Moxifloxacin Actions

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Actions of Moxifloxacin in details

infoThe action of the drug on the human body is called Pharmacodynamics in Medical terminology. To produce its effect and to change the pathological process that is happening the body and to reduce the symptom or cure the disease, the medicine has to function in a specific way. The changes it does to the body at cellular level gives the desired result of treating a disease. Drugs act by stimulating or inhibiting a receptor or an enzyme or a protein most of the times. Medications are produced in such a way that the ingredients target the specific site and bring about chemical changes in the body that can stop or reverse the chemical reaction which is causing the disease.

Pharmacology: Mechanism of Action: Moxifloxacin is a 8-methoxy-fluoroquinolone antibiotic with a broad spectrum of activity and bactericidal action. Moxifloxacin has in vitro activity against a wide range of gram-positive and gram-negative organisms, anaerobes, acid-fast bacteria and atypicals eg, Mycoplasma, Chlamydia and Legionella spp.

The bactericidal action results from the interference with topoisomerase II and IV. Topoisomerases are essential enzymes which control DNA topology and assist in DNA replication, repair and transcription.

Moxifloxacin exhibits concentration-dependent bactericidal killing. Minimum bactericidal concentrations are generally similar to minimum inhibitory concentrations (MIC). Moxifloxacin is effective against β-lactam-resistant and macrolide-resistant bacteria. Studies in animal models of infection have demonstrated the high in vivo activity.

Resistance: Resistance mechanisms which inactivate penicillins, cephalosporins, aminoglycosides, macrolides and tetracyclines do not interfere with the antibacterial activity of moxifloxacin. There is no cross-resistance between moxifloxacin and these agents. Plasmid-mediated resistance has not been observed to date.

It appears that the C8-methoxy moiety contributes to enhanced activity and lower selection of resistant mutants of gram-positive bacteria compared to the C8-H moiety. The presence of the bulky bicycloamine substituent at the C-7 position prevents active efflux, a mechanism of fluoroquinolone resistance.

In vitro studies have demonstrated that resistance to moxifloxacin develops slowly by multiple step mutations. A very low overall frequency of resistance was demonstrated (10-7 to 10-10). Serial exposure of organisms to sub-MIC concentration of moxifloxacin showed only a small increase in MIC values.

Cross-resistance among quinolones has been observed. However, some gram-positive and anaerobic organisms resistant to other quinolones are susceptible to moxifloxacin.

Pharmacokinetics: Absorption and Bioavailability: Following oral administration, moxifloxacin is absorbed rapidly and almost completely. The absolute bioavailability amounts to approximately 91%.

Pharmacokinetics are linear in the range of 50-1200 mg single dose and up to 600 mg once daily dosing over 10 days. Steady state is reached within 3 days. Following a 400-mg oral dose peak concentration of 3.1 mg/L are reached within 0.5 - 4 hrs p.a. Peak and trough plasma concentrations at steady state (400 mg once daily) were 3.2 and 0.6 mg/L, respectively.

Concomitant administration of moxifloxacin together with food slightly prolongs the time to reach peak concentrations by approximately 2 hrs and slightly reduced peak concentrations by approximately 16%. Extent of absorption remained unchanged. As AUC/MIC is most predictive for antimicrobial efficacy of quinolones, this effect is clinically not relevant. Therefore, moxifloxacin can be administered independent from meals.

After a single 400 mg 1-hr IV infusion, peak concentrations of approximately 4.1 mg/L were reached in the plasma at the end of infusion which corresponds to a mean increase of approximately 26% relative to the oral application. Exposure to drug in terms of AUC at a value of approximately 39 mg·hr/L is only slightly higher compared to the exposure after oral administration (35 mg·hr/L) in accordance with the absolute bioavailability of approximately 91%.

Following multiple IV dosing (1-hr infusion), peak and trough plasma concentrations at steady-state (400 mg once daily) were between 4.1-5.9 and 0.43-0.84 mg/L, respectively. At steady state, the exposure to drug within the dosing interval is approximately 30% higher than after the first dose. In patients, mean steady-state concentrations of 4.4 mg/L were observed at the end of a 1-hr infusion.

