Kimox, 400 mg 5 pcs.

Pharmacology

Pharmacodynamics

Mechanism of action

Inhibits topoisomerase II (DNA-gyrase) and topoisomerase IV – enzymes necessary for replication, transcription, repair and recombination of bacterial DNA. It disrupts DNA synthesis of the microbial cell and has a bactericidal effect.

The mechanism of action of fluoroquinolones including moxifloxacin is different from that of macrolides, beta-lactams, aminoglycosides or tetracyclines, so microorganisms resistant to these classes of drugs may be sensitive to moxifloxacin. Resistance to fluoroquinolones is primarily due to mutation of topoisomerase II (DNA-gyrase) or topoisomerase IV genes, reduced outer membrane permeability or efflux. Resistance to moxifloxacin in vitro develops slowly and is associated with multistep mutations. Resistance to moxifloxacin in vitro in Gram-positive bacteria occurs with a frequency of 1.8-10-9 to 1-10-11 or less.

Cross-resistance

Cross-resistance between moxifloxacin and other fluoroquinolones has been observed in Gram-negative bacteria. Gram-positive bacteria resistant to other fluoroquinolones may be sensitive to moxifloxacin. Cross-resistance between moxifloxacin and other classes of antimicrobial agents is unknown.

Moxifloxacin is active (both in vitro and by the results of clinical studies on the treatment of several infections) against most strains of the following microorganisms: Aerobic Gram-positive microorganisms – Enterococcus faecalis, Staphylococcus aureus, Streptococcus anginosus, Streptococcus constellatus, Streptococcus pneumoniae (including multi-resistant strains [MDRSP]*), Streptococcus pyogenes; aerobic gram-negative microorganisms – Enterobacter cloacae, Esherichia coli, Haemophilus influenzae, Haemophilus parainfluenzae, Klebsiella pneumoniae, Moraxella catarrhalis, Proteus mirabilis, Yersinia pestis; anaerobic microorganisms – Bacteroides fragilis, Bacteroides thetaiotaomicron, Clostridium perfringens, Peptostreptococcus spp., as well as other microorganisms – Chlamydia pneumoniae, Mycoplasma pneumoniae.

* Strains with multiple resistance to antibiotics (Multi-drug resistant Streptococcus pneumoniae, MDRSP), including strains formerly known as PRSP (Penicillin-resistant S. pneumoniae) and strains resistant to two or more of the following antibiotics: penicillin (at MPC ≥2 µg/mL), second-generation cephalosporins (e.g. cefuroxime), macrolides, tetracyclines and trimethoprim/sulfamethoxazole.

According to in vitro studies, moxifloxacin is active (MPC ≤2 µg/mL) against most (over 90%) strains of the following microorganisms: aerobic gram-positive microorganisms – Staphylococcus epidermidis, Streptococcus agalactiae, Streptococcus viridans; aerobic gram-negative microorganisms – Citrobacter freundii, Klebsiella oxytoca, Legionella pneumophyla; anaerobic microorganisms – Fusobacterium spp., Prevotella spp. Clinical significance of the obtained in vitro data is not defined, safety and efficacy of moxifloxacin in the treatment of infections caused by these pathogens in adequate and well-controlled trials has not been established.

Photosensitivity. Study of skin reaction to ultraviolet light (UVA and UVB) and visible radiation, conducted with 32 healthy volunteers (8 per group) showed that moxifloxacin shows no phototoxicity compared to placebo. Minimum erythematous dose (MED) was determined before and after administration of moxifloxacin (200 or 400 mg once daily) or placebo. The MED measured for both doses of moxifloxacin was not significantly different from placebo.

Pharmacokinetics

Absorption. When administered orally, it is well absorbed from the gastrointestinal tract. Absolute bioavailability is almost 90%. Consumption of food with high content of fat (500 calories) has no effect on absorption of moxifloxacin. Simultaneous consumption of 1 cup of yogurt has no significant effect on the degree and rate of systemic absorption (AUC). In studies with healthy volunteers it was shown that Cmax after a single oral intake of 400 mg of moxifloxacin is (3.1±1) mg/l (n=372). Plasma concentration increases in proportion to dose in the dose range up to 1200 mg (maximum single test dose when taken orally). The plasma T1/2 is (12±1.3) h and equilibrium is reached after at least three days of administration (400 mg daily).

