) | 148.4 ± 8.9 (n=92) | 141.4 ± 8.9 (n=92) |
The concentration of Sevoflurane, USP required for maintenance of general anesthesia is age-dependent (see Dosage and Administration). Sevoflurane, USP or halothane was used to anesthetize 1620 pediatric patients aged 1 day to 18 years, and ASA physical status I or II (948 Sevoflurane, USP, 672 halothane). In one study involving 90 infants and children, there were no clinically significant decreases in heart rate compared to awake values at 1 MAC. Systolic blood pressure decreased 15-20% in comparison to awake values following administration of 1 MAC Sevoflurane, USP; however, clinically significant hypotension requiring immediate intervention did not occur. Overall incidences of bradycardia [more than 20 beats/min lower than normal (80 beats/min)] in comparative studies was 3% for Sevoflurane, USP and 7% for halothane. Patients who received Sevoflurane, USP had slightly faster emergence times (12 vs. 19 minutes), and a higher incidence of post-anesthesia agitation (14% vs. 10%).
Sevoflurane, USP (n=91) was compared to halothane (n=89) in a single-center study for elective repair or palliation of congenital heart disease. The patients ranged in age from 9 days to 11.8 years with an ASA physical status of II, III, and IV (18%, 68%, and 13% respectively). No significant differences were demonstrated between treatment groups with respect to the primary outcome measures: cardiovascular decompensation and severe arterial desaturation. Adverse event data was limited to the study outcome variables collected during surgery and before institution of cardiopulmonary bypass.
Sevoflurane, USP has a nonpungent odor and is suitable for mask induction in pediatric patients. In controlled pediatric studies in which mask induction was performed, the incidence of induction events is shown below (see Adverse Reactions).
| n = number of patients. | ||
Incidence of Pediatric Induction Events | ||
Sevoflurane (n=836) | Halothane (n=660) | |
| Agitation | 14% | 11% |
| Cough | 6% | 10% |
| Breathholding | 5% | 6% |
| Secretions | 3% | 3% |
| Laryngospasm | 2% | 2% |
| Bronchospasm | <1% | 0% |
Sevoflurane, USP (n=518) was compared to halothane (n=382) for the maintenance of anesthesia in pediatric outpatients. All patients received N2O and many received fentanyl, midazolam, bupivacaine, or lidocaine. The time to eligibility for discharge from post-anesthesia care units was similar between agents (see Clinical Pharmacology and Adverse Reactions).
Sevoflurane, USP was compared to isoflurane as an adjunct with opioids in a multicenter study of 273 patients undergoing CABG surgery. Anesthesia was induced with midazolam (0.1-0.3 mg/kg); vecuronium (0.1-0.2 mg/kg), and fentanyl (5-15 mcg/kg). Both isoflurane and Sevoflurane, USP were administered at loss of consciousness in doses of 1.0 MAC and titrated until the beginning of cardiopulmonary bypass to a maximum of 2.0 MAC. The total dose of fentanyl did not exceed 25 mcg/kg. The average MAC dose was 0.49 for Sevoflurane, USP and 0.53 for isoflurane. There were no significant differences in hemodynamics, cardioactive drug use, or ischemia incidence between the two groups. Outcome was also equivalent. In this small multicenter study, Sevoflurane, USP appears to be as effective and as safe as isoflurane for supplementation of opioid anesthesia for coronary bypass grafting.
Sevoflurane-N2O was compared to isoflurane-N2O for maintenance of anesthesia in a multicenter study in 214 patients, age 40-87 years who were at mild-to-moderate risk for myocardial ischemia and were undergoing elective non-cardiac surgery. Forty-six percent (46%) of the operations were cardiovascular, with the remainder evenly divided between gastro
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Treating infections of the ear caused by certain bacteria. It may also be used for other conditions as determined by your doctor.
Cortisporin Suspension is a combination of 2 antibiotics and a corticosteroid. The antibiotics work by slowing the growth of, or killing, sensitive bacteria. The corticosteroid reduces inflammation.
