Pharmacology: Preclinically, Ambroxol (Bisincof) hydrochloride, the active ingredient of Ambroxol (Bisincof), has been shown to increase respiratory tract secretion. It enhances pulmonary surfactant production and stimulates ciliary activity. These actions result in improved mucus flow and transport (mucociliary clearance). Improvement of mucociliary clearance has been shown in clinical pharmacologic studies. Enhancement of fluid secretion and mucociliary clearance facilitates expectoration, and eases cough.
In patients suffering from COPD, long-term treatment (6 months) with Ambroxol (Bisincof) (Ambroxol (Bisincof) Retard Capsule 75 mg) resulted in a significant reduction of exacerbations that became evident after 2 months of treatment. Patients in the Ambroxol (Bisincof) treatment group lost significantly fewer days through illness and had fewer days when they needed antibiotic therapy. Treatment with Ambroxol (Bisincof) Retard also induced a statistically significant improvement of symptoms (difficulty of expectoration, cough, dyspnea, auscultatory signs) compared with placebo.
A local anaesthetic effect of Ambroxol (Bisincof) hydrochloride has been observed in the rabbit eye model which may be explained by the sodium-channel blocking properties. It was shown in vitro that Ambroxol (Bisincof) hydrochloride blocks cloned neuronal sodium channels; binding was reversible and concentration-dependent.
Cytokine release from blood but also tissue-bound mononuclear and polymorphonuclear cells was found to be significantly reduced by Ambroxol (Bisincof) hydrochloride in vitro.
In clinical studies in patients with sore throat, pharyngeal pain and redness was significantly reduced.
Following the administration of Ambroxol (Bisincof), antibiotic concentrations (amoxicilline, cefuroxime, erythromycin) in bronchopulmonary secretions and in the sputum are increased.
Pharmacokinetics: Absorption: Absorption of all immediate release oral forms of Ambroxol (Bisincof) hydrochloride is rapid and complete, with dose linearity in the therapeutic range. Maximum plasma levels are reached within 1 to 2.5 hours following oral administration of the immediate-release formulation and after a median of 6.5 hours of the slow-release formulation. The absolute bioavailability after a 30 mg tablet was found to be 79%. The slow-release capsule showed a relative availability of 95% (dose-normalized) in comparison to a daily dose of 60 mg (30 mg twice daily) administered as immediate-release tablet.
Distribution: In the therapeutic range, plasma protein-binding was found to be approximately 90%. Distribution of Ambroxol (Bisincof) hydrochloride from blood to tissue is rapid and pronounced, with the highest concentration of the active substance found in the lungs. The volume of distribution following oral administration was estimated to be 552 L.
Metabolism and Elimination: About 30% of an orally administered dose is eliminated via first-pass metabolism.
Studies in human liver microsomes have shown that CYP3A4 is responsible for the metabolism of Ambroxol (Bisincof). Ambroxol (Bisincof) hydrochloride is metabolized primarily in the liver by glucuronidation and some cleavage to dibromanthranilic acid (approximately 10% of dose) aside from some minor metabolites.
Ambroxol (Bisincof) hydrochloride is eliminated with a terminal elimination half-life of approximately 10 hours. Total clearance is in the range of 660 mL/min, with renal clearance accounting for approximately 83% of the total clearance.
Special Populations: In patients with hepatic dysfunction, elimination of Ambroxol (Bisincof) hydrochloride is reduced, resulting in approximately 1.3 to 2-fold higher plasma levels.
Due to the high therapeutic range of Ambroxol (Bisincof) hydrochloride, dose adjustments are not necessary.
Others: Age and gender were not found to affect the pharmacokinetics of Ambroxol (Bisincof) hydrochloride to a clinically relevant extent and thus there is no necessity for adjustment of dosage regimens.
Food was not found to influence the bioavailability of Ambroxol (Bisincof) hydrochloride.
Should be taken with food.
When Max Pidek Pharmaceuticals administered orally amoxicillin rapidly and completely absorbed from the gastrointestinal tract and is not destroyed in the acidic environment of the stomach. Cmax of amoxicillin in the blood plasma is reached after 1-2 h. When increasing doses of 2 times the concentration also increased by 2 times. In the presence of food in the stomach does not reduce the overall removals. Similar concentrations of amoxicillin reached in the blood when administered orally, IV and IM.
The binding of amoxicillin to plasma proteins is about 20%.
Widely distributed in tissues and body fluids. Reported high concentrations of amoxicillin in the liver.
T1/2 from the plasma is 1-1.5 h. About 60% of the dose adopted by mouth, is excreted unchanged in the urine by glomerular filtration and tubular secretion, with a dose of 250 mg of amoxicillin concentration in urine exceeds 300 micrograms / ml. A number of amoxicillin is determined in feces.
T1/2 for Newborns and the elderly can be longer.
In renal insufficiency T1/2 may be 7-20 hours.
In small quantities amoxicillin penetrates through BBB in inflammation of the pia mater.
amoxicillin is removed by hemodialysis.