Distribution. Binding to serum proteins is approximately 30-50% and is independent of the substance concentration. Vd is 1.7-2.7 l/kg. Well distributed in the tissues and body fluids, with concentrations in the tissues often exceeding the plasma concentration of the substance. After oral administration or by injection in a dose of 400 mg of moxifloxacin is found in saliva, the mucous membrane of the nose, bronchi and sinuses, subcutaneous tissues, skeletal muscle and abdominal tissues.

. High concentrations in excess of moxifloxacin levels in blood are produced in the bronchial mucosa (tissue/plasma concentration ratio (1.7±0.3), alveolar macrophages (21.2±10.0), fluid covering the respiratory epithelium (8.7±6.1) mucosa of the maxillary sinus (2.0±0.3), ethmoidal sinus (2.2±0.6), nasal polyps (2.6±0.6), abdominal tissues (2.7±08), abdominal exudate (1.6±0.7), in the contents of blisters in skin inflammation (0.9±0.2), subcutaneous tissue (0.4±0.6), skeletal muscles (0.4±0.1).

The concentrations were measured 3 h after administration of a single dose of 400 mg (except for measurements in abdominal tissue and exudate, which were taken 2 h after moxifloxacin administration, and in the sinuses, which were taken 2 h after moxifloxacin administration after 5 days of use). The elimination rate of moxifloxacin from tissues usually parallels the elimination rate from plasma.

Metabolism. Approximately 52% of the moxifloxacin dose (oral or IV) is metabolized by conjugation to form two inactive metabolites, sulfate (M1) and glucuronide (M2). M1 is approximately 38% of the dose and is excreted primarily with feces, M2 is 14% of the dose and is excreted only with the urine. Peak plasma concentrations of M2 are approximately 40% of the parent substance concentration, while plasma concentrations of M1 are typically less than 10% of the concentration of moxifloxacin.

Moxifloxacin is metabolized without involvement of the cytochrome P450 system (cytochrome P450 system activity is not affected). In vitro studies with cytochrome P450 isoenzymes show that moxifloxacin does not inhibit CYP3A4, CYP2D6, CYP2C9, CYP2C19 and CYP1A2.

Excretion. Approximately 45% of moxifloxacin (oral or IV) is excreted unchanged (of which approximately 20% in the urine, about 25% in the feces). (96±4)% of the oral dose is excreted either unchanged or as known metabolites. Total apparent clearance is (12±2) l/h, renal clearance is (2.6±0.5) l/h.

Dependence of pharmacokinetic parameters on some factors

There were no clinically significant differences in pharmacokinetics of moxifloxacin according to age, gender and race of patients.

Elderly age. No age-related changes in pharmacokinetics were observed in 16 elderly (8 men, 8 women) and 17 young (8 men, 9 women) healthy volunteers after oral administration of moxifloxacin at a dose of 400 mg for 10 days. In 16 healthy male volunteers (8 young; 8 elderly) after a single oral dose of moxifloxacin 200 mg the degree of systemic effect (AUC and Cmax) was not different in young and elderly men, T1/2 was not changed. No dose adjustment based on age is required. In large phase III studies moxifloxacin blood concentrations at the end of infusion in elderly patients after an IV infusion of 400 mg were similar to those observed in younger patients.

Paul. After oral administration of 400 mg of moxifloxacin daily for 10 days, 23 healthy men (19-75 years) and 24 healthy women (19-70 years) had mean AUC and Cmax values 8 and 16% higher in women compared with men. The differences were due to differences in body weight rather than sex.

A study of a single dose of 400 mg was conducted with 18 young men and women. A comparison of the pharmacokinetics of moxifloxacin in this study (9 women and 9 men) showed no difference in AUC or Cmax by sex. No adjustment of the dose of moxifloxacin according to sex is required.

Children. Pharmacokinetics of moxifloxacin in children has not been studied.

Race. Pharmacokinetics of moxifloxacin in equilibrium condition after daily oral intake in 400 mg dose in Japanese men was similar to that in European men and was characterized with values of Cmax 4.1 mcg /ml, AUC24 47 mcg-h /ml and T1/2 14 hours.

Renal insufficiency. No significant changes in pharmacokinetic parameters have been found in mild, moderate and severe renal dysfunction (including terminal stage). No dose adjustment is required in patients with renal impairment, including those on continuous hemodialysis and long-term ambulatory peritoneal dialysis.

