66722-44-9CC(C)NCC(O)COc1ccc(COCCOC(C)C)cc1VHYCDWMUTMEGQY-UHFFFAOYSA-NBisoprolol is a secondary amine and a secondary alcohol. It has a role as a beta-adrenergic antagonist, an antihypertensive agent, an anti-arrhythmia drug and a sympatholytic agent.
66722-44-9Pharmaceutical
Pharmaceuticals -> Used in Switzerland
Pharmaceuticals -> Antihypertensives
Pharmaceuticals
log Kow = 1.87
2.2
1.87
Breast Feeding; Lactation; Milk, Human; Antihypertensive Agents; Adrenergic Beta-Antagonists; Antiarrhythmics
Pharmaceuticals
Antianginal medicines
100-103
100 °C
9.57
9.57
9.5
pKa1 = 9.27 (secondary amine); pKa2 = 14.09 (alcohol)
안전 정보는 참고용이며, 공급업체의 물질안전보건자료(SDS), 관련 법규 및 전문가 평가를 대체하지 않습니다.
Warning
H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]
P264, P270, P301+P317, P330, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 41 reports by companies from 4 notifications to the ECHA C&L Inventory.
Warning
H302: Harmful if swallowed [Warning Acute toxicity, oral]
The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including bisoprolol fumarate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Bisoprolol fumarate/
Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.
Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.
C07AB07
C - Cardiovascular system
QC - Cardiovascular system
C07AB07
Bisoprolol decreases heart rate (chronotropy), decreases contractility (inotropy), and reduces blood pressure. The results of various clinical studies indicate that bisoprolol reduces cardiovascular mortality and all-cause mortality in patients with heart failure and decreased cardiac ejection fraction (EF).
Though the mechanism of action of bisoprolol has not been fully elucidated in hypertension, it is thought that therapeutic effects are achieved through the antagonism of β-1adrenoceptors to result in lower cardiac output. Bisoprolol is a competitive, cardioselective β1-adrenergic antagonist. When β1-receptors (located mainly in the heart) are activated by adrenergic neurotransmitters such as epinephrine, both the blood pressure and heart rate increase, leading to greater cardiovascular work, increasing the demand for oxygen. Bisoprolol reduces cardiac workload by decreasing contractility and the need for oxygen through competitive inhibition of β1-adrenergic receptors. Bisoprolol is also thought to reduce the output of renin in the kidneys, which normally increases blood pressure. Additionally, some central nervous system effects of bisoprolol may include diminishing sympathetic nervous system output from the brain, decreasing blood pressure and heart rate.
A pharmacokinetic study in 12 healthy individuals determined the mean plasma half-life of bisoprolol to be 10-12 hours. Another study comprised of healthy patients determined the elimination half-life to be approximately 10 hours. Renal impairment increased the half-life to 18.5 hours.
In patients with cirrhosis of the liver, the elimination of Zebeta (bisoprolol fumarate) is more variable in rate and significantly slower than that in healthy subjects, with plasma half-life ranging from 8.3 to 21.7 hours.
In subjects with creatinine clearance less than 40 mL/min, the plasma half-life is increased approximately threefold compared to healthy subjects.
불러오는 중…
DTXSID6022682CHEMBL645CHEBI:3127187.7 Ų [M+H]+ [CCS Type: DT; Method: single field calibrated]
192.2 Ų [M+H]+ [CCS Type: TW; Method: Major Mix IMS/Tof Calibration Kit (Waters)]
Yellow Oil
Store at 20 deg to 25 °C (68 deg to 77 °F). Protect from moisture. Dispense in tight containers.
Keep container tightly closed in a dry and well-ventilated place. Recommended storage temperature: 2 - 8 °C.
ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation; Environmental precautions: Do not let product enter drains; Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.
SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.
Product: Offer surplus and non-recyclable solutions to a licensed disposal company; Contaminated packaging: Dispose of as unused product.
Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapor or mist.
Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.
Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.
Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).
Skin protection: Handle with gloves
Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.
Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type ABEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).
Concurrent use of rifampin increases the metabolic clearance of Zebeta, resulting in a shortened elimination half-life of Zebeta. However, initial dose modification is generally not necessary. Pharmacokinetic studies document no clinically relevant interactions with other agents given concomitantly, including thiazide diuretics and cimetidine. There was no effect of Zebeta on prothrombin time in patients on stable doses of warfarin.
Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use /with Zebeta/ can increase the risk of bradycardia.