Contact your doctor or health care provider right away if any of these apply to you.
Some medical conditions may interact with Cortisporin Suspension. Tell your doctor or pharmacist if you have any medical conditions, especially if any of the following apply to you:
Some MEDICINES MAY INTERACT with Cortisporin Suspension. Because little, if any, of Cortisporin Suspension is absorbed into the blood, the risk of it interacting with another medicine is low.
Ask your health care provider if Cortisporin Suspension may interact with other medicines that you take. Check with your health care provider before you start, stop, or change the dose of any medicine.
Use Cortisporin Suspension as directed by your doctor. Check the label on the medicine for exact dosing instructions.
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All medicines may cause side effects, but many people have no, or minor, side effects. Check with your doctor if any of these most COMMON side effects persist or become bothersome:
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Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); acne-like rash; changes in hearing; decreased urination; dry, scaly, or peeling skin at the application site; continued burning or stinging; excessive hair growth; inflamed hair follicles; inflammation around the mouth; loss of hearing; muscle weakness; pain, redness, itching, irritation, or swelling not present when you began using Cortisporin Suspension; thinning, softening, or discoloration of the skin; unusual weight gain, especially in the face.
This is not a complete list of all side effects that may occur. If you have questions about side effects, contact your health care provider. Call your doctor for medical advice about side effects. To report side effects to the appropriate agency, please read the Guide to Reporting Problems to FDA.
See also: Cortisporin side effects (in more detail)
Contact 1-800-222-1222 (the American Association of Poison Control Centers), your local poison control center, or emergency room immediately.
Store Cortisporin Suspension between 59 and 77 degrees F (15 and 25 degrees C). Store away from heat, moisture, and light. Keep the container tightly closed. Keep Cortisporin Suspension out of the reach of children and away from pets.
This information is a summary only. It does not contain all information about Cortisporin Suspension. If you have questions about the medicine you are taking or would like more information, check with your doctor, pharmacist, or other health care provider.
Ovit-A may be available in the countries listed below.
Retinol is reported as an ingredient of Ovit-A in the following countries:
International Drug Name Search
Otosal may be available in the countries listed below.
Doxycycline hyclate (a derivative of Doxycycline) is reported as an ingredient of Otosal in the following countries:
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Veracor may be available in the countries listed below.
Verapamil hydrochloride (a derivative of Verapamil) is reported as an ingredient of Veracor in the following countries:
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Ossibiotic may be available in the countries listed below.
In some countries, this medicine may only be approved for veterinary use.
Oxytetracycline is reported as an ingredient of Ossibiotic in the following countries:
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Ofloxbeta may be available in the countries listed below.
Ofloxacin is reported as an ingredient of Ofloxbeta in the following countries:
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Oroken may be available in the countries listed below.
Cefixime is reported as an ingredient of Oroken in the following countries:
Cefixime trihydrate (a derivative of Cefixime) is reported as an ingredient of Oroken in the following countries:
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Orgotéine may be available in the countries listed below.
Orgotéine (DCF) is also known as Orgotein (Rec.INN)
International Drug Name Search
Glossary
| DCF | Dénomination Commune Française |
| Rec.INN | Recommended International Nonproprietary Name (World Health Organization) |
Glizid may be available in the countries listed below.
Gliclazide is reported as an ingredient of Glizid in the following countries:
International Drug Name Search
Glucose Injection BP Minijet 50%w/v
Glucose anhydrous 500 mg in 1ml.
For excipients see 6.1
Solution for injection.
The clear, colourless solution is contained in a USP Type I glass vial with an elastomeric closure. The container is specially designed for use with the IMS Minijet injector supplied.
a) As a source of energy in parenteral nutrition.
b) In severe hypoglycaemia due to insulin excess or other causes.
c) For reduction of cerebrospinal pressure and/or cerebral oedema due to delirium tremens or acute alcohol intoxication.
Glucose injection 50% w/v is strongly hypertonic and is used partly because of its dehydrating effects.
