Stopcriz pills p/o 0.4mg №10×3

Name:
Stop crisis tab. 0.4 mg No. 30 Main active ingredient Moxonidine Release form tablets Composition 1 film-coated tablet contains 0.2 mg, 0.3 mg or 0.4 mg of moxonidine. Excipients: tablet core: lactose monohydrate, povidone K25, crospovidone, magnesium stearate; tablet coating: titanium dioxide (E171), iron oxide red (E172), hydroxypropyl methylcellulose, macrogol 400.
Description:
Round, film-coated tablets. Tablets with a dosage of 0.2 mg are light pink in color. Tablets with a dosage of 0.3 mg – pink. Tablets with a dosage of 0.4 mg – dark pink. Pharmacological properties Pharmacodynamics Moxonidine has been shown to be an effective antihypertensive agent. Available experimental data suggest that the site of the antihypertensive action of moxonidine is the central nervous system (CNS). Moxonidine is a selective I1-imidazoline receptor agonist. Imidazoline-sensitive receptors are concentrated in the rostral ventrolateral part of the medulla oblongata, an area that is considered the center of regulation of the peripheral sympathetic nervous system. Stimulation of imidazoline receptors helps to reduce the activity of the sympathetic nervous system and lower blood pressure. Moxonidine differs from other sympatholytic antihypertensive drugs in its relatively low affinity for ?2-adrenergic receptors compared to I1-imidazoline receptors, which explains the lower likelihood of developing a sedative effect and dry mouth when using moxonidine. Pharmacokinetics Absorption After oral administration, moxonidine is rapidly absorbed. About 90% of the oral dose of moxonidine is absorbed in humans. Eating does not affect the pharmacokinetic properties of moxonidine. There is no effect of the first phase and bioavailability is 88%. Distribution Peak plasma concentrations of moxonidine are reached within 30-180 minutes after ingestion of the film-coated tablet. Only about 7% of moxonidine binds to plasma proteins (volume of distribution is 1.8 ± 0.4 l/kg). Metabolism 10-20% moxonidine is metabolized mainly to 4,5-dehydromoxonidine and guanidine derivatives due to opening of the imidazole ring. The hypotensive effect of 4,5-dehydromoxonidine is only 1/10 of that for moxonidine, and for guanidine derivatives it is less than 1/100. Withdrawal Moxonidine and its metabolites are almost completely excreted by the kidneys. More than 90% of the dose is excreted through the kidneys during the first 24 hours after administration, and only about 1% is excreted in the feces. The proportion of excreted unchanged moxonidine through the kidneys is about 50-75%. The mean plasma half-life is 2.2-2.3 hours, and the renal half-life is 2.6-2.8 hours. Pharmacokinetics in elderly patients Slight differences in the pharmacokinetic properties of moxonidine in healthy elderly patients and young adults age are clinically significant. Since there is no accumulation of moxonidine, there is no need to adjust the dose if renal function is normal. Pharmacokinetics in children Pharmacokinetic studies in children have not been conducted. Pharmacokinetics in patients with impaired renal function In patients with moderate renal impairment (CC 30-60 ml / min), AUC increases by 85%, and clearance decreases by 52%. For such patients, the hypotensive effect of moxonidine should be carefully monitored, especially at the beginning of treatment. In addition, the individual dose should not exceed 0.2 mg and the daily dose should not exceed 0.4 mg. Preclinical data In vitro and in vivo mutagenicity studies and one rat carcinogenicity study were negative. In studies of reproductive toxicity, no effect on fertility and teratogenic potential has been established. Embryotoxic effects have been observed in rats at doses above 3 mg/kg/day and in rabbits at doses above 0.7 mg/kg/day. In a peri- and postnatal study in rats, developmental and viability effects were seen at doses above 1 mg/kg/day. Indications for use Arterial hypertension. Contraindications – hypersensitivity to moxonidine or to any of the excipients; – angioedema in history; – sick sinus syndrome or sinoauricular blockade; – atrioventricular blockade of the 2nd and 3rd degree; – bradycardia (less than 50 beats / min at rest); – malignant arrhythmia; – heart failure; – severe ischemia of the heart or unstable angina; – severe liver failure; – chronic renal failure (CC < 30 ml / min, serum creatinine concentration > 160 μmol / l); – pregnancy or breastfeeding; – Children and adolescents under 18 years of age. Use during pregnancy and lactation There are no adequate data on the use of moxonidine in pregnant patients. Animal studies have shown reproductive toxicity. The potential risk to humans is unknown. Moxonidine should not be used during pregnancy