Zebeta should be used with care when myocardial depressants or inhibitors of AV conduction, such as certain calcium antagonists (particularly of the phenylalkylamine (verapamil) and benzothiazepine (diltiazem) classes), or antiarrhythmic agents, such as disopyramide, are used concurrently.
Zebeta should not be combined with other beta-blocking agents. Patients receiving catecholamine-depleting drugs, such as reserpine or guanethidine, should be closely monitored, because the added beta-adrenergic blocking action of Zebeta may produce excessive reduction of sympathetic activity. In patients receiving concurrent therapy with clonidine, if therapy is to be discontinued, it is suggested that Zebeta be discontinued for several days before the withdrawal of clonidine.
beta-Blockers may exacerbate the rebound hypertension which can follow the withdrawal of clonidine. If the two drugs are coadministered, the beta-blocker should be withdrawn several days before discontinuing clonidine. If replacing clonidine by beta-blocker therapy, the introduction of beta-blockers should be delayed for several days after clonidine administration has stopped.
Bisoprolol therapy has been associated with a low rate of mild-to-moderate elevations of serum aminotransferase levels which are usually asymptomatic and transient and resolve even with continuation of therapy. There have been no well documented cases of clinically apparent, acute liver injury attributable to bisoprolol. Thus, hepatotoxicity due to bisoprolol must be very rare, if it occurs at all. Most commonly used beta-blockers have been linked to rare instances of clinically apparent liver injury, typically with onset within 2 to 12 weeks, a hepatocellular pattern of liver enzyme elevations, rapid recovery upon withdrawal, and little evidence of hypersensitivity (rash, fever, eosinophilia) or autoantibody formation.
TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 140(SRC), determined from a structure estimation method(2), indicates that bisoprolol is expected to have high mobility in soil(SRC). The estimated pKa1 of bisoprolol is 9.27(3), indicating that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization from moist soil is not expected because the compound exists as a cation and cations do not volatilize. Bisoprolol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.9X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). A 37.9% of its Theoretical Oxygen Demand in 75 days using an activated sludge and the Manometric respirometry test(5) suggests that biodegradation may be a slow environmental fate process in soil(SRC).
AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 140(SRC), determined from a structure estimation method(2), indicates that bisoprolol is not expected to adsorb to suspended solids and sediment(SRC). An estimated pKa1 of 9.27(3) indicates bisoprolol will exist almost entirely in the cation form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), a BCF of 0.2(5), indicates that bioconcentration in aquatic organisms is low. Half-lives of 27.7 and 8.6 days were measured for bisopropol using two natural sediments and respective river waters(6), indicating that biodegradation may be an important environmental fate process in water(SRC).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), bisoprolol, which has an estimated vapor pressure of 2.9X10-8 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase bisoprolol may be removed from the air by wet and dry deposition(SRC). Bisoprolol exhibited half-lives of 15-70 hours when exposed to a high pressure vapor mercury lamp (250-600 nm)(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).
A common adverse effect of cardiovascular blockers is bradycardia, decreasing heart rate and strength of contraction due to its negative chronotropic and inotropic effects. Bisoprolol also decreases cardiac output; therefore, it decreases exercise capacity. Blocking beta receptors on the SA and AV node always carries a risk of heart block. It correlates less frequently with exacerbating peripheral diseases such as the Raynaud phenomenon, bronchoconstriction, and hypoglycemia than non-selective beta-blockers.
IDENTIFICATION AND USE: Bisoprolol is a beta-Adrenergic blocking agent, sometimes under the drug name Zebeta, which is indicated in the management of hypertension. It may be used alone or in combination with other antihypertensive agents. HUMAN EXPOSURE AND TOXICITY: The most common signs expected with overdosage of a beta-blocker are bradycardia, hypotension, congestive heart failure, bronchospasm, and hypoglycemia. There have been at least two reported cases where a switch from propranolol to bisoprolol resulted in worsening of arrhythmia control. An elderly person died of uncontrolled bradycardia in a hospital after being mistakenly given a higher-than-prescribed dose of bisoprolol fumarate. However, it was determined that the patient had a mutation within cytochrome P2D6, which influences metabolism of the drug. ANIMAL STUDIES: Fetotoxicity in rats occurred at 125 times the maximum recommended human dose (MRHD) of bisoprolol fumarate on a body-weight-basis, and maternal toxicity occurred at 375 times the MRHD. In rabbits, bisoprolol fumarate was not teratogenic at doses up to 12.5 mg/kg/day (31 times the MRHD based on body-weight), but increased early resorptions. The mutagenic potential of bisoprolol fumarate was evaluated in the microbial mutagenicity (Ames) test, the point mutation and chromosome aberration assays in Chinese hamster V79 cells, the unscheduled DNA synthesis test, the micronucleus test in mice, and cytogenetics assay in rats. There was no evidence of mutagenic potential in these in vitro and in vivo assays. Long-term studies were conducted with oral bisoprolol fumarate administered in the feed of mice and rats. No evidence of carcinogenic potential was seen in mice dosed up to 250 mg/kg/day or rats dosed up to 123 mg/kg/day.