Distribution: Moxifloxacin is distributed very rapidly to extravascular spaces. Exposure to drug in terms of AUC (AUCnorm= 6 kg·hr/L) is high with a volume of distribution at steady-state (Vss) of approximately 2 L/kg. In saliva, peak concentrations higher than those of plasma may be reached. In in vitro and ex vivo experiments over a range of 0.02-2 mg/L, a protein binding of approximately 45% independent from the concentration of the drug was determined. Moxifloxacin is mainly bound to serum albumin. Due to this low-value, high-free peak concentrations >10 x MIC are observed.

Moxifloxacin reaches high concentrations in tissues like lung (epithelial fluid, alveolar macrophages, biotic tissue), the sinuses (maxillary and ethmoid sinus, nasal polyp) and inflamed lesions (cantharide blister fluid) where total concentrations exceeding those of the plasma concentrations are reached. High free-drug concentrations are measured in interstitial body water (saliva, IM, SC). In addition, high drug concentrations were detected in abdominal tissues and fluids and female genital tract.

The peak concentrations and site versus plasma concentration ratios for various target tissues yielded comparable results for both modes of drug administration after a single dose of moxifloxacin 400 mg.

Metabolism: Moxifloxacin undergoes phase II biotransformation and is excreted via renal and biliary/faecal pathways as unchanged drug as well as in form of a sulfo-compound (M1) and a glucuronide (M2). M1 and M2 are the only metabolites relevant in humans, both are microbiologically inactive. Neither in in vitro nor in clinical phase I studies, metabolic pharmacokinetic interactions with other drugs undergoing phase I biotransformation involving cytochrome P-450 (CYP450) enzymes were observed.

Independent from the route of administration, the metabolites M1 and M2 are found in the plasma at concentrations lower than the parent drug. Preclinical investigations adequately covered both metabolites thus excluding potential implications with respect to safety and tolerability.

Elimination: Moxifloxacin is eliminated from plasma with a mean terminal t½ of approximately 12 hrs. The mean apparent total body clearance following 400-mg dose ranges from 179-246 mL/min. Renal clearance amounted to about 24-53 mL/min suggesting partial tubular reabsorption of the drug from the kidneys. Concomitant administration of ranitidine and probenecid did not alter renal clearance of the drug.

Mass balance of the mother compound and phase II metabolites of moxifloxacin yielded an almost complete recovery of approximately 96-98% independent from the route of administration with no indication of oxidative metabolism.

Elderly: Pharmacokinetics of moxifloxacin are not affected by age.

Gender: There was a 33% difference in the pharmacokinetics (AUC, Cmax) of moxifloxacin between male and female subjects. Drug absorption was unaffected by gender. These differences in the AUC and Cmax were attributable to the differences in body weight rather than gender. They are not considered as clinically relevant.

Interethnic Differences: Possible interethnic differences were examined in Caucasian, Japanese, Black and other ethnic groups. No clinically relevant interethnic differences in pharmacokinetics could be detected.

Children: Pharmacokinetics of moxifloxacin were not studied in paediatric patients.

Renal Impairment: The pharmacokinetics of moxifloxacin are not significantly changed by renal impairment (including creatinine clearance <30 mL/min/1.73 m2) and in patients on chronic dialysis ie, hemodialysis and continuous ambulatory peritoneal dialysis.

Liver Impairment: Moxifloxacin plasma concentrations of patients with mild to severe hepatic impairment (Child-Pugh A to C) did not reveal clinically relevant differences compared to healthy volunteers or patients with normal hepatic function, respectively.

Toxicology: Preclinical Safety Data: In a local tolerability study performed in dogs, no signs of local intolerability were seen when moxifloxacin was administered IV. After intra-arterial injection, inflammatory changes involving the peri-arterial soft tissue were observed suggesting that intra-arterial administration of moxifloxacin should be avoided.

Carcinogenicity, Mutagenicity: Although conventional long-term studies to determine the carcinogenic potential of moxifloxacin have not been performed, it has been subject to a range of in vitro and in vivo genotoxicity tests. In addition, an accelerated bioassay for human carcinogenesis (initiation/promotion assay) was performed in rats. Negative results were obtained in 4 strains of the Ames test in the HPRT mutation assay in Chinese hamster ovary cells and in the UDS assay in rat primary hepatocytes. As with other quinolones, the Ames test with TA 102 was positive and the in vitro test in the Chinese hamster v79 cells showed chromosomal abnormalities at high concentrations (300 mcg/mL). However, the in vivo micronucleus assay in the mouse was negative. An additional in vivo assay, the dominant lethal assay in the mouse, was negative as well. It is concluded that the negative in vivo results adequately reflect the in vivo situation in terms of genotoxicity. No evidence of carcinogenicity was found in an initiation/promotion assay in rats.

