ciprofloxacin reference
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(ciprofloxacin · DailyMed)
Registered Malawi · PMRA

XIPRO D EYE/EAR 0.3%/0.05% W/V SOLUTION

CIPROFLOXACIN & DEXAMETHASONE PHOSPHATE

PMPB/PL351/116 SOLUTION antiinfectives for systemic use INN generic

What it does

Ciprofloxacin is an antibiotic used to treat various bacterial infections.

Commonly used for: bacterial infections of the lungs (pneumonia), urinary tract infections (UTIs), skin infections, gastrointestinal infections

Read more in plain English ↓

Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.

Ask about this medicine

Answers come only from this medicine's registration record, BNF monograph and interaction data - not medical advice.

Medicine sourcing is available in Kenya only. We don't sell or dispense medicines - licensed pharmacies do.

Sourcing - Kenya only

Registration & product details

Registration no.
PMPB/PL351/116
Registration date
27/11/2020
Expiry date
31/03/2025
Status
Registered
Active ingredient
CIPROFLOXACIN & DEXAMETHASONE PHOSPHATE
Dosage form
SOLUTION
Strength
-
Pack size
-
Therapeutic class
-
ATC class (WHO)
J01MA - Fluoroquinolones
RxNorm RxCUI
2551
Manufacturer / MAH
-
Applicant / LTR
-
Country of origin
-

Source: Pharmacy and Medicines Regulatory Authority · fetched 2026-04-21 17:37:41 · updated 2026-09-22 04:33:03

Drug Interactions

89
Check interactions

Pharmacodynamic Warnings

Dexamethasone appears in TABLE 17: Drugs that reduce serum potassium

Severe (4)

Avapritinib - decreases exposure

Dexamethasoneispredictedtodecreasetheexposureto avapritinib.Avoid.rTheoretical

Severe Theoretical

Mifamurtide - decreases efficacy

Corticosteroidsarepredictedtodecreasetheefficacyof mifamurtide.Avoid.rTheoretical

Severe Theoretical

Quinolones - decreases absorption

Strontiumispredictedtodecreasetheabsorptionof quinolones.Avoid.oTheoretical

Severe Theoretical

Tizanidine - increases exposure

Ciprofloxacin increases the exposure to tizanidine. Avoid.

Severe Study

Moderate (40)

Aminophylline - increases exposure

Ciprofloxacin is predicted to increase the exposure to aminophylline. Adjust dose.

Moderate Theoretical

Antiepileptics - affects concentration

Ciprofloxacin affects the concentration of antiepileptics (fosphenytoin, phenytoin). Monitor concentration and adjust dose.

Moderate Study

Antipsychotics, Second Generation - increases concentration

Ciprofloxacin increases the concentration of antipsychotics, second generation (clozapine). Monitor adverse effects and adjust dose.

Moderate Study

Antipsychotics, Second Generation - increases exposure

Ciprofloxacin is predicted to increase the exposure to antipsychotics, second generation (olanzapine). Adjust dose.

Moderate Anecdotal

Clozapine - increases concentration

Ciprofloxacin increases the concentration of antipsychotics, second generation (clozapine). Monitor adverse effects and adjust dose.

Moderate Study

Unknown (45)

Agomelatine - increases exposure

Ciprofloxacin is predicted to increase the exposure to agomelatine.

Unknown Study

Anaesthetics,local - increases exposure

Ciprofloxacin is predicted to increase the exposure to anaesthetics, local (ropivacaine).

Unknown Theoretical

Anagrelide - increases exposure

Ciprofloxacinispredictedtoincreasetheexposureto anagrelide.oTheoretical

Unknown Theoretical

Antiarrhythmics - increases exposure

Ciprofloxacin slightly increases the exposure to antiarrhythmics (lidocaine).

Unknown Study

Aspirin - decreases concentration

Corticosteroids are predicted to decrease the concentration of aspirin (high-dose) and aspirin (high-dose) increases the risk of gastrointestinal bleeding when given with corticosteroids.

Unknown Study

Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact

Disclaimer: This information is sourced from Pharmacy and Medicines Regulatory Authority (Malawi). Always consult a qualified healthcare professional before using any medication.