The toxicity of cardio-selective beta-blockers occurs after ingesting a high dose of the drug, either intentionally or unintentionally. Toxicity can be asymptomatic in some patients, but treatment is always required. Patients in such cases usually present with bradycardia and hypotension. In addition, selective beta-blockers in high doses lose their selectivity, causing patients to demonstrate signs of respiratory distress, congestive heart failure, and neurological manifestations, such as confusion and mental retardation, hypoglycemia, and hyperkalemia.
Bisopropanol concentrations ranged from 0.12 to 0.16 ug/L in effluent from a sewage treatment plant in Frankfurt, Germany. Influent concentrations ranged from 0.35 to 0.49 ug/L(1). The compound was detected in 97% of samples from 90 EU wastewater treatment plant effluents, at an average concentration of 41.6 ng/L and a maximum concentration of 423 ng/L. Sampling was conducted in 2010; detection limit = 0.1 ng/L(2).
Using a structure estimation method based on molecular connectivity indices(1), the Koc of bisoprolol can be estimated to be 140(SRC). According to a classification scheme(2), this estimated Koc value suggests that bisoprolol is expected to have high mobility in soil. Log Koc values of 1.87-2.15 and 2.12 have been reported in sediments from the Burgen (0.74 total organic carbon, clay/silt 10%) and Dausenau (4.36% total organic carbon, 47% clay/silt) rivers, respectively, Germany(3), corresponding to Koc values of 74-141 and 131, respectively(SRC). However, adsorption is affected by the acidity of the soil/substrate(SRC). The estimated pKa1 of bisoprolol is 9.27(3), indicating that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).
/CASE REPORTS/ The most common signs expected with overdosage of a beta-blocker are bradycardia, hypotension, congestive heart failure, bronchospasm, and hypoglycemia. To date, a few cases of overdose (maximum: 2000 mg) with bisoprolol fumarate have been reported. Bradycardia and/or hypotension were noted. Sympathomimetic agents were given in some cases, and all patients recovered.
/CASE REPORTS/ An elderly person died of uncontrolled bradycardia in a hospital. The doctor had prescribed 1.35 mg of bisoprolol fumarate orally, but a nurse mistakenly gave the patient 10 mg of the drug 9 hours prior to her death. Bisoprolol was detected in her blood by liquid chromatography-mass spectrometry at a concentration of 176 ng/mL. Even if the patient had chronic heart failure, this concentration is double the expected value. This patient was found to have a mutation within cytochrome P2D6, with thymidine substituted for cytosine at position 100 and cytosine for guanine at position 4180, causing proline to serine and threonine to serine amino acid substitutions. This mutation in the intermediate metabolizer allele reportedly reduces enzyme activity by half. However, in addition to the type of cytochrome P450 allelic variant, the amount of enzyme product influences metabolism of this drug. In this case, the high blood concentration of bisoprolol was only partly attributable to an error in prescription; its concentration was inexplicably high.
/CASE REPORTS/ Propranolol in slow-release form has been the first-line treatment in long QT (LQT) until it was withdrawn from the market. We describe two cases where a switch to bisoprolol resulted in worsening of arrhythmia control: A man with LQT2, asymptomatic on propranolol, experienced syncope after switching to bisoprolol 5 mg daily. He switched back to propranolol and has remained asymptomatic during subsequent 12 months. A man with classical Jervell Lange-Nielsen syndrome, previous gangliectomy, and ICD implantation, switched to bisoprolol 5 mg daily. Four months later he experienced a tachycardia storm. He switched back to propranolol and has remained free from arrhythmias during subsequent 12 months.
Bisopropol not detected in bream (Abramis brama) and roach (Rutilus rutilus) from Lake Haapajarvi, Finland, caught on May 24, 2010. The lake receives effluent from a wastewater treatment plant via the Rakkolanjoki river. It was not detected in the same species that were sampled on July 1, 2011 from Lake Saimma in southern Finalnd, which is not influenced by municipal waste water(1).