Hepatic impairment. Dose adjustment is not recommended in mild, moderate and severe hepatic impairment (Child Pugh grades A, B and C). However, due to metabolic disorders associated with hepatic failure, which may lead to prolongation of the QT interval, moxifloxacin should be used with caution in these patients.

Preclinical toxicology

Carcinogenicity. No long-term animal studies have been conducted to evaluate the carcinogenic effects of moxifloxacin.

Mutagenicity. Mutagenicity or genotoxicity was not observed in a number of in vitro tests, including Ames test (using 4 bacterial strains of TA 98, TA 100, TA 1535, TA 1537), test with hypoxanthine-guanine phosphoribosyltransferase of Chinese hamster ovary cells, as well as in vivo (including micronucleus test in mice). Mutagenic activity was revealed (as for other quinolones) in Ames test using bacterial strain TA 102, probably caused by blockade of DNA-gyrase. It showed clastogenic activity in V-79 test for chromosomal aberrations, but did not cause atypical DNA synthesis in rat hepatocyte culture.

The effect on fertility. No effect of moxifloxacin on fertility was detected in male and female rats when administered orally at doses greater than 500 mg/kg/day (approximately 12-fold greater than MRDH, in terms of body surface area) or intravenously at doses of 45 mg/kg/day (approximately identical to MRDH, in terms of body surface area, mg/m2). Small effects on sperm morphology (head and tail separation) in male rats and on the sexual cycle of female rats were observed when doses of 500 mg/kg/day were administered orally.

Toxicology and/or pharmacology in animals

The quinolones cause arthropathy in young growing animals. In studies in dogs, pups have been shown to develop arthropathy on oral administration of moxifloxacin at doses ≥30 mg/kg/day (approximately 1.5 times the MRDH) for 28 days. Oral administration to mature monkeys and rats at doses of 135 and 500 mg/kg/day, respectively, was not accompanied by manifestations of arthropathy.

Some quinolones have proconvulsant activity that is enhanced when combined with NSAIDs. In the study on mice no increase of acute toxicity or potential toxic effect on CNS (including seizures) were found after oral administration of moxifloxacin in dose of 300 mg/kg together with administration of NSAIDs (diclofenac, ibuprofen, fenbufen).

In studies on dogs it was shown that at plasma concentrations of moxifloxacin, 5 times higher than therapeutic levels in humans, prolongation of QT interval was observed. The main mechanism of QT interval prolongation (data from electrophysiological studies) is the inhibition of rapid activating component of delayed (delayed) rectifying potassium current. Simultaneous infusion of sotalol against the background of moxifloxacin administration in dogs led to a more pronounced prolongation of the QT interval c than when taking moxifloxacin alone at the same dose (30 mg/kg).

There were no signs of local intolerance in dogs when administered moxifloxacin by IV injection. Inflammatory changes affecting the periarterial soft tissues have been observed following an IV/a injection of moxifloxacin, suggesting that IV administration should be avoided.

Clinical Studies

The efficacy of moxifloxacin for systemic use has been evaluated in a number of clinical studies.

Acute bacterial sinusitis

The efficacy of moxifloxacin (400 mg once daily orally for 10 days) in treating patients with acute bacterial sinusitis was evaluated in a double-blind, controlled clinical trial conducted in the United States. The clinical efficacy of moxifloxacin (cure plus improvement) was 90%; the primary efficacy analysis was performed on days 7-21 after therapy.

In addition, studies were conducted to obtain bacteriological data to assess microbiological eradication in adult patients when treated with moxifloxacin (400 mg orally, once daily for 7 days). All patients (n=336) underwent an abdominal puncture. The clinical efficacy rate (eradication) at day 21-37 after treatment was 97% (29/30) for Streptococcus pneumoniae, 83% (15/18) for Moraxella catarrhalis, and 80% (24/30) for Haemophilus influenzae.

The exacerbation of chronic bronchitis

. According to the results of a large-scale randomized double-blind controlled clinical trial conducted in the United States, the clinical efficacy of moxifloxacin in the treatment of exacerbations of chronic bronchitis (oral dose of 400 mg once daily for 5 days) was 89% (222/250 patients), with the initial assessment of results on days 7-17 after therapy. The degree of microbiological eradication was: for Streptococcus pneumoniae and Haemophilus parainfluenzae 100% (16/16), Haemophilus influenzae 89% (33/37), Moraxella catarrhalis 85% (29/34), Staphylococcus aureus 94% (15/16), Klebsiella pneumoniae 90% (18/20).