Hypertonic solutions of glucose should be administered via a central vein. The dose is variable and depends upon the indication, clinical condition and size of the individual.
The rate of utilisation of glucose varies considerably from patient to patient. In general, the maximal rate has been estimated at 500-800mg/kg body weight/hour. If the patient's capacity to utilise glucose is exceeded, glycosuria and diuresis will occur.
Adults, elderly, children over 6 years:
Hypoglycaemia: 20-50ml of a 50% w/v solution, repeated as necessary according to the patient's response, by slow intravenous injection, e.g. 3ml/minute. After 25g of glucose has been given, it is advisable to interrupt the injection and evaluate the effect. The exact dose required to relieve hypoglycaemia will vary. After the patient responds, supplemental oral feeding is indicated to avoid relapse, especially after insulin shock therapy.
Acute alcoholism: 50ml of glucose 50% w/v solution should be administered intravenously. Unmodified insulin (20 units) and thiamine hydrochloride (100mg) should be added to the infusion.
The intravenous use of strongly hypertonic solutions of glucose is contraindicated in patients with anuria, intracranial or intraspinal haemorrhage, or delirium tremens if the patient is already dehydrated.
Known sensitivity to corn or corn products, hyperglycaemic coma, or ischaemic stroke.
Hypertonic solutions of glucose should be administered via a large central vein to minimise the damage at the site of injection.
Use with caution in patients with diabetes mellitus, severe undernutrition, carbohydrate intolerance, thiamine deficiency, hypophosphataemia, haemodilution, sepsis and trauma. Rapid infusion of hypertonic glucose solution may lead to hyperglycaemia. Patients should be observed for signs of mental confusion or loss of consciousness.
Prolonged use in parenteral nutrition may affect insulin production; blood and urine glucose should be monitored. Fluid and acid-base balance and electrolyte status should also be determined during therapy with dextrose.
None known.
Intravenous glucose may result in considerable foetal insulin production, with an associated risk of rebound hypoglycaemia in the new-born. Infusion should not exceed 5-10g/hour during labour or Caesarean section.
This preparation is intended for use only in emergencies.
Anaphylactoid reactions have been reported in patients with asthma and diabetes mellitus.
Local pain, inflammation, irritation, thrombophlebitis and fever may occur.
Hypokalaemia, hypomagnesaemia or hypophosphataemia may result from the use of hypertonic solutions via the intravenous route.
Prolonged or rapid administration of hyperosmotic (>5%) solutions may lead to dehydration.
The administration of glucose without adequate levels of thiamine (which form the coenzyme systems in its metabolism), may precipitate overt deficiency states, e.g. Wernicke's encephalopathy.
Excess glucose infusion produces increased CO2, which may be important in respiratory failure, and stimulates catecholamine secretion.
The patient becomes hyperglycaemic and glycosuria may occur. This can lead to dehydration, hyperosmolar coma and death.
Treatment: The infusion should be discontinued and the patient evaluated. Insulin may be administered and appropriate supportive measures taken.
Glucose, the natural sugar occurring in the blood, is the principle source of energy for the body. It is readily converted to fat and is also stored in the liver and muscles as glycogen. When a rapid rise in blood sugar is demanded by the body, glycogen is quickly liberated as d-glucose. When the supply of glucose is insufficient, the body mobilises fat stores which are converted to acetate with production of energy by the same oxidative pathways employed in the combustion of glucose.
It may decrease body protein and nitrogen losses. Glucose is also the probable source of glucuronic acid with which many foreign substances and their metabolites combine to form excretion products. It probably provides the basic substances required for the formation of hyalluronates and chondroitin sulphates, the supporting structures of the organism. It can be converted to a pentose essential for the formation of nucleic acids by the cells.
Glucose is metabolised to carbon dioxide and water with the release of energy.
Not applicable since glucose has been used in clinical practice for many years and its effects in man are well known.