AEROBIC: Half-lives of 27.7 and 8.6 days were measured for bisopropol (5 ug dissolved in methanol) using two natural sediments and respective river water of low anthropogenic impact from the Baybreach and Unterbach streams, respectively, near Dausenau, Germany(1). Bisoprolol, present at 50 mg/L, reached 37.9% (75.4% with added carbon source of NaAc) of its Theoretical Oxygen Demand in 75 days using an activated sludge from a sewage treatment plant in Jyvaskyla, Finland and the Manometric respirometry test (OECD test 301F). Based on these results, bisoprolol is considered moderately biodegradable under aerobic conditions(2).
ANAEROBIC: Bisoprolol, present at 1000 mg/L (methane evolution) showed a methane production of 15.7 mL in 161 days using a digester sludge inoculum at 31.5 g/L from a sewage treatment plant in Jyvaskyla, Finland. An averaged of 28% removal was observed using an initial bisoprolol concentration of 100 ug/L. Based on these results, bisoprolol is considered moderately persistent under anaerobic conditions(1).
Benchmark Dataset for the Liver Toxicity Knowledge Base (LTKB)
bisoprolol
Zebeta®
Beta blockers
3
less-DILI-concern drugs
The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including bisoprolol fumarate, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Bisoprolol fumarate/
The plasma elimination half-life is 9-12 hours and is slightly longer in elderly patients, in part because of decreased renal function in that population.
The pharmacokinetic properties of bisoprolol-(14)C were studied in Wistar rats, beagle dogs, and Cynomolgus monkeys. ... The plasma half-life of the unchanged drug was approximately 1 hr in rats, 3 hr in monkeys, and 5 hr in dogs.
In dogs, bisoprolol has ... a half life of 4 hours
Approximately 50% of the bisoprolol dose is eliminated by non-renal pathways. Bisoprolol is metabolized through oxidative metabolic pathways with no subsequent conjugation. Bisoprolol metabolites are polar and, therefore, really eliminated. Major metabolites found in plasma and urine are inactive. Bisoprolol is mainly metabolized by CYP3A4 (95%), whereas CYP2D6 plays a minor role. The CYP3A4-mediated metabolism of bisoprolol appears to be non-stereoselective.
... In humans, the known metabolites are labile or have no known pharmacologic activity. ... Bisoprolol fumarate is not metabolized by cytochrome P450 II D6 (debrisoquin hydroxylase).
The plasma concentrations and urinary excretions of bisoprolol enantiomers in four Japanese male healthy volunteers after a single oral administration of 20 mg of racemic bisoprolol were evaluated. The AUC(infinity) and elimination half-life of (S)-(-)-bisoprolol were slightly larger than those of (R)-(+)-bisoprolol in all subjects. The metabolic clearance of (R)-(+)-bisoprolol was significantly (P < 0.05) larger than that of (S)-(-)-bisoprolol (S/R ratio: 0.79+/-0.03), although the difference was small. In contrast, no stereoselective in vitro protein binding of bisoprolol in human plasma was found. An in vitro metabolic study using recombinant human cytochrome P450 (CYP) isoforms indicated that oxidation of both bisoprolol enantiomers was catalyzed by the two isoforms, CYP2D6 and CYP3A4. CYP2D6 metabolized bisoprolol stereoselectively (R > S), whereas the metabolism of bisoprolol by CYP3A4 was not stereoselective. The S/R ratio of the mean clearance due to renal tubular secretion was 0.68, indicating a moderate degree of stereoselective renal tubular secretion. These findings taken together suggest that the small differences in the pharmacokinetics between (S)-(-)- and (R)-(+)-bisoprolol are mainly due to the stereoselectivity in the intrinsic metabolic clearance by CYP2D6 and renal tubular secretion.
The pharmacokinetic properties of bisoprolol-(14)C were studied in Wistar rats, beagle dogs, and Cynomolgus monkeys. ... The metabolism of bisoprolol was studied in the same three animal species and in humans. The major metabolites are the products of O-dealkylation and subsequent oxidation to the corresponding carboxylic acids. ...
Y41JS2NL6U
BISOPROLOL
Mechanisms of Action [MoA] - Adrenergic beta-Antagonists
Established Pharmacologic Class [EPC] - beta-Adrenergic Blocker
Bisoprolol is a beta-Adrenergic Blocker. The mechanism of action of bisoprolol is as an Adrenergic beta-Antagonist.
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.
Drugs that bind to and block the activation of ADRENERGIC BETA-1 RECEPTORS.