About ciprofloxacin

Ciprofloxacin is an antibiotic used to treat various bacterial infections.

What it treats

  • bacterial infections of the lungs (pneumonia)
  • urinary tract infections (UTIs)
  • skin infections
  • gastrointestinal infections

How it works

It works by stopping the growth of bacteria in the body.

Who it's for

Ciprofloxacin is for adults and children who need treatment for bacterial infections.

Drug class

Quinolones

AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.

About dexamethasone

Dexamethasone is a corticosteroid used to treat various conditions by reducing inflammation and suppressing the immune system.

What it treats

  • inflammation
  • allergic reactions
  • certain cancers
  • autoimmune diseases (e.g., lupus)
  • skin conditions (e.g., eczema)

How it works

It works by mimicking the effects of hormones produced by the adrenal glands, helping to decrease inflammation and control the immune response.

Who it's for

It is prescribed for adults and children with specific health issues that require inflammation control or immune suppression.

Drug class

Corticosteroids

Cautions

  • • Be cautious if taking medications that lower potassium levels.

AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.

Clinical monograph: Ciprofloxacin

BNF-referenced

Ciprofloxacin is a broad-spectrum antibiotic belonging to the fluoroquinolone class, effective against a wide range of both Gram-negative and Gram-positive bacteria. It works primarily by inhibiting bacterial DNA gyrase and topoisomerase IV, enzymes crucial for DNA replication and transcription. This inhibition leads to the death of susceptible bacteria, making ciprofloxacin a valuable option in treating various bacterial infections, including urinary tract infections, respiratory infections, and skin infections.

Indications

  • Bacterial infections
  • Urinary tract infections
  • Respiratory tract infections
  • Skin and soft tissue infections
  • Acute pyelonephritis
  • Severe diabetic foot infections
  • Anthrax (treatment and post-exposure prophylaxis)
  • Disseminated gonococcal infection (unlicensed)

Mechanism of action

Ciprofloxacin acts on bacterial topoisomerase II (DNA gyrase) and topoisomerase IV. It binds to the alpha subunits of DNA gyrase, preventing the supercoiling of bacterial DNA, which is essential for DNA replication. This inhibition leads to bacterial cell death. Ciprofloxacin exhibits bactericidal activity during both logarithmic and stationary growth phases, particularly against organisms like Escherichia coli and Pseudomonas aeruginosa.

Pharmacodynamics

Ciprofloxacin is characterized by its potent activity against many Gram-negative and some Gram-positive bacteria, achieved through its mechanism of action on DNA gyrase and topoisomerase IV. It binds with significantly higher affinity to bacterial DNA gyrase compared to mammalian enzymes, thus minimizing potential side effects. There is no cross-resistance between ciprofloxacin and other antibiotic classes, which enhances its use in cases of antibiotic resistance. Additionally, ciprofloxacin is under investigation for potential effects against malaria, cancers, and AIDS.

Pharmacokinetics

Ciprofloxacin is rapidly absorbed after oral administration, with bioavailability around 70-80%. It is widely distributed in body tissues and fluids, including the lungs, liver, kidneys, and prostate. The drug undergoes hepatic metabolism and is primarily excreted via the kidneys, with a half-life of about 4 hours. Dosing adjustments may be necessary in renal impairment. Ciprofloxacin's pharmacokinetic profile supports its efficacy in treating systemic infections.

Contra-indications

  • Hypersensitivity to ciprofloxacin or other quinolones
  • Concurrent use with tizanidine

Adverse effects

  • Nausea
  • Diarrhea
  • Headache
  • Dizziness
  • Tendon rupture
  • QT interval prolongation
  • Photosensitivity
  • Rash
  • Superinfection

Interactions

  • Severe: ciprofloxacin + tizanidine (increases exposure)
  • Moderate: ciprofloxacin + aminophylline (increases exposure)
  • Moderate: ciprofloxacin + antiepileptics (affects concentration)
  • Moderate: ciprofloxacin + fosphenytoin (affects concentration)
  • Moderate: ciprofloxacin + phenytoin (affects concentration)
  • Moderate: ciprofloxacin + antipsychotics (increases concentration)
  • Moderate: ciprofloxacin + clozapine (increases concentration)
  • Moderate: ciprofloxacin + olanzapine (increases exposure)
  • Moderate: ciprofloxacin + dopaminereceptor agonists (increases exposure)