ECG: At high concentrations, moxifloxacin is an inhibitor of the delayed rectifier potassium current of the heart and may thus cause prolongations of the QT-interval. Toxicological studies performed in dogs using oral doses of ≥90 mg/kg leading to plasma concentrations ≥16 mg/L caused QT-prolongations, but no arrhythmias. Only after very high cumulative IV administration of >50-fold the human dose (>300 mg/kg), leading to plasma concentrations of ≥200 mg/L (>30-fold the therapeutic level after IV administration), reversible, nonfatal ventricular arrhythmias were seen.

Arthrotoxicity: Quinolones are known to cause lesions in the cartilage of the major diarthodial joints in immature animals. The lowest oral dose of moxifloxacin causing joint toxicity in juvenile dogs was 4 times the maximum recommended therapeutic dose (400 mg/50 kg person) on a mg/kg basis with plasma concentrations 2-3 times higher than those at the recommended therapeutic dose.

Reprotoxicity: Reproductive studies performed in rats, rabbits and monkeys indicate that placental transfer of moxifloxacin occurs. Studies in rats (per OS and IV) and monkeys (per OS) did not show evidence of teratogenicity or impairment of fertility following administration of moxifloxacin. Skeletal malformations were observed in rabbits that had been treated with an IV dose of 20 mg/kg. This study result is consistent with the known effects of quinolones on skeletal development. There was an increase in the incidence of abortions in monkeys and rabbits at human therapeutic concentrations. In rats, decreased foetal weights, an increased prenatal loss, a slightly increased duration of pregnancy and an increased spontaneous activity of some male and female offspring was observed at doses which were 63 times the maximum recommended dose on a mg/kg basis with plasma concentrations in the range of the human therapeutic dose.

Microbiology: Effect on the Intestinal Flora in Humans: In 2 volunteer studies, the following changes in the intestinal flora were seen following oral dosing with moxifloxacin. E. coli, Bacillus spp, Bacteroides vulgatus, Enterococci and Klebsiella spp, were reduced as were the anaerobes Bifidobacterium, Eubacterium and Peptostreptococcus. These changes returned to normal within 2 weeks. Clostridium difficile toxin was not found.

In Vitro Susceptibility Data: Gram-Positive Bacteria: Sensitive: Streptococcus pneumoniae including multi-drug resistant Streptococcus pneumoniae (MDRSP) strains, penicillin-resistant S. pneumoniae (PRSP) and strains resistant to ≥2 of the following antibiotics: Penicillin (MIC ≥2 mcg/mL), 2nd generation cephalosporins (eg, cefuroxime), macrolides, tetracyclines and trimethoprim/sulfamethoxazole; Streptococcus pyogenes (group A)*, Streptococcus milleri, Streptococcus mitior, Streptococcus agalactiae, Streptococcus dysgalactiae, Streptococcus anginosus*, Streptococcus constellatus*, Staphylococcus aureus (including methicillin-sensitive strains)*, Staphylococcus cohnii, Staphylococcus epidermidis (including methicillin-sensitive strains), Staphylococcus haemolyticus, Staphylococcus hominis, Staphylococcus saprophyticus, Staphylococcus simulans, Corynebacterium diphtheriae, Enterococcus faecalis* (vancomycin, gentamycin, susceptible strains only). Intermediate: Staphylococcus aureus (methicillin/ofloxacin resistant strains)+, Staphylococcus epidermidis (methicillin/ofloxacin resistant strains)+.

Gram-Negative Bacteria: Sensitive: Gardnerella vaginalis, Haemophilus influenzae (including β-lactamase negative and positive strains)*, Haemophilus parainfluenzae*, Moraxella catarrhalis (including β-lactamase negative and positive strains)*, Bordetella pertussis, Escherichia coli*, Klebsiella pneumoniae*, Klebsiella oxytoca, Enterobacter aerogenes, Enterobacter agglomerans, Enterobacter cloacae*, Enterobacter intermedius, Enterobacter sakazaki, Proteus mirabilis*, Proteus vulgaris, Morganella morganii, Providencia rettgeri, Providencia stuartii. Intermediate: Pseudomonas aeruginosa, Pseudomonas fluorescens, Burkholderia cepacia, Stenotrophomonas maltophilia, Neisseria gonorrhoea*.