Water for Injection
Glucose solutions which do not contain electrolytes should not be administered concomitantly with blood through the same infusion set as haemolysis and clumping may occur.
3 years.
Store below 25°C.
The solution is contained in a USP type I glass vial with an elastomeric closure which meets all the relevant USP specifications. The product is available as 10ml and 50ml.
The container is specially designed for use with the IMS Minijet injector. Do not use the injection if crystals have separated.
International Medication Systems (UK) Ltd
208 Bath Road
Slough
Berkshire
SL1 3WE
UK
PL 03265/0008R
Date first granted: 28 February 1991
Date renewed: 28 February 1996
April 2001
POM
Onemer may be available in the countries listed below.
Ketorolac tromethamine (a derivative of Ketorolac) is reported as an ingredient of Onemer in the following countries:
International Drug Name Search
Etomidate Injection is a sterile, nonpyrogenic solution. Each milliliter contains Etomidate, 2 mg, propylene glycol 35% v/v. The pH is 6.0 (4.0 to 7.0).
It is intended for the induction of general anesthesia by intravenous injection.
The drug Etomidate is chemically identified as (R)-(+)-ethyl-1-(1-phenylethyl)-1H-imidazole -5-carboxylate and has the following structural formula:
Molecular weight: 244.29
Etomidate is a hypnotic drug without analgesic activity. Intravenous injection of Etomidate produces hypnosis characterized by a rapid onset of action, usually within one minute. Duration of hypnosis is dose dependent but relatively brief, usually three to five minutes when an average dose of 0.3 mg/kg is employed. Immediate recovery from anesthesia (as assessed by awakening time, time needed to follow simple commands and time to perform simple tests after anesthesia as well as they were performed before anesthesia), based upon data derived from short operative procedures where intravenous Etomidate was used for both induction and maintenance of anesthesia, is about as rapid as, or slightly faster than, immediate recovery after similar use of thiopental. These same data revealed that the immediate recovery period will usually be shortened in adult patients by the intravenous administration of approximately 0.1 mg of intravenous fentanyl, one or two minutes before induction of anesthesia, probably because less Etomidate is generally required under these circumstances (consult the package insert for fentanyl before using).
The most characteristic effect of intravenous Etomidate on the respiratory system is a slight elevation in arterial carbon dioxide tension (PaCO2). See also ADVERSE REACTIONS.
Reduced cortisol plasma levels have been reported with induction doses of 0.3 mg/kg Etomidate. These persist for approximately 6 to 8 hours and appear to be unresponsive to ACTH administration.
The intravenous administration of up to 0.6 mg/kg of Etomidate to patients with severe cardiovascular disease has little or no effect on myocardial metabolism, cardiac output, peripheral circulation or pulmonary circulation. The hemodynamic effects of Etomidate have in most cases been qualitatively similar to those of thiopental sodium, except that the heart rate tended to increase by a moderate amount following administration of thiopental under conditions where there was little or no change in heart rate following administration of Etomidate. However, clinical data indicates that Etomidate administration in geriatric patients, particularly those with hypertension, may result in decreases in heart rate, cardiac index, and mean arterial blood pressure. There are insufficient data concerning use of Etomidate in patients with recent severe trauma or hypovolemia to predict cardiovascular response under such circumstances.
Clinical experience and special studies to date suggest that standard does of intravenous Etomidate ordinarily neither elevate plasma histamine nor cause signs of histamine release.
Limited clinical experience, as well as animal studies, suggests that inadvertent intra-arterial injection of Etomidate, unlike thiobarbiturates, will not usually be followed by necrosis of tissue distal to the injection site. Intra-arterial injection of Etomidate is, however, not recommended.
Etomidate induction is associated with a transient 20 to 30% decrease in cerebral blood flow. This reduction in blood flow appears to be uniform in the absence of intracranial space occupying lesions. As with other intravenous induction agents, reduction in cerebral oxygen utilization is roughly proportional to the reduction in cerebral blood flow. In patients with and without intracranial space occupying lesions, Etomidate induction is usually followed by a moderate lowering of intracranial pressure, lasting several minutes. All of these studies provided for avoidance of hypercapnia. Information concerning regional cerebral perfusion in patients with intracranial space occupying lesions is too limited to permit definitive conclusions.