Precautions

  • Risk of arthropathy in children
  • History of tendon disorders
  • Concurrent use of drugs that prolong the QT interval
  • Ensure adequate hydration to prevent crystalluria
  • Monitor for signs of superinfection

Pregnancy

Avoid in pregnancy due to potential risk of arthropathy in animal studies; safer alternatives should be considered.

Breast-feeding

Ciprofloxacin is excreted in breast milk; caution is advised when administered to nursing mothers.

Storage

Store at room temperature, away from moisture and heat. Protect from light.

Formulations

  • Oral tablet: 250 mg, 500 mg, 750 mg
  • Intravenous infusion: 400 mg/200 mL
  • Eye drops: concentration may vary
BNF 85 (British National Formulary) p.636 BNF 85 (British National Formulary) p.1306 BNF 85 (British National Formulary) p.1332 BNF for Children 2019-2020 p.383 BNF for Children 2019-2020 p.722 BNF for Children 2019-2020 p.736 PubChem / pathway

AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.

Clinical monograph: Dexamethasone

BNF-referenced

Dexamethasone is a synthetic corticosteroid with potent anti-inflammatory and immunosuppressive properties. It has predominantly glucocorticoid activity and is used to treat various inflammatory and allergic conditions. Its mechanisms include decreasing vasodilation and permeability of capillaries, inhibiting leukocyte migration, and altering gene expression related to inflammation. Dexamethasone is administered orally or via injection, and it is important to manage dosing carefully to avoid potential side effects.

Indications

  • Suppression of inflammatory and allergic disorders
  • Adjunctive treatment of suspected bacterial meningitis
  • Reduction of peri- and neonatal morbidity and mortality in preterm birth
  • Management of severe croup
  • Congenital adrenal hyperplasia
  • COVID-19 requiring supplemental oxygen

Dosage

Adults: For adults, the typical dosing varies by condition

Mechanism of action

Dexamethasone binds to the glucocorticoid receptor, leading to changes in gene expression that result in decreased inflammatory and immune responses. It inhibits phospholipase A2, reducing the formation of pro-inflammatory mediators, and promotes anti-inflammatory genes like interleukin-10. The drug also inhibits neutrophil apoptosis and demargination, contributing to its anti-inflammatory effects. Its glucocorticoid activity results in significant immunosuppression at higher doses.

Pharmacodynamics

Dexamethasone's pharmacodynamics involve the modulation of inflammatory responses through glucocorticoid receptor binding. It inhibits pro-inflammatory signals while promoting anti-inflammatory signals. The duration of action varies based on the administration route, and careful dosing is required to avoid suppression of the hypothalamic-pituitary-adrenal axis and increased infection risk. The drug has a wide therapeutic window, allowing for higher doses than the body's natural production.

Pharmacokinetics

Dexamethasone is well-absorbed after oral administration, with peak plasma concentrations typically occurring within 1-2 hours. It is extensively metabolized in the liver, primarily through hepatic cytochrome P450 enzymes. The elimination half-life ranges from 3 to 4 hours, although it may be longer in certain populations. The drug is excreted mainly in urine as metabolites. The pharmacokinetics can be affected by factors such as liver function and co-administered medications.