Anaerobes: Sensitive: Bacteroides distasonis, Bacteroides eggerthii, Bacteroides fragilis*, Bacteroides ovatus, Bacteroides thetaiotamicron*, Bacteroides uniformis, Fusobacterium spp, Peptostreptococcus spp, Porphyromonas spp, Porphyromonas anaerobius, Porphyromonas asaccharolyticus, Porphyromonas magnus, Prevotella spp, Propionibacterium spp, Clostridium perfringens*, Clostridium ramosum.

Atypicals: Sensitive: Chlamydia pneumoniae*, Chlamydia trachomatis**, Mycoplasma pneumoniae*, Mycoplasma hominis, Mycoplasma genitalum, Legionella pneumophila*, Coxiella burnettii.

Note: */**Clinical efficacy has been demonstrated for susceptible isolates in approved clinical indications.

+Moxifloxacin showed in vitro activity with MIC values in the susceptible range in methicillin-resistant staphylococci expressing only the MecA gene. The use of moxifloxacin is not recommended if these strains are identified.

The frequency of acquired resistance may vary geographically and with time for certain species. However, for moxifloxacin, this has not been observed to date. Local area information on resistance of organisms is desirable, particularly when treating severe infections. The previously mentioned information is provided as a guide on the probability of an organism being susceptible to moxifloxacin.

Comparison of pharmacokinetic/pharmacodynamic surrogates for IV and oral administration of a moxifloxacin 400-mg single dose.

In patients requiring hospitalisation AUC/MIC90 parameters >125 and Cmax/MIC90 of 8-10 is predictive for clinical cure. In outpatients, these surrogate parameters are generally smaller ie, AUC/MIC90 >30-40.

The following table provides the respective pharmacokinetic/pharmacodynamic surrogates for IV and oral administration of moxifloxacin 400 mg calculated from single dose data.

How should I take Moxifloxacin?

Take this medicine only as directed by your doctor. Do not take more of it, do not take it more often, and do not take it for a longer time than your doctor ordered.

This medicine comes with a Medication Guide. Read and follow the instructions carefully. Ask your doctor if you have any questions.

Swallow the tablet whole with a glass of water. Do not split, crush or chew it. This medicine may be taken with or without food.

Take this medicine at the same time each day.

Drink plenty of fluids with this medicine to help prevent some unwanted effects.

If you are taking aluminum or magnesium-containing antacids, iron supplements, multivitamins, didanosine (Videx®), sucralfate (Carafate®), or zinc, do not take them at the same time that you take this medicine. It is best to take these medicines at least 4 hours before or 8 hours after taking moxifloxacin. These medicines may keep moxifloxacin from working properly.

Keep using this medicine for the full treatment time, even if you feel better after the first few doses. Your infection may not clear up if you stop using the medicine too soon.


The dose of this medicine will be different for different patients. Follow your doctor's orders or the directions on the label. The following information includes only the average doses of this medicine. If your dose is different, do not change it unless your doctor tells you to do so.

The amount of medicine that you take depends on the strength of the medicine. Also, the number of doses you take each day, the time allowed between doses, and the length of time you take the medicine depend on the medical problem for which you are using the medicine.

  • For oral dosage form (tablets):
    • For infections:
      • Adults—400 milligrams (mg) once every 24 hours.
      • Children—Use and dose must be determined by your doctor.

Missed Dose

If you miss a dose of this medicine, take it as soon as possible. However, if it is almost time for your next dose, skip the missed dose and go back to your regular dosing schedule. Do not double doses.


Store the medicine in a closed container at room temperature, away from heat, moisture, and direct light. Keep from freezing.

Keep out of the reach of children.

Do not keep outdated medicine or medicine no longer needed.

Ask your healthcare professional how you should dispose of any medicine you do not use.

Moxifloxacin administration

infoAdministration of drug is important to know because the drug absorption and action varies depending on the route and time of administration of the drug. A medicine is prescribed before meals or after meals or along with meals. The specific timing of the drug intake about food is to increase its absorption and thus its efficacy. Few work well when taken in empty stomach and few medications need to be taken 1 or 2 hrs after the meal. A drug can be in the form of a tablet, a capsule which is the oral route of administration and the same can be in IV form which is used in specific cases. Other forms of drug administration can be a suppository in anal route or an inhalation route.