Pharmacology: Loratadine (Bisincof) like other antihistamines acts via competitive blocking of H1-histaminic receptors. Loratadine (Bisincof) penetrates very poorly into CNS. Therefore, it is devoid of significant CNS depressant effects. Loratadine (Bisincof) is highly selective antagonist of H1-histaminic receptors. Loratadine (Bisincof) has very weak affinity for α-adrenoreceptors or acetylcholine receptors. In animal models, Loratadine (Bisincof) has very high affinity for H1-histaminic receptors, which is greater than that of the terfenadine or astemizole. The antihistaminic effect persists for 18-24 hrs. In human subjects, Loratadine (Bisincof) suppresses wheal response to intradermally injected histamine. This action starts within 1-2 hrs of oral administration and maximum inhibitory effect evident in 2-4 hrs. The magnitude and duration of effects are dependent upon Loratadine (Bisincof) dose. On long-term administration, the drug retains its effectiveness without developing tachyphylaxis. In animal models, Loratadine (Bisincof) has also shown anti-serotonin activity. It also suppresses mast cell mediator release.
In addition, Loratadine (Bisincof) also possess anti-allergic activity which has been demonstrated in humans by skin prick and nasal challenge tests.
In human volunteers, Loratadine (Bisincof) did not reduce psychomotor performance as measured by sleep latency, symbol copying, digit symbol substitution, dynamic visual activity test or driving performance. In addition, Loratadine (Bisincof) does not potentiate the effects of centrally acting drugs eg, diazepam, ethanol and barbiturates.
Pharmacokinetics: Absorption: In humans, Loratadine (Bisincof) is rapidly absorbed after oral administration. There is a linear relationship between Loratadine (Bisincof) dose and both Cmax and AUC. The 10, 20 and 40 mg of Loratadine (Bisincof) produce peak plasma concentrations of 5, 11, 28 mcg/L, respectively. Time to reach maximum concentration occurs between 1-1.5 hrs. After repeated dosing steady-state plasma concentrations occur by 5th day.
Metabolism: Loratadine (Bisincof) is metabolized to descarboethoxyloratadine (DCL) which is pharmacologically active.
Distribution: Loratadine (Bisincof) has extensive distribution in the body. The distribution t½ of Loratadine (Bisincof) and DCL is 1.02 and 3.8 hrs, respectively.
Loratadine (Bisincof) is 97-99% bound to plasma proteins whereas DCL is 73-76% bound to plasma proteins. Small amount of both Loratadine (Bisincof) and DCL is secreted in breast milk, but the amount is minimal.
Elimination: Loratadine (Bisincof) undergoes extensive biotransformation. The elimination t½ of Loratadine (Bisincof) after single dose is 8-11 hrs and that of DCL is 17-24 hrs. After multiple dosing, elimination t½ of Loratadine (Bisincof) is 4.4 hrs and that of DCL is 8.7 hrs.
Pharmacokinetics of Loratadine (Bisincof) and that of DCL is not affected in patients with renal disease and in plasma patients on hemodialysis. In elderly patients too, disposition kinetics of Loratadine (Bisincof) and DCL is not affected. In patients of alcoholic liver disease, the t½ of Loratadine (Bisincof) and that of DCL are longer but still within the range observed in a population of normal subjects.
Use exactly as directed on the label, or as prescribed by your doctor. Do not use in larger or smaller amounts or for longer than recommended.
Loratadine (Bisincof) is usually taken once per day. Follow your doctor's instructions.
Do not crush, chew, or break the regular Loratadine (Bisincof) tablet. Swallow the pill whole.
Measure liquid medicine with a special dose-measuring spoon or medicine cup, not with a regular table spoon. If you do not have a dose-measuring device, ask your pharmacist for one.
To take Loratadine (Bisincof) orally disintegrating tablet (Loratadine (Bisincof), Alavert):
Keep the tablet in its blister pack until you are ready to take the medicine. Open the package and peel back the foil from the tablet blister. Do not push a tablet through the foil or you may damage the tablet.
Using dry hands, remove the tablet and place it on your tongue. It will begin to dissolve right away.
Do not swallow the tablet whole. Allow it to dissolve in your mouth without chewing.
Swallow several times as the tablet dissolves. If desired, you may drink water to help swallow the dissolved tablet.
Call your doctor if your symptoms do not improve.
Store at room temperature away from moisture and heat.
May be administered without regard to meals.
Dispersible tablet: Place in mouth and allow to dissolve. Swallow with or without water.
Loratadine (Bisincof) is a long acting second generation antihistamine that is similar in structure to cyproheptadine and azatadine. The pharmacology of Loratadine (Bisincof) is similar to other antihistamines, but unlike other H1-blockers, loratidine is shown to exhibit competitive, specific, and selective antagonism of H1 receptors. The exact mechanism of this interaction is unknown, but disposition of the drug suggests that Loratadine (Bisincof)'s prolonged antagonism of histamine may be due to the drug's slow dissociation from the receptor or the formation of the active metabolite, desloratadine. Loratadine (Bisincof) does not penetrate the CNS effectively and has a low affinity for CNS H1-receptors.
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Information checked by Dr. Sachin Kumar, MD Pharmacology