Contra-indications

  • Systemic fungal infections
  • Hypersensitivity to dexamethasone or any component of the formulation
  • Active tuberculosis
  • Cautious use in patients with peptic ulcer disease

Adverse effects

  • Oedema
  • Hypotension
  • Increased susceptibility to infections
  • Mood changes
  • Cushing's syndrome
  • Hyperglycemia
  • Gastrointestinal perforation
  • Osteoporosis
  • Adrenal suppression

Interactions

  • Severe interaction with avapritinib (decreases exposure)
  • Moderate interaction with mitotane (decreases exposure)
  • Moderate interaction with monoclonal antibodies (decreases exposure)
  • Moderate interaction with tocilizumab (decreases exposure)
  • Moderate interaction with aprepitant (increases exposure)
  • Moderate interaction with netupitant (increases exposure)
  • Moderate interaction with rifampicin (decreases exposure)
  • Unknown interaction with cobicistat (increases exposure)
  • Unknown interaction with caspofungin (decreases concentration)
  • Unknown interaction with idelalisib (increases exposure)

Precautions

  • Use with caution in patients with a history of tuberculosis
  • Monitor for signs of infection due to immunosuppressive effects
  • Consider dose adjustments in hepatic impairment
  • Taper dosage to avoid withdrawal symptoms after prolonged use
  • Monitor blood glucose levels in diabetic patients

Pregnancy

Dexamethasone is classified as a pregnancy category C drug. It should only be used if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Dexamethasone is excreted in breast milk. Caution is advised when administering to breastfeeding women, and the risks versus benefits should be considered.

Storage

Store at room temperature (15-30 degrees Celsius), protect from light, and keep out of reach of children.

Formulations

  • Tablet (6 mg)
  • Solution for injection (3.3 mg/1 ml)
  • Dexamethasone sodium phosphate solution for injection (6.6 mg/2 ml)
BNF 85 (British National Formulary) p.772 BNF 85 (British National Formulary) p.1289 BNF 85 (British National Formulary) p.1296 BNF for Children 2019-2020 p.477 BNF for Children 2019-2020 p.714 PubChem / pathway

AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.

Molecular reference: Ciprofloxacin

PubChem CID 2764

Molecular formula: C17H18FN3O3

Mechanism of action

Ciprofloxacin acts on bacterial topoisomerase II (DNA gyrase) and topoisomerase IV. Ciprofloxacin's targeting of the alpha subunits of DNA gyrase prevents it from supercoiling the bacterial DNA which prevents DNA replication. The mechanism by which ciprofloxacin's inhibition of DNA gyrase or topoisomerase IV results in death in susceptible organisms has not been fully determined. Unlike beta-lactam anti-infectives, which are most active against susceptible bacteria when they are in the logarithmic phase of growth, studies using Escherichia coli and Pseudomonas aeruginosa indicate that ciprofloxacin can be bactericidal during both logarithmic and stationary phases of growth; this effect does not appear to occur with gram-positive bacteria (e.g., Staphylococcus aureus). In vitro studies indicate that ciprofloxacin concentrations that approximate the minimum inhibitory concentration (MIC) of the drug induce filamentation in susceptible organisms; high concentrations of the drug result in enlarged or elongated cells that may not be extensively filamented. Although the bactericidal effect of some fluoroquinolones (e.g., norfloxacin) evidently requires competent RNA and protein synthesis in the bacterial cell, and concurrent use of anti-infectives that affect protein synthesis (e.g., chloramphenicol, tetracyclines) or RNA synthesis (e.g., rifampin) inhibit the in vitro bactericidal activity of these drugs, the bactericidal effect of ciprofloxacin is only partially reduced in the presence of these anti-infectives. This suggests that ciprofloxacin has an additional mechanism of action that is independent of RNA and protein synthesis. Ciprofloxacin usually is bactericidal in action. Like other fluoroquinolone anti-infectives, ciprofloxacin inhibits DNA synthesis in susceptible organisms via inhibition of the enzymatic activities of 2 members of the DNA topoisomerase class of enzymes, DNA gyrase and topoisomerase IV. DNA gyrase and topoisomerase IV have distinct essential roles in bacterial DNA replication. DNA gyrase, a type II DNA topoisomerase, was the first identified quinolone target; DNA gyrase is a tetramer composed of 2 GyrA and 2 GyrB subunits. DNA gyrase introduces negative superhelical twists in DNA, an activity important for initiation of DNA replication. DNA gyrase also facilitates DNA replication by removing positive super helical twists. Topoisomerase IV, another type II DNA topoisomerase, is composed of 2 ParC and 2 ParE subunits. DNA gyrase and topoisomerase IV are structurally related; ParC is homologous to GyrA and ParE is homologous to GyrB. Topoisomerase IV acts at the terminal states of DNA replication by allowing for separation of interlinked daughter chromosomes so that segregation into daughter cells can occur. Fluoroquinolones inhibit these topoisomerase enzymes by stabilizing either the DNA-DNA gyrase complex or the DNA-topoismerase IV complex; these stabilized complexes block movement of the DNA replication fork and thereby inhibit DNA replication resulting in cell death. ... Ciprofloxacin is cytotoxic to a variety of cultured mammalian cell lines at concn that deplete cells of mtDNA. The IC50 values for ciprofloxacin varied from 40-80 ug/ml depending on the cell line tested. Cytotoxicity required continuous exposure of cells to drug for 2-4 days, which corresponded to approx three or four cell doublings. Shorter times of drug exposure did not cause significant cytotoxicity. In addition, cells became drug resistant when they were grown under conditions that bypassed the need for mitochondrial respiration. Resistance was not due to a decr in cellular drug accumulation, ... /indicating/ that ciprofloxacin cytotoxicity is caused by the loss of mtDNA encoded functions. Analysis of mtDNA from ciprofloxacin treated cells revealed the presence of site specific, double stranded DNA breaks. ... Exonuclease protection studies indicated that the 5'-, but not the 3', ends of the drug induced DNA breaks were tightly assoc