May be taken with or without food.

Moxifloxacin pharmacology

infoPharmacokinetics of a drug can be defined as what body does to the drug after it is taken. The therapeutic result of the medicine depends upon the Pharmacokinetics of the drug. It deals with the time taken for the drug to be absorbed, metabolized, the process and chemical reactions involved in metabolism and about the excretion of the drug. All these factors are essential to deciding on the efficacy of the drug. Based on these pharmacokinetic principles, the ingredients, the Pharmaceutical company decides dose and route of administration. The concentration of the drug at the site of action which is proportional to therapeutic result inside the body depends on various pharmacokinetic reactions that occur in the body.


Moxifloxacin, given as an oral tablet, is well absorbed from the gastrointestinal tract. The absolute bioavailability of moxifloxacin is approximately 90 percent. Co-administration with a high fat meal (i.e., 500 calories from fat) does not affect the absorption of moxifloxacin.

Consumption of 1 cup of yogurt with moxifloxacin does not significantly affect the extent or rate of systemic absorption (AUC).

Mean Steady-State Plasma Concentrations of Moxifloxacin Obtained With Once Daily Dosing of 400 mg Either

Orally (n=10) or by I.V. Infusion (n=12)


Moxifloxacin is approximately 30-50% bound to serum proteins, independent of drug concentration. The volume of distribution of moxifloxacin ranges from 1.7 to 2.7 L/kg. Moxifloxacin is widely distributed throughout the body, with tissue concentrations often exceeding plasma concentrations. Moxifloxacin has been detected in the saliva, nasal and bronchial secretions, mucosa of the sinuses, skin blister fluid, subcutaneous tissue, skeletal muscle, and abdominal tissues and fluids following oral or intravenous administration of 400 mg. Moxifloxacin concentrations measured post-dose in various tissues and fluids following a 400 mg oral or I.V. dose are summarized in the following table. The rates of elimination of moxifloxacin from tissues generally parallel the elimination from plasma.


Approximately 52% of an oral or intravenous dose of moxifloxacin is metabolized via glucuronide and sulfate conjugation. The cytochrome P450 system is not involved in moxifloxacin metabolism, and is not affected by moxifloxacin. The sulfate conjugate (M1) accounts for approximately 38% of the dose, and is eliminated primarily in the feces. Approximately 14% of an oral or intravenous dose is converted to a glucuronide conjugate (M2), which is excreted exclusively in the urine. Peak plasma concentrations of M2 are approximately 40% those of the parent drug, while plasma concentrations of M1 are generally less than 10% those of moxifloxacin.

In vitro studies with cytochrome (CYP) P450 enzymes indicate that moxifloxacin does not inhibit CYP3A4, CYP2D6, CYP2C9, CYP2C19, or CYP1A2, suggesting that moxifloxacin is unlikely to alter the pharmacokinetics of drugs metabolized by these enzymes.


Approximately 45% of an oral or intravenous dose of moxifloxacin is excreted as unchanged drug (~20% in urine and ~25% in feces). A total of 96% ± 4% of an oral dose is excreted as either unchanged drug or known metabolites. The mean (± SD) apparent total body clearance and renal clearance are 12 ± 2 L/hr and 2.6 ± 0.5 L/hr, respectively.

Special Populations


Following oral administration of 400 mg moxifloxacin for 10 days in 16 elderly (8 male; 8 female) and 17 young (8 male; 9 female) healthy volunteers, there were no age-related changes in moxifloxacin pharmacokinetics. In 16 healthy male volunteers (8 young; 8 elderly) given a single 200 mg dose of oral moxifloxacin, the extent of systemic exposure (AUC and Cmax) was not statistically different between young and elderly males and elimination half-life was unchanged. No dosage adjustment is necessary based on age. In large phase III studies, the concentrations around the time of the end of the infusion in elderly patients following intravenous infusion of 400 mg were similar to those observed in young patients.


The pharmacokinetics of moxifloxacin in pediatric subjects have not been studied.


Following oral administration of 400 mg moxifloxacin daily for 10 days to 23 healthy males (19-75 years) and 24 healthy females (19-70 years), the mean AUC and Cmax were 8% and 16% higher, respectively, in females compared to males. There are no significant differences in moxifloxacin pharmacokinetics between male and female subjects when differences in body weight are taken into consideration.