Efficacy of moxifloxacin (oral dosage of 400 mg once daily) in the treatment of patients with clinically and radiographically documented community-acquired pneumonia was evaluated in a randomized, double-blind, controlled clinical trial conducted in the United States. The clinical efficacy of moxifloxacin was 95% (184/194), with an initial efficacy assessment in most patients on days 14-35 at follow-up visits.

A randomized, double-blind, controlled clinical trial conducted in the United States and Canada evaluated the efficacy of moxifloxacin when administered sequentially, v/v, then orally, in a dose of 400 mg once daily for 7-17 days in patients with a confirmed diagnosis of community-acquired pneumonia. The clinical efficacy of moxifloxacin was 86% (157/182), with primary efficacy analysis in most patients on day 7-30 after the end of therapy.

In an open-label study outside the United States, the clinical efficacy of moxifloxacin was 93% (241/258) on day 5-7 and 84% (216/258) 21-28 days after completion of treatment.

. Combined data of 4 researches suggest that degree of clinical effectiveness of moxifloxacin is 85% in relation to Staphylococcus aureus, 92% – in relation to Klebsiella pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, 93% – in relation to Chlamydia pneumoniae, 94% – in relation to Streptococcus pneumoniae, 96% – in relation to Mycoplasma pneumoniae.

Out-of-hospital pneumonia caused by strains of Streptococcus pneumoniae with multiple resistance to antibiotics (see “Indications”). The clinical and bacteriological efficacy of moxifloxacin was 95% (35/37).

Uncomplicated infections of the skin and its appendages.

According to the results of a randomized double-blind controlled clinical trial conducted in the USA, in the treatment of skin infections (uncomplicated abscesses – 30%, furuncles – 8%, cellulitis – 16%, impetigo – 20%, other skin infections – 26%) the effectiveness of moxifloxacin (oral administration in a dose of 400 mg once daily for 7 days) was 89% (108/122).

Complicated infections of the skin and its appendages

The efficacy of moxifloxacin was evaluated in two randomized controlled clinical trials with the active drug. In a double-blind trial conducted primarily in North America, the clinical efficacy of moxifloxacin (sequential IV followed by oral administration at a dose of 400 mg once daily for 7-14 days) was 77.2% (125/162). In a second open international study, the clinical efficacy of moxifloxacin in a dose of 400 mg once daily for 7-21 days was 80.6% (254/315). Treatment success rates varied according to the type of diagnosis, ranging from 61% in patients with infected ulcers to 90% in patients with complicated rust inflammation.

The clinical efficacy of moxifloxacin was 82.2% (106/129) against Staphylococcus aureus (methicillin-sensitive strains), 81.6% (31/38) against Esherichia coli, 91.7% (11/12) against Klebsiella pneumoniae, 81.8% (9/11) against Enterobacter cloacae.

Complicated intra-abdominal infections

The efficacy of moxifloxacin has been evaluated in two randomized controlled clinical trials with the active drug. A double-blind study conducted in North America in the treatment of patients with intraabdominal infections such as peritonitis, abscess, appendicitis with perforation, and intestinal perforation reported 79.8% (146/183) effectiveness of moxifloxacin (sequential IV followed by oral administration at a dose of 400 mg once daily for 5-14 days). In a second open-label international study, the efficacy of moxifloxacin (400 mg once daily for 5-14 days c) was 80.9% (199/246).

Plague

The efficacy studies of moxifloxacin could not be conducted in people with pneumonic plague for ethical and feasibility reasons. Therefore, approval of this indication was based on an animal efficacy study and supportive pharmacokinetic data in adult humans and animals.

A randomized, blind, placebo-controlled study was conducted in an animal model of African green monkey pneumonic plague. Twenty monkeys (10 males and 10 females) were exposed to a mean inhalation dose (±standard deviation) of (100±50) LD50 (range 92 to 127 LD50) of Yersinia pestis aerosol (strain CO92). The MPC of moxifloxacin for the Y. pestis strain used in this study was 0.06 µg/mL. Development of a persistent fever of at least 4 h was used as a trigger for initiating a 10-day administration of either moxifloxacin or placebo. All of the animals studied had fever and bacteremia with Y. pestis prior to observation. Ten of 10 (100%) animals receiving placebo died of the disease between 83 and 139 h (115±19) after infection. Ten of 10 (100%) animals receiving moxifloxacin survived for 30 days after study completion. Compared with the placebo group, mortality was significantly lower in the moxifloxacin group (survival difference: 100% with two-sided 95% CI (66.3%, 100%), p<0.0001 value).