Pharmacodynamics

Ciprofloxacin is a second generation fluoroquinolone that is active against many Gram negative and Gram positive bacteria. It produces its action through inhibition of bacterial DNA gyrase and topoisomerase IV. Ciprofloxacin binds to bacterial DNA gyrase with 100 times the affinity of mammalian DNA gyrase. There is no cross resistance between fluoroquinolones and other classes of antibiotics, so it may be of clinical value when other antibiotics are no longer effective. Ciprofloxain and its derivatives are also being investigated for its action against malaria, cancers, and AIDS.

Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.

Molecular reference: Dexamethasone

PubChem CID 5743

Molecular formula: C22H29FO5

Mechanism of action

The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels. Corticosteroids diffuse across cell membranes and complex with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA, and stimulate transcription of mRNA and subsequent protein synthesis of enzymes ultimately responsible for anti-inflammatory effects of topical application of corticosteroids to the eye. In high concentrations which may be achieved after topical application, corticosteroids may exert direct membrane effects. Corticosteroids decrease cellular and fibrinous exudation and tissue infiltration, inhibit fibroblastic and collagen-forming activity, retard epithelial regeneration, diminish postinflammatory neovascularization and reduce toward normal levels the excessive permeability of inflamed capillaries. /Corticosteroids (Otic)/ Glucocorticoids are capable of suppressing the inflammatory process through numerous pathways. They interact with specific intracellular receptor proteins in target tissues to alter the expression of corticosteroid-responsive genes. Glucocorticoid-specific receptors in the cell cytoplasm bind with steroid ligands to form hormone-receptor complexes that eventually translocate to the cell nucleus. There these complexes bind to specific DNA sequences and alter their expression. The complexes may induce the transcription of mRNA leading to synthesis of new proteins. Such proteins include lipocortin, a protein known to inhibit PLA2a and thereby block the synthesis of prostaglandins, leukotrienes, and PAF. Glucocorticoids also inhibit the production of other mediators including AA metabolites such as COX, cytokines, the interleukins, adhesion molecules, and enzymes such as collagenase. /Glucocorticoids/ Corticosteroids diffuse across cell membranes and complex with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA (chromatin), and stimulate transcription of messenger RNA (mRNA) and subsequent protein synthesis of various inhibitory enzymes responsible for the anti-inflammatory effects of topical corticosteroids. These anti-inflammatory effects include inhibition of early processes such as edema, fibrin deposition, capillary dilatation, movement of phagocttes into the area, and phagocytic activities. Later processes, such as capillary production, collagen deposition, and keloid formation also are inhibited by corticosteroids. The overall actions of topical corticosteroids are catabolic. /Corticosteroids (topical)/

Pharmacodynamics

Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Dexamethasone's duration of action varies depending on the route. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections.

Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.

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