A 400 mg single dose study was conducted in 18 young males and females. The comparison of moxifloxacin pharmacokinetics in this study (9 young females and 9 young males) showed no differences in AUC or Cmax due to gender. Dosage adjustments based on gender are not necessary.


Steady-state moxifloxacin pharmacokinetics in male Japanese subjects were similar to those determined in Caucasians, with a mean Cmax of 4.1 µg/mL, an AUC24 of 47 µg•h/mL, and an elimination half-life of 14 hours, following 400 mg p.o. daily.

Renal Insufficiency

The pharmacokinetic parameters of moxifloxacin are not significantly altered in mild, moderate, severe, or end-stage renal disease. No dosage adjustment is necessary in patients with renal impairment, including those patients requiring hemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD).

In a single oral dose study of 24 patients with varying degrees of renal function from normal to severely impaired, the mean peak concentrations (Cmax) of moxifloxacin were reduced by 21% and 28% in the patients with moderate (CLCR≥ 30 and ≤ 60 mL/min) and severe (CLCRless than30 mL/min) renal impairment, respectively. The mean systemic exposure (AUC) in these patients was increased by 13%. In the moderate and severe renally impaired patients, the mean AUC for the sulfate conjugate (M1) increased by 1.7-fold (ranging up to 2.8-fold) and mean AUC and Cmax for the glucuronide conjugate (M2) increased by 2.8-fold (ranging up to 4.8-fold) and 1.4-fold (ranging up to 2.5-fold), respectively.

The pharmacokinetics of single dose and multiple dose moxifloxacin were studied in patients with CLCRless than 20 mL/min on either hemodialysis or continuous ambulatory peritoneal dialysis (8 HD, 8 CAPD). Following a single 400 mg oral dose, the AUC of moxifloxacin in these HD and CAPD patients did not vary significantly from the AUC generally found in healthy volunteers. Cmax values of moxifloxacin were reduced by about 45% and 33% in HD and CAPD patients, respectively, compared to healthy, historical controls. The exposure (AUC) to the sulfate conjugate (M1) increased by 1.4- to 1.5-fold in these patients. The mean AUC of the glucuronide conjugate (M2) increased by a factor of 7.5, whereas the mean Cmax values of the glucuronide conjugate (M2) increased by a factor of 2.5 to 3, compared to healthy subjects. The sulfate and the glucuronide conjugates of moxifloxacin are not microbiologically active, and the clinical implication of increased exposure to these metabolites in patients with renal disease including those undergoing HD and CAPD has not been studied.

Oral administration of 400 mg QD moxifloxacin for 7 days to patients on HD or CAPD produced mean systemic exposure (AUCss) to moxifloxacin similar to that generally seen in healthy volunteers. Steady-state Cmax values were about 22% lower in HD patients but were comparable between CAPD patients and healthy volunteers. Both HD and CAPD removed only small amounts of moxifloxacin from the body (approximately 9% by HD, and 3% by CAPD). HD and CAPD also removed about 4% and 2% of the glucuronide metabolite (M2), respectively.

Hepatic Insufficiency

No dosage adjustment is recommended for mild, moderate, or severe hepatic insufficiency (Child-Pugh Classes A, B, or C). However, due to metabolic disturbances associated with hepatic insufficiency, which may lead to QT prolongation, moxifloxacin should be used with caution in these patients. (See



  1. EPA DSStox. "Moxifloxacin: DSSTox provides a high quality public chemistry resource for supporting improved predictive toxicology.". (accessed September 18, 2017).
  2. NCIt. "Moxifloxacin: NCI Thesaurus (NCIt) provides reference terminology for many systems. It covers vocabulary for clinical care, translational and basic research, and public information and administrative activities.". (accessed September 18, 2017).


The results of a survey conducted on for Moxifloxacin are given in detail below. The results of the survey conducted are based on the impressions and views of the website users and consumers taking Moxifloxacin. We implore you to kindly base your medical condition or therapeutic choices on the result or test conducted by a physician or licensed medical practitioners.

User reports

1 consumer reported administration

When best can I take Moxifloxacin, on an empty stomach, before or after food? website users have also released a report stating that Moxifloxacin should be taken With a meal. In any case, this may not be the right description on how you ought to take this Moxifloxacin. Kindly visit your doctor for more medical advice in this regard. Click here to see other users view on when best the Moxifloxacin can be taken.
With a meal1

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