Preliminary data suggests that Etomidate will usually lower intraocular pressure moderately.
Etomidate is rapidly metabolized in the liver. Minimal hypnotic plasma levels of unchanged drug are equal to or higher than 0.23 mcg/mL; they decrease rapidly up to 30 minutes following injection and thereafter more slowly with a half-life value of about 75 minutes. Approximately 75% of the administered dose is excreted in the urine during the first day after injection. The chief metabolite is R-(+)-1-(1-phenylethyl)-1H-imidazole-5-carboxylate acid, resulting from hydrolysis of Etomidate, and accounts for about 80% of the urinary excretion. Limited pharmacokinetic data in patients with cirrhosis and esophageal varices suggest that the volume of distribution and elimination half-life of Etomidate are approximately double that seen in healthy subjects.
(Reference: H. Van Beem, et. al., Anaesthesia 38 (Supp 38:61-62, July 1983).
In clinical studies, elderly patients demonstrated decreased initial distribution volumes and total clearance of Etomidate. Protein binding of Etomidate to serum albumin was also significantly decreased in these individuals.
Reduced plasma cortisol and aldosterone levels have been reported following induction doses of Etomidate. These results persist for approximately 6 to 8 hours and appear to be unresponsive to ACTH stimulation. This probably represents blockage of 11 beta-hydroxylation within the adrenal cortex.
(References: 1. R.J. Fragen, et. al., Anesthesiology 61:652-656, 1984. 2. R.L. Wagner & P.F. White, Anesthesiology 61:647-651, 1984. 3. F.H. DeJong, et. al., Clin. Endocrinology and Metabolism 59:(6):1143-1147, 1984, and three additional drafts of Metabolic Studies, all submitted to NDA 18-228 on April 1, 1985).
Etomidate injection is indicated by intravenous injection for the induction of general anesthesia. When considering use of Etomidate, the usefulness of its hemodynamic properties (see CLINICAL PHARMACOLOGY) should be weighed against the high frequency of transient skeletal muscle movements (see ADVERSE REACTIONS).
Intravenous Etomidate is also indicated for the supplementation of subpotent anesthetic agents, such as nitrous oxide in oxygen, during maintenance of anesthesia for short operative procedures such as dilation and curettage or cervical conization.
Etomidate is contraindicated in patients who have shown hypersensitivity to it.
INTRAVENOUS Etomidate SHOULD BE ADMINISTERED ONLY BY PERSONS TRAINED IN THE ADMINISTRATION OF GENERAL ANESTHETICS AND IN THE MANAGEMENT OF COMPLICATIONS ENCOUNTERED DURING THE CONDUCT OF GENERAL ANESTHESIA.
BECAUSE OF THE HAZARDS OF PROLONGED SUPPRESSION OF ENDOGENOUS CORTISOL AND ALDOSTERONE PRODUCTION, THIS FORMULATION IS NOT INTENDED FOR ADMINISTRATION BY PROLONGED INFUSION.
Do not administer unless solution is clear and container is undamaged. Discard unused portion (see DOSAGE AND ADMINISTRATION).
No carcinogenesis or mutagenesis studies have been carried out on Etomidate. The results of reproduction studies showed no impairment of fertility in male and female rats when Etomidate was given prior to pregnancy at 0.31, 1.25 and 5 mg/kg (approximately 1X, 4X, and 16X human dosage).
Etomidate has been shown to have an embryocidal effect in rats when given in doses 1 and 4 times the human dose. There are no adequate and well-controlled studies in pregnant women. Etomidate should be used during pregnancy only if the potential benefit justifies the potential risks to the fetus. Etomidate has not been shown to be teratogenic in animals. Reproduction studies with Etomidate have been shown to:
Decrease pup survival at 0.3 and 5 mg/kg in rats (approximately 1X and 16X human dosage) and at 1.5 and 4.5 mg/kg in rabbits (approximately 5X and 15X human dosage). No clear dose-related pattern was observed.