Bisoprolol is well absorbed in the gastrointestinal tract. The bioavailability of bisoprolol is about 90% due to the minimal first-pass effects. Absorption is unaffected by food intake. Peak plasma concentrations of bisoprolol are attained within 2-4 hours and steady-state concentrations are achieved within 5 days of administration. In a pharmacokinetic study, the mean peak concentration of bisoprolol was 52 micrograms/L. Cmax at steady state concentrations of bisoprolol is 64±21 ng/ml administered at 10 mg daily. The area under the curve (AUC) following oral administration of 10mg bisoprolol ranged from 597 to 661 ug/L x h. Following intravenous administration of the same dosage, the AUC was 672 ug/L x h.
Bisoprolol is eliminated equally by both renal and hepatic pathways. About 50% of an oral dose is excreted unchanged in the urine with the remainder of the dose excreted as inactive bisoprolol metabolites. Under 2% of the ingested dose is found to be excreted in the feces.
The volume of distribution of bisoprolol is 3.5 L/kg. The mean volume of distribution was found to be 230 L/kg in heart failure patients, which was similar to the volume of distribution in healthy patients. Bisoprolol is known to cross the placenta.
Total body clearance in healthy patients was determined to be 14.2 L/h. In patients with renal impairment, clearance was reduced to 7.8 L/h. Hepatic dysfunction also reduced the clearance of bisoprolol.
Beagles were treated with bisoprolol, a beta 1-selective adrenoceptor antagonist, for 30 days with the following daily doses: oral: 30 mg/kg; conjunctival: 0.5% solution (approx. 0.04 mg/kg) and 5% solution (approx. 0.4 mg/kg). Drug concentrations were determined in plasma and various eye tissues on days 1, 16, and 30, and on day 59, i.e. on day 29 of the follow-up period. Bisoprolol concentrations in plasma and most eye tissues were considerably higher after oral than after conjunctival treatment. The highest tissue concentrations were observed in the iris (+ciliary body) and retina (+choroid) with tissue/plasma concentration ratios between 100 and 150 after oral and 1000 to 3000 after conjunctival instillation (5% solution). In plasma no accumulation of the drug was observed which is in accordance with its plasma half-life of 4 to 5 hr. In contrast to this, concentrations in the iris and retina increased from day 1 to day 16 and 30 by 3 to 8 times and the half-life of bisoprolol in these tissues was estimated to be between 3 to 5 days.
The pharmacokinetic properties of bisoprolol-(14)C were studied in Wistar rats, beagle dogs, and Cynomolgus monkeys. Bisoprolol is well absorbed in these species; independent of the route of administration (IV or PO), 70-90% of the (14)C-dose was recovered in urine. Fecal excretion was approximately 20% in rats and less than 10% in dogs and monkeys. Rats excreted approximately 10% of the dose in bile after IV as well as after oral administration. The plasma half-life of the unchanged drug was approximately 1 hr in rats, 3 hr in monkeys, and 5 hr in dogs. The bioavailability was 40-50% in monkeys, approximately 80% in dogs, and 10% in rats. Studies in rats have shown that the drug is rapidly taken up by the tissues. After IV administration, high levels of radioactivity were found in lung, kidneys, liver, adrenals, spleen, pancreas, and salivary glands. After oral administration, the highest concentration occurred in the liver and kidneys. With the exception of plasma and liver, unchanged bisoprolol was the major radioactive constituent in all tissues studied. Both the blood-brain and placental barriers were penetrated, but only to a small degree. No accumulation of radioactivity in tissues was observed after repeated dosing (1 mg/kg/day). The metabolism of bisoprolol was studied in the same three animal species and in humans. The major metabolites are the products of O-dealkylation and subsequent oxidation to the corresponding carboxylic acids. The amount of bisoprolol excreted unchanged in the urine is 50-60% of the dose in humans, 30-40% in dogs, and approximately 10% in rats and monkeys.
MEDICATION
Adrenergic beta-1 Receptor Antagonists; Antihypertensive Agents; Sympatholytics
Use (kg; approx.) in Germany (2009): >7500
Table: Bisoprolol Fumarate Preparations [Table#8328]
Table: Bisoprolol Fumarate Combination Preparations [Table#8329]
용도Cardensiel is an intermediate in the synthesis of 3,3''-(Isopropylazanediyl)bis(1-(4-((2-isopropoxyethoxy)methyl)phenoxy)propan-2-ol) (I824005), which is an impurtiy of Bisoprolol (B510500), a selective β-adrenergic blocker. Used as an antihypertensive.