The mean plasma concentrations of moxifloxacin associated with a statistically significant improvement in survival compared with placebo, in an African green monkey model of pneumonic plague, achieved or exceeded those in adult humans when administered in the recommended oral and intravenous regimens. The mean (±standard deviation) plasma Cmax and total plasma exposure (AUC) in adults treated with 400 mg v/v were (3.9±0.9) µg/ml and (39.3±8.6) µg-h/ml, respectively. The mean (±standard deviation) plasma Cmax and AUC0-24 in monkeys after a one-day simulated dosing regimen simulating the achievement of AUC0-24 in humans at the 400 mg dose were (4.4±1.5) mcg/mL and (22±8) mcg-h/mL, respectively.

Indications

Infectious inflammatory diseases caused by microorganisms sensitive to moxifloxacin:

Active ingredient

Composition

How to take, the dosage

Interaction

Special Instructions

In some cases hypersensitivity and allergic reactions may develop already after the first use of the drug and the physician should be informed immediately. Very rarely even after the first use of the drug anaphylactic reactions may progress to life-threatening anaphylactic shock. In these cases the treatment with moxifloxacin should be stopped and necessary medical measures (including anti-shock measures) should be started immediately.

When using moxifloxacin some patients may show prolongation of the QT interval. Moxifloxacin should be used with caution in women and elderly patients. Since women compared to men have a longer QT interval, they may be more sensitive to the medicines prolonging the QT interval. Older patients are also more susceptible to QT interval medications.

Long QT interval prolongation is associated with an increased risk of ventricular arrhythmias, including polymorphic ventricular tachycardia. The degree of QT interval prolongation may increase with increasing drug concentration, so the recommended dose should not be exceeded. However, in patients with pneumonia the correlation between plasma concentration of moxifloxacin and prolongation of QT interval was not noted.

When using moxifloxacin the risk of ventricular arrhythmias may increase in patients with conditions predisposing to arrhythmias. In this regard, moxifloxacin is contraindicated in:

– changes in the electrophysiological parameters of the heart, expressed in prolongation of the QT interval: congenital or acquired documented prolongation of the QT interval, electrolyte abnormalities, especially uncorrected hypokalemia;

– clinically significant bradycardia;

– clinically significant heart failure with reduced left ventricular ejection fraction;

– a history of rhythm disturbances with clinical symptoms;

– use with other QT interval-prolonging medications (see

– use with other QT interval lengthening drugs (see section “Interaction with other medicinal products”).

Moxifloxacin should be used with caution:

– in patients with potentially antiarrhythmic conditions, such as acute myocardial ischemia and cardiac arrest;

– in patients with cirrhosis (because the risk of QT interval prolongation cannot be excluded in this category of patients).

When taking moxifloxacin it was reported about the cases of fulminant hepatitis, potentially leading to liver failure (including fatal cases) (see section “Adverse effects”). The patient should be informed that in case of symptoms of liver failure it is necessary to consult a physician before continuing treatment with moxifloxacin.

When taking moxifloxacin it was reported about the cases of bullous skin lesions (Stevens-Johnson syndrome or toxic epidermal necrolysis) (see section “Side effects”). The patient should be informed that in case of symptoms of skin lesions or mucous membranes it is necessary to consult a physician before continuing treatment with moxifloxacin.

The use of quinolone drugs is associated with a possible risk of seizures. Moxifloxacin should be used with caution in patients with diseases of the CNS and with disorders of the CNS which predispose to seizures or reduce the threshold for seizure activity. The use of broad-spectrum antibacterial agents, including moxifloxacin, is associated with the risk of pseudomembranous colitis.

This diagnosis should be kept in mind for patients who developed severe diarrhea during treatment with moxifloxacin. In this case appropriate therapy should be administered immediately. Drugs which inhibit intestinal peristalsis are contraindicated in the development of severe diarrhea.

Moxifloxacin should be used with caution in patients with myasthenia gravis due to possible exacerbation of the disease.