Increase slightly the number of stillborn fetuses in rats at 0.3 and 1.25 mg/kg (approximately 1X and 4X human dosage).
Cause maternal toxicity with deaths of 6/20 rats at 5 mg/kg (approximately 16X human dosage) and 6/20 rabbits at 4.5 mg/kg (approximately 15X human dosage).
There are insufficient data to support use of intravenous Etomidate in obstetrics, including Caesarean section deliveries. Therefore, such use is not recommended.
It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when Etomidate is administered to a nursing mother.
There are inadequate data to make dosage recommendations for induction of anesthesia in pediatric patients below the age of ten (10) years; therefore, such use in not recommended (see also DOSAGE AND ADMINISTRATION).
Clinical data indicates that Etomidate may induce cardiac depression in elderly patients, particularly those with hypertension (see CLINICAL PHARMACOLOGY and OTHER ADVERSE OBSERVATIONS, Circulatory System.).
Elderly patients may require lower doses of Etomidate than younger patients. Age-related differences in pharmacokinetic parameters have been observed in clinical studies (see CLINICAL PHARMACOLOGY and DOSAGE AND ADMINISTRATION).
This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection and it may be useful to monitor renal function.
Induction doses of Etomidate have been associated with reduction in plasma cortisol and aldosterone concentrations (see CLINICAL PHARMACOLOGY). These have not been associated with changes in vital signs or evidence of increased mortality; however, where concern exists for patients undergoing severe stress, exogenous replacement should be considered.
The most frequent adverse reactions associated with use of intravenous Etomidate are transient venous pain on injection and transient skeletal muscle movements, including myoclonus:
a. Most movements are bilateral. The arms, legs, shoulders, neck, chest wall, trunk and all four extremities have been described in some cases, with one or more of these muscle groups predominating in each individual case. Results of electroencephalographic studies suggest that these muscle movements are a manifestation of disinhibition of cortical activity; cortical electroencephalograms, taken during periods when these muscle movements were observed, have failed to reveal seizure activity.
b. Other movements are described as either unilateral or having a predominance of activity of one side over the other. These movements sometimes resemble a localized response to some stimuli, such as venous pain on injection, in the lightly anesthetized patient (averting movements). Any muscle group or groups may be involved, but a predominance of movement of the arm in which the intravenous infusion is started is frequently noted.
c. Still other movements probably represent a mixture of the first two types.
Skeletal muscle movements appear to be more frequent in patients who also manifest venous pain on injection.
Hyperventilation, hypoventilation, apnea of short duration (5 to 90 seconds with spontaneous recovery), laryngospasm, hiccup and snoring suggestive of partial upper airway obstruction have been observed in some patients. These conditions were managed by conventional countermeasures.
Hypertension, hypotension, tachycardia, bradycardia and other arrhythmias have occasionally been observed during induction and maintenance of anesthesia. One case of severe hypotension and tachycardia, judged to be anaphylactoid in character, have been reported.
(Reference: M. Sold and A. Rothhammer, Anaesthesist 34:208-210, 1985. Submitted to NDA 18-228 on 16 May 1985).
Geriatric patients, particularly those with hypertension, may be at increased risk for the development of cardiac depression following Etomidate administration (see CLINICAL PHARMACOLOGY).
Postoperative nausea and/or vomiting following induction of anesthesia with Etomidate is probably no more frequent than the general incidence. When Etomidate was used for both induction and maintenance of anesthesia in short procedures such as dilation and curettage, or when insufficient analgesia was provided, the incidence of postoperative nausea and/or vomiting was higher than that noted in control patients who received thiopental.
Overdosage may occur from too rapid or repeated injections. Too rapid injection may be followed by a fall in blood pressure. No adverse cardiovascular or respiratory effects attributable to Etomidate overdose have been reported.