unless absolutely necessary. Moxonidine should not be used during lactation as the drug passes into breast milk. Breastfeeding should be discontinued if moxonidine therapy is essential. Dosage and administration Adults (and the elderly) Treatment should begin with the lowest dose of moxonidine (0.2 mg) taken in the morning. Three weeks later, if necessary, the dose is increased to 0.4 mg and taken in one (morning) or two doses (morning and evening) until a satisfactory effect is achieved. If after the next three weeks the response to treatment is still unsatisfactory, the dose can be increased to a maximum of 0.6 mg divided into morning and evening doses. Do not exceed a single dose of moxonidine equal to 0.4 mg and a daily dose of 0.6 mg. Meal does not affect the pharmacokinetic properties of moxonidine, so the tablets can be taken regardless of the meal. Tablets must be taken with sufficient liquid. Children Moxonidine should not be used in children and adolescents under 18 years of age as there is limited clinical experience in this age group. Patients with renal insufficiency For patients with moderate renal impairment (CC> 30 ml / min, but < 60 ml / min), a single dose should not exceed 0.2 mg, and the daily dose should not exceed 0.4 mg of moxonidine. Patients with hepatic impairment No studies have been conducted in patients with hepatic impairment. Moxonidine is not extensively metabolized by the liver, so little effect on pharmacokinetics is expected. Dosing in patients with mild to moderate hepatic insufficiency is the same as in adult patients. Treatment should not be stopped suddenly. The drug should be stopped within 2 weeks. Side effects The most common side effects are dry mouth, dizziness, weakness and drowsiness. These symptoms often improve after the first few weeks of treatment. Adverse reactions observed during placebo-controlled clinical trials involving n = 886 patients taking moxonidine are listed by system organ class and, depending on the frequency, are classified as follows: very frequent (? 1/10), frequent (? 1 / 100, <1/10), infrequent (?1/1000, <1/100), rare (?1/10000, <1/1000), very rare (<1/10000), frequency not established (cannot be established according to available data). Cardiac disorders: infrequent - bradycardia. Ear and labyrinth disorders: infrequent - ringing in the ears. Nervous system disorders: common - headache*, dizziness, vertigo, drowsiness; infrequent - fainting *. Vascular disorders: infrequently - hypotension (including orthostatic hypotension). Gastrointestinal disorders: very common - dry mouth; frequent - diarrhea, nausea, vomiting, dyspepsia. Violations of the skin and subcutaneous fat: frequent - rash, itching; infrequent - angioedema. General violations: frequent - asthenia; infrequent - edema. Skeletal muscle and connective tissue disorders: common - back pain; infrequent - pain in the neck. Mental disorders: frequent - sleep disorders; infrequent - increased excitability. * No increase in frequency compared to placebo was observed. Overdose Symptoms. There are several reports of acute non-fatal overdose with moxonidine 19.6 mg. The following signs and symptoms have been observed: headache, sedation, drowsiness, hypotension, dizziness, asthenia, bradycardia, dry mouth, vomiting, fatigue, and epigastric pain. In case of severe overdose, careful monitoring of the patient's condition is recommended, especially in case of impaired consciousness and respiratory depression. Potentially, a short-term increase in blood pressure, tachycardia, hyperglycemia is also possible. Treatment. There are no specific antidotes. In case of hypotension, restoration of circulating blood volume by the administration of fluid and dopamine is recommended. Bradycardia can be treated with atropine. Alpha-adrenergic antagonists may reduce or eliminate transient hypertension in moxonidine overdose. Interaction with other drugs Simultaneous use of moxonidine and other antihypertensive drugs leads to an additive effect. Since tricyclic antidepressants may reduce the effect of centrally acting antihypertensive drugs, co-administration of tricyclic antidepressants with moxonidine is not recommended. Moxonidine may enhance the effect of tricyclic antidepressants (simultaneous administration should be avoided), tranquilizers, alcohol, hypnotics and sedatives. Moxonidine moderately improves cognitive impairment in patients receiving lorazepam. Moxonidine may increase the sedative effect of benzodiazepines when used concomitantly. Moxonidine is excreted by tubular secretion. Interaction with other agents that are excreted by tubular secretion cannot be ruled out. Storage conditions Store at a temperature not exceeding 30 ° C. Buy Stopcriz tablets p/o 0.4 mg No. 10x3