With quinolones including moxifloxacin therapy the development of tendinitis and tendon rupture is possible especially in the elderly and patients receiving glucocorticosteroids. Cases have been described that occurred within a few months after completion of treatment. At the first symptoms of pain or inflammation at the site of injury, the drug should be discontinued and the affected limb should be unloaded. Photosensitivity reactions have been reported with quinolones.

But during the preclinical and clinical studies, as well as during the use of moxifloxacin in practice photosensitivity reactions were not observed. Nevertheless, patients receiving moxifloxacin should avoid exposure to direct sunlight and ultraviolet light.
The use of the drug in tablet form for oral administration is not recommended in patients with complicated inflammatory diseases of the pelvic organs (such as those associated with tubo-ovarian or pelvic abscesses).

The use of moxifloxacin is not recommended for the treatment of infections caused by strains of Staphylococcus aureus resistant to methicillin (MRSA). In the case of suspected or confirmed MRSA infections, treatment with appropriate antibacterial agents should be prescribed (see section “Pharmacodynamics”).

The ability of moxifloxacin to inhibit the growth of mycobacteria may cause in vitro interaction of moxifloxacin with the test for Mycobacterium spp. leading to false-negative results when analyzing samples from patients who are treated with moxifloxacin during this period.

In patients treated with quinolones, including moxifloxacin, cases of sensory or sensorimotor polyneuropathy leading to paresthesias, hypoesthesias, dysesthesias or weakness have been described. Patients who are treated with moxifloxacin should be warned about the need to immediately consult a physician before continuing treatment in case of symptoms of neuropathy, including pain, burning, tingling, numbness or weakness (see section “Side effects”).

Psychiatric reactions may occur even after the first prescription of fluoroquinolones, including moxifloxacin. In very rare cases, depression or psychotic reactions progress to suicidal thoughts and behavior with a tendency to self-harm, including suicide attempts (see section “Side effects”). In the case of development of any side effects on the central nervous system, including mental disorders it is necessary to immediately cancel moxifloxacin and initiate appropriate therapy. In these cases it is recommended to switch to therapy with another antibiotic other than fluoroquinolones if possible. Caution should be exercised when prescribing moxifloxacin to patients with psychosis and/or with a history of psychiatric disorders.

Because of the high prevalence and increasing incidence of infections caused by Neisseria gonorrhoeae resistant to fluoroquinolones during the treatment of patients with pelvic inflammatory diseases should not be conducted monotherapy with moxifloxacin, except in cases when the presence of resistant to fluoroquinolones N. gonorrhoeae is excluded. If there is no way to exclude the presence of fluoroquinolone-resistant N. gonorrhoeae, it is necessary to consider supplementing empirical therapy with moxifloxacin with an appropriate antibiotic that is active against N. gonorrhoeae (e.g., cephalosporin).

As with other fluoroquinolones, during the use of moxifloxacin changes in blood glucose concentrations were observed, including hypo- and hyperglycemia. During the therapy with moxifloxacin dysglycemia occurred more frequently in elderly patients and patients with diabetes receiving concomitant therapy with oral hypoglycemic agents (e.g., sulfonylureas) or insulin.

When using moxifloxacin in such patients the risk of hypoglycemia increases, up to hypoglycemic coma. It is necessary to inform patients about the symptoms of hypoglycemia (confusion, dizziness, “wolfish” appetite, headache, nervousness, palpitations or rapid pulse, pale skin, sweating, trembling, weakness). If a patient develops hypoglycemia, it is necessary to immediately discontinue treatment with moxifloxacin and begin an appropriate therapy. In these cases it is recommended to switch to therapy with another antibiotic other than fluoroquinolones, if possible. During treatment with moxifloxacin in elderly patients with diabetes mellitus it is recommended to monitor closely the concentration of glucose in blood.

Patients with a family history or actual deficiency of glucose-6-phosphate dehydrogenase are prone to hemolytic reactions during treatment with quinolones. Moxifloxacin should be administered with caution in these patients.

The tablets contain the dye sunset yellow (E 110), which may cause allergic reactions.

Fluoroquinolones, including moxifloxacin, may impair patients’ ability to drive and engage in other potentially dangerous activities requiring increased attention and rapid psychomotor reactions due to the effect on the CNS and visual impairment.

Synopsis

Contraindications

Side effects

Overdose

Pregnancy use

Similarities