In the event of suspected or apparent overdosage, the drug should be discontinued, a patent airway established (intubate, if necessary) or maintained and oxygen administered with assisted ventilation, if necessary.
The LD50 of Etomidate administered intravenously to rats is 20.4 mg/kg.
Etomidate injection is intended for administration only by the intravenous route (see CLINICAL PHARMACOLOGY). The dose for induction of anesthesia in adult patients and in children above the age of ten (10) years will vary between 0.2 and 0.6 mg/kg of body weight, and it must be individualized in each case. The usual dose for induction in these patients is 0.3 mg/kg, injected over a period of 30 to 60 seconds. There are inadequate data to make dosage recommendations for induction of anesthesia in patients below the age of ten (10) years; therefore, such use is not recommended. Geriatric patients may require reduced doses of Etomidate.
Smaller increments of intravenous Etomidate may be administered to adult patients during short operative procedures to supplement subpotent anesthetic agents, such as nitrous oxide. The dosage employed under these circumstances, although usually smaller than the original induction dose, must be individualized. There are insufficient data to support this use of Etomidate for longer adult procedures or for any procedures in pediatric patients; therefore, such use is not recommended. The use of intravenous fentanyl and other neuroactive drugs employed during the conduct of anesthesia may alter the Etomidate dosage requirements. Consult the prescribing information for all other such drugs before using.
Etomidate injection is compatible with commonly administered pre-anesthetic medications, which may be employed as indicated. See also CLINICAL PHARMACOLOGY, ADVERSE REACTIONS, and dosage recommendations for maintenance of anesthesia.
Etomidate hypnosis does not significantly alter the usual dosage requirements of neuromuscular blocking agents employed for endotracheal intubation or other purposes shortly after induction of anesthesia.
Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
To prevent needle-stick injuries, needles should not be recapped, purposely bent, or broken by hand.
Etomidate Injection 20 mg/10 mL is supplied as follows:
NDC Number Packaging
0069 - 0006 - 01 Carton of 10 x 10 mL Single-dose vials
Etomidate Injection 40 mg/20 mL is supplied as follows:
NDC Number Packaging
0069 - 0006 - 03 Carton of 10 x 20 mL Single-dose vials
Store at 20º to 25º C (68º to 77º F). [see USP Controlled Room Temperature].
Discard unused portion.
Rx Only
Made in India
Pfizer Labs
Division of Pfizer Inc
New York, NY 10017
May 2011
1016382
NDC 0069-0006-02
10 mL Single Dose Vial
Etomidate injection
20 mg/10 mL
(2 mg/mL)
For Intravenous Use
Discard Unused Portion
Rx only
Contains 10 of NDC 0069-0006-02
Rx only
10 x 10 mL Single Dose Vials
Etomidate injection
20 mg/10 mL
(2 mg/mL)
For Intravenous Use
Pfizer Injectables
NDC 0069-0006-04
20 mL Single Dose Vial
Etomidate injection
40 mg/20 mL
(2 mg/mL)
For Intravenous Use
Discard Unused Portion
Rx only
Pfizer Injectables
Contains 10 of NDC 0069-0006-04
Rx only
10 x 20 mL Single Dose Vials
Etomidate injection
40 mg/20 mL
(2 mg/mL)
For Intravenous Use
Pfizer Injectables
| Etomidate Etomidate injection | ||||||||||||||||||||||||
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| Marketing Information | |||
| Marketing Category | Application Number or Monograph Citation | Marketing Start Date | Marketing End Date |
| ANDA | ANDA078289 | 02/03/2012 | |
| Labeler - Pfizer Laboratories Div Pfizer Inc. (134489525) |
| Registrant - AGILA SPECIALTIES PRIVATE LIMITED (650548014) |
| Establishment | |||
| Name | Address | ID/FEI | Operations |
| AGILA SPECIALTIES PRIVATE LIMITED | 676199117 | Analysis, Manufacture, Sterilize, Pack | |
